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BDS 2 > BDS5002: HHD > Flashcards

BDS5002: HHD Flashcards

1
Q

Define macule, papule, nodule

A

Macule: localised area of colour or textural change in skin
Papule: small solid elevation of skin <5mm in diameter
Nodule: papule but >5mm

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2
Q

Describe finger clubbing

A

Change in shape of D end of fingers and nail

Caused by lung, heart and GI disease
Inflammatory bowel disease
Lung cancer
Asbestosis 
Congenital heart disease
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3
Q

Describe nail pitting

A

Small indents/depressions in surface of nail

Caused by:
Psoriasis
Lichen planus
Alopecia areata

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4
Q

Describe koilonychia

A

Spoon shaped nail

Caused by:
Fe deficiency anaemia
Raynaud’s phenomenon
Systemic lupus erythematsus

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5
Q

Describe Beau’s lines

A

Transverse depressions in nail usually reflect poor growth

Caused by
Raynaud’s phenomenon
Trauma

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6
Q

Describe splinter haemorrhages

A

Tiny blood clots, tend to run vertically

Caused by
Trauma
IE 
Lupus
Rheumatoid disease 
Psoriasis
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7
Q

Describe herpetic whitlow

A

Swelling, reddening, tenderness of infected finger
Associated pyrexia (inc. temp.) and lymphadenopathy
Initially vesicles form, may burst and coalesce

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8
Q

Describe paronychia

A

Localised, superficial irritation of epidermis bordering nails

Caused by infection, chemical irritation or moisture

Acute: staphylococcus aureus
Chronic: yeasts and bacteria; candida sp and gram- bacilli

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9
Q

What are the most common cutaneous malignancies?

A
  1. Basal cell carcinoma
  2. Squamous cell carcinoma
  3. Malignant melanoma
  4. Cutaneous lymphoma
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10
Q

What are the common predisposing factors of B/SCC?

A 
UV radiation, skin type I/II
Arsenic
Ionising radiation
Burn/vaccination scars
Immunosuppression
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11
Q

What is BCC?

A

Locally invasive cancer of epidermal basaloid cells

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12
Q

Describe the presentation of BCC

A

Spontaneous ulcer that fails to heal
Non-healing asymptomatic lump or sore spot that grows slowly

Nodular: most common, HandN; pearly papule w/ rolled edge, telangiectasia and central depression w or w/o ulceration

Superficial: slow growing, scaly pink patch or plaque

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13
Q

What is the prognosis of BCC?

A

Most grow slowly and are non-aggressive
If long standing or neglected may behave like ‘rodent ulcers’; destroy skin and deep tissue
Rarely metastasise

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14
Q

What is SCC?

A

Malignant tumour of keratinocytes

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15
Q

Where is SCC most common?

A

Sun exposed sites; HandN, forearm, hand, lower lip

Starts in area of actinic keratosis as small papule; ulcerates and crusts

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16
Q

What are malignant melanomas?

A

Malignant tumours of melanocytes

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17
Q

What are the common predisposing factors for malignant melanomas?

A

UV radiation, skin type I/II
Pre-existing melanocytic lesions; multiple banal naevi, dysplastic/atypical naevi, congenital naevi
Family history of naevi or melanomas

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18
Q

How is malignant melanoma diagnosed?

A 
Changes to naevi or pigmented lesion
Recent inc. size
Irregular outline
Colour variation
Erythema at edge
Crusting, oozing, bleeding 
Commonly itchy
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19
Q

Describe the prognosis of malignant melanoma

A

Depth dependent
<1.49mm 93% 5yr survival
1.5-3.49mm 67%
>3.5mm 38%

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20
Q

What is the primary treatment for malignant melanomas?

A

Surgical excision w/ adequate clearance margin

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21
Q

What is psoriasis?

A

Chronic, noninfectious relapsing inflammatory condition due to inc. cycling epidermal cells

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22
Q

What are the predisposing factors of psoriasis?

A 
Koebner phenomenon 
Infection: streptococcal sore throats leading to guttate psoriasis 
Drugs: B-blockers, Li, antimalarials 
Stress
Sunlight: only 10% cases 
Alcohol
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23
Q

Describe the presentation of psoriasis

A

Well demarcated red scaly patches topped w/ silvery scales

Pitting or onycholysis of nails

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24
Q

What is psoriatic arthropathy/arthritis?

A

Arthritis associated w/ psoriasis
D arthritis: most common; interphalangeal joints of hands and feet
Rheumatoid like arthritis
Mutilans: severe arthritis
Ankylosis spondylitis (spine) or sacroiliitis (sacroiliac joints)

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25
Q

What are the treatments for psoriasis?

A 
Coal tar
Corticosteroids
Retinoids 
VitD
Ciclosporin
Monoclonal AB
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26
Q

What are the dental aspects of psoriasis?

A

Associated w/ geographic tongue, drug induced gingival hyperplasia and ulceration
Destructive TMJ disease

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27
Q

What is eczema?

A

Pattern of non-infective inflammatory response characterised by spongiosis in acute stage and lichenification in chronic stage

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28
Q

Name endogenous eczema types

A

Atopic
Seborrhoeic
Venous

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29
Q

Describe seborrhoeic eczema/dermatitis

A

Found near sebaceous glands, around many hair follicles; scalp, face, neck
Red, scaly rash
May have exudation and crusting if severe

Immunosuppressed pts most at risk; w/ HIV
Associated w/ yeast Pityrosporum ovale

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30
Q

Describe the treatment of seborrhoeic eczema

A

Topical combinations of anitfungals w/ weak corticosteroids

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31
Q

What are the types of exogenous eczema?

A

Contact irritant
Contact allergic
Infective

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32
Q

Describe contact dermatitis/eczema

A

Precipitated by exogenous factor
If allergic; due to type IV hypersensitivity
May be irritant through damage to skin barrier

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33
Q

What is the treatment plan for eczema?

A
  1. Identify aetiology
  2. Treat 2ndary infection
  3. Emollients and soap substitutes
  4. Topical corticosteroids; hydrocortisone (weak) don’t damage skin
  5. Immunosuppressants
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34
Q

What are the dental aspects of eczema?

A

Association w/ atopy
Perioral dermatitis
Exfoliative cheilitis
Oral allergy syndrome

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35
Q

What is atopy?

A

Inherited tendency to develop; eczema, asthma, hay fever, urticaria, dermographism w/ high levels IgE (allergic Ig)

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36
Q

Define Ag and immunogen

A

Ag: toxin/foreign substance that triggers immune response when recognised/bound to Ab; produce Ab

Immunogen: molecule that triggers immune response

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37
Q

Define adjuvant

A

Substance that enhances Ab response

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38
Q

Define vaccine and toxoid

A

Vaccine: antigenic substance that provides immunity against 1/+ disease

Toxoid: toxin from pathogen that is no longer toxic but still antigenic

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39
Q

Define Ab titre

A

Amount Ab in blood

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40
Q

Discuss passive immunisation and give examples of vaccines given

A

Natural: trans-placental material IgG protects newborn
Artificial p: injection of preformed Ab derived from serum of man or animals

Protect at short notice for limited period
Homologous (human) 3-6mns; heterogeneous (animal) wks

Horse antitoxins: diphtheria, botulism
Pooled Ig; range diseases, HepA
Specific Ig: HepB, rabies, varicella-zoster, tetanus

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41
Q

Discuss how active immunisation works

A

Natural: follows sub/clinical infection
Artificial: vaccination

Induced by using inactivated/attenuated live organisms or their products
Protective by stim. Ab production

BCG vaccination promotes cell mediated immunity

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42
Q

Discuss the characteristics of an ideal vaccine

A
  1. Promotes effective immunity
  2. Confers lifelong protection
  3. Safe (no side effects)
  4. Stable
  5. Cheap
  6. Good and effective
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43
Q

Discuss the 3 different types of active vaccine

A
  1. Toxoids: useful when symptoms due to 1 toxin; inactivated toxin to retain antigenicity but lose toxicity; diphtheria, tetanus
  2. Inactivated: killed organism stim. Ab production; typhoid, influenza
  3. Attenuated: live w/ red. virulence still immunogenic; multiply in body, mimic natural infection w/ Ab production w/o symptoms; MMR, yellow fever
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44
Q

Compare the primary and secondary immune response

A

Primary: slow, primarily IgM, levels rapidly return to normal, Ab titre small

Secondary: rapid, IgG, Ab titre much higher

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45
Q

Discuss different administration routes of vaccines w/ examples

A

Mouth: colonise gut, promote local and humoral Abs; oral polio vaccine

Subcutaneous, intramuscular: anterolateral thigh, upper arm; all except BCG

Intradermal: BCG

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46
Q

Discuss the possible complications of vaccines

A

Side effects: local (pain, erythema), general (fever, malaise)

Anaphylactic shock

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47
Q

What are the 5 main contraindications for vaccines?

A
  1. Previous local or general reaction
  2. Acute illness
  3. No live vaccine if immunosuppressed
  4. No live vaccine if pregnant
  5. No BCG vaccine to HIV/AIDs pts
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48
Q

Define sterilisation, disinfection, antiseptic, asepsis

A

Sterilisation: removal/inactivation of ALL microorganisms; viruses, bacteria and spores, fungi and spores

Disinfection: removal/inactivation of SOME microorganisms; doesn’t usually include bacterial spores

Antiseptic: destroys/inhibits growth; can be applied to living tissue

Asepsis: free from microorganisms

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49
Q

What are the 4 main methods of sterilisation?

A
  1. Heat
  2. Irradiation
  3. Gas
  4. Filtration
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50
Q

Describe the relationship b/w T and temp. in relation to heat sterilisation

A

Higher temp., hold time dec. to achieve sterilisation

Indirect

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51
Q

Discuss moist heat sterilisation

A

Autoclave

Highly effective
Temps >100degrees
Conditions attained by raising pressure of steam in pressure vessel
Steam must be saturated (max. amount H2O as vapour) and dry (no H2O droplets)

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52
Q

Discuss dry heat sterilisation

A

Incineration: effective for pathological waste, surgical dressings, needle

Red heat: points of forceps held in flame

Flaming: direct exposure for few secs

Hot air: for materials which; can withstand high temp for prolonged period; are affected by contact w/ steam

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53
Q

Discuss irradiation sterilisation

A

Ionising radiation incl. gamma, X-ray, accelerated electrons

Commercial sterilisation single use items; plastic syringes

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54
Q

Discuss gas and filtration sterilisation

A

Gas: ethylene oxide; highly penetrative and non-corrosive; commercial sterilisation single use items

Filtration: useful remove bacteria from fluids; 0.22microm filter removes bacteria not viruses

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55
Q

Why are indicators important for sterilisation and give examples biological and non-biological indicators

A

Determine whether sterilisation has occurred

Biological: Bacillus spp. cultures
- after use, strips cultured, any growth = sterilisation failed

Non-biological

  • externally calibrated thermocouple linked to T monitor
  • autoclave tape, Brownes’ tubes; reached correct temp
  • TST (temp, steam, time) indicator strips
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56
Q

3 main sources of infection and 3 main transmission routes

A

Sources

  • pt suffering from infectious disease
  • pt in prodromal stage of certain infection
  • individuals who are carriers

Transmission

  • direct contact of tissues w/ skin or body fluids
  • droplets containing infectious agent
  • via contaminated instruments which haven’t been rendered safe for use
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57
Q

Define anaemia

A

Condition in which the total no. RBCs or Hb in the blood is red.

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58
Q

What is mean corpuscular vol?

A

MCV is av. vol. RBCs

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59
Q

What are the predisposing factors for anaemia?

A

Dec. Production RBC

  • Fe, VitB12, folate deficiencies
  • marrow infiltration; cancer
  • chronic disease; rheumatoid, cancer

Inc. destruction RBC
- haemolytic anaemia; disorders RBC membrane/enzyme/Hb or immune destruction

Loss RBCs; bleeding

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60
Q

What are the main classifications of anaemia?

A

Microcytic: MCV < 76
- Fe deficiency, thalassaemia

Normocytic: MCV 76-96

  • cancer
  • chronic disease

Macrocytic: MCV >96

  • VitB12, folate deficiency
  • alcohol, drugs, liver disease
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61
Q

Explain how Fe deficiency can cause anaemia

A

Fe in haem; no haem = no Hb

Defective Hb synthesis causes red. RBC maturation so RBCs small and red. Hb

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62
Q

How must an Fe deficiency be confirmed?

A

Full blood count, blood film
Serum ferritin (storage form Fe) dec.
Serum Fe dec.; total Fe binding capacity inc.

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63
Q

Causes of Fe deficiency and treatments

A

Causes

  • pre-menopausal F: menorrhagia
  • M/post-menopause: GIT bleeding; ulcer, cancer

Treatment: replace Fe

  • diet
  • oral Fe (best)
  • avoid blood transfusion
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64
Q

Discuss nomocytic anaemia

A

Marrow infiltration
Chronic disease: inflammation, infection, cancer

Caused by inflammatory cytokines 
Process
- red. RBC lifespan
- poor marrow response to erythropoietin
- red. erythropoiesis
- inflammatory cytokines interfere w/ Epo production and actions
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65
Q

How can a VitB12 or folate deficiency lead to megaloblastic anaemia?

A

Required for DNA synthesis
Synthesis impaired; delayed maturation erythroblast nucleus
Cells fail to divide leading to large cells

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66
Q

Causes of B12 deficiency

A

Nutritional: esp. vegans
Malabsorption
- gastric: pernicious anaemia, partial/whole gastrectomy
- intestinal: Ileal disease, Crohn’s, tapeworm

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67
Q

Discuss pernicious anaemia

A

Autoimmune: autoantibodies against gastric mucosa and intrinsic factor
Causes gastric atrophy, red. acid and IF secretion

Clinical

  • glossitis
  • mild jaundice
  • peripheral neuropathy
  • post., lat. column damage
  • dementia
  • optic atrophy
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68
Q

Discuss causes and features of folate deficiency

A

Nutritional: old age, poverty, alcoholism
Malabsorption: coeliac, Crohn’s
Excess utilisation: pregnancy, lactation, haemolytic anaemia, psoriasis
Other: anticonvulsants, antifolate drugs

Clinical

  • glossitis
  • mild jaundice
  • no neurology
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69
Q

Discuss haemolytic anaemia

A 
Due to shortened RBC survival: <120d
Clinical
- pallor, anaemia
- jaundice
- gallstones
- splenomegaly
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70
Q

Discuss lab findings for haemolytic anaemia

A 
FBC: Hb low; MCV low/normal/high
Haptoglobin 
DAT +ve: immune
RBC breakdown
- inc. serum unconjugated bilirubin
- inc. urinary urobilinogen
- inc. serum LDH
RBC production
- inc. reticulocytes in blood
- inc. RBCs in marrow
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71
Q

Discuss heredity spherocytosis

A

Congenital: autosomal dominant
Disorder RBC membrane

Chronic HA
Spherocytes in peripheral blood

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72
Q

Discuss sickle cell disease

A 
Congenital HA; disorder Hb structure 
Point mutation in globin gene
Causes
Dec. O2 conc.
- Hb forms long rod structure
- RBC sickle
- inc. rigid
Block microcirculation 
- ischaemia
- pain
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73
Q

Discuss glucose-6-phosphate dehydrogenase deficiency

A 
Congenital HA x-linked; enzyme disorder
G6P reverses oxidation Hb, RBC membrane
Clinical
- neonatal jaundice
- acute haemolysis w/ oxidant drugs or fava beans
- RBCs oxidised and damaged
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74
Q

Discuss acquired haemolytic anaemia

A

Autoimmune anaemia
Self-reacting IgG attaches to RBC
Removed by spleen; extravascular haemolysis

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75
Q

What is haemostasis?

A

Complex interaction of vessels, platelets, von Williebrand Factor, clotting factors to stop bleeding

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76
Q

Describe the 2 mechanisms of haemostasis

A

Primary

  • vascular response; reflex vasoconstriction
  • platelet plug formation via vWF

Secondary

  • clotting factors circulate in inactive form
  • tissue factor released on injury to blood vessel activated extrinsic pathway
  • exposure to collagen activates intrinsic pathway
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77
Q

What are the types of haemostatic disorders based on haemostasis mechanisms?

A

Primary

  • vascular disorders
  • vWF disease (can be secondary)
  • platelet disorders

Secondary
- clotting factor disorders

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78
Q

What are the types of haemostatic disorders based on if congenital/acquired?

A

Congenital

  • vWD (1/2)
  • Haemophilia A and B (2)

Acquired

  • thrombocytopenia (1)
  • platelet dysfunction associated w/ drugs (1)
  • antiplatelet (1)
  • anticoagulants (2)
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79
Q

Discuss vascular disorders in relation to haemorrhagic disorders

A

Rarely cause severe bleeding
Hereditary haemorrhagic telangiectasia; autosomal dominant
Clinical: telangiectasia on skin and mucous membranes
Dental
- bleeding from oral surgery not troublesome
- regional LA; risk deep tissue bleeding

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80
Q

What is the function of Von williebrand factor?

A

Mediates platelet adhesion to damaged endothelium
Stabilises and transports factor 8
Mediates platelet aggregation

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81
Q

Discuss vWD

A

Caused by vWF deficiency, not sex linked
Clinical
- problems of either 1/2 haemostasis or both
- bruising, epistasis
- prolonged bleeding during surgical, dental work
- GI bleed and menorrhagia freq.

Management

  • desmopressin; stim. release vWF and F8; mild
  • vWF replacement; severe
  • anti-fibrinolytic drugs slow/prevent plug breakdown
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82
Q

Discuss dental relevance of vWD

A

Prolonged oozing post XLA, bleeding into muscles/joints
Avoid regional LA; infiltration safer
Avoid aspirin/NSAIDs; co-codamol safer

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83
Q

Discuss platelet deficiency disorders

A

Hereditary: Bernard-Soulier syndrome

Megakaryocyte suppression

  • chemotheraputic agents
  • viruses: mumps, HIV

Bone marrow failure: aplastic anaemia, lymphoma, leukaemia, metastases

Splenomegal; sequestration of platelets

Inc. destruction

Autoimmune: idiopathic thrombocytopenia purpura

  • cytotoxic drugs
  • diseases: disseminated intravascular coagulation, lupus, malaria
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84
Q

What is the dental relevance of platelet deficiency disorders?

A

Thrombocytopenia: find out platelet count, request FBC pretreatment
Refer to GO/haematologist for management
Risk spontaneous bleeding if PC<20000mm3

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85
Q

Discuss platelet dysfunction disorders

A

Antiplatelets: aspirin, NSAIDs, clopidogrel, dipyridamole

  • all except NSAIDs act irreversibly, permanently on lifespan of RBC
  • NSAIDs reversible and cleared in 1/2d

vWD

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86
Q

Discuss the dental relevance of platelet dysfunction disorders

A

Minor dental procedures continue medications
Never stop medications w/o consulting GP
Anti-platelets: stop 7d pre-surgery, resume 1-2d postoperative
NSAIDs: stop 24hrs before, resum next day
Post-XLA bleeding: compressive packing, sutures, absorbable haemostatic agents

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87
Q

Describe clinical features of platelet disorders

A

Easy bruising and bleeding

  • petechiae
  • purpura
  • ecchymosis
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88
Q

Discuss haemophilia A and B

A

Deficiency CF 8 and 9, respectively
Categorised by CF levels

Clinical

  • mild: bleed minimally, associated w/ surgery
  • moderate: bleed after minor injury; require urgent attention
  • severe: bleed v often w/ or w/o provocation
  • haemorrhage appears to stop, intractable oozing follows; bleeding into deep tissues, muscles, joints, facial spaces

Management

  • desmopressin: inc. production F8
  • CF replacement therapy; CF concentrate from plasma, commercially available recombinant factor
  • anti-fibrinolytic; tranexamic acid, epsilon-amino caproic acid
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89
Q

Discuss dental relevance of haemophilia A and B

A

Significant risk haemorrhage post surgery or LA
Ensure adequate CF levels
Postoperative: monitor haematoma formation; swelling, hoarseness, dysphagia
HandN trauma: prophylactic CF8 replacement
- red. risk bleeding into cranial cavity/fascial spaces of neck

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90
Q

Discuss anticoagulant therapy

A

Thrombosis or significant risk of thrombosis

Indications: atrial fibrillation, cardiac valvular disease, ischaemic heart disease

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91
Q

Discuss use of warfarin

A

Oral medication
Inhibit VitK dependent CF (2,7,9,10)
Monitored via international normalised ratio (INR)/prothrombin time
Reversed w/ fresh frozen plasma/VitK
Narrow therapeutic range, freq. monitoring and dose adjustment

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92
Q

Discuss dental relevance of warfarin

A

Measure INR within 24hr surgery; <4 refer
Interactions: metronidazole, macrolides, azole antifungals, NSAIDs
Inc. risk significant bleeding
Minimise: avoid use concurrent medications, seek alternatives

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93
Q

Discuss herparin

A

Inhib. CF2 and 10
Short-lived anticoagulant effects
Standard and low MWt herparins
Monitored via activated partial thromboplastin time

Standard: IV; immediate management acute thromboembolic event
LMWH: SC; non-hospitalised ambulatory pts

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94
Q

Define determinant, receptor and specificity

A

Determinant: smallest unit Ag from which Ab can be made from or T-cell respond to

Receptor: molecule/complex of molecules which possess at least 1 recognition site

Specificity: ability of R to distinguish identity of determinant recognised from other determinants

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95
Q

Describe non-immunological defences

A 
Intact epithelium: muco-ciliary escalator 
Cough reflex
Bladder emptying
pH vagina, skin
Normal flora: OC, GIT, vagina, skin
Bile, sebum
Desquamation, swallowing reflex
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96
Q

Describe activation of innate immune system

A

Microorganism breach mucosal barrier
Recognised by Rs on cell surface
Engagement of Rs trigger engulfment and destruction of bacteria
Cytokines released: affect other cells
Chemokines: attract other cells bearing chemokine Rs
Local inflammation bring other cells of immune system
Complement cascade proteins: coat bacteria, target for destruction

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97
Q

Discuss molecules of innate immune system

A

Lysozyme: destroy our surface bacteria
Pepsin-digestive enzyme: hydrolyses proteins
Complement plasma proteins: coat bacteria, mark for phagocytosis
- Recruitment inflammatory cells
- Opsonisation of pathogens
- Kill pathogens
Cytokines, chemokines: cell-cell communication; modulators of immune response
Antimicrobial: cryotidins, defensins; damage cell membranes

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98
Q

Discuss circulation of lymphocytes

A

Naive lymphocyte -> lymph node through blood
Ag from infection site -> lymph node via lymphatics
Lymphocyte and lymph -> blood via thoracic duct

Adhesion molecules on surface interact w/ ligands on endothelial cells
- multiple: selectins, bound chemokines, integrins
Expression specific adhesion molecules restrict destination of cell

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99
Q

Discuss activation of adaptive immune response

A

Immature DCs migrate through bloodstream, survey local environment for pathogens
Carry Ag to lymph nodes, mature DC present Ag to T-cells in form can read
Express Ag and co-stimulatory molecule on surface; if don’t have both = no T cell stim.

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100
Q

Discuss memory and tolerance in active immunity

A

Memory: Expansion of Ag specific clone after encounter w/ Ag
- enhanced specific immune responses following repeated exposure

Tolerance: delete auto-reactive cells soon after development

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101
Q

Distinguish b/w Ab, cytokines, complement

A

Ab: high ply specific, effect function of adaptive immune response

Cytokines: non-specific chemical mediators, innate and adaptive

Complement: system plasma proteins act together to attack EC forms of pathogens

  • can occur spontaneously (innate)
  • or pathogen specific Ab binding pathogen (adaptive)
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102
Q

Discuss myeloid derived immune system cells

A

Macrophages: phagocytosis, activation bacterial mechanisms, Ag presentation

Dendritic cell:

  • immature: phagocytosis/Ag uptake peripheral
  • mature: Ag presentation to T cells

Neutrophil: phagocytosis, activation bacterial mechanisms

Eosinophils: killing Ab-coated parasites

Mast: release granules containing histamine, active agents

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103
Q

Discuss natural killer cells

A

Lymphoid derived
Release lyric granules kill some virus infected cells
Lack Ag specific Rs

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104
Q

Discuss clonal selection

A

Lymphocytes that encounter their specific Ag will survive, differentiate, proliferate

Lymphocytes bear specific Ag R w/ unique specificity
R occupation activate lymphocyte
Differentiated effect cells from activated lymphocyte bear identical R
If bear self molecule R will be deleted at early stage of development

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105
Q

Discuss histamine

A

Vasoactive amine stored in mast cells
Release: Ag bind IgE on mast cell surface
Vasodilation and smooth muscle contraction
Some symptoms of immediate hypersensitivity

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106
Q

Discuss leukotrienes

A

Lipid mediators of inflammation derived from arachidonic acid
Produced by macrophages and mast cells

Smooth muscle contraction
Inc. vascular permeability
Stim. mucous secretion

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107
Q

Discuss prostaglandins

A 
Lipid metabolites of arachidonic acid
Same effect as leukotrienes 
- smooth muscle contraction
- inc. vascular permeability 
- stim. mucous secretion
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108
Q

Discuss chemokines

A

Small chemo-attractant molecules stim. migration and activation of cells
- esp. lymphocytes and phagocytic cells
Central roll in inflammatory response
Rs used by viruses to enter cells

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109
Q

Discuss interferons

A

Alpha: prod. leukocytes, DC; antiviral, inc. MHC I expression
Beta: from fibroblasts; “
Gamma: T and NK cells; macrophage activation, inc. MHC and Ag processing, Ig class switching, suppression Th2

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110
Q

Discuss tumour necrosis factor (TNF)

A

Alpha: prod. macrophage, NK, T cells; promote inflammation, endothelial cell activation
Beta: T and B cells; lymph node development

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111
Q

Discuss interleukins

A

1: prod. macrophages, epithelial cells; fever, T and macrophages activation
2: T cells; T cell proliferation
4: T and mast; B activation, IgE switch induce differentiation -> Th2
5: T and mast; eosinophil growth and differentiation
6: T, macrophages, endothelial; T and B differentiation, acute phase protein production, fever

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112
Q

Discuss erythropoiesis

A

Production of RBCs

Controlled by -ve feedback
Stim. by
- hypoxia 
- high altitude
- inc. exercise
- loss lung tissue due to emphysema
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113
Q

What is polycythaemia?

A

Overproduction of RBCs

Inc. viscosity and BP, dec. flow rate blood w/ dec. O2 delivery

Can lead to embolism, heart failure, stroke

  • primary: cancer of erythropoietic cell line in red bone marrow
  • secondary: from dehydration, emphysema, altitude
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114
Q

Discuss general aetiology if anaemia

A

Deficiency: Fe, Vit B12, folic acid, Coeliac/Crohn’s disease
Bone marrow aplasia
Inc. destruction: sickle cell, Thalassaemia, G6PDH, hereditary spherocytosis
Other: chronic disease, acute blood loss, renal failure, malignancy

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115
Q

Discuss Fe deficiency anaemia

A

Symptoms

  • early; none
  • late; tiredness, dyspnoea, palpitations, tachycardia, conjunctiva pallor

Dental

  • sore tongue
  • atrophic glossitis
  • candidiasis
  • angular stomatitis
  • aphthous-like ulceration
  • pallor of oral mucosa
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116
Q

Discuss B12 deficiency anaemia

A

Causes

  • pernicious anaemia; autoantibody to gastric parietal cell
  • partial gastrectomy
  • Crohn’s/Coeliac (malabsorption)

Dental

  • depapillated, beefy red tongue
  • angular chellitis

Neurological

  • circumoral and peripheral tingling, numbness
  • specific for B12

Special investigations

  • Serum B12
  • intrinsic Ab/gastric anti-parietal Ab

Treatment: month IM B12

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117
Q

Discuss folate deficiency anaemia

A

Causes

  • chronic alcoholism
  • drugs; cytotoxic, phenytoin, HIV/AIDS

Symptoms: same as B12 w/o neurological

Treatment: daily oral intake folic acid

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118
Q

Discuss sickle cell anaemia

A

Problem w/ Hb formation

Clinical

  • painful crises: infarcts bone, CNS, spleen, lungs
  • haematological crises
  • chronic anaemia
  • chronic hyperbilirubinaemia; jaundice, gall stones
  • susceptible to infection; meningococci, pneumococci
  • sequestration syndrome; spleen - septicaemia

Dental

  • painful infarcts in jaw or osteomyelitis
  • hypercemetosis
  • excessive overjet/bite; haemopoietic maxilla
  • hypomineralised teeth
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119
Q

Discuss aplastic anaemia

A

V rare
Cause
- non-functioning bone marrow
- pancytopenia; leukopenia, thrombocytopenia, anaemia
- idiopathic: exposure benzene, irradiation, hepatitis

Clinical

  • anaemia
  • susceptibility infection
  • bleeding

Dental
- oral manifestations similar to leukaemia

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120
Q

Discuss general management of anaemia

A

Eliminate underlying disease
Replacement therapy
- Fe: ferrous sulphate, ferrous fumerate
- folate
- IM B12
Blood transfusion: acute haemolysis/blood loss
Erythropoietin: chronic renal failure, anaemia chronic disease

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121
Q

General symptoms of respiratory diseases

A

Key

  • dyspnoea
  • cough
  • sputum
  • haemoptysis (coughing blood)
  • chest pain

Other

  • wheeze; asthma
  • stridor; harsh, rattling sound due to narrow trachea and larynx
  • fever, rigor, night sweats (TB, infection, cancer)
  • dysphonia
  • weight loss
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122
Q

General signs of respiratory disease

A 
Hand
- tar staining
- peripheral cyanosis 
- tremor; fine (beta blocker) or flapping (CO02 retention)
- finger clubbing 
Lymphadenopathy 
Tracheal deviation 
Chest well deformity 
Inc. jugular venous pressure
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123
Q

Define asthma

A

Common chronic inflammatory condition of airways

Airway hyper responsiveness causes reversible (spontaneous or w/ therapy) airflow obstruction

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124
Q

2 classifications of asthma

A

Extrinsic (allergic)

  • classical asthma, childhood onset
  • precipitants incl. allergens in animal fur/feather, drugs (NSAIDs, ABs), food (nuts, milk), mites, moguls
  • history of other allergic diseases; food allergy, hay fever, eczema
  • often remit by teenage years

Intrinsic

  • adult onset, middle age, non-allergic
  • more progressive, less responsive to therapy
  • triggers; stress, gastro-oesophageal reflux
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125
Q

Compare extrinsic and intrinsic asthma

A 
Onset: childhood; adult
Allergy: allergic; not
Family history: present; absent
Freq.: common; rare 
Predisposition form IgE: present; absent
COPD: none; chronic bronchitis 
Pathogenesis: IgE mediated mast cell degranulation; mast cell instability, airway hyper-responsivity 
Progression: improves; worsens
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126
Q

Pathogenesis of asthma

A 
Bronchoconstriction
Cellular inflammation and infiltration 
Mucosal oedema 
Mucus hypersecretion and exudate in airway lumen
Airway remodelling:
- smooth muscle and goblet cell hypertrophy 
- epithelial damage 
- inc. collagen deposit
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127
Q

Discuss clinical features asthma

A

May be absent in well controlled pts

Wheeze
Dyspnoea
Cough
Chest tightness
Become distressed, anxious, tachycardic
Red. chest expansion, use accessory respiratory muscles
Symptoms intermittent; worse at night, early morning

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128
Q

Discuss investigations into diagnosing asthma

A

Peak expiratory flow rate (PEFR): diurnal variation, lowest values early morning
- if improvement after bronchodilator = asthma
- no improvement and smoker = COPD
Spirometry: FEV:FVC red.
Blood test: eosinophilia, inc. IgE
Chest X-ray: rule out other causes; pneumothorax

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129
Q

Discuss management of asthma

A 
Pt education 
Smoking cessation
Avoid triggers; irritants, allergens
Stepwise approach based on severity 
Drugs
- O2
- short/long term beta-2 agonists
- mast cell stabilisers
- leukotriene R antagonist
- corticosteroids
- anti-IgE monoclonal Ab (omalizumab)
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130
Q

Discuss dental relevance of asthma

A

Pt attend w/ usual medication
GA, sedation avoided
Elective care deferred in severe cases
Triggers: NSAIDs, penicillin, stress, anxiety
Gastro-oesophageal reflux common
Medication: thrush, dry mouth, adrenal suppression common w/ systemic corticosteroids
Emergencies: acute severe or life threatening

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131
Q

Define and discuss risk of COPD

A

Chronic obstructive pulmonary diseases: progressive, poorly reversible airflow limitation associated w/ persistent inflammatory response of lungs

Risk

  • smoking: major, pack year dependent
  • air pollutants: in/outdoor
  • occupational dusts and chemicals
  • alpha-1-antitrypsin deficiency: early onset COPD
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132
Q

Discuss chronic bronchitis

A

COPD

Airway obstruction from chronic mucosal inflammation, mucus gland hypertrophy, mucus hypersecretion, bronchospasm
Persistent cough and sputum production on most days for 3/12 in 2 consecutive yrs

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133
Q

Discuss emphysema

A

Dilation of airspaces distal to terminal bronchioles w/ destruction of alveoli and red. alveolar SA for gaseous exchange
Red. elastic recoil, collapse and red. total lung capacity

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134
Q

Discuss diagnosis and management of COPD

A 
Diagnosis: FEV/FVC <0.7; FEV <80% predicated (NICE)
Management 
- smoking cessation
- weight loss
- exercise
- vaccination; influenza, pneumococcal 
- non-invasive ventilation
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135
Q

Discuss clinical features of COPD

A 
Dyspnoea, wheeze
Persistent cough, sputum 
Fatigue
Weight loss
Red. exercise tolerance
Cyanosis 
Use accessory muscles
Flapping tremor 
Tachypnoea
Tachycardia
Barrel chest
Red. chest expansion
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136
Q

Discuss dental relevance of COPD

A

Treat upright
Always bring inhaler w/
Cough can make treatment difficult
Rubber dam can further obstruct breathing (mouth breathers)
Best treat under LA, avoid bilateral mandibular or P injections
Avoid GA, sedation
Medication: thrush, dry mouth, adrenal suppression w/ systemic corticosteroids

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137
Q

What is pneumonia?

A

Acute infection of lung parenchyma, usually bacterial associated w/ high morbidity and mortality

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138
Q

Risk factors of pneumonia

A

Smoking
Chronic lung/heart disease
Alcohol
Immunosuppression

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139
Q

Clinical features and complications of pneumonia

A

Clinical

  • cough, sputum
  • fever
  • chest pain
  • lung abscess
  • dyspnoea
  • pyrexia
  • tachypnoea
  • tachycardia
  • empyema
  • red. lung expansion
  • plural rub

Complications

  • lung abscess
  • empyema
  • respiratory failure
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140
Q

Management and dental relevance of pneumonia

A

Management

  • alcohol, tobacco avoidance
  • analgesics and antipyretic relieve symptoms
  • broad spectrum antimicrobial
  • prophylaxis: smoking cessation, influenza immunisation

Dental

  • defer all treatment
  • GA contraindicated
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141
Q

What is tuberculosis?

A

Chronic granulomatous infection caused by M. tuberculosis

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142
Q

Risk factors of TB

A 
Homeless
Prison
HIV
Alcoholism 
IV drug use
Migrants, asylum seekers
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143
Q

Clinical features TB

A

Initial infection: subclinical; latent many yrs until individual immunosuppressed
Active: shortly after infection if immunosuppressed

Chronic cough
Sputum
Haempotysis
Weight loss
Night sweats
Fever
Lymphadenopathy 
Loss appetite
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144
Q

Discuss diagnosis and treatment of TB

A

Diagnosis

  • chest X-ray
  • sputum microscopy; Ziehl-Neelsen stain for acid fast bacilli
  • sputum culture; gold standard, takes several wks
  • biopsy affect organs; histological hallmark caseating granulomata
  • notifiable disease; contact tracing

Treatment; 4 drugs for 6/12

  • initial: isoniazid, rifampicin, ethambutol, pyrazinamide 2/12
  • continuation: isoniazid, rifampicin 4/12
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145
Q

Discuss dental relevance of TB

A 
Contagious, treatment deferred
Red. splatter and aerosols; min. coughing, avoid ultrasonic, use rubber dam
PPE
Avoid GA
Possible drug interactions 
Tuberculous ulcers
Cervical lymphadenopathy
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146
Q

Lung cancer aetiology

A 
Smoking: 20% smokers, cessation dec. risk w/ time, passive 
Asbestosis 
Radon
Arsenic
Coal tar
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147
Q

Clinical features lung cancer

A 
Haemoptysis
Chest pain
Persistent cough
Dyspnoea
Unexplained weight loss
Recurrent chest infections
Hoarseness 
Wheeze, stridor
Finger clubbing 
Cervical lymphadenopathy
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148
Q

Discuss lung cancer investigations and management

A

Investigations

  • chest X-ray
  • CT and PET scan
  • bronchoscopy
  • sputum cytology
  • biopsy

Management

  • TNM tumour staging
  • surgery
  • radiotherapy; palliative care, chemotherapy
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149
Q

Prognosis of lung cancer

A

Non-small cell: 50% 2yr survival w/o spread, 10% w/ spread

Small cell: 3/12 median survival if untreated , 1-1.5yr if treated

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150
Q

Dental relevance of lung cancer

A

Smoking common risk for oral and lung cancer
Metastasis to oro-facial region; cervical lymphadenopathy, jaw paraestheisa
LA safe, GA and sedation if absolutely necessary
Chemotherapy; immunosuppressed

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151
Q

What is cystic fibrosis?

A

Autosomal recessive hereditary disorder of metabolism
Defect in CF transmembrane conductance regulator (CFTR) protein that regulates Cl, Na transport across membrane of exocrine glands

Characterised by

  • dec. excretion Cl into airway lumen
  • inc. Na reabsorption into epithelial
  • inc. viscosity and stasis of secretions
  • recurrent bronchopulmonary infection -> bronchiectasis
  • pancreatic duct obstruction and fibrosis: insufficiency w/ malabsorption and bulky, foul smelling stool
  • gallstones, DM, cirrhosis, pancreatitis
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152
Q

Discuss clinical features and complications of CF

A

Clinical

  • persistent cough
  • wheeze
  • haemoptysis
  • finger clubbing
  • cyanosis
  • dyspnoea

Complications

  • recurrent chest infections
  • pneumothorax
  • bronchiectasis
  • cor pulmonale
  • nasal polyps
  • infertility
  • gallstones
  • DM
  • biliary cirrhosis
  • stunted growth
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153
Q

How is CF diagnosed?

A

Na, Cl in sweat >60mmol/L

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154
Q

Management of CF

A

Drugs: bronchodilators, prophylactic antimicrobial
Vaccination: measles, whooping cough, influenza
Diet: low fat intake, adequate vitamins
Lung transplant in severe cases

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155
Q

Dental relevance of CF

A

Recurrent sinusitis
Enamel hypoplasia
Major salivary gland swelling and xerostomia
Delayed development and eruption
GA contraindicated; poor respiratory function

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156
Q

Main types of mucocutaneous lesions

A

Lichen planus
- vulvovaginal-gingival syndrome
Lichenoid reaction
Lupus erythematous

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157
Q

What is lichen planus?

A

Oral, cutaneous and genital disease
Thought to be immunologically mediated
Premalignant condition

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158
Q

Discuss natural history of L.P.

A

Chronic oral lesions: 4-25yr, 7yr av.
Skin lesions active 18/12 av.

70-77% skin LP have oral
10-30% oral LP have skin

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159
Q

Oral presentation of LP

A

Reticular; white lines
Erythematous (atrophic); thinning of mucosa, superficial reddening
Erosive; ulcerative
Symmetrical; both skin and oral lesions
B/L mucosa, tongue, gingiva (rarely P/L mucosa)
- areas of inc. friction; O line = Keobner phenomenon

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160
Q

Variants of LP

A 
Papular
Reticular
Plaque-like
Atrophic
Erosive (ulcerative)
Bullous
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161
Q

Discuss extra-oral presentation of LP

A

Cutaneous, purple polygonal pruritic papules
Dystrophic nails
Lichen planopilaris (hair) -> scarring alopecia

Ocular, nasal, laryngeal, oesophageal, gastric, bladder

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162
Q

Discuss cutaneous LP

A

Mainly flexor surfaces of wrists, shins
Symmetrical distribution
Koeber phenomenon

Papules red turning violaecous
Flat topped, polygonal, few mm diameter

Wickham’s striae: surface network fine white striations

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163
Q

Discuss other sites of LP

A

Nails: longitudinal grooving and pitting reversible, possible nail loss
Hair: follicular but permanent scarring alopecia common

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164
Q

Discuss vulvovaginal-gingival syndrome

A

Type of LP

Often unrecognised
Usually ulcerative and symptomatic
Progressive vulval disease leading to scarring
Reports of malignant transformation

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165
Q

Discuss lichenoid drug reaction

A

Bi/unilateral disease
May be ulcerative
No pathognomonic histological features
Diagnosis: withdrawal of drug

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166
Q

What 10 drugs are commonly associated w/ oral lichenoid reactions?

A
  1. B-blockers; atenolol
  2. ACE inhibitors; captopril
  3. Diuretics; furosemide
  4. Methyldopa
  5. Oral hypoglycaemics; tolazamide
  6. NSAIDs; ibuprofen
  7. Gold salts; rheumatoid arthritis
  8. Penicillamine
  9. Antimalarials; doxycycline
  10. Allopurinol; gout
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167
Q

Discuss clinical features of lichenoid reaction

A

Soreness as in LP esp. erosive form
Often indistinguishable from LP
Asymmetric distribution if due to reaction to local materials
More likely to be erosive form and affect palate and tongue

Resolves on stopping implicated drug

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168
Q

Discuss oral contact hypersensitivity reactions

A 
Subgroup of OLR
Individual sensitised to component of DM
- amalgam alloy, Ni, Hg, Au, BisGMA
Lesion confined to area in direct contact w/ restoration 
\+ve response to patch test
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169
Q

Discuss systemic lupus erythematosus

A

Multi-systemic autoimmune disease
Autoantibodies (ANA) generated against variety autoantigens
Involves vascular and connective tissues

Multisystem involvement w/ serological or haematological changes
Malar rash
Photosensitivity discoid lesions, diffuse alopecia, vasculitis
Sun expose: may trigger acute systemic flares

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170
Q

Discuss discoid lupus erthematosus

A

Scaly atrophic plaques in sun exposed skin
May involve oral and genital mucosa, skin, hair

Round/oval plaques: red, scaly w/ keratin plugs
Scarring may cause alopecia

Management: potent topical or intralesional corticosteroids, antimalarials

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171
Q

Define vesicle and bulla

A

Vesicle: small, fluid-filled blister <5mm

Bulla;p: large, fluid-filled blister >5mm

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172
Q

Discuss varicella zoster virus

A

Human herpes virus 3 HHV3

Causes chicken pox and shingles

1ry infection: chickenpox in non-immune
Recurrence: reactivation as shingles; may be sign of underlying malignancy, immunosuppression

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173
Q

Discuss chickenpox

A

1ry infection HHV3

Itchy, maculopapular rash back, chest, face
Initial site upper respiratory tract as droplet infection
May have oral vesicles/ulceration on palate/fauces

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174
Q

Discuss shingles and post herpetic neuralgia

A

Complication of shingles

Recrudescence of latent HHV3 from DRG or CN ganglia present since initial infection as chickenpox
Probably many reactivations throughout life but controlled by competent cell-mediated immunity

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175
Q

What is dermatitis herpetiformis?

A

Chronic pruritic papulovesicular rash causing small blisters on urticated base on buttocks, elbows and knees
Associated w/ gluten sensitive enteropathy (Coeliac disease)

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176
Q

Oral presentation of dermatitis herpetiformis

A

Transient, superficial blisters -> tender, nonspecific ulcers (~70%)

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177
Q

Discuss clinical features of dermatitis herpetiformis

A

Smaller bullae and vesicles

Associated w/ Coeliac disease

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178
Q

Treatment of dermatitis herpetiformis

A

Gluten free diet and dapsone

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179
Q

Aetiology of erythema multiforme

A

Infection: HSV, Hep, mycoplasma, bacterial, fungal, parasites
Drug: anti-epileptic (phenytoin), penicillin, NSAIDs, anti-fungals, barbiturates
Systemic: lupus, malignancy, pregnancy
Idiopathic: 50% cases

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180
Q

What is erythema multiform?

A

Skin condition thought to be caused by immune mediated type 3 hypersensitivity

Causes target/iris lesions, erythematous papule blisters
Common sites: extremities (palms, soles) and mucous membranes

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181
Q

Clinical features of erythema multiforme

A

Oral lesions

  • bullae or erythematous base break rapidly into irregular ulcers, bleed and from crusts
  • lips more freq., gingiva rare

Skin macules and papules, central pale area surrounded by oedema and bands of erythema
- iris type but can also be bullae

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182
Q

Discuss pemphigus vulgaris

A

Chronic, organic specific autoimmune blistering disease

Circulating and bound IgG autoantibodies directed against adhesion proteins of desmosomes causing dissolution cell-cell adhesion

Leads to intraepithelial blisters affecting skin and mucosa

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183
Q

Discuss oral presentation of pemphigus vulgaris

A

Oral bullae; fragile, short lived
Large, shallow non-healing ulcers typical
Palate, buccal mucosa and gingiva most commonly affected

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184
Q

Discuss cutaneous pemphigus

A

Large non-healing erosions and ulcers of skin
May appear 3-4/12 after mouth lesions

Management

  • topical corticosteroids; mouthwashes
  • systemic corticosteroids; prednisolone
  • steroid-sparing agents; azathioprine, mycophenolate mofetil
  • IV Igs
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185
Q

Discuss mucous membrane pemphigoid

A

Rare, autoimmune blistering disease common in middle age/elderly

Circulating and bound Abs against basement membrane zone
Predominately mucosal disease: urogenital, conjunctiva, larynx, oesophagus
- rarely skin, if scalp will lead to alopecia

Full thickness epithelium lifts off underlying connective tissue
Large, tense bullae (blood filled) breakdown to chronic, painful erosions

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186
Q

Management of mucous membrane pemphigoid

A 
Topical corticosteroids 
Oral 
- prednisolone
- dapsone
- tetracyclines
- azathioprine 
- cyclophosphamide
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187
Q

Discuss bullous pemphigoid

A

Common in elderly
Oral lesions only 10% cases
Initial urticarial eruption precedes onset of blistering
Large, tense blisters involving skin of limbs, trunk, flexures

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188
Q

Management of bullous pemphigoid

A

Systemic prednisolone +/- azathioprine
Self limiting in 50% cases
Systemic corticosteroids stopped after 2yr

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189
Q

Corticosteroid side effects

CUSHINGOID

A 
Cataracts
Ulcers
Skin: striae, thinning, bruising 
Hypertension/Hirsutism/Hyperglycaemia
Infections
Necrosis
Glycosuria 
Osteoporosis/Obesity
Immunosuppression 
Diabetes
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190
Q

Define acute inflammation

A

Response of living tissue to injury

All purpose defence mechanism

  • contain and isolate injury
  • destroy or neutralise injury
  • resolve injury (may become chronic)
  • heal and repair
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191
Q

Exogenous and endogenous causes of acute inflammation

A

Exogenous

  • trauma; stabbing
  • infection; dermatitis
  • chemicals; acid attack
  • temp.
  • radiation; UV

Endogenous

  • anoxia; lack O2, infarct
  • Ab/Ag complexes
  • body chemicals; stomach acids
  • metabolic products; urate crystals -> gout
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192
Q

5 Cardinal Signs of Acute inflammation (macroscopic changes)

A 
Redness
Swelling
Heat
Pain
Loss of function
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193
Q

Discuss the microscopic changes seen during acute inflammation

A 
Initial construction then dilation of vessels
Inc. blood flow and permeability 
Formation of exudate
Migration of leukocytes through wall
Oedema
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194
Q

Discuss impact of inc. permeability in acute inflammation

A

Enhances migration of cells
Dilution of toxins
Stim. lymphatic/immune response
Deposition of proteins; fibrin to form mechanical barrier

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195
Q

Mechanisms involved in migration of WBCs from blood to tissue

A

Margination: move to periphery, no longer mixed w/ RBCs
Pavementing: adhere to endothelial cells of vessels
Diapedesis: pass through endothelial cells to reach tissue

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196
Q

Discuss neutrophil polymorphs

A

Main cell of inflammation; goes hand in hand w/

1st cell to arrive
Predominant for 1st 6-24hr
Most common
Mobile, phagocytic, respond to chemotaxis
Segmented nucleus, granular cytoplasm full of granules containing enzymes

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197
Q

Discuss eosinophils and basophils/mast cells

A

Eosinophils

  • esp. allergy and helminth infections
  • bilobed nucleus, red granules

Basophils/mast cells

  • esp. early
  • blue/purple cytoplasm
  • degranulate w/ release vasoactive amines
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198
Q

Discuss monocytes/macrophages

A

Same cell; monocyte when inside, macrophage when reach tissue

Circulating tissue
2nd main cell of inflammation 
Predominant after 24hr
Mobile, phagocytic, respond to chemotaxis
Attacks and clears up
Bean shaped nucleus, copious cytoplasm
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199
Q

Discuss neutrophil chemotaxis

A

Conc. gradient neutrophil is drawn up due to

  • bacteria
  • fungi
  • immune complexes
  • toxins
  • complement components
  • lipoxygenase products
  • WBC breakdown products
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200
Q

Discuss phagocytosis

A

Recognition and attachment

  • mechanical contact
  • opsonisation

Engulfment

  • pseudopods
  • phagosomes

Killing and degradation
- lysosomal contents

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201
Q

Discuss clinical features of acute inflammation

A 
Pyrexia
Drowsiness 
Lethargy 
Leukocytosis
Dec. appetite
Acute phase proteins
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202
Q

Discuss resolution of acute inflammation

A

Clearance of injury
Clearance of any inflammatory cells and mediators
Replacement of injured cells
Normal function resumed

Can be spontaneous or w/ treatment

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203
Q

Discuss repair outcome of acute inflammation

A

If tissue lost is unable to regenerate
Replaced w/ granulation tissue and fibrosis
Likely will have less than ideal function

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204
Q

Discuss chronic inflammation

A

If Acute inflammation injury can’t be dealt w/

Or repeated episodes

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205
Q

Discuss suppurative inflammation

A

Pus: more exaggerated form acute inflammation
Abscess: walled-off and surrounded by fibrous rim

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206
Q

Discuss septicaemia

A

If organism gains access to lymphatic then blood or blood directly
Inflammatory response heightened
Mortality high

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207
Q

Possible outcomes of tissue loss and destruction

A 
Inflammation (all cases)
Regeneration
Repair w/ fibrosis
Persistence of cavity or gap
Permanent loss
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208
Q

Define regeneration and repair

A

Regeneration: replacement injured cells by parenchymal cells of same type via proliferation
Repair: replacement of injured cells by granulation tissue and ultimately fibrous scar

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209
Q

Discuss general features of wound healing

A 
Would w/ escape of blood
Haemostasis 
Inflammation
Macrophages remove debris
Cells regenerate if possible
Angiogenesis
Fibroblasts move in, proliferate, lay down collagen
Scar
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210
Q

Discuss haemostasis role in tissue repair

A

Stops bleeding

Vasoconstriction endothelial cell activation
Platelets adhere, become activated, aggregate
Coagulation cascade forms fibrin clot

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211
Q

3 groups cells can be divided into

A

Labile: skin, gut mucosa, bone marrow
- continue to proliferate throughout life, replace cells that are destroyed

Stable: kidney, liver, endocrine, bone marrow
- turn over at low level normal circumstances, capable rapid replication if req.

Permanent: cardiac muscle, neurons, striated/skeletal muscle
- incapable mitotic division or organised proliferation

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212
Q

Why might labile/stable cells not be able to regenerate?

A

Architecture structure may be lost

Intact basement membrane req. for regeneration of most tissues

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213
Q

3 tissues capable of regenerating all constituents

A

Liver
Bone
Bone marrow

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214
Q

Discuss the granulation tissue

A 
Proliferation of new capillaries (angiogenesis)
Fibroblasts 
- synthesis ECM and collagen
- proliferate and chemotactic in response to mediators; collagen, macrophage chemokines
Myofibroblasts
Macrophages
- clear debris
- secrete growth factors
- stim. endothelial and fibroblasts
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215
Q

Discuss angiogenesis

A

Degradation: enzymatic degradation of basement membrane of parent vessels

Migration: endothelial cells towards stimulus

Proliferation: endothelial cells into cords

Maturation: and lumen formation (initially leaky)

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216
Q

Discuss remodelling of wound after repair/regeneration

A 
Macrophages clear debris
Inc. amount collagen laid down
Vessels disappear
Fibrous tissue
Collagen cross-linking
Contraction myofibroblasts 
Fibrous scar
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217
Q

Compare 1ry and 2ry intention healing

A

1ry: simple incision/cut
- initial bleeding, inflammation
- edge brought together easily
- epithelial cells proliferate, meet on surface whilst granulation tissue forms in underlying clot
- scar

2ry

  • edges can’t be approximated
  • more bleeding, inflammation
  • more granulation tissue
  • granulation tissue on surface as epithelium takes time to cover
  • wound contraction (myofibroblasts)
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218
Q

Discuss fracture healing

A

As usual have; bleeding, clot formation, periosteal disruption, inflammation, granulation tissue then

  • cartilage forms in granulation tissue from chondrocytes
  • bridges gap (provisional callus)
  • calcification and ossification by osteoblasts (fibrocollagenous callus then bony callus)
  • remodelling by osteoblasts/clasts
  • woven bone becomes lamellar
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219
Q

What is special about fracture healing ?

A

Only situation where granulation tissue leads to regeneration

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220
Q

Control of repair

A

Growth factors
- activation and proliferation fibroblasts
- angiogenesis and epithelial cell regeneration
Cell-cell/cell-matrix interactions (contact inhibition)
ECM synthesis and collagenisation (fibronectin, proteoglycans)

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221
Q

Factors affecting healing

A

Systemic

  • age
  • nutrition
  • DM
  • steroids
  • chronic illness (renal failure)
  • haematological disorder

Local

  • infection
  • foreign material
  • blood supply
  • type of tissue
  • extent of injury
  • mobility
  • radiation
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222
Q

Discuss mycobacterium

A 
Aerobic
Curved/straight rods
Non-motile
Acid fast: cell wall contains waxy lipids (mycolic acids)
- stain red on green background
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223
Q

Distinguishing factors of mycobacterium tuberculosis

A

Slow growing
Colonies visible to eye ~8wks from clinical material
Colonies ‘rough, buff (yellow), tough’
Limited growth temp. 35-37

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224
Q

What is TB and it’s aetiology?

A

Chronic granulomatous disease

Aetiology

  • M. tuberculosis: human
  • M. bovis: human and mammal
  • M. africanum: human, equatorial Africa
  • M. microti: vole (seldom)
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225
Q

Discuss pathogenesis of TB

A

M. tuberculosis survival within alveolar macrophages
Clinical features due to immune felines mediated tissue destruction and other pathological characteristics

1ry: immune system surrounds organism (forms cavity), protects body, bacteria sits dormant
Post 1ry: reactivation of dormant bacteria (immunosuppressed)

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226
Q

Significance of immunocompromised pt and TB

A

Bacteria much more likely to reactivate

Cavity formation rare as lack immune response to 1ry infection

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227
Q

Discuss transmission of TB

A

Inhalation of cough droplets from infectious individuals
Only sputum +ve individuals are infectious
Esp. within households and areas over-crowding

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228
Q

How can the spread of TB be controlled?

A

Early detection: emphasis on rapid diagnosis
Effective therapy of pt
Red. over-crowding
Vaccination

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229
Q

Discuss vaccination for TB

A

Bacille Calmetter-Guerin (BCG)

  • live, attenuated strain M. bovis
  • intracutaneous injection
  • variable efficacy
Purified Protein Derivative (PPD) skin test 
- intracutaneously = Mantoux test 
- lack inflammatory response = BCG req.
- limited usefulness distinguishing
— active disease
— quiescent infections
— previous BCG vaccination 
— other mycobacterium infection
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230
Q

How is TB diagnosed?

A 
Microscopy: acid-fast bacilli seen w/ ZN staining 
Culture: slow, not ideal
Specimens
- sputum
- washings, biopsy
- gastric aspirates
- CSF, urine, pleural fluid
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231
Q

Treatment of TB

A

Long, drawn out, compliance problems

Intensive phase; 2/12

  • rifampicin
  • isoniazid
  • pyrazinamide (and/or ethambutol)

Continuous phase 9/12

  • rifampicin
  • isoniazid
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232
Q

Discuss upper respiratory tract infections

A

Involve

  • nose
  • paranasal sinuses
  • middle ear
  • laryngeal, epiglottal tissues
  • post. pharynx
  • tonsils

Mainly bacteria and viruses
Colds, sore throats economic burden

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233
Q

Discuss lower respiratory infections

A

Freq. bacteria; viruses, fungi, mycoplasmas, pneumocystis

Fever, productive cough, chest pain

Pneumonia; life threatening
- inflammation bronchial and alveolar spaces -> anoxia -> altered cardio-pulmonary functions -> morbidity/mortality

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234
Q

Discuss respiratory infections below larynx

A

Bronchitis

  • acute: mycoplasma pneumoniae
  • chronic: H. influenzae, S. pneumoniae

Bronchiectasis

  • H. influenzae
  • Ps. aeruginosa

Whooping cough: B. pertussis

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235
Q

Discuss 2ry pneumonia

A

Predisposing

  • chronic bronchial disease
  • compromised pt
  • CF

Pathogens

  • S. pneumoniae
  • Haemophilus influenzae
  • Branhamella catarrhalis
  • fungal infections
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236
Q

Discuss Haemophilus species

A 
Facultative anaerobes 
CO2 enhance growth
Catalase and oxidase +ve
Gram -ve rod, coccobacillus or filamentous 
Req. X (haemin) and/or V (NADP) factor
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237
Q

Discuss the carriage and pathogenesis of haemophilus influenzae

A

Carriage
- URT, nasopharynx/throat

Pathogenesis
- possibly penetration of submucosa of nasopharynx

Otitis media (inflammation ear): pathogenesis unclear, caused by non-typable strains

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238
Q

Discuss the virulence and diagnosis of haemophilus influenzae

A

Virulence

  • capsule; antiphagocytic
  • pili (fimbrae); attach to epithelial cells
  • IgA protease
  • other cell membrane components

Diagnosis

  • high no. in sputum
  • blood culture; pt w/ invasive disease
  • Ag detection (type b disease)
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239
Q

Discuss non-invasive haemophilus influenzae disease

A

Often non-encapsulated strains
Often predisposition; viral, anatomical
Local infection; otitis media, sinusitis
Can give chronic obstructive airway disease

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240
Q

Discuss treatment of haemophilus influenzae

A

Ampicillin resistance; use cefotaxime (cephalosporin)

Vaccine: capsular polysaccharide preparations used

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241
Q

Discuss general features of Corynebacterium diphtheriae

A

Cause diphtheria
Aerobic/facultative anaerobic
Gram +ve rods; diphtheroids or coryneforms

Strains: gravis, intermedius, mitis

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242
Q

Discuss epidemiology and pathogenesis of corynebacterium diphtheriae

A

Epidemiology

  • person-person spread via nasopharyngeal secretions
  • resists desiccation, survive weeks in dust (hospital)

Pathogenesis
- elicit inflammatory exudate and cause necrosis of faucial mucosa
- infection spread to post-nasal cavity of larynx, cause respiratory obstruction
— and clotting of exudate which becomes adherent (pseudomembrane)
- prod. powerful toxin into bloodstream
— affinity for heart muscle, nerve endings, adrenal glands
- death from asphyxia or toxin-mediated cardiac damage

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243
Q

Discuss the Elek test

A

Test to differentiate b/w toxigenic and non-toxic strains corynebacterium diphtheriae

-ve control non-toxic, strain from pt, +ve control toxigenic
Filter paper soaked in anti-toxin
Lines of precipitation indicate +ve reaction thus toxigenic strain

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244
Q

Discuss treatment and vaccination for corynebacterium diphtheriae

A

Treatment

  • pt isolation
  • ABs; penicillin, tetracycline, clindamycin
  • early anti-toxin therapy
Vaccine
- diphtheria toxoid 
- DTP
— diphtheria toxoid
— tetanus toxoid
— whooping cough whole killed cells
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245
Q

Causative species and risk of bacterial sialadenitis

A

Sialadenitis: inflammation salivary gland

Causative

  • S. aureus
  • alpha-haemolytic strep.
  • anaerobes

Risk

  • dehydration
  • red. salivary flow
  • anaerobes
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246
Q

Clinical features and diagnosis of bacterial sialadenitis

A

Clinical

  • acute or chronic
  • painful, tender
  • swelling
  • purulent discharge from duct orifice
  • erythematous of overlying skin
  • fever, malaise, leukocytosis

Diagnosis

  • history and clinical findings
  • microbiology of pus
  • after resolution acute phase; investigate correctable salivary gland abnormalities
  • recurrent parotitis childhood; sialography show multiple sialectasis within parotid gland
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247
Q

Management of bacterial sialadenitis

A 
AB: flucloxacillin, amoxicillin-clavulanate, clindamycin 
Inc. fluid intake 
Surgical drainage (severe)
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248
Q

Causative species and risk of acute necrotising ulcerative gingivitis

A

Causative: strict anaerobic bacteria

Risk

  • poor OH
  • smoking
  • stress
  • malnutrition
  • vit deficiency
  • immunodeficiency
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249
Q

Clinical features and diagnosis of acute necrotising ulcerative gingivitis

A

Clinical

  • rapid development
  • painful ulceration
  • gingival margin and inter-dental papillae
  • halitosis
  • widespread

Diagnosis

  • clinical
  • gram-stained smear; fusobacteria, medium sized sprochetes, acute inflammation
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250
Q

Management of acute necrotising ulcerative gingivitis

A 
Mechanical cleaning; scaling, debridement 
OH
Metronidazole 200mg 3x 3d 
Amoxicillin 500mg 3x 5d
Chlorhexidine 2x
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251
Q

What is noma (cancrum oris/necrotising ulcerative stomatitis/fusospirochetal gangrene)?

A

Gangrene of face and mouth

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252
Q

Causative species and risk of noma

A

Causative

  • fusobacterium necrophorum
  • prevotella intermedia
  • alpha-haemolytic strep.
  • pseudomonas

Risk

  • ANUG
  • malnutrition
  • poor OH
  • debilitation after severe illness
  • immunosuppression
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253
Q

How is noma spread?

A

Through muscle and bone

NOT through anatomic spaces of head and neck

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254
Q

Causative species and risk of actinomycosis

A

Causative: actinomyces

Risk

  • caries and XLA
  • gingivitis and gingival trauma
  • poor OH
  • immunocompromised
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255
Q

Clinical features of actinomycosis

A

Chronic, long standing
Cervicofacial; CNS/thoracic/abdominal/pelvic less freq.

Swelling @ angle of mandible -> multiple draining sinuses
Abscess formation
Draining sinus tracts
Fistula and tissue fibrosis

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256
Q

Diagnosis and treatment actinomycosis

A

Diagnosis
- aspirated pus w/ aggregates actinomyces forming yellow particles (sulphur granules)

Treatment

  • surgical tissue + removal dead tissue
    • Long course penicillin or erythromycin
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257
Q

Discuss staphylococcus mucositis

A

Causative: S. aureus

Risk

  • elderly
  • semi-comatose
  • dehydration
  • Crohn’s

Clinical

  • start; oral discomfort, mucosal erythema
  • progress; widespread crusting, mucosal bleeding

Treatment

  • regular oral lavage
  • anti-staphylococcal AB
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258
Q

Discuss TB

A

Causative: mycobacterium tuberculosis
Spread on droplets of sputum

IO Lesion

  • ulcer on dorsal tongue w/ irregular, raised borders
  • calcified lymph nodes of previous infection may appear radio-opaque

Diagnosis

  • histopathology
  • Ziehl-Neelsen stain
  • microbiology culture LJ media and prolonged incubation
  • molecular microbiology
  • tuberculin skin test

Treatment
- systemic anti-tuberculous chemotherapy; rifampicin, isoniazide, ethambutol, pyrazinamide

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259
Q

Causative species, spread and treatment of syphilis

A

Causative: treponema pallidum

Transmission: sexual contact, vertical, blood transfusion

Treatment: penicillin

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260
Q

Discuss 1ry syphilis

A

Highly infectious firm nodule @ site of inoculation
Breakdown after few days leaving painless ulcer w/ indurated margins

Usually on genitals
Lymphadenopathy

Resolves 3-12wks

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261
Q

Discuss 2ry syphilis

A

Highly infectious maculopapular rash
Mucosal ulcers
Condylomata lata (warts on genitals)

Lymphadenopathy
Febrile illness
Malaise

6wk post-1ry infection
Resolves 2-6wks

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262
Q

Discuss 3ry syphilis

A

3-15yr after infection

Gummatous, CV, neuro-syphilis

Oral lesions

  • gumma (necrotic, painless ulcer) on palate
  • leukoplakia of dorsum tongue
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263
Q

Discuss congenital syphilis

A

Infected mother w/ 1/2ry infection pass to developing foetus

Causes
- nasal deformity; saddle nose
- Hutchinson’s triad
— interstitial keratitis
— deafness
— notched/screwdriver shaped incisors, mulberry shaped molars
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264
Q

What is ischaemic heart disease?

A

Spectrum of disorders resulting from imbalance b/w myocardial need for O2 and adequacy of supply

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265
Q

Aetiology of IHD

A

95% caused by atheroma of coronary arteries

Remainder by vasculitides (inflammation vessel) and arterial vasospasm

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266
Q

What is atheroma?

A

Same as atherosclerosis

Disease of large and medium sized arteries
Build up of lipid w/ subsequent mural changes
- fatty streaks
- atheromatous plaques

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267
Q

IHD risk factors

A 
Hypertension 
Hyperlipidaemia
Smoking 
DM
Age
Gender
Familial predisposition 
Obesity 
Insufficient exercise
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268
Q

Pathogenesis of IHD

A

Encrustation; platelet thrombi over injured endothelium

Imbibition; low grade inflammation leads to inc. plasma filtration

Reaction to injury; endothelial injury w/ inc. permeability and macro/smooth muscle accumulation

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269
Q

Complications of IHD

A

Ulceration
Fissuring
Haemorrhage
Thrombosis

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270
Q

Epidemiology of IHD

A

M>F
Peak
- M 55-64
- F 70-80

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271
Q

4 Clinical syndromes of IHD

A

Sudden death; unexpected death within 1h cardiac symptoms

Myocardial infarct
Angina
Chronic IHD

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272
Q

Discuss sudden death in IHD

A

Atheroma w/ complicated plaque

Death due to arrhythmias

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273
Q

Compare stable and unstable angina

A

Stable

  • crushing central pain
  • occurs after exercise
  • relieved by rest/vasodilator (GTN)
  • caused by low flow in coronary arteries
  • may result in minor patchy fibrosis
  • usually stable (T1) plaque

Unstable

  • sudden onset
  • increasing intensity
  • unresponsive to rest/vasodilator
  • usually T2 plaque
  • may progress; MI or sudden death
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274
Q

4 types of atheroma plaque

A

T1: static; stays similar/slow growing, predict symptoms
T2: dynamic; changes due to complications

Concentric: narrowed vessel whole way round
Eccentric: large lump on 1 side

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275
Q

3 types of myocardial infarct

A

Regional, transmural
Regional, subendocardial
Circumferential, subendocardial

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276
Q

Discuss regional, transmural MI

A 
Whole thickness of myocardium
Usually T2 plaque w/ thrombosis
90% have arterial occlusion 
Flow often re-established 
Persistent occlusion likely result in fatal outcome
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277
Q

Discuss regional, subendocardial MI

A

Confined inner 1/3 ventricle and well defined area
Rapid lysis of occlusive thrombus
Significant collateral supply to outer ventricle

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278
Q

Discuss circumferential, subendocardial MI

A

Caused by general under-perfusion due to

  • moderate hypotension on background of triple vessel disease
  • severe hypotension and normal vessels
  • other factors; severe anaemia
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279
Q

Macroscopic changes seen in IHD

A 
6-12h inapparent 
12-24h pallor
>24h well defined yellowed, softened area
5-7d red rim
>7d scar tissue
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280
Q

Short term complications IHD

A 
Dysrhythmias/arrhythmia; sudden death
Cardiogenic shock
LVF
DVT
Cardiac rupture; haemopericardium
Papillary muscle failure; mitral regurgitation 
Pericarditis 
Mural thrombosis
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281
Q

Long term complications IHD

A 
LVF
Sudden death/arrhythmia
Aneurysm
Dressler's syndrome
Recurrent infarction
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282
Q

Discuss valvular HD

A

Stenosis

  • failure of valve to open fully preventing forward flow
  • abnormality cusps
  • chronic

Regurgitation

  • failure of valve to close allowing backward flow
  • abnormality cusps or supporting structures
  • acute or chronic
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283
Q

Describe infective endocarditis

A

Colonisation of heart valves by infectious agent
Req. bacteraemia/septicaemia
Immunosuppression predisposes
Clinical: fever, changing heart murmurs

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284
Q

Epidemiology of IE

A

Congenital (esp. small VSD) and rheumatic HD
Artificial valve
Congenital defects: floppy mitral/calcified aortic valve
Neutropenia
Immunodeficiency/suppression
IV drug use

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285
Q

Discuss subacute IE

A 
Background of valvular/CHD
Insidious onset
May recover w/ treatment
Low virulence organisms; S. viridans
Vegetation less bulky, inflammation less destructive
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286
Q

Discuss acute IE

A 
Usually previously normal heart
Virulent organisms: S. aureus, fungi
High mortality 
Mitral>Aortic>>>Tricuspid
Bulky vegetations w/ severe necrotising inflammation
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287
Q

Morphology of IE

A

Friable, bulky, bacteria laden vegetations
Single or multiple
1mm -> cms
May perforate or erode leaflet

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288
Q

Cardiac complications of IE.

A 
Valvular insufficiency or stenosis 
Myocardial abscess
Suppurative pericarditis 
Dehiscence of artificial valve
Emboli of coronary arteries
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289
Q

Systemic embolic complications of IE

A

L: brain, spleen, kidneys
R: lungs, possibly w/ 2ry abscess formation

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290
Q

Renal complications IE

A

Renal infarction or emboli (2ry abscess)

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291
Q

Discuss acute rheumatic fever

A

Recurrent inflammatory disease in childhood
Follows pharyngeal infection by group A strep.
Immunologically mediated, not direct bacterial invasion
Usually resolves
- can lead to chronic valve disease

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292
Q

Symptoms and pathology of acute rheumatic fever

A

Symptoms

  • fever
  • migratory polyarthritis
  • pancreatitis
  • subcutaneous nodules
  • erythema marginatum
  • Sydenham’s chorea

Pathology

  • small, friable vegetations on valves (endocardium)
  • microscopy: Aschoff bodies in myo- and pericardium (small collections of epithelioid macrophages)
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293
Q

Discuss chronic rheumatic fever

A

10y+ after acute

Likelihood inc. w/ early age, severity and no. recurrences

Stenosis; via fibrous scarring or calcification valves w/ bridges b/w commissures
Regurgitation; via fibrous scarring chordae tendinae

Caused by organisation of endocardial inflammation

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294
Q

Discuss congenital HD

A

6-8/1000 live births
Genetic and environmental influences
- drugs
- infections; rubella

Ventricular septal defect 33%
Atrial septal defect 5%

Leads to shunts, obstruction or failure

Risk for IE

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295
Q

4 steps of immune system

A
  1. Immunological recognition (surveillance)
    - detection of infection or damage
    - innate immune cells and lymphocytes (adaptive)
  2. Induction of immune effector functions (activation and specificity)
    - T helper/cytotoxic
    - B cells
  3. Immune regulation
    - induction of Tregs and down-regulating feedback mechanisms (cytokines)
  4. Induction immunological memory
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296
Q

Discuss Ag presenting cells (APC)

A

Highly specialised cells

Process Ag and display peptide fragments on surface w/ molecules req. for T cell activations

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297
Q

3 main APCs

A

Dendritic cell

  • recognise microbial Ag through innate R; pattern recognition receptor recognise pathogen associated molecular pattern
  • found in lymphoid tissue

Macrophages

  • specialise in internalising EC pathogens
  • tissue resident, mature forms in circulation

B cells

  • directly bind some Ag through B cell R
  • Ag specific R allows internalising large amounts Ag

Phagocytic (DC, M) engulf Ag and destroy them in IC compartment (phago-lysosome)

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298
Q

Compare exogenous and endogenous Ag

A

Exogenous: endocytosed by APC via Ag R/Ab/C3b/non-specifically

  • non/self
  • endosome merges w/ lysosome, contents digested by enzymes
  • oligopeptide fragments inserted groove MHC class 2 molecules in endosome wall
  • MHC class 2 + fragments pass to cell surface in vacuole wall, recognised by CD4 T-cell

Endogenous: synthesise within APC

  • self (proteins) or non-self (viruses)
  • proteins manufactured in APC broken up by proteasome in cytoplasm
  • oligopeptide fragments transported in ER, inserted groove MHC class 1
  • MHC class 1 + fragment pass to cell surface in vacuole wall, refinished by CD8 T-cell
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299
Q

Steps in Ag processing and presentation

A

Exogenous Ag recognised by R on APC surface, taken into IC compartments

  • R usually pattern recognition R (PRR); toll-like Rs
  • recognise pathogen associated molecular pattern on microbe surface

Degraded by lysozyme into peptides, bind MHC molecules for presentation to T cells

All Ag processed into peptides before presentation to T cells

B cells express Ab on surface specific for Ag
- bind Ag and internalise immune complex; degrade protein, re-express on surface in binding groove MHC class 2
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300
Q

Discuss role of MHC molecules in Ag recognition

A

MHC molecules bind Ag fragments, express on surface and present to appropriate cells

Class 1: on all nucleated cells

  • present Ag, identify most body cells as self
  • Class 1-Ag complex detected by cytotoxic T cells (CD8+)

Class 2: only on APCs

  • don’t induce Ab production
  • req. for communication w/ B and macrophages
  • class 2-Ag complex detected by helper T cells (CD4+)
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301
Q

Role of CD4 and 8 T-lymphocytes in Ag recognition

A

Actually T cell R that recognises Ag, different for each clone T cell, only recognise Ag bound to MHC

CD4: recognition Ag on MHC class 2 (exogenous Ag)

  • outcomes
  • infected macrophage activated and kill IC bacteria
  • T cell recognise Ag on B; B activated, turn into plasma cell, specific Ab produced

CD8: recognition Ag on MHC class 1 (endogenous Ag)

CD3: signals recognition to interior of T cells

Accessory molecules covey signals important for activation

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302
Q

What cytokines do Th1 and Th2 produce? What are their functions?

A

Th1: IL2
- T cell proliferation

Th2

  • IL4: B-cell activation, IgE switch induces differentiation -> Th2
  • IL5: eosinophil growth and differentiation
  • IL6: TandB differentiation, acute phase protein production, fever
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303
Q

Structure of Ab

A

2 light chains; variable and constant regions
2 heavy chains; variable and constant regions
Hinge; flexibility
Disulphide bond; hold light and heavy together
- position is characteristic of isotope
Variable amounts carb

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304
Q

General functions of Ab (4)

A

Neutralisation: prevent bacterial adherence
Opsonisation: coat bacteria, target for phagocytosis
Complement: enhance opsonisation, lyse some bacteria
Ab dependent cellular toxicity: kill infected cell

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305
Q

Isotypes of Ab

A

IgG: complement activation, placental Ig

IgM: macroglobulin, form pentamers, complement

IgA: dimers, high MWt secreted forms

IgD

IgE: mast cell activation

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306
Q

Compare T in/dependent Ag

A

T independent

  • Ab response doesn’t req. Th
  • many are polysaccharides
  • at high conc.; polyclonal B cell response made, Ab non-specific (IgM)
  • low conc. more specific Ab made

T dependent

  • req. Th
  • switch from IgM to other classes (IgG/A)
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307
Q

Discuss B cell activation signals

A

1st: Ag binds Ag R on B cell

2nd
For TD Ag
- delivered by Th; recognises fragment Ag bound to MHC C2 on surface B
For TI Ag
- deliver Ag itself
— direct binding to innate R (TLR) OR
— extensive cross-linking of membrane IgM

interaction of CD40 and CD40L contributes essential part 2nd signal
B cell carries CD40

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308
Q

Discuss possible fates of activated B cells

A 
Th cells stimulates proliferation through secretion cytokines 
Cytokines drive class switching, proliferation and differentiation B cells

Mutations in variable region affect fate

  • low affinity BCR = apoptosis
  • high affinity BCR = inc. chance activation and survival form plasma or memory cell
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309
Q

Define chronic inflammation

A

Inflammatory response of prolonged ration whose extended time course is provoked by persistence of causative stimulus to inflammation in tissue

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310
Q

When does chronic inflammation arise?

A

From progression of acute if original stimulus persists
After repeated episodes of acute
De novo if causative agent produces only mild acute response

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311
Q

Etiological agents of chronic inflammation

A

Infectious organisms which

  • avoid/resist host defences; TB
  • have ability to persist; due to location, pleural abscess, joint infection

Irritant, non-living foreign material
- in surgical and trauma wounds

Autoimmune: rheumatoid arthritis
Unknown: Crohn’s disease

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312
Q

4 effector cells of chronic inflammation

A

Lymphocytes

  • activate and can be activated by macrophages
  • B: humoral response, prod. Ab
  • T: cytotoxic response, CD8+

Plasma cells: prod. Ab

Macrophages

  • derived from blood monocytes
  • stim. by chemokines and chemotactic agents released by T
  • digest/kill cell, digest ECM, stim. fibroblasts and CT, angiogenesis, recruitment

Fibroblasts

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313
Q

What is granulomatous inflammation?

A

Distinctive chronic inflammation reaction w/ predominant cell activated macrophage

Granuloma: collection of epithelioid macrophages surrounded by lymphocytes and occasionally plasma cells

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314
Q

Describe appearance of granulomatous inflammation

A

Caseating necrosis central sphere
Surrounded by Langhans giant cells and macrophages
Fibroblasts and few lymphocytes on periphery

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315
Q

Examples of granulomatous inflammation

A

Bacterial: TB, leprosy, syphilis, cat-scratch disease
Parasitic: schistosomiasis
Fungal: cyptococcus
Inorganic dusts: silicosis (dust w/ silica)
Unknown: Sarcoidosis, Crohn’s

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316
Q

Discuss autoimmune disorders in relation to chronic inflammation and give 2 examples

A

Occurs when breakdown in tolerance; ability of body to distinguish self and non-self
Often production/presence of Ab to which body reacts

Rheumatoid arthritis

  • associated w/ rheumatoid factors
  • joint destruction and deformity due to chronic inflammatory response in joint synovium

Hashimoto’s Thyroiditis

  • disease of thyroid
  • goitre and hypothyroidism
  • Ab to TSH R in thyroid gland
  • massive chronic inflammatory response within thyroid w/ glandular destruction and endocrine disturbance
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317
Q

Discuss hypersensitivity in relation to chronic inflammation

A

T1: anaphylactic

  • results of IgE in response to allergen
  • release of histamine and inflammatory mediators, subsequent inflammation

T2
- results of circulating Ab attaching to specific body tissues leading to inflammation
- Goodpastures syndrome
— reaction b/w Ab, basement membrane, endothelium of capillaries in glomerulus in kidney and lungs
— chronic inflammation w/ damage to kidney and lungs

T3

  • deposition of Ab-Ag complexes within vessel walls and tissues, subsequent inflammation and tissue damage
  • SLE glomerulopathy due to deposition within glomerulus

T4

  • cell mediated, sensitised T cells
  • stimulate macrophages and other chronic cells
  • TB, rejection of organ grafts
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318
Q

Possible outcomes of chronic inflammation

A

Healing by scarring
Perforation (of ulcer)
Chronicity: recurrent
Depends on local factors, host immune response, persistent disease

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319
Q

Discuss herpes simplex virus and the different types

A

Enveloped, dsDNA

Alpha herpes: HSV1,2 and VZV
Beta herpes: CMV, HHV6,7 and simian herpes 8
Gamma: EBV, HHV8

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320
Q

Causative virus and clinical features primary herpetic gingivostomatitis

A

Causative: HSV1/2

Clinical

  • intraepithelial vesicles rupture; blood, crusted lip, widespread painful ulcers
  • gingiva swollen and erythematous
  • pyrexia, headache
  • cervical lymphadenopathy
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321
Q

Diagnosis and treatment of primary herpetic gingivostomatitis

A

Diagnosis; clinical +

  • isolation, culture HSV
  • serology: 4 fold inc. IgG, presence IgM
  • immunofluorescence, PCR
  • biopsy: multi-nucleated giant cells

Treatment

  • limit contact w/ lips, mouth; red. spread
  • supportive therapy; chlorhexidine, analgesic, soft diet
  • acyclovir; severe, immunocompromised
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322
Q

Discuss herpes labiallis

A

Reactivation HSV (IO reactivation)

Trigger

  • sunlight
  • trauma
  • stress
  • fever
  • malnutrition
  • immunosuppression

Clinical

  • prodrome tingling, burning
  • vesicle ruptures; erosion crust and heal w/o scar

Treatment

  • education; infectivity
  • topical acyclovir red. severity and duration
  • suncream red. recurrence
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323
Q

3 other common HSV viruses

A

Eczema herpeticum
Erythema multiforme
Herpetic whitlow

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324
Q

Discuss chicken pox

A

Causative: varicella zoster virus
Transmission: direct or droplet

Clinical

  • fever
  • maculopapular rash become vesicular then pustular
  • scab
  • itchy skin lesions; successive crops back, chest, abdomen, face, scalp
  • mucous membrane lesions; ulcers w/ erythematous halo hard palate, pillars fauces, uvula
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325
Q

What is shingles? Clinical features, diagnosis, treatment

A

Reactivation VZV

Clinical

  • prodrome: severe pain and parathesia
  • vesicles on erythematous base, scab, heal w/o scar
  • unilateral
  • skin, mucous membrane lesions: max./mand. divisions involved
  • progressive and disseminated in immunocompromised

Diagnosis; clinical +

  • vesicular fluid for VZV and viral culture
  • smear for immunofluorescence
  • specific IgM, inc. IgG

Treatment

  • self limiting
  • supportive therapy
  • high dose acyclovir ASAP
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326
Q

Complication of shingles

A

Post-herpetic neuralgia

Clinical: severe shooting pain or constant burning sensation

Diagnosis: history + clinical

Treatment

  • carbamazepine, phenytoin, gabapentine not effective
  • surgical not effective
  • transcutaneous electric nerve stim. effective some cases
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327
Q

Discuss Ramsay Hunt Syndrome

A

VZV affecting motor nerve; geniculate ganglion of facial nerve

Clinical

  • ipsilateral LMN facial palsy
  • vesicular rash external ear
  • loss of taste ant. 2/3 tongue
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328
Q

What is infectious mononucleosis? Pathogenesis and clinical features

A

Glandular fever caused by Epstein-Barr virus

EBV infect B cell, T react to B and become atypical lymphocytes (Downey cells)
- lymphoid proliferation in blood, spleen, lymph nodes

Clinical

  • lymph node enlargement
  • fever
  • pharyngeal inflammation
  • petechiae in palate
  • gingival bleeding, ulcers
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329
Q

Diagnosis and management infectious mononucleosis

A

Diagnosis

  • EBV serology, IgM to viral capsid Ag
  • +ve monospot slide test

Management

  • supportive; bed rest, antipyretic
  • hospitalisation; severe cases w/ hepatic/splenic involvement
  • NO amoxicillin
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330
Q

3 other diseases caused by Epstein-Barr virus

A 
Burkitt's lymphoma 
Nasopharyngeal carcinoma 
Oral hairy leukoplakia 
- HIV/immunocompromised
- asymptomatic, demarcated corrugated white lesion, flat/plaque-like/papillary-villous 
- clinical + biopsy diagnosis
- improve underlying immunosuppression
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331
Q

Discuss hand, foot and mouth disease

A

Group A coxsackievirus disease
Causative; A16 (4, 5, 9, 10)

Clinical

  • macular and vesicular eruptions hands, feet, mucosa of pharynx, soft palate, buccal sulcus, tongue
  • variable degrees systemic upset
  • resolves 7-10d

Diagnosis; clinical +

  • virus culture; saliva, faeces, vesicle fluid
  • detection Ab

Management

  • self limiting
  • supportive therapy
  • chlorhexidine
  • analgesic
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332
Q

Discuss herpangina

A

Causative; coxsackie A1 2 3 4 5 6 8 10 16 22 B3
Droplet transmission

Clinical

  • malaise, fever, dysphagia, sore throat
  • vesicular eruption soft palate, fauces, tonsils
  • diffuse erythematous pharyngitis
  • release 7-10d

Diagnosis; clinical +

  • back of mouth lesion distribution
  • virus culture
  • detection Ab

Management

  • bed rest
  • antiseptic mouthwash
  • fluid intake
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333
Q

Discuss causative species and clinical features mumps

A

Paramyxoviridae virus

Transmission; direct or droplet

Clinical

  • fever, malaise, headache, chills
  • pre-auricular pain, swelling
  • bilateral; affect parotid and submandibular
  • swelling; 2-3d after onset
  • resolve 10d
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334
Q

Complications, diagnosis, management of mumps

A

Complications

  • meningitis
  • encephalitis
  • transient deafness
  • epididymo-orchitis
  • oophoritis
  • pancreatitis
  • nephritis

Diagnosis; clinical +

  • detection IgM
  • virus culture

Management; rest, fluid, analgesic

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335
Q

Compare verruca vulgaris and condyloma acuminatum

A

Verruca vulgaris; HPV2,4

  • autoinnoculation from fingers
  • white warty lesion w/ granular surface producing cauliflower-like appearance
  • labial and palate mucosa, lingual frenulum

Condyloma acuminatum; HPV6,11,60

  • soft papillary lesion
  • direct contact w/ venereal warts
  • labial and lingual mucosa, multiple lesions
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336
Q

Diagnosis and management of papillomavirus

A

Diagnosis; clinical +

  • histopathology
  • immunostaining detect HPV

Management
- excision

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337
Q

Predisposing, clinical features, diagnosis and management pseudomembranous candidosis

A

Predisposing

  • infant, elderly
  • Fe deficiency
  • HIV
  • AB/steroid therapy

Clinical

  • soft creamy-yellow patches, wiped off
  • erythematous mucosa

Diagnosis; smear for microscopy, swab for culture

Management

  • eradicate predisposing
  • antifungal; polyene, azoles
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338
Q

Discuss chronic hyperplastic candidosis

A

Predisposing; tobacco + same as pseudomembranous candidosis
Clinical: thickened, irregular, smooth white plaques @ commissures and dorsum tongue

Diagnosis

  • histopathology; candidal hyphae within keratin layers hyperplastic epithelium
  • chronic inflammatory infiltrate

Management

  • red. predisposing
  • antifungal, surgery, cryotherapy, laser
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339
Q

Compare acute and chronic erythematous candidosis

A

Acute
Predisposing; systemic AB, inhaled steroid, immunosuppression
Clinical; painful red areas oral mucosa
Diagnosis; smear microscopy, swab culture
Management
- predisposing; stop AB, rinse mouth after inhaler
- antifungal

Chronic
Predisposing; denture
Clinical; erythematous mucosa w/ margins corresponding periphery appliance
Diagnosis; smear, swab mucosa and appliance
Management
- appliance hygiene; mechanical cleaning, soak antiseptic
- remove appliance at night
- antifungal

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340
Q

Discuss median rhomboid glossitis

A

Clinical; smooth, well demarcated erythematous area b/w ant. 2/3 and post. 1/3 tongue

Diagnosis; microscopy and culture

Management
- predisposing, antifungal

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341
Q

Discuss angular cheilitis

A

Causative; candida, staphylococcus, streptococcus

Clinical; erythema and yellow crusting corner/s mouth

Management

  • eradication reservoir microorganism
  • antifungal or antistaphylococcus
  • investigation underlying cause; DM, hematinic deficiency
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342
Q

Discuss chronic mucocutaneous candidiasis

A

Rare group disorders characterised by persistent superficial candidal infection of mucosal surfaces, skin and nails
Oral lesions resemble chronic hyperplastic candidosis

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343
Q

Anatomy of lower GIT

A

Small intestine; digestion and absorption

  • duodenum
  • jejunum
  • ileum

Large intestine; recovery H2O, electrolytes and formation, storage, expulsion faeces

  • colon
  • ascending, transverse, descending segments

Rectum, anus

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344
Q

Common diseases of small intestine

A

Coeliac

Crohn’s

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345
Q

Features of malabsorption

A 
Diarrhoea or steatorrhoea (fatty stools)
Abdominal discomfort/pain
Nutritional deficiencies
- weight loss
- failure to thrive
- anaemia
- lassitude
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346
Q

Clinical features and causes steatorrhoea

A

Clinical

  • bulky stool
  • float
  • greasy/fatty/frothy
  • foul smell
  • difficult to flush

Causes

  • Coeliac/Crohn’s
  • CF
  • pancreatitis/cancer
  • liver disease
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347
Q

What is Coeliac disease?

A

Gluten sensitive enteropathy, non-tropical sprue
Strong genetic background
Permanent intolerance/hypersensitivity/toxic reaction to alpha-gliadin component of gluten

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348
Q

Clinical findings of coeliac disease

A

Dental hypoplasia

  • enamel defects obvious: symmetrically and chronologically distributed
  • mostly mild; rough surface w/ horizontal grooves or shallow pits

Villous atrophy (malabsorption)

  • glossitis, burning mouth
  • angular cheilitis
  • tiredness
  • malaise
  • easy bruising

Inflammation

  • crampy abdominal pain
  • bloating

Steatorrhoea
Weight loss
RAS
Exacerbation LP

Assoaciacted autoimmune disease: Sjogrens, DM
Malignant disease: oesophageal + oropharyngeal SCC, NHL, small novel adenocarcinoma

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349
Q

Investigations for Coeliac disease

A 
FBC: anaemia
Haematinics screen: low B12, folate, Fe
Stool examination; excess fat
Serology; detect
- anti-gliadin and anti-endomysial Ab
- tissue transglutaminase
Endoscopy: villous atrophy
SI biopsy (gold standard): villous atrophy

Repeat after 3mnth GFD

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350
Q

Associated diseases of Coeliac disease

A

Dermatitis herpetiformis
Linear IgA disease
Selective IgA deficiency

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351
Q

Discuss management of Coeliac disease

A

GFD for life only treatment

  • substitute wheat flour w/ potato, rice, soy flour
  • GF bread, pasta, pastries
  • GF beer, lager

Correct nutritional deficiencies: B12, Ca, folate

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352
Q

Dental relevance Coeliac disease

A

Anaemia may predispose
Untreated pt may have bleeding tendencies
May complicate GA

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353
Q

Clinical features of Crohn’s on mouth region

A 
Perio-oral and lip swelling
RAS
Angular stomatitis 
Mucosa tags or cobble-stoning of mucosa
Atypical ulcers; large, linear, ragged
Lesions associated w/ nutritional deficiencies
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354
Q

Clinical features Crohn’s of SI area

A

Abdominal pain; pancreatitis
Abnormal bowel habits; constipation, diarrhoea
Weight loss
Malabsorption

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355
Q

Clinical feature Crohn’s of LI

A

Non-bloody diarrhoea >6wk
Bleeding and pain released to defecation
Intestinal obstruction due to stricturing disease

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356
Q

Clinical features Crohn’s disease of perianal area

A

Anal tags
Anal fistulae, fissure
Anal abscess formation

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357
Q

Extra-intestinal feature Crohn’s disease

A

Musculoskeletal

  • arthritis
  • ankylosing spondylitis

Skin

  • erythema nodosum
  • psoriasis
  • pyoderma gangrenosum
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358
Q

Investigation for Crohn’s disease

A

FBC: anaemia, microcytosis, thrombocytopenia
Inflammatory markers: inc. erythrocytes sedimentation rate, C-reactive protein
Haematinic screen: dec. folate, ferritin, Fe, B12, K, Zn
Faecal calprotectin inc.
Stool microscopy; exclude infective diarrhoea

Radiological

  • lower GI endoscopy: sigmoidoscopy/colonoscopy
  • MRI and CT scanning
  • barium follow through

Histological
- mucosal biopsies; non-caesating granuloma

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359
Q

Management of Crohn’s in 1ry and 2ry care

A

1ry: refer adult pt <40 w/
- diarrhoea >6wk
- abdominal pain w/ weight loss
- raised faecal calprotectin
- unexplained vit B12, folate deficiencies

2ry: individualised

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360
Q

Management of Crohn’s

A

Diet: exclude offending substance
- benzoates/cinnamonaldehyde, E-preservatives

Life: smoking, stress, exercise, balanced diet, well hydrated

Correct nutritional deficiencies

Anti-inflammatory drugs: sulfasalazine, mesalazine
Immunomodulators: prednisolone, methotrexate, azathioprine

Biological therapy: anti-TNFalpha; infliximab, Adalimumab

Surgery: drain abscess, repair fistulae and fissures

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361
Q

Dental relevance of Crohn’s

A

Stress can precipitate acute flare-up; min. stress
Avoid AB for oral infections which can aggravate diarrhoea
Evaluate history steroid use esp. major dentistry indicated
Delay routine dentistry during flare-up

Oro-facial granulomatosis May precede GI manifestations

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362
Q

What is ulcerative colitis?

A

Diffuse inflammation superficial layers of colon mucosa
Affect part or whole of LI
Clinical course ranges from persistent to relapsing and remitting

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363
Q

Clinical features ulcerative colitis

A

Abdominal pain
Bloody diarrhoea
Pus
Intermixed mucus w/ or w/o systemic toxicity

Systemic toxicity

  • fever
  • anorexia, weight loss
  • anaemia
  • inc. ESR, CRP
Joint pain
Conjunctivitis 
Finger clubbing
Erythema nodosum
Pyoderma gangrenosum
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364
Q

Investigations and management ulcerative colitis, complications

A

Investigations and management
- similar to Crohn’s, focus on colon

Complications

  • carcinoma of colon
  • inc. risk if early onset or chronic disease (>10y)
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365
Q

Discuss pseudomembranous colitis

A

Occurs after high dose or prolonged oral AB use
Elderly or debilitated pt most at risk
Lincomycin and clindamycin commonly implicated
Associated w/ proliferation Clositridum difficille
Manifests as painful diarrhoea and mucus passage in stool
Treatment: oral metronidazole or vancomycin

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366
Q

What is IBS? Discuss aetiology and clinical findings

A

Functional bowed disorders

Aetiology; unknown

  • infection
  • stressful life event
  • anxious personality

Clinical; usually look healthy

  • crampy abdominal pain relieved by defecation or flatulence
  • bloating or abdominal distension
  • altered bowel habits
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367
Q

Discuss management and dental aspect IBS

A

Management

  • reassurance
  • stress relieve
  • high fibre diet
  • anti-spasmodics; mebeverine
  • CBT
  • antidepressants

Dental; psychogenic oral symptoms

  • burning mouth
  • persistent idiopathic facial pain
  • sore tongue
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368
Q

Discuss Peutz-Jegher’s Syndrome

A 
Autosomal dominant conditions 
Characterised by
Mucocutaneous hyperpigmentation
- macules on lips and B mucosa 
- occasionally macules circumorally
GI hamartomatous polyps

Complications

  • intestinal obstruction
  • abdominal pain
  • GI bleeding
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369
Q

Define antimicrobial, antibiotic, bactericidal, bacteriostatic

A

Antimicrobial: drug w/ activity against microorganism
- anti-bacterial/fungal/viral/parasitic

AB: chemical compound made by microorganism that inhibits/kills other microorganism at low conc.; doesn’t include synthetic agents

Bactericidal: kill bacteria
Bacteriostatic: inhibit growth

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370
Q

8 features of idea antimicrobial

A
  1. Selective toxicity against microbial target
  2. Minimal toxicity to host
  3. Cidal activity
  4. Long plasma half life
  5. Low binding to plasma protein
  6. Good tissue distribution
  7. Oral and parenteral preparations
  8. No adverse interactions w/ other drugs
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371
Q

Discuss mechanisms of action and resistance of antimicrobials

A 
Action
- inhibit synthesis 
— cell wall
— nuclei acid
— folate
— protein 
- disruption of cytoplasmic membrane 
Resistance
- production enzymes
— beta-lactamases, aminoglycoside-modifying, chloramphenicol acetyl transferase 
- alteration
— outer membrane permeability 
— target sites; penicillin binding protein
— metabolic pathway 
- efflux pumps
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372
Q

4 principles of antimicrobial stewardship

A
  1. Promotes appropriate use of antimicrobials
  2. Improve pt outcomes
  3. Red. microbial resistance
  4. Dec. spread of infections by multi-drug-resistant organisms
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373
Q

5 common groups of antibacterials in dentistry

A
  1. Penicillins
  2. Macrolides
  3. Lincosamides
  4. Tetracyclines
  5. Nitroimidazoles
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374
Q

6 groups of penicillin

A
  1. Benzylpenicillin
  2. Orally absorbed; penicillin V
  3. Anti-staphylococcal; floxacillin
  4. Extended spectrum; amoxicillin
  5. Anti-pseudomonal; ticracillin
  6. Beta-lactamase-resistant
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375
Q

Mechanism of action and resistance of penicillins

A

Action
- inhibit cell wall synthesis
— bind PBP
— inhibit transpeptidation of peptidoglycan

Resistance

  • Beta-lactamases
  • failure to penetrate outer membrane gram-
  • efflux
  • low affinity binding to target PBP
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376
Q

Discuss side effects penicillins

A

Allergic reaction: anaphylactic reaction, hypersensitivity
GI: diarrhoea, enterocolitis
HA, neutropenia, thrombocytopenia
Renal: interstitial nephritis, Haemorrhagic cystitis
CNS: encephalopathy, seizures

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377
Q

Common macrolides

A

Erythromycin
Clarithromycin
Azithromycin

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378
Q

Mechanism of action and resistance, activity of macrolides

A

Action

  • inhibit RNA-dependent protein synthesis (50S)
  • bacteriostatic

Resistance

  • dec. outer membrane permeability
  • efflux
  • alteration RNA
  • enzymatic inactivation by phosphotransferases

Activity

  • gram+
  • mycoplasma
  • legionella
  • chlamydia
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379
Q

Side effects macrolides

A 
GIT symptoms
Skin rash
Fever
Eosinophilia 
Cholestatic jaundice
Transient hearing loss
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380
Q

Mechanism of action and resistance, activity of lincosamides

A

Action
- inhibit RNA-dependent protein synthesis (50S)

Resistance

  • dec. outer membrane permeability
  • alteration rRNA and 50S ribosomal proteins of R sites
  • inactivation by transferase

Activity

  • gram+
  • anaerobes
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381
Q

Common lincosamides

A

Clindamycin

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382
Q

Side effect lincosamides

A

C. difficile colitis
Allergic reaction
Transient hepatitis
Neutropenia, thrombocytopenia

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383
Q

Common tetracyclines

A

1st gen

  • tetracycline
  • chlortetracycline
  • oxytetracycline

2nd
- doxycycline

3rd
- tigecycline

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384
Q

Mechanism of action and resistance, activity of tetracyclines

A

Action

  • inhibit bacterial protein synthesis (30S)
  • bacteriostatic

Resistance

  • efflux
  • ribosomal protection protein
  • enzymatic inactivation

Activity; broad spectrum; gram+/-, IC organisms

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385
Q

Side effects tetracyclines

A 
GIT symptoms 
Allergic reaction
Photosensitivity 
Pigmentation; skin, nail, sclera
Deposition in growing bone and teeth
Hepatotoxicity 
Exacerbate renal impairment 
Superinfection
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386
Q

Common nitroimidazoles

A

Metronidazole

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387
Q

Mechanism of action and resistance, activity metronidazole

A

Action
- interact w/ nuclei acids and proteins causing breakage, destabilisation, cell death

Resistance: rare

Activity: anaerobes, facultative anaerobes, Protozoa

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388
Q

Side effect nitroimidazoles

A 
Metallic taste
GIT symptoms
Peripheral neuropathy 
Disulfiram-like reaction w/ alcohol
- nausea, vomiting, flushing, tachycardia, hypotension, confusion
Allergic reaction
Genitourinary: dark urine, dysuria, cystitis, incontinence 
Inc. effect warfarin
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389
Q

2 families of common antifungals

A

Polyenes

Azoles

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390
Q

Common polyenes

A

Amphotericin (IV)

Nystatin (oral)

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391
Q

Discuss polyenes

A

Action

  • interact w/ ergosterol, form transmembrane ion channel
  • inc. membrane permeability; cell contents leak, cell death

Resistance

  • intrinsic such as in dermatophytes
  • acquired rare

Selective action on fungi, human sterol = cholesterol

Nystatin used only topically on skin, mucous membranes

Side effects (amphotericin)

  • anaphylaxis
  • nephrotoxicity
  • GIT upset
  • muscle and joint pain
  • pain
  • anaemia
  • CV toxicity
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392
Q

2 groups of azoles

A

Imidazoles

  • ketoconazole
  • miconazole
  • clotimazole

Tiazoles

  • itraconazole
  • fluconazole
  • voriconazole
  • posaconazole
  • ravuconazole
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393
Q

Discuss azoles

A

Action: inhibit synthesis ergosterol

Ketoconazole associated w/ fatal hepatotoxicity
Imidazoles contraindicated in hepatic impairment, pregnancy, breast feeding

Fluconazole

  • cause abnormal LFT
  • dose red. in renal impairment
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394
Q

5 targets for antivirals

A
  1. Attachment
  2. Entry
  3. Uncoating
    - amantadine, rimantadine for influenza
  4. Nucleic acid synthesis
    - nucleoside analogues
    - non-nucleoside polymerase inhibitors
    - non-nucleoside reverse transcriptase inhibitors
  5. Assembly and release
    - protease and neuraminidase inhibitors
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395
Q

Discuss acyclovir

A

Effective against HSV, VZV

Resistance

  • associated w/ red. thymidine kinase activity
  • rare in immunocompetent pt
Side effects
- skin irritation topically
- high dose IV
— nephrotoxicity 
— GIT disturbance 
— confusion 
— hallucinations
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396
Q

General characteristics of staphylococcus genus

A

Gram+ cocci, arranged in grape-like clusters
Non-motile, non spore forming, catalase+
0.5-1.0 micron diameter
An/aerobic metabolism
Resistant dry conditions and high salt conc.
Mainly found skin and mucous membranes

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397
Q

Classification of staphylococci

A

Coagulase+

  • aureus
  • aureus var. anaerobius
  • delphini
  • intermedius

Coagulase-

  • epidermidis
  • haemolyticus
  • lugdunensis
  • saprophyticus
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398
Q

4 main diagnostic features of S. aureus

A
  1. Colonies pigmented: carotenoid pigments; golden-yellow, fawn, cream
  2. Prod. EC coagulase (coagulase+)
  3. Prod. nucleases that break down DNA (DNase+)
  4. Prod. cell surface-associated enzyme; clumping factor or bound coagulase
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399
Q

Common infections caused by S. aureus

A

Pyogenic (pus producing)

  • boils, carbuncles
  • abscesses
  • wound (surgical) infection
  • septicaemia
  • endocarditis
  • osteomyelitis
  • impetigo
  • mastitis
  • pneumonia

Toxin-mediated

  • scaled skim syndrome
  • pemphigus neonatorum
  • toxic shock syndrome
  • food poisoning
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400
Q

Pathogenesis of S. aureus

A

Opportunistic pathogen

  • lowered host resistance
  • damaged skin/mucous membranes
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401
Q

Discuss enterotoxins/pyrogens exotoxins and epidermolytic toxins/exfoliatins in relation to S. aureus

A

Toxins produced by S. aureus

Enterotoxins/pyrogenic exotoxins (super Ag)

  • heat stable proteins; induce nausea, vomiting, diarrhoea
  • most commonly contaminated food; meats, custard filled pastries, ice cream, potato salad

Epidermolytic toxins/exfoliatins

  • A and B toxins cause blistering disease
  • pemphigus neonatorum; distended blisters
  • impetigo; flattened blisters
  • scalded skin syndrome; extensive area skin lost
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402
Q

Discuss toxic shock syndrome toxin in relation S. aureus

A

TSST-1

Causes toxic shock syndrome
Associated w/ highly absorbent tampons

Vaginal colonisation w/ S. aureus; multiplication and toxin production

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403
Q

Discuss haemolysins and Panton-Valentine Leucocidin in relation to S. aureus

A

Toxins produced by S. aureus

Haemolysins; alpha, beta, gamma, delta

  • cytotoxic: lysis RBC, phagocytic and tissue cells
  • alpha: skin infections; dermonecrotic

Panton-Valentine Leucocidin

  • destroys WBC; inc. resistance to phagocytosis
  • associated w/ community acquired MRSA
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404
Q

Discuss hyaluronidase and other enzymes in relation to S. aureus virulence

A

Hyaluronidase (spreading factor)
- break down IC ground substance (hyaluronic acid) of tissues

Other

  • lipases
  • proteases
  • coagulases
  • DNase
  • phosphatases
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405
Q

Discuss the other virulence factors of S. aureus

A

Cell wall polymers

  • peptidoglycan: inhibit inflammatory response
  • lipoteichoic acid: interact w/ toll-like Rs

Cell surface protein

  • protein A: reacts w/ Fc region IgG
  • clumping factor: binds fibrinogen
  • fibronectin-binding protein: binds fibronectin
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406
Q

Discuss epidemiology of Staphylococcal infections

A

Sources

  • infected lesions; pus, dried exudate discharge from wound
  • carriers; spread from carriage site (nose, moist skin)
  • animals

Modes

  • exogenous; outside source
  • endogenous; carriage site; nose, minor lesions

Cross infection

  • closed communities; hospitals
  • direct contact, air-borne dust and droplet nuclei
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407
Q

Discuss diagnosis of staphylococcal infections

A

Pus from abscesses, wounds, burns
Sputum from pneumonia cases
Faeces/vomit suspected food poisoning
Blood suspected bacteraemia; septic shock, osteomyelitis, endocarditis
Mid-stream urine suspected cystitis, pyelonephritis
Ant. nasal/perineal swabs

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408
Q

Discuss AB resistance in staphylococcus and methods to over come

A
  1. Prod. penicillinase (Beta-lactamase)
    - inactivate by opening beta-lactam ring
    - methicillin, cloxacillin stable to penicillinase
  2. Mutation PBP in bacterial cell envelope
    - mecA gene encodes mutant PBP; PBP2a low affinity beta-lactam AB
  3. Glycopeptide resistant (vancomycin, teicoplanin)
    - transfer of vanA coding for glycopeptide resistance
    - glycopeptide-intermediate S. aureus; thickened cell wall

Combination of 2 streptogramins (Synercid) and linezolids

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409
Q

Discuss methicillin resistant S. aureus (MRSA)

A

Resistant: all Beta-lactam AB, gentamicin, erythromycin, tetracycline
Strains resistant to vancomycin
Synercid now approved when fail respond to vancomycin

Predominantly hospital pathogens in debilitated pt esp. ICU
- multiple courses AB and invasive devices
Problem in community; Long-stay institutions

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410
Q

Characteristics of coagulase- staphylococci

A 
Morphologically similar to S. aureus 
Often non-pigmented
DNase-
Majority carry coagulase- staph. as normal skin flora
Normally don’t cause infection 
Infect pt w/ defective resistance; colonising implants
- CSF shunts
- IV lines and cannulae 
- cardiac valves
- pacemakers
- artificial joints
- vascular graft
- catheters
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411
Q

Infections caused by coagulase- staph.

A 
Infected prostheses, implants
Ventriculitis; shunt associated
Peritonitis 
Septicaemia 
Endocarditis; prosthetic valve
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412
Q

Discuss pathogenesis and treatment of coagulase- staph.

A

Pathogenesis

  • few known virulence factors
  • form adherent biofilms on surface polymers used for implants/prostheses

Treatment

  • resistant: penicillin, penicillinase-resistant penicillins, gentamicin, erythromycin, chloramphenicol
  • vancomycin resistance rare
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413
Q

Discuss fungi and mycoses

A

Fungi

  • diverse group eukaryotes
  • moulds: branching filaments (hyphae) form interwoven mass, sores
  • yeasts: budding
  • dimorphic fungi: mycelial or yeast phase depending on growth conditions

Mycoses

  • mostly moulds; some yeasts, many dimorphic
  • highly pathogenic: Histoplasma capsilatum
  • opportunistic: Candida and Aspergillus spp.
  • form and severity depend on degree exposure, site and method entry, level immunocompetence
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414
Q

3 types of mycoses

A
  1. Superficial mycoses
  2. Subcutaneous
  3. Systemic
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415
Q

Discuss superficial mycoses

A

Skin, hair, nail, mucous membranes

Ringworm: complex of disease caused by moulds
Dermatophytes: affect keratinous tissues (stratum corneum), colonise and digest keratin
Yeast: Candida spp. (esp. C. albicans); generally endogenous can be sexually transmitted

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416
Q

Discuss subcutaneous and systemic mycoses

A

Subcutaneous

  • involve skin: subcutaneous tissues and bone
  • slow, localised spread
  • mainly tropical regions; mycetoma, sporotrichosis

Systemic

  • inhalation airborne mould spores
  • mainly Americas: blastomycosis, histoplasmosis
  • opportunistic pathogen more widespread
  • immunocompromised
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417
Q

Discuss diagnosis and treatment of mycoses

A

Diagnosis

  • clinical observation + lab investigations
  • microscopy, isolation of causal fungus in culture, serological tests

Treatment

  • most antifungals act on sterol components of cell membrane
  • wide variation in activity
  • most for topical use; few administered systemically
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418
Q

Discuss ringworm

A

Superficial mycoses

Scalp and feet
3 genera dermatophytes 
- Trichoohyton
- Microsporum
- Epidermophyton

Peeling/trauma epidermis probably necessary for infections
- irritation, erythema, oedema, some vesiculation

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419
Q

Discuss superficial candidiasis

A

Candida spp. commensals 50% popn.
Carriage rate inc. w/ age and pregnancy
Overgrowth and infection: normal micro flora altered or resistance lowered

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420
Q

Discuss acute pseudomembranous and chronic mucocutaneous candidiasis

A

Acute pseudomembranous

  • new-born, elderly/debilitated, immunocompromised
  • white plaques become confluent to form pseudomembrane

Chronic mucocutaneous
- rare condition esp. children and elderly

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421
Q

Discuss acute atrophic and chronic atrophic candidiasis

A

Acute atrophic
- use of broad spectrum AB allows yeast overgrowth
— tongue and cheek mucosa become thin, inflamed

Chronic atrophic
- red, inflamed, swollen mucosa under denture

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422
Q

Discuss chronic hyperplastic candidiasis and angular cheilitis

A

Chronic hyperplastic candidiasis
- leukoplakia
— thickened epithelium penetrated by C. albicans hyphae

Angular cheilitis
- eroded condition of angle(s) of mouth

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423
Q

6 predisposing factors for oral candidiasis

A
  1. Local: trauma, occlusion, maceration
  2. Saliva: xerostomia, Sjögren’s syndrome, radiotherapy, cytotoxic therapy
  3. Diet: high carb
  4. Physiological: young, elderly
  5. Hormonal: DM, hypothyroidism, hyperparathyroidism, hypoadrenocorticism
  6. Nutrition: hypovitsminosis, Fe deficiency, malnutrition
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424
Q

Discuss vaginal candidiasis and skin infections

A

Superficial mycoses

Vaginal candidiasis

  • white lesion on epithelium vulva, vagina, cervix
  • itching, soreness, white discharge

Skin infection

  • moist sites: axillae, groin, perineum, submammary folds
  • napkin dermatitis in infants
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425
Q

Discuss systemic candidiasis

A

May be localised
- urinary tract, liver, endocarditis, meninges, peritoneal cavity
Or widely disseminated
- septicaemia
Usually follows overgrowth commensals yeast (C. albicans) in association w/ serious abnormality of host

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426
Q

Discuss actinomyces

A

Branching gram+ rod-shaped filamentous bacteria
Facultative anaerobes

Most spp. commensals mouth
- cause actinomycosis

Species

  • israelii; actinomycosis
  • meyeri, naeslundii, odontolyticus; rarely cause actinomycosis
  • odontolyticus; isolated from deep caries
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427
Q

Clinical features actinomycosis

A

Chronic infection
Multiple abscesses dam granulomas
Tissue destruction, extensive fibrosis, formation sinuses

Actinomycetes form mycelia embedded in protein/polysaccharide matrix and surrounded by zone gram-

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428
Q

Discuss diagnosis and treatment actinomycosis

A

Diagnosis

  • crushed sulphur granules stained reveal gram+ mycelia and zone acid-fast clubs
  • fluorescent antiserum, culture, biochemical test
Treatment
- sensitive to AB
— penicillin or tetracycline
- penetration of drugs into fibrotic disease tissue poor
- surgical debridement
— red. scarring/deformity
—hasten healing
— dec. recurrence
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429
Q

Discuss the mucosal immune system

A

Exposure to environment; constant exposure to foreign matter
- constant antigenic challenge
Large SA specialised for absorption
Resident microflora parent at most mucosal epithelial
Main route of entry for infectious microorganism

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430
Q

Compare systemic and mucosal immune system

A

Systemic: largely sterile environment, vigorous reposts to microbial invasion

Mucosal: constant exposure

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431
Q

5 factors that contribute to OC health (Immunology)

A
  1. Integrity of oral mucosa
  2. Lymphoid tissue
  3. Saliva
  4. GCF
  5. Humoral and cellular immunity
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432
Q

Discuss non-specific defence mechanisms in OC

A

pH (5.7-7); varies b/w individuals, within individuals
Temp.; variation depending on foods/drinks
Saliva; nutrient source but poor culture medium
- organic nutrients
- proteins, carbs, vitamins
- antibacterial substances
- lysozyme, lactoperoxidse (kills bacteria in reaction involving Cl-, H2O2)

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433
Q

Discuss 3 physical barrier factors of mucosal barrier in OC (non-specific defence)

A

Adherent mucin layer

  • sticky slipper gel; allows transit of nutrients, not bacterial products or toxins
  • secreted constantly from salivary glands
  • effective in trapping bacteria for prolonged exposure to hot antibacterial substances

Desquamation

  • shedding of cells
  • rate related to microbial burden

Epithelial Ab R
- secretory component R on B epithelium, anchor SIgA/bacteria complexes then shed w/ cells

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434
Q

Discuss innate cells of OC immunity

A

Phagocytise

  • macrophages; mature monocytes leave circulation
  • neutrophils; short lived, not in healthy tissues

NK; recognise cells infected by virus

  • activated by cytokines secreted by macrophages or in response to interferon
  • infected cell killed when perforin insert into membrane
  • form pores and granzymes enter infect cell, induce apoptosis

Dendritic

  • Langerhans, Interdigitating, Follicular dendritic
  • recognition microbial Ag through innate R
  • process and present Ag to T
  • follicular in specialised areas lymph nodes, present un-modified Ag to B cells
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435
Q

Discuss 7 innate molecules of OC immunity

A

TLR

  • expressed on oral epithelium
  • pattern recognition Rs recognise PAMP

Agglutinin; from complexes w/ SIgA
Histatins; neutralisation toxins, chelation, protease and cytokine inhibition
Cystatins; cysteine protease inhibition
Lysozyme; destroy outer surface bacteria
Peroxidases; bactericidal
Lactoferrin; bacteriostatic due to Fe deprivation

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436
Q

7 antimicrobial substances of saliva

A
  1. SIgA; inhibit adherence, agglutinates, virus neutralisation
  2. Lactoferrin
  3. Lysozyme
  4. Agglutinins
  5. Myeloperoxidase
  6. Salivary peroxidase
  7. Leukocytes
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437
Q

Discuss mechanism of action of OC Ab

A

Both

  • virus neutralisation
  • enzyme and toxin neutralisation
  • inhibit adherence
  • agglutination

IgG

  • complement activation
  • opsonisation

SIgA

  • immune exclusion
  • IC neutralisation
  • virus excretion
  • interact w/ non-specific factors; lysozyme, lactoferrin, peroxidases
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438
Q

Briefly outline non/specific factors of OC immunity

A

Non-specific

  • mucosal barrier
  • innate cells (macrophages, neutrophils, NK, DC)
  • innate molecules; histatins, lysozyme, cystatins, peroxidases, lactoferrin

Specific

  • SIgA
  • IgG, IgM
  • effector T cells
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439
Q

4 functions of kidneys

A

Excretion of metabolites and drugs
Regulation normal body fluid vols. and electrolyte balance
Regulation acid-base balance
Endocrine functions

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440
Q

Discuss pre-renal, renal and post-renal factors causing acute renal failure

A

Pre-renal

  • hypotension: haemorrhage/severe burns
  • renal thrombosis
  • sepsis
  • drugs causing shutdown: NSAIDs, ACEIs

Renal

  • ABs: gentamicin, amphotericin
  • analgesic OD: aspirin, NSAIDs, paracetamol
  • multiple organ failures
  • interstitial nephritis

Post-renal: obstruction urine flow

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441
Q

Discuss chronic renal disease

A

Not specific as several causes
Characterised: kidney damage, red, GFR for 3/+ mnths
Result: progressive loss kidney function through 5 stages (early, mild, moderate, severe, end-stage)

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442
Q

Discuss common and rare causes of chronic renal disease

A

Common

  • longstanding hypertension
  • DM
  • chronic pyelonephritis
  • chronic glomerulonephritis
  • polycystic renal disease
  • urinary tract obstruction
  • renal artery stenosis

Rare

  • SLE
  • amyloid
  • multiple myeloma
  • gout
  • Pb poisoning
  • long term drug: analgesic, gold, penicillamine, cyclosporine
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443
Q

When do symptoms of CRD manifest?

A

Kidney function <25%

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444
Q

Discuss blood and immune symptoms of CRD

A

Anaemia: toxic suppression bone marrow/dec. erythropoietin
Purpura/bleeding tendency: abnormal platelet prod./defective vWF/dec. thromboxane
Lymohopenia: infection susceptibility

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445
Q

Discuss the GI and metabolic symptoms of CRD

A

GI

  • anorexia
  • nausea, vomiting

Metabolic

  • inc. nitrogenous compounds: azotemia/uraemia
  • renal osteodystrophy: PO retention -> dec. plasma Ca2+ -> inc. PTH activity
  • active vitD deficiency
  • polyuria, polydipsia, glycosuria
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446
Q

Discuss neuromuscular symptoms of CRD

A 
Headaches
Confusion 
Sensory disturbances
Tremors
Peripheral neuropathy
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447
Q

Discuss CV symptoms CRD

A

Hypertension
Congestive heart disease
Atheroma
Peripheral vascular disease

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448
Q

Discuss skin features of CRD

A

Pruritus
Bruising
Infection

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449
Q

Discuss special investigations for diagnosing CRD

A

Urine: red/white cell casts, urate crystals
RBC
- red. RBC; anaemia
- impaired platelet function; inc. bleeding time

Biochemistry

  • inc. urea, creatinine
  • inc. K+, metabolic acidosis
  • inc. PO43- -> dec. Ca2+ -> inc. PTH

Ultrasound: size, obstruction

Biopsy

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450
Q

Discuss general management of CRD

A

Aim: slow down/halt progression to end-stage

Anaemia: erythropoietin (epoietin)
Hypertension: ACEI (captopril)
Fluid retention; diuretics (furosemide)
Hyperohosohataemia: CaCO3
Hypocalcaemia: Ca2+ supplement/VitD3
Metabolic acidosis: NaHCO3
CV risk: aspirin, statins, smoking cessation
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451
Q

Discuss peritoneal dialysis and haemodialysis

A

Peritoneal

  • peritoneal membrane act as natural semi-permeable membrane
  • less efficient haemodialysis, carried out more freq.
  • relatively easy, carried out @ home
  • travel w/: continuous ambulatory peritoneal fistula

Haemodialysis

  • vascular access for introduction of infusion lines; arteriovenous fistulas
  • pt dialysed 3x/wk for 3hr each session
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452
Q

Discuss renal transplantation

A

Indicated suitable pt w/ end stage CRD
1st choice children, pt w/ diabetic nephropathy
Transplanted kidney usually sited in right iliac fossa
Req. lifelong immunosuppressant (cyclosporine, azathioprine, corticosteroid)

Complications

  • rejection
  • immunosuppression induced infection/malignancy
  • inc. risk ischaemic heart disease
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453
Q

Dental relevance of general renal disease pt

A

Treatment best day after dialysis; heparin worn off, max. benefit form dialysis
Ensure careful haemostasis during surgical procedure
Odontogenic infection treated vigorously
Prescription drugs excreted by kidney adjusted post consultation w/ renal physician
Avoid
- systemic fluorides
- aspirin, NSAIDs
LA safe unless severe bleeding tendency

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454
Q

Dental relevance of haemodialysis CRD pt

A 
Haemodialysis can predispose BBV; hepB/C
IV cannulation or taking blood
- avoid arteriovenous fistulas arm min. risk
— fistula infection
— thrombophlebitis
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455
Q

Discuss dental relevance of renal osteodystrophy

A

Loss of lamina dura on X-ray
Brown tumours on gingiva
Osteomalacia

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456
Q

Dental relevance of kidney transplant pt

A

Pt taking steroids may need steroid cover for stressful procedure
More susceptible to infection; treat before transplant
- carefully monitor and aggressively treat infections
Cyclosporine; inc. risk gingival hyperplasia
Inc. risk opportunistic infection (TB)

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457
Q

Discuss symptoms and clinical feature of nephrotic syndrome

A

Glomerular damage

  • massive proteinuria
  • hypoalbuminaemia
  • hypercholesterolaemia

Clinical

  • facial oedema, ascites
  • predisposed to infections w/ S. pneumoniae, H. influenzae; loss IgG urine
  • loss cholecalciferol binding protein -> vitD deficiency
  • loss antithrombin 3, inc. CF -> hypercoagukability -> thrombosis

Long term corticosteroid therapy problematic

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458
Q

General characteristics of streptococci

A 
Gram+, chain-forming cocci
1.0microm diameter
Facultative anaerobes 
Catalase-
Fastidious culture req.
Fermentative
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459
Q

Discuss serological classification of strep.

A

Lancefield groups
Group specific carb Ag in cell wall; som useful as species markers
Grouping reactions by precipitin reactions b/w acid extract test strep. and Lancefield group antisera

Some strep. serologically heterogeneous; non-groupable strains or strains w/ several different grouping carb Ags

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460
Q

Discuss 3 different types of haemolysis seen in strep

A 
Beta: zone complete RBC clearing
- streptolysin O
— lyses erythrocytes
— cytotoxic neutrophils, platelets, cardiac tissue
— inactivated by O2
- streptolysin S
— lyses erythrocytes 
— lucocidial
— non-inactivated by O2

Alpha: zone partial RBC clearing; incl. strep. viridans group

Gamma: no haemolysis (non-haemolytic)

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461
Q

Main diseases associated w/ S. pyogenes

A

URT: Acute tonsillitis, pharyngitis

Skin: impetigo, erysipelas

Toxin mediated: scarlet fever

Systemic: septicaemia, toxic shock

Post streptococcal infection: rheumatic fever, acute glomerulonephritis

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462
Q

Discuss virulence factors of S. pyogenes

A

Surface components; M protein
C5a peptidase; inhibit phagocytosis
EC products; toxins

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463
Q

Discuss the 7 toxins produced by S. pyogenes

A

Erythrogenic toxins (SPE A B C); phage mediated

  • cause rash of scarlet fever
  • pyrogenic
  • cytotoxic
  • immunosuppressive

Streptolysins (O, S): beta haemolysis

Streptokinase (A, B); fibrinolysis

  • prevent fibrin formation
  • catalyse plasminogen to plasmin
  • prevent localisation of infection

Deoxyribonucleases (A B C D)
- hydrolyse nucleic acids and nucleoproteins for own metabolism

Hyaluronidase

  • breakdown hyaluronic acid in connective tissue
  • important spread pathogen through tissues

NADase

Enzymes: amylase, proteinase, lipase

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464
Q

Discuss upper respiratory tract S. pyogenes infection

A

Strep throat -> acute tonsillitis, pharyngitis

Invasion via URT to tonsils, other lymphoid tissues of pharynx
Infections accompanied by fever
May spread to paranasal sinuses, middle ear (otitis media)

Inc.; osteomyelitis, meningitis, peritonsillar anscess

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465
Q

Discuss erysipelas and impetigo

A

Skin infections by S. pyogenes

Erysipelas

  • acute spreading skin lesion; oedema, erythema
  • possible spread from strep throat or direct infection abrasion/wound
  • episodic: same area, possibly hypersensitivity reaction

Impetigo

  • discrete crusted lesions
  • skin-skin transmission
  • prevalent unhygienic conditions and in institutions
  • can lead to acute glomerulonephritis
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466
Q

Discuss scarlet fever

A

Toxin mediated S. pyogenes infection

Strep throat and generalised erythema
Due to erythrogenic toxins
Desquamation of tongue (red strawberry tongue) and later skin

Incidence, severity dec.; improved social conditions, ABs

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467
Q

Discuss rheumatic fever

A

Post streptococcal complication

Fever, polyarthritis, carditis

Cause

  • chronic heart lesion due to streptolysins and proteinase
  • immunological phenomena

Cross reaction b/w Pyogenes Ag and human heart tissue
Delayed hypersensitivity

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468
Q

Discuss acute glomerulonephritis

A

Post streptococcal complication

Common, acute nephritis due to pyogenes in URT and/or skin lesions

Can be epidemic/outbreak in institutions
Immunological similarity b/w glomerular basement membrane and pyogenes cell membrane Ags

Abs prod.: Ag-Ab complement complexes formed

Result: inflammation, fibrin deposition, tissue destruction

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469
Q

Discuss main diseases caused by S. agalactiae

A 
Main strep pathogen neonates, young 
Early onset
- causes
— early membrane rupture
— prolonged labour
— prematurity 
— Grp B presence in birth canal
- septicaemia, shock; death if untreated

Late onset

  • infection from adult carriers or baby-baby (nosocomial)
  • purulent meningitis
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470
Q

Main diseases associated w/ S. pneumoniae

A

LRT -> inflammation reaction -> lung congestion and consolidation

  • hypoxaemia
  • pleurisy
  • empyema (lung necrosis, abscess)

Meningitis

  • high mortality
  • invasion via blood stream from pharynx

Bacteraemia
- predisposing
— mucus entrapment; anaesthesia, convulsions, head trauma
- 2ry infection respiratory tract

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471
Q

Discuss characteristics of viridans strep

A

Oral strep

Haemolytic and serological heterogeneity (alpha, gamma, rarely beta); identified by biochemical tests
Have characteristic niches within OC

Culture

  • mutans; hard glucans
  • sanguinis; hard glucans
  • salvivarius; mucoid, hard fructans
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472
Q

Discuss strep mutans group

A

Isolated from carious lesions, IE

Mutans
Sobrinus

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473
Q

Characteristics of S. mutans important to dental caries

A

Adhesins; bind to tooth
- lipoteichoic acid; react w/ tooth pellicle components
- cell wall associated proteins/polypeptides
— glucosyl transferase; direct adhesion or via glucan synthesis
— glucan binding protein B; promote co-adhesion during plaque development
— Ag I/II; bind pellicle R on tooth surface

Prod. in/soluble EC polysaccharides from sucrose
Prod. IC polysaccharides as reserve carb source
Acidogenic; ferment wide range carbs rapidly form lactic acid
Acidouric; survive and grow at low pH

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474
Q

Discuss S. mutans anti-caries therapy

A

Colonise OC w/ genetically modified S. mutans strain unable to produce lactic acid

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475
Q

Discuss Ag I/II and it’s role in caries

A

Cell wall anchored protein family
Present on surface of other oral and non-oral strep

Involved in

  • biofilm formation
  • platelet aggregation
  • tissue invasion
  • immune modulation

S. mutans; recognises salivary glycoproteins
- Ab against AgI/II prevent mutans adherence

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476
Q

How can Ag I/II potentially play a role in caries prevention?

A

Caries vaccinations

Production of monoclonal Abs for prevention of S. mutans tooth colonisation

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477
Q

Discuss members of S. mitis group

A

Parasanguinis, pneumoniae

Sanguinis

  • prod. ECP glucan, form hard, adherent colonies on sucrose agar
  • prod. IgA-protease clear SIgA

Gordonii

  • isolated: IE vegetations
  • important member plaqu community

Mitis; main plaque pioneering species

  • isolated; IE vegetations
  • causes septicaemia in neutropenia pt

Orlais; main plaque pioneering species

  • isolated; IE
  • septicaemia in neutropenic pt
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478
Q

Discuss strep salivarius group

A

Salivarius

  • main plaque pioneering species
  • preferentially colonises tongue
  • prod. ECP; fructans or levan
  • prod. large mucoid colonise
  • not significant pathogen
Vestibularis
- colonise vestibular mucosa
- don’t prod. ECP
- prod. urease, H2O2
— raise local pH
— contribute salivary peroxidase activity
— inhibit competing bacteria
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479
Q

Discuss strep anginosus group

A

Intermedius, anginosus, constellatus

Isolated plaque, mucosal surfaces
Associated w/ purulent infections (abscesses) of OC, sometimes involving major organs

Characteristics

  • serological heterogeneity
  • alpha, beta, gamma haemolysis prod. by different strains
  • don’t prod. polysaccharides
  • Intermedius; intermedilysin (cytotoxin) role undetermined
  • prod. glycosidases; cleave carb residues off host cell glycoproteins
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480
Q

Discuss strep virulence factors in relation to IE

A

Bind fibronectin; surface protein host cells incl. heart endothelium
Prod. ECO
Bind platelets (platelet aggregation associated protein prod. by strep)
Bind collagen via PAAP; collagen exposed due to tissue damage
Expression of tissue degrading proteinases

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481
Q

Define commensal, carriage, pathogen, opportunistic pathogen, virulence

A

Commensal: organism that benefits from relationship w/ host but is neither beneficial nor harmful to host

Carriage: person asymptomatically carries pathogenic organism which can be spread to another person

Pathogen: microorganism capable of causing infection

Opportunistic pathogen: organism that causes disease when disturbance in homeostasis b/w host and commensal

Virulence: quantitative ability of pathogen to cause disease

482
Q

Define endemic, epidemic, outbreak and pandemic

A

Endemic: always present in popn. at more-or-less constant level (may be cyclic)

Epidemic: higher than normal level in popn., usually much higher than endemic, usually short term; flu

Outbreak: localised inc. in incidence; E. coli food poisoning

Pandemic: epidemic spreading b/w continents; cholera

483
Q

4 common instances when opportunistic pathogens arise

A

Immunocompromised pt
Organism moved to site do not normally colonise
ABs or other therapies
Dietary imbalances; plaque related diseases

484
Q

Discuss the sources of infections

A

Endogenous: within; normal flora invade

Exogenous: from outside

  • contact w/ other human
  • zoonoses: animal pathogen
  • organisms in environment; H2O, soil
  • fomites: inanimate environment
485
Q

2 types of ways in which infections are spread

A

Horizontal: organism transmitted b/w individuals
Vertical: mother to offspring in utero/around birth

486
Q

Discuss vertical transmission

A

Congenital infections
- via mothers’s blood and by crossing placenta
— congenital syphilis, rubella, toxoplasmosis
- acquired shortly before/during delivery
— HSV, HBV

487
Q

Discuss attachment and invasion of bacteria

A

Invading organisms must adhere to host tissue to colonise body

Neisseria gonorrhoeae attach genital mucosa via fimbriae (non-fimbrinate isolates non-pathogenic)

Haemophilus influenzae attach via haemagglutinin Ag

488
Q

3 main ways in which pathogens evade the immune system

A

Overcome immune defence
Avoid destruction by phagocytes
Motility

489
Q

Discuss how pathogens overcome immune defence

A

Respiratory bacteria secrete IgA protease which degrades Ig

S. pyogenes express protein A which binds Ig preventing opsonisation and activation of complement

490
Q

Discuss how bacteria avoid phagocytosis

A

S. pneumoniae has a polysaccharide capsule which inhibits uptake by polymorphs

Some bacteria (mycobacterium tuberculosis) survive inside host macrophages

491
Q

Discuss motility as a means to evade immune defence

A

Ability to move enhances pathogenicity

- flagellae of S. typhimurium

492
Q

Discuss bacterial enzymes used to damage host cells

A

Coagulase: walling off of staph lesions (S. aureus)
Proteases: porphyromonas gingivalis

Bacteria express proteases, nucleases, lipases, glycosidases

493
Q

Discuss exotoxins used by bacteria to damage host

A

Classic gram+ bacteria

  • clostridium tetani toxin
  • corynebacterium diptheriae toxin

Streptolysins (S. pyogenes); lysosomal discharge, kill polymorphs, inhibit chemotaxis
Strep erythrogenic toxin (pyogenes) -> scarlet fever
S. aureus enterotoxin -> diarrhoea
Bibrio cholerae enterotoxin; stim. adenylate cyclise -> watery diarrhoea

Highly toxic: act at specific sites
Neutralised by antitoxin
Often destroyed by heat

494
Q

Discuss endotoxins used by bacteria to damage host cell

A

Endotoxins from cell wall gram- bacteria produce IL-1 and TNF causing fever and shock

495
Q

Discuss some of the lab investigations used to identify bacterial infections

A

Culture: gold standard

Microscopy: light (bacteria), electron (viruses)
Immunofluorescence
Colourimetric
Nucleic acid extraction/PCR amplification/sequencing technology

Serological

  • 4 fold inc. Ab titre or presence IgM
  • useful when hard to presumptive bacteria or for viral infections
496
Q

6 factors affecting transmissibility of bacteria

A 
Ability to survive
Ability to find alternative host
Shedding capacity
Infectivity
Virulence
Ability to evade immune response
497
Q

Discuss bacterial ability to survive in relation to transmissibility

A

Resist drying, UV: enterovirus

H2O: Legionella, Giardia

Soil: Clostridium tetanii

498
Q

Discuss shedding capacity in relation to bacterial transmissibility

A

How easily bacteria spread

Respiratory: influenza, measles, M. tuberculosis
Skin-contact: HSV, S. aureus
Faecal-oral: HAV, salmonella typhimurium
Blood, body fluids: HIV, HBV, syphilis

499
Q

Compare active and carrier infection

A

Active: clinically unwell

Carrier: looks well but chronically infected

  • may not be aware infected
  • HBV
500
Q

Common modes of infection transmission

A 
Respiratory/droplet
Faecal-oral
Skin/mucous membrane
Blood
Fomites
Zoonoses
Sexual transmission
Salivary 
Insect
501
Q

Discuss skin/mucous membrane spread of infection

A

Skin usually good barrier to most infection
May occur via direct contact or via fomites (shared towels)

Usually occurs through abrasion in epidermis

  • impetigo; GrpA strep
  • cellulitis; spreading infection, S. pyogenes
502
Q

Discuss salivary spread of infection

A 
Some infections (HSV) transferred directly by contact w/ infected secretions 
Others transmitted from saliva via bite breaking through skin
503
Q

Discuss sexual transmission of infection

A

Usually b/w sexual partners

  • neisseria gonorrhoea (gonorrhoea)
  • treponema pallidum (syphilis)

Infant @ birth via birth canal

  • congenital syphilis
  • GrpB strep
504
Q

Discuss respiratory spread of infections

A

Aerosolisation of secretions dependent on

  • amount infective discharge
  • size aerosol droplets
  • resistance of pathogens to drying/inactivation by UV

May also be transmitted by secretions on hands or fomites (handkerchiefs)

505
Q

Discuss faecal-oral route of transmission

A

Important means of spread esp. where poor hygiene practised

May involve direct or finger to mouth spread
Use of night soil as fertiliser or faecal contamination of food/water

Salmonella spp., Shigella spp., HAV

506
Q

Discuss blood-borne transmission of infection

A

May occur from direct transmission through use of blood products or dirty needles
- HIV, HBV

May occur via insect host; malaria via female anopheles mosquito

507
Q

Discuss zoonotic transmission of infection

A

Animal-human
Animals that have natural reservoirs to humans

Zoonotic diseases; salmonella, rabies

508
Q

Discuss insect spread of infection

A

Winged insects vectors for many infections; malaria

Fleas: wingless insects
- jump long distances; bubonic plague

509
Q

Discuss fomite spread of infection

A

Fomites; inanimate objects that can carry, transmit infection

Soft toys, shared towels, handkerchiefs

510
Q

What are nosocomial infections?

A

Hospital acquired infections

511
Q

Common nosocomial infections

A

UTI
Wound/skin and soft tissue infections
Respiratory tract infections

512
Q

Discuss how nosocomial infections can be prevented

A

Isolating pt w/ known resistant organism infection if possible
Strict adherence to sensible infection control procedures
- isolation if necessary
Hand washing b/w pts

513
Q

Clinical features lobar pneumonia

A 
High grade fevers w/ rigors 
Productive cough
Rusty sputum 
Pleuritic chest pain
Signs of consolidation
514
Q

Discuss pathology of lobar pneumonia

A

Lobar distribution, 4 stages

Congestion (24h): vessels engorged, alveolar oedema, heavy, red lungs

Red hepatisation (2-4d): outpouring of neutrophils and RBCs into alveoli, red, solid, airless ‘liver-like’ lungs

Grey hepatisation (4-8d): fibrin and macrophages replace neutrophils and RBCs, grey solid airless lung

Resolution (8-10d): gradual return to normal

515
Q

Complications of lobar pneumonia

A

Most cases resolve

Rarely suppurative (abscess, empyema) esp. w/ Klebsiella or Staph infections

516
Q

4 typical clinical settings of bronchopneumonia

A
  1. Chronic debilitating illness
  2. 2ry to viral infections
  3. Infancy
  4. Old age
517
Q

Causative species of bronchopneumonia

A

Low virulence bacteria

  • staph
  • S. viridans
  • H influenzae
  • coliforms
518
Q

Pathology of bronchopneumonia

A

Bilateral, basal, patchy
Grey or grey-red spots of consolidation

Microscopically: Acute inflammatory infiltrate in bronchioles and alveoli

519
Q

Complications of bronchopneumonia

A

Death; usually terminal event/complicating event in other debilitating illness or old age

Resolution
Scarring
Abscess/empyema (rare)

520
Q

Discuss interstitial/atypical pneumonia

A 
Mycoplasmal or viral 
Inflammation restricted to alveolar septa or interstitial tissues 
Atypical; no alveolar exudate 
Clinical
- general rather than localised symptoms
- out of proportion to signs 
Variable clinical course, usually mild
521
Q

Discuss pulmonary TB

A

Infection by M. tuberculosis
Occurs early childhood
Airborne from ‘open cases’
Clinical: disease represents reinfection or reactivation

522
Q

Discuss 1ry TB

A

Response to 1st contact w/ tubercle bacteria
Usually asymptomatic
Ghon complex: typically 1cm focus in midzone w/ draining lymph node
Heals w/ fibrosis and calcification

523
Q

Discuss 2ry TB

A

Reinfection or reactivation

Usually apical, about 3cm at clinical presentation

524
Q

Discuss microscopic findings of TB

A

Characteristic changes resulting from T4 hypersensitivity
Granulomas w/ caseating necrosis, Langhan’s giant cells, epithelioid macrophages
Ziehl-Neelsen stain reveals characteristic acid-fast bacilli

525
Q

Complications of pulmonary TB

A

Progressive fibrocavitary TB
- gradually destroys lungs through necrosis, cavitation and fibrosis

Miliary TB
- blood borne dissemination within lung or throughout body
- seed-like foci consisting of granulomas
— meninges, bone marrow, liver, any organ

526
Q

Discuss chronic obstructive pulmonary diseases

A

Group of diseases characterised by obstruction to airflow
- intermittent, reversible, irreversible

Cf restrictive diseases; no obstruction but inhibition to lung expansion

527
Q

Discuss chronic bronchitis

A

Clinical definition
- productive cough >3mnth 2 consecutive yr
Mucous gland hypertrophy, hypersecretion +/- infection
Progressive
Hypoxia, hypercapnia, cyanosis-prone
Blue bloater

528
Q

Discuss emphysema

A

Pathological definition
- permanent dilatation of airways D to terminal bronchioles
Centriacinar/panacinar/irregular
Elastin destruction -> loss elastic recoil
Tend to hyperventilate; blood gases normal
Pink puffers

529
Q

Discuss bronchial asthma

A

Inc. irritability of bronchial tree
Paroxysms of reversible bronchospasm
Commonest; atopic caused by T1 hypersensitivity to common allergens (pollen, dust)
Others: aspirin-induced, occupational, infection

530
Q

Discuss bronchiectasis

A

Permanent dilatation of bronchi and bronchioles w/ necrosis of walls
Usually follows obstruction or childhood viral pneumonia
Airways become saclike, filled w/ foul-smelling pus
Chronic paroxysmal cough, brought on by change in posture
Copious foul-smelling sputum
Complications
- abscess
- amyloid
- fibrosis
- clubbing
- cor pulmonale

531
Q

Aetiology of lung (bronchogenic) cancer

A 
Directly caused by cigarette smoking 
Other factors
- asbestos 
- mineral dusts
- radiation
- pollution
- scarring
532
Q

Classifications of lung cancers

A

Histological

  • squamous cell carcinoma
  • adenocarcinoma
  • small cell (oat cell) carcinoma
  • large cell carcinoma

Clinical

  • small cell
  • non-small cell
533
Q

Compare small cell and non-small cell lung carcinoma

A

Small cell

  • not treatable surgically; usually widely disseminated @ diagnosis
  • chemotherapy

Non-small cell
- surgically treatable

534
Q

Clinical features of lung cancer

A

Local: cough, haemoptysis, pain
General: weight loss, clubbing, hypertrophic pulmonary osteoarthropathy
Paraneoplastic syndromes: ectopic hormone production by tumour cells
- hypercalcaemia
- SIADH

535
Q

Lung cancer prognosis

A

Depends on staging

5yr survival <10%

536
Q

Discuss occupational lung disease

A

Diseases caused by inhalation of dust particles, mineral or organic substances over many yr due to occupational exposure

Diffuse interstitial
Restrictive disease

537
Q

2 mechanisms by which occupational lung diseases occur

A
  1. Scarring from chronic irritation; inert substances
    - coal workers’ pneumoconiosis
  2. Hypersensitivity
    - organic dusts
538
Q

Examples of occupational lung disease

A

Coal workers’ pneumoconiosis
- anthracosis, macules, progressive massive fibrosis

Silicon

  • silicosis
  • Caplan’s Syndrome

Asbestos

  • asbestosis
  • pleural plaques
  • caplan’s Syndrome
  • mesothelioma
  • cancer; lung, liver, stomach, colon

Organic dusts

  • farmers’ lung
  • bagassosis
  • byssinosis
  • bird breeder’s lung
539
Q

Discuss pulmonary oedema

A

Disease of vascular origin

Haemodynamic, usually cardiogenic
Heavy, wet lungs
Alveolar pink granular fluid, may contain haemosiderin-laden macrophages (heart failure cells)
Resolution or ‘brown induration, (long standing)

540
Q

Discuss diffuse alveolar damage

A

Disease of vascular origin

Acute respiratory distress syndrome

Oedema caused by damage to alveolar capillary endothelium
Shock, trauma, sepsis, viral infection, radiation, noxious gases

Rapidly developing life-threatening respiratory insufficiency
Oedema fluid and fibrinous membranes line alveoli

Doesn’t resolve, proceed to severe scarring

541
Q

Discuss emboli and infarction

A

Disease of vascular origin

Pulmonary arteries occluded by circulating clots usually from lower limb veins in bed-ridden

Large saddle emboli

  • immediately fatal
  • lodge @ bifurcation of pulmonary trunk

Small emboli

  • lodge peripherally
  • characteristic wedge shaped infarcts
542
Q

Discuss pulmonary hypertension

A

Disease of vascular origin

Pulmonary circulation is low pressure

Inc. pressure can be 2ry to

  • COPD
  • left heart vascular disease
  • recurrent thrombi emboli

Causes right ventricle hypertrophy and failure
- chronic cor pulmonale

543
Q

3 main groups of WBCs and members of groups

A

Granulocytes

  • neutrophils; phagocytose (granular)
  • eosinophils; inflammatory response, immunity (granular)
  • basophils, mast cells; release histamine (granular)

Mononuclear phagocytes

  • macrophage; phagocytose
  • monocytes; phagocytose (agranular)
  • dendritic cell; gather, present Ags

Lymphocytes; phagocytose (agranular)

544
Q

2 types of WBC disorders

A

Inc. WBC; leukocytosis >11x10^9/L

  • inc. production; leukaemia, myeloproliferative diseases
  • reactive leucocytosis; 2ry to infection/inflammation
  • medications; prednisolone

Dec. WBC; leukopenia <4x10^9/L

  • 2ry to aplastic anaemia
  • cyclic neutropenia
  • drugs; chemotherapy
  • overwhelming bacterial/viral infection (HIV)
  • radiation; 2ry to radiotherapy
545
Q

What is leukaemia? What are the 2 types?

A

Leukaemia: malignant proliferation of WBCs

Acute; proliferation of immature blast cells
Chronic; proliferation of mature cells

546
Q

Discuss ALL, AML and CML, CLL

A

Types of leukaemia

Acute lymphoblastic leukaemia (lymphoblasts)
- children
- poor prognosis adults
Acute myeloid leukaemia (myeloblasts)
- adults
- poor prognosis adults and children

Chronic myeloid leukaemia (myelocytes)
- associated w/ Philadelphia chromosome
Chronic lymphocytic leukaemia (lymphocytes)

547
Q

Discuss acute leukaemia and clinical presentation

A

Rapid accumulation of dysfunctional, immature cells in blood and bone marrow
Red. no. normal, functioning, mature W/RBCs and platelets

Clinical

  • short history feeling unwell
  • may present neutropenic fever or bleeding
  • organ infiltration may occur; skin, gums, testes, meninges
  • blood film; leucocytosis: circulating blasts and cytopenia
548
Q

Discuss chronic leukaemia and clinical presentation

A

Progresses slowly permitting bone marrow to retain ability to produce more mature functional cell lines

Often asymptomatic
Usually accidental finding during routine exam
Both forms more common in adults

Clinical

  • often diagnosed incidentally
  • usually long-term history non-specific symptoms (weight loss, nausea)
  • splenomegaly common
  • lymphadenopathy common in CLL
  • blood film; leucocytosis; circulating mature lymphocytes or myeloid cells
549
Q

Discuss management of leukaemias

A

Adjunct supportive therapy; compensate for lack of functioning cells

  • red cell transfusion
  • platelet transfusion
  • granulocyte colony stimulating factor

Specific

  • chemotherapy
  • radiotherapy
  • bone marrow transplantation
550
Q

Dental relevance of leukaemia

A

Mucosal bleeding; dec. platelets
(Bleeding tendency)
Inc. susceptibility to infections; dec. functioning WBCs
Gingival enlargement; dysfunctional WBC infiltrating organs

551
Q

Types of lymphomas

A

Hodgkin’s
Non-Hodgkin’s
Burkitt’s
Multiple myeloma

552
Q

What is a lymphoma?

A

Malignant proliferation of lymphocytes within nodal and extra-nodal sites
Solid tumours

553
Q

What is Hodgkin’s lymphoma?

A

Dysfunctional B cell resulting in accumulation of abnormal B cell

Characterised by presence of Reed-Sternberg cells in biopsy (mutated B cells, huge)

554
Q

Risk factors of Hodgkin’s lymphoma

A

M>F
Immunocompromised
+ve family history
History of infectious mononucleosis

555
Q

Clinical features of Hodgkin’s lymphoma

A 
Progressive, painless enlargement of lymph nodes (esp. neck)
Tiredness/weakness/fatigue
Anorexia, weight loss
Fever, night sweats 
Bone pain
Pruritus
Flu-like symptoms
556
Q

Special investigations for diagnosing Hodgkin’s lymphoma

A

Lymph node biopsy: presence of Reed-Sternberg cells (mutated B cells)
FBC, CT, MRI, PET scans

557
Q

Discuss the staging of Hodgkin’s lymphoma

A

1: 1 lymph node region or 1 extralymphatic site
- A: absence of B symptoms
- B: fever, night sweats, weight loss

2: 2/+ lymph node regions on same side diaphragm, may incl. localised extralymphatic site
3: lymph nodes of both sides diaphragm, may incl. spleen or localised extralymphatic sites
4: diffuse extralymphatic disease; liver, bone marrow, skin, lung

558
Q

Discuss treatment options for Hodgkin’s lymphoma

A

Radiation therapy: stage 1/2
Combined chemotherapy: stage 3/4
Bone marrow transplant: recurrent lymphoma

559
Q

Dental relevance of Hodgkin’s lymphoma

A

Infections
Mucositis/ulceration due to cytotoxic drugs
Anaemia
Bleeding tendencies
Painless enlarged cervical lymph nodes
Impaired respiratory function (pulmonary fibrosis from irradiation)

Lymphomas rarely form in OC or oropharynx
LA regional blocks avoided if bleeding tendencies
Conscious sedation if req., GA in hospital

560
Q

Discuss non-Hodgkin’s lymphoma

A

More common
Poor prognosis
Occur # @ any age; >60 common

B or T cell associated subtypes
Aggressive (high grade) and non-aggressive (low grade) subtypes

Greater propensity for extra-nodal sites (GIT, CNS)
Usually multi-focal

Symptoms, dental aspects, diagnosis, staging same as Hodgkin’s

561
Q

Discuss Burkitt’s lymphoma

A

Associated w/ previous Epstein-Barr virus infection (infectious mononucleosis; glandular fever)

Endemic; African children and young adults
- Boys>Girls
- jaw swelling
Sporadic; Western world
- M>F
- inc. incidence in HIV/AIDs
- symptoms/diagnosis/staging/treatment same as Hodgkin’s

562
Q

What is multiple myeloma?

A

Proliferation of malignant plasma cell

563
Q

Discuss malignant myeloma

A

Over abundance of monoclonal paraproteins (M-proteins)
- monoclonal Ig prod. in excess by clonal proliferation of plasma cells

Unknown aetiology
- possibly genetic

Common around 60
M>F
More prevalent in Africans

564
Q

Clinical features of multiple myeloma

A 
Amyloidosis (tongue)
Anaemia 
Petechiae/ecchymosis
Bleeding
Infections
Blood hyperviscosity 
Bone pain 
Osteoporosis 
Hypercalcaemia
Renal damage
565
Q

Special investigations for diagnosing multiple myeloma

A 
FBC, renal function, bone profile 
Total body bone survey 
Urine Bence-Jones protein 
Serum protein electrophoresis 
Bone marrow aspiration
X-ray affected bone 
CT/MRI
566
Q

Dental relevance of multiple myeloma

A

Management of
- manifestations of leukaemias/lymphomas
- oral complications of chemo- and radiotherapy
- multiple myeloma check IV bisphosphonates
— risk osteonecrosis (MRONJ)

567
Q

Discuss reactive leucocytosis

A

Causes

  • disease
  • infection
  • neoplastic condition

Evaluate w/ WBC differential count
Changes to WBC differential
- establish differential diagnosis
- guide treatment

568
Q

Discuss WBC differential count patterns

A

Inc. neutrophils
- acute bacterial infection

Inc. lymphocytes, dec. neutrophils
- viral infection

Inc. monocytes

  • chronic bacterial infection
  • acute exacerbation of chronic inflammation (TB)

Inc. eosinophils

  • allergies
  • parasitic infection
  • Hodgkin’s lymphoma

Inc. basophils

  • chronic myeloid lymphoma
  • polycythemia
569
Q

Briefly outline functions of liver

A

Metabolic: detoxification and breakdown of toxins, hormones, drugs

Synthesis

  • bile
  • protein
  • carb
  • lipid
  • RBCs
  • clotting factors

Storage

570
Q

Outline responses of liver to injury

A 
Hepatocyte degeneration and IC accumulations
Hepatocyte necrosis and apoptosis 
Inflammation 
Regeneration 
Fibrosis
571
Q

4 common symptoms of liver disease

A

Jaundice
Oedema
Ascites
Cerebral dysfunction

572
Q

What is jaundice?

A

Raised serum bilirubin w/ bilirubin deposited in tissues

Characterised by yellowing of skin and eyes

573
Q

5 stages in bilirubin metabolism

A
  1. Haem from RBC breakdown
  2. Oxidised to biliverdin, reduced to bilirubin
  3. Bilirubin bound to serum albumin, transported to liver
  4. Bilirubin conjugated in liver become H2O soluble, excreted in bile
  5. Gut bacteria deconjugate to produce urobiliogen; excreted in faeces, urine
574
Q

Classification of causes of jaundice

A

Site: pre-, intra-, post-hepatic
Type: conjugated, unconjugated

575
Q

Discuss pre-, intra- and post-hepatic causes of jaundice

A

Pre-hepatic
- express bilirubin production
— haemolytic anaemia, internal bleeding, ineffective erythropoiesis

Intra-hepatic; physiological jaundice of newborn

  • diffuse hepatocellular disease; impaired conjugation
  • intra-hepatic bile duct disease; dec. excretion
  • drugs; red. uptake/impaired excretion

Post-hepatic
- extra-hepatic biliary obstruction
— gallstones, pancreatic cancer, extra-hepatic biliary atresia, biliary strictures

576
Q

Discuss oedema/ascites and cerebral dysfunction symptoms of jaundice

A

Oedema/ascites
- hepatic causes
— portal hypertension
— hypoalbuminaemia

Cerebral dysfunction 
- hepatic encephalopathy associated w/ raised serum ammonia, regarded as disorder of neurotransmission 
- symptoms 
— disturbances in consciousness
— rigidity 
— hyperreflexia
— asterixis
577
Q

What is hepatitis?

A

Inflammation of liver following injury

578
Q

4 common causes of hepatitis

A

Viral
Alcohol
Drugs/toxin
Autoimmune

579
Q

Discuss the 5 types of viral hepatitis

A

A: faecal-oral spread; not chronic

B: parenteral spread; chronic 5-10%

C: parenteral spread; chronic >50%

Delta hepatitis virus/D

  • defective RNA virus; infective if encapsulated by HBV
  • co-infection; fulminant disease (severe, sudden onset)
  • superinfection; chronic progressive disease

E: waterborne; not chronic

580
Q

Discuss acute hepatitis

A

Initially Mostly non-specific symptoms; nausea, vomiting
Specific symptoms; loss appetite, jaundice, dark urine
Small proportion develop acute liver failure

Macroscopy; mild hepatomegaly, congestion

Microscopy

  • scattered foci of lobular necrosis and inflammation
  • apoptotic bodies (councilman bodies)
  • hepatocyte ballooning and necrosis
  • disruption of architecture (lobular disarray)
  • inflammation of portal tracts
581
Q

What is chronic hepatitis?

A

Necroinflammatory disease in which hepatocytes are target of attack

582
Q

Discuss chronic hepatitis

A

May be asymptomatic or non-specific
Lab evaluation
Extensive damage may lead to cirrhosis, portal hypertension

Clinically
- symptomatic, biomedical, histological evidence of disease >6mnth

583
Q

Causes of chronic hepatitis

A

B/B+D
C
Autoimmune hepatitis
Drug-induced hepatitis

584
Q

Histology of chronic hepatitis

A

Inflammation; predominately lymphocytic

  • portal
  • periportal interface hepatitis (piecemeal necrosis); active disease
  • lobular

Hepatocyte necrosis

  • bridging necrosis; portal to central/portal-portal
  • confluent necrosis; larger area

Fibrosis
- portal/periportal/bridging and eventually cirrhosis

585
Q

What is cirrhosis?

A

Irreversible end stage liver disease

586
Q

Histology of cirrhosis

A

Fibrosis
Nodules; regenerative hepatocytes surrounded by fibrosis
Disruption of vascular architecture and blood flow

587
Q

Causes of cirrhosis

A

Alcohol
Viral hepatitis (B, C, D)
Autoimmune hepatitis
1ry/2ry biliary cirrhosis

Metabolic

  • haemochromatosis; overload of Fe
  • Wilson’s disease; Cu poisoning
  • alpha-1-antitrypsin deficiency

Drugs
Idiopathic
Venous outflow obstruction

588
Q

Complications of cirrhosis

A

Hepatic failure
Hepatic encephalopathy
Portal hypertension
Oesophageal varices; massive haemorrhage

589
Q

Discuss hepatic encephalopathy as complication of cirrhosis

A

Mechanism

  • portal blood bypasses liver
  • toxic or metabolic effect on brain
  • ammonia, bacteria, altered GABA level

Clinically
- ranges from subtle psychiatric disturbances to coma

590
Q

Possible effects of portal hypertension

A

Ascites
Portal-systemic venous shunts
Splenomegaly (congestive)

591
Q

Discuss ascites as result of portal hypertension

A

Mechanisms

  • high intra-sinusoidal pressure
  • leakage from hepatic lymphatics
  • hypoalbuminaemia
  • Na, H2O retention
592
Q

Discuss portal-systemic venous shunts as result of portal hypertension

A

Oesophagus; varices
Rectum; haemorrhoids
Falciform ligament
Ant. abdominal wall (caput medusae)

593
Q

Discuss alcoholic liver disease

A

Alcoholic steatosis

  • fatty change; soft, yellow liver
  • fibrosis

Alcoholic hepatitis

  • fatty change
  • fibrosis
  • hepatocyte necrosis
  • inflammation
  • +/- Mallory’s hyaline; Fe deposition

Alcoholic cirrhosis

594
Q

Discuss 1ry and 2ry liver tumours

A 
1ry
- benign; liver cell adenoma 
- malignant 
— hepatocellular carcinoma
— cholangiocarcinoma
— angiosarcoma
— hepatoblastoma

2ry (metastatic)
- source
— carcinoma; colorectal, stomach, pancreas, breast
— malignant melanoma

595
Q

Discuss liver metastases

A

Sources

  • carcinoma
  • multiple melanoma

Morphology

  • hepatomegaly
  • typically multiple nodules
596
Q

Aetiology of hepatocellular carcinoma

A

Hepatitis B/C virus
Haemochromatosis
Aflatoxin
Age, gender, alcohol

597
Q

Discuss clinical presentation of hepatocellular carcinoma

A

Abdominal pain, weight loss, hepatomegaly
Raised serum alpha-feto protein
Metastases occur late; lungs
Survival <6mnths
- death due to cachexia, varices, encephalopathy

598
Q

Discuss the macroscopy and microscopy of hepatocellular carcinoma

A 
Macroscopy; hepatomegaly 
- 3 patterns
— unifocal mass; yellow/white, soft, haemorrhage, necrotic 
— multifocal
— diffusely infiltrative

Microscopy

  • well-differentiated tumours resemble normal liver trabeculae
  • poorly differentiated tumours mimic metastases
599
Q

What is dysphagia?

A

Difficulty swallowing

Req. urgent investigation unless short duration or associated w/ sore throat

600
Q

Causes of dysphagia

A

Mechanical block

  • malignant stricture; pharyngeal, oesophageal, gastric cancer
  • benign structure; oesophageal web/ring
  • extrinsic pressure; lung cancer, retrosternal goitre, aortic aneurysm, left atrial enlargement
  • pharyngeal pouch

Motility disorders

  • achalasia
  • systemic sclerosis
  • myasthenia gravis
  • bulbar/pseudobulbar palsy

Other

  • oesophagitis
  • globus hystericus (anxiety swallowing)
601
Q

What is Patterson-Kelly Syndrome?

A

Rare condition characterised by dysphagia, post-cricoid webs, are deficiency anaemia, glossitis and inc. incidence of pharyngeal and oral carcinoma

602
Q

Discuss achalasia

A

Lower oesophageal sphincter fails to reflex due to degeneration of myenteric plexus

Symptoms; dysphagia, regurgitation, substernal cramps, weight loss

Investigation
- Ba swallow shows tapered, dilated lower oesophagus

Risk factor for oesophageal cancer

603
Q

What is Gastro-oesophageal reflux (GORD)?

A

Reflux of stomach contents causing troublesome symptoms w/ @ least 2 episodes heart burn /wk
Associated w/ dysfunction of lower oesophageal sphincter

604
Q

Predisposing factors of GORD

A 
Hiatus hernia
Lower oesophageal sphincter hypotension 
Loss of oesophageal peristaltic function 
Gastric acid hypersecretion
Delayed gastric emptying 
Overeating
Smoking, alcohol
Abdominal obesity 
Drugs; tricyclics, anticholinergics, nitrates
Systemic sclerosis
H. pylori
605
Q

Discuss oesophageal and extra-oesophageal symptoms of GORD

A

Oesophageal

  • heartburn
  • belching
  • acid brash
  • water brash
  • odynophagia

Extra-oesophageal

  • nocturnal asthma
  • chronic cough
  • laryngitis
  • sinusitis
606
Q

Complications of GORD

A 
Oesophaitis
Ulcers
Benign strictures
Oesophageal adenocarcinoma
Fe deficiency anaemia
607
Q

Discuss some of the treatments for GORD

A

Lifestyle

  • weight loss
  • smoking cessation
  • raise head in bed
  • small regular meals
  • avoid hot, caffeinated drinks, alcohol, acidic fruits
  • avoid drugs affecting oesophageal motility or damage mucosa

Medications

  • antacids; alginates (Gaviscon)
  • H+ pump inhibitor; lansoperazole

Surgery; nissen fundoplication
- only if severe and refractory to medical measures

608
Q

Dental relevance of GORD

A

Unpleasant taste
Erosion
Exacerbated by treatment w/ NSAIDs (damage mucosa)

609
Q

What is hiatus hernia?

A

Condition in which proximal stomach herniates into thorax

50% symptomatic GORD
30% >50
More common obese women

610
Q

What are the 2 types of hiatus hernia?

A

Sliding

Rolling

611
Q

Compare sliding and rolling hiatus hernia

A

Sliding; 80%

  • Gastro-oesophageal junction slides into chest
  • often associated w/ acid reflux
  • LES less competent

Rolling; 20%

  • Gastro-oesophageal junction remains in abdomen
  • bulge of stomach herniates into chest alongside oesophagus
  • para-oesophageal hernia
  • acid reflux uncommon
  • may strangulate
612
Q

2 investigations to diagnose hiatus hernia

A

Ba swallow

Upper GI endoscopy

613
Q

Discuss treatment of hiatus hernia

A 
Lose weight 
Treat reflux symptoms 
Surgical repair if
- intractable symptoms despite max. medical therapy 
- complications 
- rolling hernia (even is asymptomatic)
614
Q

Discuss Barrett’s oesophagus

A

Precancerous condition

Chronic reflux oesophagitis -> normal oesophageal squamous epithelium replaced by columnar gastric epithelium

Continuous or patchy

Premalignant lesion; metaplasia may occur
40 fold inc. risk adenocarcinoma

Not associated w/ H. pylori

615
Q

Risk factors of oesophageal carcinoma

A 
Alcohol, smoking, obesity 
Achalasia
GORD, Barrett's oesophagus 
Tylosis 
PVS (Plummer-Vinson/Patterson-Kelly Syndrome)
Low Vit A and C
Nitrosamines exposure
616
Q

Clinical presentation of oesophageal carcinoma

A 
Hoarseness, cough 
Dysphagia
Weight loss 
Retrosternal pain
Lymphadenopathy (occ)
617
Q

Dental relevance of oesophageal carcinoma

A

Inc. chance develop 2nd cancer HandN
May occur 2ry to PVS
Rare; may have tylosis and oral leukoplakia

618
Q

What is dyspepsia?

A

Indigestion

Nonspecific group of symptoms related to upper GIT

619
Q

Symptoms of dyspepsia

A

Epigastric pain
- related to specific foods, hunger, time of day
- bloating and fullness after meals
Heartburn

Anaemia (Fe deficiency)
Loss of weight 
Anorexia
Recent onset w/ progressive symptoms 
Melaena/haematemesis
Swallowing difficulty
620
Q

What is peptic ulceration and risk factors

A

Ulcer + break in continuity of epithelial surface

Risk

  • H pylori
  • drugs; aspirin, NSAID, corticosteroid
  • smoking, stress
621
Q

Compare gastric and duodenal ulceration

A

Gastric

  • mainly elderly
  • lesser curve of stomach
  • asymptomatic
  • epigastric pain related to meals, relieved by antacids
  • weight loss
Duodenal 
- 4x more common
- may asymptomatic 
- epigastric pain before eating or @ night
— relieve by eating or drinking milk
622
Q

Risk factors for gastric cancer

A 
Alcohol, smoking
H pylori
Dietary salt and preservatives
Dietary fruit and veg 
Pernicious anaemia
623
Q

Presentation of gastric cancer

A

Vague and nonspecific

Dysphagia
Nausea
Malaena
Anaemia

624
Q

Discuss investigations for gastric cancer

A

Endoscopy and biopsy of 1ry tumour
- 6 biopsy samples from mass and adjacent tissue

Staging may involve endoscopic ultrasonography, CT abdomen (for liver metastases), PET

625
Q

What are haematemesis and malaena? Causes of both

A

Haematemesis; vomiting blood, coffee ground or fresh red
Malaena; Black, tarry stool

Causes

  • gastritis or gastric erosion
  • peptic ulcers
  • duodenitis, oesophagitis
  • drugs: NSAID, aspirin, corticosteroids, warfarin, thrombolytics
  • Mallory-Weiss tear
  • oesophageal varices
  • malignancy
626
Q

Discuss oesophageal varices

A

Dilated collateral veins @ sites of Porto-systemic anastomosis
Cause: portal hypertension
Most common in lower oesophagus, also stomach

Associated w/ liver cirrhosis
Variceal bleeding may develop, 30-50%mortality/episode

627
Q

What is Mallory-Weiss tear/Syndrome?

A

Forceful or long term vomiting or coughing resulting in bleeding via oesophageal tear

Tear involved mucosa and submucosa but not underlying muscular layer

628
Q

Associations of Mallory-Weiss tear

A 
Alcoholism 
Eating disorder
Hyperemesis
Gravidarum (prolonged vomiting)
Epileptic convulsion 
NSAID abuse
629
Q

Discuss the healing and treatment of Mallory-Weiss tear

A

Usually heals w/o treatment +/- PPI or H2 antagonist

Bleeding usually stops 24-48h

Treatment

  • endoscopy; cauterisation or injection of adrenaline
  • surgical management
  • embolisation (occ)
630
Q

Discuss initial management of upper GI bleed

A 
Protect airway, high flow O2
Resuscitate (ABC)
2 large bore cannulae 
FBC, UandE, LVT, crossmatch, clotting
IV fluids and omeprazole 
Catheter 
Transfuse
Urgent endoscopy
631
Q

Define obligate and facultative anaerobes and anaerobiosis

A

Obligate: unable to grow in presence of O2; req. low red./oxidation potential (Eh)

Facultative: grow under an/aerobic conditions; E. coli, staphylococci, streptococci

Anaerobiosis: life in absence of O2

632
Q

List methods of anaerobic cultivation

A 
Anaerobic jars
Gas-generating sachets 
Anaerobic cabinets 
Roll-tube/Hungate 
Robertons Cooked meat medium
633
Q

Discuss anaerobic jars

A

Vacuum/replacement method
Vacuum pump remove air
Replace atmosphere w/ gas mix; 80% N2, 10% H2, 10% CO2
Incl. Pd catalyst

634
Q

Discuss gas-generating sachets

A

Anaerogen sachets
O2 absorbed
CO2 produced
No catalyst or H2O

635
Q

Discuss anaerobic cabinets

A

Complete working chamber for organism
Contains atmosphere; 80% N2, 10% H2, 10% CO2
Pass materials in/out via air lock

636
Q

List important gram+ anaerobes

A

Cocci: peptostreptococci

Spore forming rods: clostridium

Non-spore forms:g

  • propionibacterium
  • eubacterium
  • actinomyces
  • bifidobacterium
637
Q

List important gram- anaerobes

A

Cocci: veillonella

Rods and filaments

  • bacteriodes
  • fusobacterium
  • porphyromonas
  • prevotella
  • campylobacter

Spirochaetes

  • spirochaeta
  • treponema
638
Q

Discuss dentoalveolar/PA abscess

A

Abscess develop around apices of teeth w/ necrotic and infected root canals

Oral strep, many anaerobes (predominately obligate)

639
Q

Discuss osteomyelitis

A

Rare disease
Inflammation of jaw bone cavity

Gram- anaerobes, streptococcus spp.

640
Q

Discuss chronic marginal and acute ulcerative gingivitis

A

Chronic marginal

  • inflammation confined to soft tissues of gingiva as result of plaque
  • no particular species

Acute ulcerative

  • grey gingival pseudomembrane, easily removed reveal bleeding area, destruction of interdental papillae
  • Spirochaetes (treponema spp.), prevotella intermedia, fusobacterium spp.
641
Q

Discuss periodontitis

A

Gingival inflammation extending to deeper tooth supporting structures
Destruction of PDL and alveolar bone
Porphyromonas gingivalis, prevotella intermedia, AA, capnocytophaga spp.

642
Q

Discuss pericoronitis

A

Inflammation of soft tissues surrounding crown of PE tooth

Prevotella intermedia, fuscobacterium nucleatum

643
Q

Discuss peri-implantis

A

Inflammation around implant systems replacing missing teeth

Prevotella intermedia
Porphyromonas gingivalis

644
Q

Discuss actinomycosis and sialadenitis

A

Actinomycosis

  • formation chronic granuloma w/ swelling
  • chronic; multiple discharging sinuses observed
  • actinomyces israelii

Sialadenitis

  • infection salivary glands
  • strep spp., Staph aureus, gram- anaerobes
645
Q

Discuss general features of Clostridium spp.

A

Gram+, large anaerobic spore forming rods
Prod. endospores; enable to survive adverse conditions (soil, skin)
Found: human/animal intestine, soil, H2O, decaying animal/plant matter
Pathogenic spp. prod. potent exotoxins

646
Q

List important diseases and which clostridium causes them

A

Botulism; C. botulinum

Gas gangrene; perfringens, novyi, septicum

Food poisoning; perfringens

Tetanus; tetani

Pseudomembranous colitis; difficle

647
Q

Discuss tetanus

A

Caused by C. tetani

Usually follows contamination of deep wound/injury
Spores in soil and general environment

Tetani prod. tetanospasmin (neurotoxin), tetanolysin (haemolysin)

Causes

  • trismus
  • dysphagia
  • muscle spasms
  • death by cardiac/respiratory failure

Prevention

  • immunisation w/ tetanus toxoid
  • passive immunisation; human tetanus Ig
648
Q

Discuss botulism

A

Caused by C. Botulinum

Following ingestion of pre-formed toxin food (processed meats, canned foods)

Prod. extremely potent neurotoxins (types A-G)
- human A B E

Causes

  • vomiting
  • thirst
  • muscle paralysis
  • death by cardiac/respiratory failure

Prevention
- rigorous control of processed foods

649
Q

Discuss gas gangrene

A

Polymicrobial infection of wounds
May involve C. perfringens, novyi, septicum

Caused by histotoxic clostridia that prod. range lethal and necrotising toxins

3 stages

  • contamination
  • clostridia cellulitis
  • myonecrosis

Gas formed in tissues

Causes

  • shock
  • fever
  • delirium
  • coma
  • death

Treatment: amputation

Prevention: proper wound management

650
Q

Discuss benefits of normal gut flora

A

Competition against pathogens; nutrients, niches
Attenuation mucosal immune response to pathogens (control inflammation)
Enhance integrity of mucosal barrier; provide nutrients for colonic epithelium
Aid epithelial turnover; red. bacterial adherence and no’s.
Maintenance gut mucus layer
Metabolism toxic compounds
Prod. folate and VitK from dietary precursors
Prod. luminal IgA; protect against microbial translocation through epithelium

651
Q

Outline composition of normal gut flora

A

Stomach: low pH, bile; usually sterile

SI

  • jejunum; small no. enterococci, lactobacilli
  • ileum; small no. Enterobacteriaceae, gram- anaerobes (bacteriodes fragilis)
LI
- gram-
— bacteriodes fragilis 
— fusobacterium nucleatum
— escherichia 
—salmonella
— shigella
— proteus
— klebsiella
-gram+
— sporing: clostridium 
— nonsporing: actinomyces, lactobacillus
652
Q

Discuss diarrhoeal diseases

A 
Major cause illness and death LEDC
Socioeconomic factors
- clean water
- sewage disposal 
- food quality/balance

Mechanisms
Invasive; salmonella enteritis, Shigella dysenteriae
- cramps in abdomen, pus and blood in stool
- bacterial invasion of intestinal tissues and resulting necrosis
Exotoxin; staph and clostridial food poisoning, Vibrio cholerae (cholera)
- secretion in food; live bacteria not necessary

653
Q

Discuss general features of escherichia spp. and conditions caused by E. coli

A

Gram- rods, lactose fermenter

Fimbriae: important in adhesion to host cells
Pili: conjugation allow gene transfer

Conditions

  • GI infections
  • UTI
  • septic infections (abscess, wounds)
  • neonatal meningitis
654
Q

4 pathotypes of E. Coli

A

Enterooathogenic (EPEC)
Entertoxigenic (ETEC)
Entero-invasive (EIEC)
Vero enterocytoxigenic (VTEC)

655
Q

Discuss enteropathogenic E. Coli

A

Adherence and effacing lesions of intestine
Acute enteritis in infants
High mortality
Non-invasive

Virulence: adherence to epithelium, cytoskeletal rearrangement; Ca2+ and electrolyte loss

656
Q

Discuss entertoxigenic E. Coli

A

Adherence to SI epithelium
Toxin mediated diarrhoea
Brief illness, vomiting, abdominal cramps, loose stools
Acute enteritis (all ages); travellers diarrhoea

Virulence: toxin causes adenylate cyclase ribosylation and cAMP accumulation; leads to fluid secretion

657
Q

Discuss entero-invasive E. coli

A

Causes dysentery-like disease
Invasive w/ bacteria entering LI epithelial and multiplying

Virulence: epithelial invasion; destruction and spread

658
Q

Discuss vero cytotoxigenic E. coli

A

Infection can lead to renal failure in severe cases
Produces vero toxin/Shiga-like toxins 1 (VT1) and 2 (VT2)
Causes Haemorrhagic colitis

Virulence: vero toxin
- A and B subunits
— A enzymatic, B R binder
- inhibits rRNA and therefore protein synthesis

659
Q

Discuss general features and pathogenesis of salmonella genus

A

Gram- bacilli, non-lactose fermenter
Inhabit animal intestine

Pathogenesis

  • ingestion; infectious dose varies
  • bacteria attach to epithelium of ileum mucosa, invade and multiply
660
Q

Discuss enteric fevers and outline pathogenesis

A

Caused by salmonella typhi (typhoid fever), paratyphi (paratyphoid fever)

Transmitted by contaminated food/water
- thus control by public health measure (clean drinking water, careful food regulations)

Initial fever and constipation ->
Bacteria spread from gut -> blood and lymphatic
Liver, spleen, gall bladder, kidneys involved ->
Further spread via blood

Symptoms

  • fever, malaise
  • pyrexia
  • anorexia
  • diarrhoea or constipation
  • hepatomegaly, splenomegaly
661
Q

Discuss gastroenteritis

A

Caused by salmonella

From: meat, eggs, human/animal carrier (S. enteritidis)

Symptoms

  • cramps
  • diarrhoea
  • fever
  • vomiting
  • dehydration
  • renal failure; young/elderly
662
Q

Discuss shigella and condition caused by spp.

A

Gram- rods, non-lactose fermenter

S. dysenteriae, flexneri, boydii

  • cause bacillary dysentery
  • freq. bloody, mucopurulent stools

Pathogenesis

  • invade LI epithelial
  • cells die, inflammation follows

Spread: faecal-oral (poor hygiene)
Control: inc. hygiene, dec. overcrowding

663
Q

Discuss Klebsiella bacteria

A

Gram- rods, lactose fermenter
Large mucoid colonies

Infections

  • UTI
  • severe bronchopneumonia and lung abscess
  • serious cause nosocomial infections; surgical wounds
664
Q

Discuss proteus bacteria

A

Gram-, non-lactose fermenter

Causes

  • UTI infants
  • wound infections
  • surgical infections
665
Q

Discuss general features of Vibrio spp.

A

Gram- rods
Comma shaped
Motile-polar flagellum

666
Q

Discuss Vibrio cholerae

A 
Causes cholera
Symptoms 
- vomiting
- cramps
- rice water stools
- rapid dehydration
- death; 12-24h if untreated

Enterotoxin prod.; ribosylation of adenylate cyclase regulator; inc. cAMP
H2O and electrolyte outflow into bowel

Spread: contaminated H2O/food
- overcrowded communities w/ poor hygiene
Control: public health measures

667
Q

Discuss Vibrio parahaemolyticus

A

Causes explosive diarrhoea
Common Japan, Singapore (raw seafood)
Symptoms abate ~3d

668
Q

Discuss pseudomonas aeruginosa

A

Opportunistic pathogen

Nosocomial infections: kitchen/food, staff hands, pts
Carriers; up to 30% hospital pt acquire; rapid spread possible

Exogenous infections: wounds, eyes, burns
Endogenous: immunocompromised

669
Q

Discuss campylobacter spp and infections caused

A

C. jejuni, coli; gram- rods, slender spiral

Most common cause infective diarrhoea MEDC

From; animals and birds (poultry)
Invasive in jejunum and ileum
- abdominal pain
- diarrhoea
- fever
- nausea
670
Q

Discuss helicobacter pylori

A

Gram- rod

Colonises stomach in gastric mucosa
- can cause gastritis

~25% popn. thought to be carriers
Important in peptic ulceration
V high urease producer

671
Q

Outline some of the underlying causes of STIs in the UK

A

More tolerance to sexual diversity, behaviour
Inconsistent use of condoms
High levels asymptomatic infection
Poor access to GUM clinics, sexual health services
Clinics running @ capacity; less efficient for partner notification, behavioural counselling

672
Q

Discuses the causative agent of gonorrhoea

A

Neisseria gonorrhoeae

Human pathogen, acute and relatively easy to treat
Gram-, aerobic cocci (pairs)
Catalase, oxidase+
Virulent strains have pili; attachment to host, evade phagocytosis
No serological classification
Not a commensal

673
Q

Discuss clinical presentation of gonorrhoea

A

Purulent infection of mucous membranes of urethra, cervix (rectal, pharyngeal)
Purulent discharge, dysuria
Microscopy; bacteria inside polymorphonuclear cells of inflammatory exudate

674
Q

Complications of gonorrhoea

A

Epididymitis

  • inflammation of epididymis; spread to testicle
  • possibly infarction -> necrosis

Salpingitis

  • inflammation of Fallopian tube
  • pelvic inflammation disease and sterility

Purulent conjunctivitis newborn; blindness

Disseminated gonorrhoea
- painful joints, fever, skin lesions

675
Q

Discuss treatment and control of gonorrhoea

A

Treatment
- penicillin; slow release IM injection
— tetracycline, ceftriaxone
- beta-lactamase mediated resistance

Control

  • inc. incidence since 60s; oral contraception, changing attitudes, travel
  • barrier contraception most effective
676
Q

Discuss the causative agent of syphilis

A

Treponema pallidum

Spirochaete; spiral shaped, rigid cell
Motile; polar flagella enclosed in outer membrane

Visible through dark ground microscopy

677
Q

Discuss the pathogenesis of syphilis

A

Treponema pallidum enter by penetration of intact mucosa or abraded skin

Has 1, 2, 3ry stages

678
Q

Discuss 1ry, 2ry, 3ry syphilis

A

1ry

  • bacteria multiply at entry site
  • lesion (chancre) ~3wks; painless, freq. on external genitalia
  • heals ~6wks

2ry; 2-12wks later

  • macular or pustular lesions/rash; esp. trunk, extremities
  • highly infectious lesions
  • flu-like illness

3ry; 3-30yrs later

  • slow, progressive destructive inflammatory disease
  • can affect any organ
  • neurosyphilis
  • cardiovascular
  • gummatous; bone and skin lesions
679
Q

Discuss latent and congenital syphilis

A

Latent

  • no clinical manifestations
  • serological evidence persists
  • some 2ry relapse
  • late latent infection; non-infectious

Congenital

  • in-utero transmission go foetus after 1st 3/12 pregnancy
  • possibly foetal death
  • congenital abnormalities/deformities
  • facial and tooth deformities arising few yrs later (silent infection)
680
Q

Discuss the diagnosis of syphilis

A 
Clinical 
Microscopy; 1/2ry lesions 
Serological 
Non-specific; cardiolipin Ab test
- 1ry screen
- confirmation by specific tests
- Ab reacting to cardiolipin from beef heart (similar to treponemal Ag)

Specific
- T. pallidum immobilisation test; Live treponemes immobilised by pt Ab

681
Q

Discuss treatment and control of syphilis

A

Treatment
- penicillin
— tetracycline, erythromycin, chloramphenicol

Control

  • incidence dec. since ABs
  • barrier contraception
  • indexing cases/contacts and treatment of them
682
Q

Discuss causative agent of chlamydia

A

Chlamydia trachomatis

Obligate intracellular parasites

Elementary bodies: live outside host, initiate infection
Attachment, entry
Reticulate bodies: intracellular multiplication, new EB produced infect adjacent cells

683
Q

Discuss clinical manifestations of chlamydia

A 
Urethritis 
Cervicitis 
Proctitis 
Epididymitis
Conjunctivitis
684
Q

Discuss diagnosis and treatment of chlamydia

A

Diagnosis

  • cell culture growth
  • immunofluorescent staining
  • direct Ab detection

Treatment: tetracycline

685
Q

Briefly discuss viral STIs

A

HIV

Herpes simplex; HSV1 oropharyngeal, HSV2 venereal

  • 1ry lesion on external genitalia 3-7d after infection
  • gives rise to painful ulcers
  • resolves but virus travels up sensory nerve endings
  • can recur on reactivation

HepB

  • homosexual men
  • IV drug use; tattooing, piercings
  • illness mainly due to immune response

Papilloma

  • genital warts 1-6/12 on penis, vulva, perianal regions
  • some types associated w/ cervical cancer
686
Q

Discuss aetiology of UTIs

A

Usually ascending bacterial infection

Urethra -> bladder -> kidney -> urinary tract -> bloodstream (septicaemia)

Less commonly reach kidney through haematogenous route

687
Q

Outline some predisposing factors of UTIs

A 
Disruption of urine flow; catheter, pregnancy, prostatic hypertrophy 
F; shorter urethra
Sexually active
Prevention of complete bladder emptying 
Reflux of urine
DM
688
Q

Discuss the virulence factors of some common UTI agents

A

E. Coli

  • particular pili for adherence to urethral, bladder epithelium
  • capsular polysaccharides; cause pyelonephritis, resist phagocytosis
  • haemolysin; membrane damaging

Proteus mirabilis; urease significant in pyelonephritis

689
Q

Discuss clinical features of UTIs

A 
Lower
- acute; dysuria, pain
- cloudy urine; pus cells and bacteria 
— possibility of chromic inflammatory changes in bladder, prostate, periurethral glands 
- prostatitis; Acute, chronic

Upper

  • difficult to diagnose as district from lower
  • lower and fever due to kidney involvement (pyelonephritis)
  • recurrent pyelonephritis leads to renal damage
690
Q

Discuss the diagnosis of UTI

A

Bacteriuria: midstream urine >10^5/ml
Contaminated <10^4/ml and >1 species
Infected >10^5/ml and only 1 species

Catheter pt significant when any bacteria no. isolated

Collection

  • MSU midstream
  • catheter urine
  • supra-pubic aspirate
691
Q

Treatment of UTI

A

Trimethoprim, ampicillin 5d

If resistant; cephaloxin

692
Q

Define hypersensitivity, autoreactivity, autoimmunity

A

Hypersensitivity: loss of tolerance; overreactive, immune response w/ pathological outcome

Autoreactivity: acting against own cells/tissues

Autoimmunity: loss of tolerance; response to self Ags and pathological consequences

693
Q

Define atopy and allergy

A

Atopy: inherited tendency to over produced IgE, likely present as allergy or asthma

Allergy: hypersensitivity of immune system to molecule in environment that most people do not react to

694
Q

Discuss immunodeficiency

A

Loss of function

1ry; rare; congenital or inherited

2ry; common

  • acquired as consequence of disease and treatment
  • mainly affecting phagocyte and lymphocyte function
695
Q

Contributing factors to 2ry immunodeficiency

A 
Ageing
Malnutrition 
Tumours
Cancer chemotherapy 
Trauma
Infection
696
Q

Discuss ageing as contributing factor to 2ry immunodeficiency

A

Memory T cells no. inc. but less able to expand
Fewer naive T enter pool due to involution of thymus
Immune repertoire of T and B cells dec.; dec. quality of response

Elderly less able to respond to vaccination
Inc. infections

697
Q

Discuss malnutrition as contributing factor to 2ry immunodeficiency

A

Calorie malnutrition; body protects important organs, immune system less important

Lack certain dietary elements (Fe, Zn); immune system not supported

698
Q

Discuss and cytotoxic therapy as contributing factor to 2ry immunodeficiency

A

Direct effect of tumour on immune system by immune regulatory or immunosuppressive molecules; transforming growth factor beta

Cytotoxic drugs and irradiation
- kill cells incl. stem and rapidly dividing in 1ry lymphoid tissues (marrow, thymus)

699
Q

Discuss trauma and infection as contributing factors to 2ry immunodeficiency

A

Trauma

  • burn victims, post-operative; less able to deal w/ pathogens
  • inc. infections due to immunosuppressive molecules; glucocorticoids

Microbes

  • measles
  • malaria
  • HIV; dec. T cell function and Ag processing
700
Q

Outline types of hypersensitivity reaction

A

I immediate: response to extrinsic allergens; IgE and mast cell mediated

II cytotoxic: IgG/M recognise cell surface components

III immune complex driven: complex deposited on tissues

IV delayed: T cell driven, APC present self Ag

V stimulatory

701
Q

Discuss type I hypersensitivity reaction

A

Immediate hypersensitivity

IgG directed against harmless environmental/food Ag; pollen, peanut protein
Result in release of pharmacological mediators by IgE sensitised mast cells
Prod. acute inflammation w/ symptoms asthma/rhinitis

Extreme cases: anaphylactic shock

  • vasodilation
  • smooth muscle contraction
702
Q

Effect of mast cell activation

A

GIT: inc. fluid secretion, peristalsis

Airways: dec. diameter, inc. mucus secretion

Blood vessels: inc. blood flow, permeability

703
Q

Discuss molecules released by mast cells

A

Tryptase, chymase: remodel connective tissue matrix

Toxic mediator
Histamine, heparin: toxic to parasite, inc. vascular permeability, smooth muscle contraction

Cytokine
IL-4/13: stim., amplify Th2 response
IL-3/5: eosinophil production, activation
TNF-alpha: inflammation, cytokine production, endothelium activation

Chemokine
CCL3: attract monocytes, macrophages, neutrophils

Lipid mediators
Leukotrienes C/D/E4: smooth muscle contraction, inc. vascular permeability, mucus secretion
Platelet activating factor: attract leukocytes, amplify lipid mediator production, activate neutrophils, eosinophils, platelets

704
Q

Discuss molecules released by eosinophils

A

Enzyme
Eosinophil peroxidase: toxic; catalysing halogenation, histamine release
Eosinophil collagenase: remodel connective tissue matrix

Toxic protein
Major basic protein: toxic to parasite/mammalian, histamine release
Eosinophil cationic protein: toxic parasite, neurotoxin
Eosinophil-derived neurotoxin: neurotoxin

Cytokine
IL-3/5: eosinophil production, activation
TGF-alpha/beta: epithelial proliferation, myofibroblast formation

Chemokine
IL-8: influx leukocytes

Lipid mediators
Leukotrienes C/D/E4: vascular permeability, smooth muscle contraction, mucus secretion
PAF: amplify lipid mediator, attract leukocytes, activate neutrophils, eosinophils, platelets

705
Q

Discuss type II hypersensitivity

A

IgG/M react against cell surface and ECM Ags
Damage cells/tissues by activating complement, binding and activating cells carrying Fc Rs

Target auto-Ag

  • basement membrane lung
  • AChR (myasthenia gravis)
  • erythrocytes (haemolytic anaemia)

Drug induced: penicillin bind RBC cause IgG mediated damage to cells

Dental: pemphigus, pemphigoid

706
Q

Discuss type V hypersensitivity

A

Variation type II
Ab mediated

Auto-Ab directed against hormone Rs
Function to stimulate, similar to natural ligand

Graves’ Disease: Ab to thyroid stim. hormone causing overactive thyroid

707
Q

Discuss type III hypersensitivity

A

Immune complexes formed every time Ab and Ag meet (normally removed by phagocytes)
Form in
- circulation causing systemic disease; Arthus reaction
- local sites; Farmers’ Lung (inhalation)

Persistent infection can lead to complex deposition in kidney (Strep. nephritis)

Reactivity to self-Ag can result in autoimmune disease that is immune complex mediated (lupus)

708
Q

Discuss type IV hypersensitivity

A

Occurs 24h after exposure
T cell mediated + dendritic, macrophages, cytokines

Contact hypersensitivity (skin)

  • nickel in watch strap
  • plant material; poison ivy

Dental

  • contact; lipstick
  • lichenoid reaction B mucosa to amalgam
  • oral facial granulomatosis; Oral Crohn’s
709
Q

List non-autoimmune bone disorders by inherited and acquired

A

Inherited

  • osteogenesis imperfecta
  • cleidocranial dysplasia
  • osteopetrosis

Acquired

  • osteomalacia, rickets
  • osteoporosis
  • osteomyelitis
  • Paget’s disease of bone
  • Reiter’s Syndrome
  • osteoarthritis
  • fibrous dysplasia
710
Q

Discuss general features of osteogenesis imperfecta

A

Rare, autosomal dominant condition characterised by brittle bones susceptible to #
Gene closely related to dentinogenesis imperfecta
Defective T1 collagen formation
Osteoblasts active but small; mainly woven bone formation

711
Q

Clinical features of osteogenesis imperfecta

A

Multiple #s of minimal impact
Bone distortion of healing; gross deformity, dwarfism
Parietal/frontal bossing: eversion upper part ear
Sometimes present w/ cardiac complications
Deafness, blue sclera, easy bruising, week/loose tendons/ligaments, hernias

712
Q

Discuss diagnosis and management of osteogenesis imperfecta

A

Diagnosis: clinical +

  • +ve family history
  • X-ray
  • skin biopsy
  • DNA-based sequencing

Management: no cure

  • supportive therapy: dec. #s, cope w/ disability, maintain overall health
  • bisphosphonates; prevent bone loss
713
Q

Discuss dental relevance of osteogenesis imperfecta

A

Handle pt carefully
Don’t confuse w/ physical abuse
Min. force, support jaw, ensure haemostasis
Chest deformities may contraindicate surgery
Dentinogenesis imperfecta
Bisphosphonates

714
Q

Discuss cleidocranial dysplasia

A

Rare, autosomal dominant trait on chromosome 6

Defect of membrane bone formation; skull, clavicle

715
Q

Clinical features of cleidocranial dysplasia

A

Absent/defective clavicle
Prognathic mandible due to maxillary hypoplasia
Depressed nasal bridge
Parietal, frontal, occipital bossing
Kyphoscoliosis, pelvic abnormalities may be associated

716
Q

Diagnosis and dental relevance of cleidocranial dysplasia

A

Diagnosis: clinical + X-ray

Dental

  • facial anomalies
  • hyperdontia, supernumerary teeth
  • deciduous retention; delayed/failed permanent retention
  • twisted roots, malformed crowns
  • dentigerous cyst; associated w/ unerrupted/PE crowns
717
Q

General features of osteopetrosis

A

Rare genetic disorder characterised by excessive bone density
Defective osteoclastic activity and remodelling
Dense but weak, fragile bones; heal normally
Severity varies

718
Q

Clinical features of osteopetrosis

A

None (mild)

Bone pain, #s, osteomyelitis (severe)
Infection, anaemia
Cranial neuropathies
Epilepsy, learning disability (rare)

719
Q

Discuss investigations for osteopetrosis

A

X-ray: dense (marble-like) bone appearance

Ca, PO usually normal

720
Q

Dental relevance of osteopetrosis

A 
Frontal bossing, hypertelorism
Trigeminal or facial neuropathies 
Jaw #
Delayed eruption
Osteomyelitis
721
Q

What are osteomalacia and rickets? Discuss common risk factors

A

Rickets: child; inadequate mineralisation of bone framework
Osteomalacia: failed mineralisation of replacement bone in normal bone turnover

Risk

  • VitD deficiency
  • pigmented skin, sun cream, concealing clothing, elderly, institutionalised
  • Ca2+ malabsorption
  • renal disease
  • drugs
  • pregnancy, lactation
722
Q

Clinical features and investigations of osteomalacia and rickets

A

Clinical

  • weak, hypotonic muscles
  • bone pain, #s
  • deformity, impaired growth (children)
  • hypocalcaemia, tetany, seizures
  • swellings @ costochondral junctions
Investigations 
- X-ray: pseudo-fracture 
- biochemical
— Ca, PO low/normal
— ALP raised
— PTH raised
— 25-OHVitD low
723
Q

Management and dental relevance of osteomalacia and rickets

A

Management

  • treat underlying cause
  • VitD, Ca2+ supplements

Dental
- delayed eruption (severe)
- if associated w/ malabsorption Syndrome
— May cause VitK deficiency, 2ry hyperparathyroidism

724
Q

Discuss osteoporosis

A

Common condition usually in elderly
Diminished bone mass; fragility, inc. risk #
Inadequate peak bone mass and/or ongoing bone loss
Usually spine, forearm, hips

725
Q

Modifiable and non-modifiable risk factors of osteoporosis

A

Modifiable

  • smoking, alcohol
  • low dietary Ca2+
  • insufficient VitD
  • lack physical activity
  • immobility
  • drugs: steroids, anticonvulsants, anticoagulants

Non-modifiable

  • old age
  • F: post-menopause
  • race: Caucasian, Asians
  • family history
726
Q

Clinical features and investigations for osteoporosis

A

Clinical

  • # : thoracic and Lu bar vertebrae, head of femur, D radius
  • kyphosis and height shrinkage

Investigations
- bone density by DEXA;

727
Q

Management and dental relevance of osteoporosis

A

Management

  • modifiable risk avoidance
  • dietary advice: Ca2+, VitD intake
  • bisphosphonates

Dental

  • GA contraindicated; deformed chest, vertebral collapse
  • jaw osteoporosis can cause excessive alveolar bone loss esp. Fs
  • bisphosphonates and BRONJ
728
Q

What is osteomyelitis? Distinguish b/w haematogenous and direct/contiguous source

A

Infection of bone
Staph. most common; also H. influenzae, salmonella

Haematogenous

  • bacteria seeding from blood
  • usually 1 species bacteria
  • primarily in children
  • common @ high vascular, rapidly growing metaphysis of growing bone

Direct

  • local infection caused by trauma/surgery
  • multiple bacteria
729
Q

Clinical features osteomyelitis

A

Fever, localised bone pain, erythema

If in jaw

  • deep seated boring pain w/ swelling, trismus, regional lymphadenopathy
  • lower lip paraesthesia
  • teeth tender, may be mobile
  • pus discharge from gingival crevice or several sinuses if cortical plate penetrated
730
Q

Diagnosis and treatment osteomyelitis

A

Diagnosis: history and clinical findings +

  • X-ray: marked bony destruction late stages
  • blood: leukocytosis w/ neutrophilia, raised erythrocyte sedimentation rate

Treatment
- ABs: floxacillin and fusidic acid 4-6wks starting IV

731
Q

Dental relevance of osteomyelitis

A

Can affect jaws

Acute: adult, mandible mostly, several causes, little radiographic change
Chronic
- 2ry inadequate treatment acute
- de novo from low virulent bacteria or radiotherapy complication
- marked radiographic change

Delay all elective treatment until complete resolution
Impact of underlying condition on dental treatment

732
Q

Discuss Paget’s disease of bones

A

Progressive bone enlargement and deformity from osteoblastic/clastic overactivity

Inc. abnormal bone resorption followed by weaker new bone formation (chaotic repair and renewal)
Inc. local bone blood flow and fibrous tissue

Sites: thoracic/lumbar spine, tibia, femur, pelvis, skull

733
Q

Clinical features of Paget’s disease

A

Asymptomatic (early stage)
Hands and feet usually spared

Pain: hips, knees
Deformity: skull enlargement, bowed tibia
Pathological #s
Cranial nerve compression
High output cardiac failure due to bone hypervascularity if widespread

Osteosarcoma (rare)

734
Q

Discuss diagnosis and treatment of Paget’s disease

A

Diagnosis

  • X-ray
  • radionuclide bone scans
  • raised ALP; normal Ca, PO

Treatment: bisphosphonates

735
Q

Dental relevance of Paget’s disease

A

Pt may develop heart failure; avoid GA
Hypercementosis complicate XLA
Gross symmetrical widening of alveolar ridges
Poor blood supply may predispose to chronic osteomyelitis
Hearing, sight, smell may deteriorate
Osteosarcoma in jaw (rare)

736
Q

Discuss osteoarthritis and risk factors for it

A 
Most common form arthritis 
Characterised by
- degeneration of articular cartilage
- thickening of exposed underlying bone 
- development of peri-articular cysts
- joint deformation

Risk

  • age, gender
  • genetics
  • obesity
  • # through joint
  • congenital joint dysplasia
  • Paget’s disease, gout
737
Q

Clinical features of osteoarthritis

A 
Joint pain; worse on movement 
Joint stiffness
Deformity
Loss of function 
Herberden's nodes (hard/bony swellings in distal interphalangeal joints)
738
Q

Management of osteoarthritis

A 
Refuser exercise
Weight control
Good footwear
Walking stick
Heat/cold

Drugs: NSAID, antidepressant, intra-articular injections
Surgery

739
Q

Dental relevance of osteoarthritis

A

Access complicated by age and immobility
Bleeding tendency due to aspirin
Red. manual dexterity; poor OH
TMJ involvement

740
Q

Discuss Reiter’s Syndrome

A

Triad of arthritis, urethritis, conjunctivitis
Follow gut infections (salmonella) or STI (chlamydia)
Reactive arthritis begins ~1-2wks post infection

Management

  • no specific diagnostic test
  • WCC and ESR raised
  • ABs, NSAID, steroid injection, physiotherapy

Dental

  • migratory glossitis-like pattern lesion on mucosa
  • ulceration
741
Q

Discuss fibrous dysplasia and compare monostotic and polyostotic

A

Replacement of area of bone by fibrous tissue
Localised swelling affecting single bone (monostotic) or several bones (polyostotic)
Lesions start in childhood, stabilises by adult

Monostotic

  • more common
  • affects F
  • often involves jaws, esp. maxilla

Polyostotic

  • may be unilateral
  • may involve 50% of skeleton
  • 50% have abnormal skin hyper-pigmentation
  • Albright syndrome
742
Q

Diagnosis and management of fibrous dysplasia

A

Diagnosis

  • X-ray: ground glass appearance
  • Ca, PO normal; ALP raised

Management

  • self-limiting; cease progression post puberty
  • bisphosphonates treatment may have implications
  • testolactone for precocious puberty of Albrights
  • surgery; correct residual cosmetic defect
  • endocrine conditions may complicate treatment
743
Q

Dental relevance of fibrous dysplasia

A

Facial bones freq. involved monostotic type
- 25% polyostotic
Hyperthyroidism and DM may be associated w/ polyostotic type

744
Q

Discuss autoimmunity/autoimmune disease

A 
Immune system recognition failure/malfunction 
Abs and T cells produced and directed against self
Initiated by
- defect in immunological tolerance
- presence of sequestrated Ags
- infection; viruses
- drugs; methyldopa
- chemicals
745
Q

Discuss rheumatoid arthritis

A

Chronic multi-system autoimmune disease
Characterised by auto-Ab (rheumatoid factor, an IgM) directed against IgG

Immune complex formation -> complement activation, synovial inflammation, destructive joint disease

Genetically predisposed
Environmental factors (virus, smoking) trigger and maintain inflammation
746
Q

Joints commonly involved in rheumatoid arthritis

A

Wrists, elbow, shoulder
Hips, knees, ankles
Upper cervical spine

Index and middle metacarpophalangeal joints
Proximal interphalangeal joints
Metatarsophalangeal

747
Q

Clinical features of acute rheumatoid arthritis

A 
Insidious onset
Systemic features
- early morning stiffness affected joint
- generalised afternoon fatigue
- malaise
- weight loss
- generalised weakness
- occasional low-grade fever

Joint; symmetrical
- pain, swelling, stiffness

748
Q

Clinical features chronic rheumatoid arthritis

A

Joints held in flexion to min pain
- joint capsular deviation
- flexion contractures
— ulnar deviation of fingers
— swan-neck, Boutonnière deformities
Stretching of joint capsule; joint instability
Wrist synovitis compressing median nerve; carpal tunnel

749
Q

Extra-articular clinical features rheumatoid arthritis

A

Pulmonary fibrosis, pleurisy
Pericarditis, myocarditis, vasculitis, valvulitis
Atlantoaxial subluxation, spinal cord compression
Lymphadenopathy
Uveitis
Anaemia

750
Q

Investigations for rheumatoid arthritis

A

Serology

  • rheumatoid factor +ve (sensitive)
  • anti-CCP/ACPA+ (specific)

Elevated ESR, CRP

X-rays

  • soft tissue swelling
  • narrowing of joint space
  • joint erosion

FBC

  • normocytic anaemia
  • neutropenia
  • thrombocytosis

Hyoergammaglobulinaemia

751
Q

Management of rheumatoid arthritis

A

Symptom modifying drugs
- acetaminophen, NSAID, intra-articular corticosteroids

Disease-modifying anti-rheumatic drugs
- methotrexate, gold, antimalarials, sulfasalazine, cyclosporine

Surgery: joint replacement

Supportive

  • smoking cessation, rest, good nutrition, tolerable exercise
  • splints, appliances: red. pain, preserve function, facilitate mobility
752
Q

Dental relevance of rheumatoid arthritis

A

Sudden extension of neck; atlanto-axial subluxation
Red. manual dexterity; poor OH
Drugs; ulcers, lichenoid reaction
TMJ; painless restricted opening
Sjogren syndrome; xerostomia, candidiasis, caries, sialadenitis

753
Q

Discuss ankylosing spondylitis

A

Seronegative spondyloarthropathy
Genetic predisposition, environmental factors may play role
Affects axial skeleton (spine) and large peripheral joints

754
Q

Clinical features of ankylosing spondylitis

A

Insidious

Early

  • nocturnal lower back pain, morning stiffness
  • para-spinal muscle spasm
  • worsening pain, tenderness in sacroiliac region due to sacroilitis

Late

  • hip involvement; severe hip arthritis
  • kyphosis
  • loss of lumbar lordosis
  • bent-forward posturing

Recurrent Acute uveitis
Aortic insufficiency, angina, pericarditis
Compromised pulmonary function, red. chest expansion
Achilles and patellar tendinitis

755
Q

Investigations for ankylosing spondylitis

A

X-ray
Early; symmetric
- subchondral erosions; sclerosis or later narrowing, eventual fusion of sacroiliac joints
- upper lumbar vertebrae squaring w/ sclerosis at corners
- spotty ligamentous calcification
Late
- bamboo spine appearance from prominent syndesmophytes
- diffuse para-spinal ligamentous calcification
- osteoporosis

FBC
Inflammatory markers/acute phase reactants

756
Q

Treatment of ankylosing spondylitis

A

Goal

  • pain relief
  • maintain joint range of motion
  • prevent end-organ damage
757
Q

Dental relevance of ankylosing spondylitis

A

Avoid GA: restricted mouth opening, respiratory and cardiac complications

TMJ involvement

Pt difficulty placing neck on headrest

758
Q

Discuss psoriatic arthritis

A

D interphalangeal joints toes and fingers
May also affect spine and sacroiliac joints
Resembles RA

Diagnosis; clinical +

  • ESR normal
  • X-ray helpful, blood tests unhelpful

Management

  • drugs; similar to RA
  • analgesic, NSAID, intra-articular corticosteroid
  • anti-TNF; control arthritis and skin lesions

Dental

  • rarely affect TMJ
  • mucosa psoriasis occasionally seen histologically
  • methotrexate/anti-TNF may cause ulcers
759
Q

Discuss Sjögren’s syndrome

A

Autoimmune exocrinopathy characterised by

  • lymphocyte infiltration in salivary and lacrimal glands
  • progressive acinar destruction in salivary and lacrimal glands

1ry (Sicca Syndrome)

  • xerostomia
  • dry eyes (keratoconjunctivitis sicca)

2ry

  • dry mouth, eyes
  • connective tissue disease
760
Q

Investigations and dental relevance of Sjorgen’s syndrome

A

Investigations
Serology: antinuclear ABs, inc. ESR, hypergammaglobulinaemia
Oral: sialometry, labial gland biopsy
Imaging: sialography, salivary scintiscanning

Dental

  • xerostomia; candidiasis, caries, dysphonia, sialadenitis
  • early onset lymphocytic infiltration: parotid gland swelling
  • late onset: indicative of progression to lymphoma
  • 2ry SS: anaemia
761
Q

Causes and histological features of oesophagitis

A

Causes

  • GORD
  • other chemical stimuli
  • infection: Candida, HSV, cytomegalovirus (CMV)
  • eosinophilic oesophagitis

Histology

  • ulceration
  • inflammatory cells
  • epithelial hyperplasia
762
Q

Discuss Barrett’s oesophagus

A

Columnar metaplasia: stratified squamous epithelium replaced by gastric/intestinal type columnar epithelium

Prolonged reflux increases risk
M>F

Prevalence rising

763
Q

Types of oesophageal tumours

A

Benign

  • squamous papilloma
  • leiomyoma

Malignant

  • adenocarcinoma
  • SCC
764
Q

Symptoms and clinical features of oesophageal carcinoma

A

Symptoms

  • dysphagia
  • weight loss

Clinical

  • aspiration pneumonia
  • fistulas
765
Q

Macroscopic features and microscopic types of oesophageal carcinoma

A

Macroscopic

  • polyp/exophytic
  • central ulcer
  • infiltrating

Microscopic

  • adenocarcinoma 60%
  • SCC 35%
  • other 5%
766
Q

Aetiology and general features of oesophageal adenocarcinoma

A

Aetiology

  • Barrett’s oesophagus; 30-40x inc.
  • factors associated w/ GORD; obesity, alcohol, hiatus hernia
  • genetic factors

Histology: similar to gastric adenocarcinoma
5yr survival 32%

767
Q

Risk factors and general features of oesophageal SCC

A

Risk

  • geographic: Russia, Iran
  • tobacco, alcohol
  • dietary: nitrates, nitrosamines, vit deficiency
  • oesophagitis
  • achalasia
  • genetic conditions; tylosis

Site

  • U1/3 10%
  • M1/3 65%
  • L1/3 25%

Symptoms present late
Locally invasive; pleura, pericardium
5yr survival 5-10%

768
Q

What is chronic gastritis?

A

Chronic inflammation of gastric mucosa

Common
Often asymptomatic

Classified by histology, aetiology, distribution

769
Q

Histological features and complications of H pylori associated chronic gastritis

A

Histology

  • chronic inflammatory cells
  • neutrophils
  • H pylori visible
  • atrophy and intestinal metaplasia w/ T

Complications

  • peptic ulceration
  • gastric carcinoma
  • gastric lymphoma
770
Q

4 other types of chronic gastritis

A

Autoimmune

  • fundus > antrum
  • atrophy common

Granulomatous: TB, Crohn’s, sarcoidosis
Chemical: NSAID, alcohol, Nike reflux
Radiation

771
Q

Common sites of peptic ulceration

A

Stomach

Duodenum

772
Q

Predisposing factors and complications of peptic ulceration

A

Predisposing

  • NSAID
  • H pylori
  • alcohol
  • Zollinger-Ellison syndrome (gastric acid hypersecretion)

Complications

  • bleeding
  • perforation
  • obstruction
773
Q

Types of stomach polyps and tumours

A

Non-malignant

  • polyps: fundic gland polyp, hyperplastic polyp
  • adenoma: potentially malignant

Potentially/Malignant

  • adenocarcinoma
  • lymphoma
  • GI stromal tumour
  • carcinoid/endocrine tumour
774
Q

Risk factors for gastric carcinoma

A

Chronic gastritis, intestinal metaplasia

  • H pylori
  • autoimmune

Diet: nitrates, nitrosamines, lack fruit/veg
Smoking
Hereditary: early gastric cancer
Adenoma

775
Q

Clinical features and spread of gastric carcinoma

A

Clinical

  • weight loss
  • vomiting
  • abdominal pain

Spread

  • local: pancreas
  • metastasis; lymph noises, liver, lungs
  • peritoneal seeding
  • transcoelomic; to ovaries

5yr survival 5-15%

776
Q

Discuss Coeliac disease

A

Immune reaction to gliadin
Serum anti-gliadin and anti-endomysial Abs

Histology: flat, small Bowen mucosa (villous atrophy)

Diagnosis

  • histology, serology (Ab+)
  • improvement w/ GF diet

Complications

  • Fe/folate malabsorption; anaemia
  • Ca malabsorption; osteoporosis
  • VitD malabsorption; osteomalacia
  • T cell lymphoma
777
Q

Types of small intestine tumour

A

Benign: hamartomas, hyperplastic polyps

Potentially/malignant

  • carcinoid/endocrine tumour
  • GIST
  • Lymphoma
  • adenocarcinoma
778
Q

Discuss small intestine carcinoid/endocrine tumour

A

Usually incidental
May obstruct
Characteristic histology w/ expression of endocrine markers

May prod. hormones

  • carcinoid Syndrome: diarrhoea, wheezing, flushing,p
  • Zollinger-Ellison syndrome: multiple upper GI ulcers
779
Q

Discuss acute appendicitis

A

Common
Central abdominal pain followed by R iliac fossa pain
May perforate and cause peritonitis
Surgical emergency

Histology

  • ulceration of mucosa
  • neutrophil rich inflammatory infiltrate through wall
780
Q

Discuss Crohn’s disease

A

Chronic inflammatory disorder
Characterised by crampy abdominal pain w/ diarrhoea
Can occur anywhere in GIT

781
Q

Macroscopic features of Crohn’s

A 
Discontinuous involvement; 'skip' lesions 
Thickening of wall
Strictures
Linear ulcers
Fistulas w/ bowel, skin, other organs
Perianal fissures, fistulas
782
Q

Extra-intestinal complications of Crohn’s

A

Polyarthritis/sacroilitis/ankylosing spondylitis
Uveitis
Erythema nodosum

783
Q

Histology of Crohn’s disease

A

Transmural chronic inflammation
Non-necrotising granulomas
Ulcers

784
Q

Discuss ulcerative colitis

A

Chronic inflammatory disorder
Affects large bowel
Characterised by bloody and freq. diarrhoea

785
Q

Macroscopic appearance and histology of ulcerative colitis

A

Macroscopic

  • continuous; starts distally, spreads proximal
  • erythema, granularity, ulceration of mucosa, pseudopolyps

Histology

  • diffuse chronic inflammation of mucosa
  • mucosal architectural distortion
786
Q

Complications of ulcerative colitis

A

Extra-intestinal

  • arthritides
  • 1ry sclerosing cholangitis
  • cholangiocarcinoma

Intestinal
- toxic megacolon
- dysplasia and colorectal carcinoma
— proportional to extent, duration of disease

787
Q

Discuss diverticular disease

A

Large intestine disease
Most common >60, sigmoid colon
Outpouchings of mucosa through walk @ weak points
Associated w/ low fibre diet

788
Q

Complications of diverticular disease

A

Peri-diverticular abscess
Stricture
Perforation, peritonitis

789
Q

Discuss colorectal carcinoma

A

60-70yo

Clinical

  • rectal bleeding
  • change in bowel habit
  • weight loss, malaise

Macroscopic

  • polypoid
  • ulcerated

Histology
- well/moderately/poorly differentiated

790
Q

Common bacterial agents detected in oral cavity

A 
Cocci
Gram+
- enterococcus
- peptostreptococcus
- streptococcus 
Gram-
- branhamella
- neisseria
- veillonella
Rods
Gram+
- actinomyces
- bifidobacterium
- corynebacterium
- lactobacillus 
Gram-
- porphyromonas
- prevotella
- aggregatibacter 
- fusobacterium
791
Q

Discuss common fungal and viral agents found in oral cavity

A

Fungal; Candida spp.

  • C. albicans largest proportion oral fungi
  • 50% popn. carry

Viral

  • HSV1: most common
  • cytomegalovirus: saliva most individuals
  • Hep, HIV: saliva asymptomatic individuals
  • Coxsackie, papilloma: associated w/ lesions
792
Q

How are oral infections classified?

A
  1. Bacterial, fungal, viral
  2. Endo/exogenous
  3. Hard/soft tissue
793
Q

Discuss endogenous and exogenous classification of oral infections

A

Endogenous: caused by microorganisms normally found in mouth

Exogenous

  • microorganism not normally found in oral cavity
  • 1ry infections: HSV, 1ry syphilis
  • 2ry manifestations: TB, viral infections
794
Q

4 examples of bacterial hard tissue oral infections

A

Caries: S. mutans, lactobacilli

Abscesses: oral strep., gram- anaerobes (prevotella, porphyromonas, fusobacterium, treponema)

Dry socket: various incl. actinomyces spp.

Osteomyelitis: staph aureus, others

795
Q

5 examples endogenous soft tissue oral infections

A

PD disease: AA, porphyromonas, prevotella

Acute ulcerative gingivitis: fusobacterium, treponema, prevotella intermedia

Pericoronitis: Porohyromonas gingivalis, prevotella intermedia

Sialadenitis: staph aureus, oral strep.

Actinomycosis: actinomyces Israelii

796
Q

3 examples exogenous soft tissue oral infections

A

Gonorrhoea: neisseria gonorrhoeae

Syphilis: treponema pallidum

Tuberculosis: mycobacterium tuberculosis

797
Q

Example of fungal soft tissue oral infection

A

Candidiasis: C. albicans, Candida spp.

798
Q

Examples of 1ry and 2ry viral soft tissue oral infections

A

1ry

  • herpetic stomatitis: HSV
  • herpes zoster: Varicella-Zoster
  • herpangia: Coxsackie A
  • Oral warts: papilloma

2ry

  • hand, foot, mouth disease: Coxsackie A
  • glandular fever: Epstein-Barr
799
Q

How do disturbances to oral microflora allow for oral infection to arise?

A

Allow for:

Selective overgrowth of endogenous species; candidiasis in AIDS pt
Displacement of endogenous species: actinomycosis following trauma to mucosa/jaws
Introduction of exogenous species: TB lesions following trauma to mucosa

800
Q

Physiological predisposing factors for oral infection

A

Old age, infancy: dec. Abs, saliva flow; candidiasis, root caries
Pregnancy: unknown mechanism; gingivitis

801
Q

How is trauma a predisposing factor for oral infections ?

A

Local: loss of tissue integrity; various opportunistic infections
General: general debilitation, dehydration; candidiasis

802
Q

Malnutrition, endocrine disorders and AIDs as predisposing factors to oral infections

A

Malnutrition: Fe/folate deficiency; candidiasis

Endocrine disorder: unknown mechanisms; fungal infections

AIDs: red. host immune defence; opportunistic, candidiasis

803
Q

AB therapy, chemotherapy, oral malignancies as predisposing factors to oral infections

A

AB: loss of colonisation resistance, selection of resistant flora; candidiasis, opportunistic

Chemotherapy: xerostomia, local mucosal effect; candidiasis, caries

Oral malignancies: xerostomia, loss of muscular function; candidiasis, caries

804
Q

Discuss antibiotics used in treatment of oral infections

A

Metronidazole

  • inc. activity against anaerobes
  • pt warned re effects alcohol, metallic taste

Amoxicillin

  • broad spectrum, good oral absorption, interferes cell wall synthesis
  • predisposes to candidiasis

Tetracycline; AB of choice

  • broad spectrum, significant risk exacerbating renal failure
  • not given pt history/renal disease, children <12, pregnant/breastfeeding
805
Q

Discuss topical antifungals used in treatment of oral infections

A

Nystatin

  • polyene, not absorbed by gut
  • pastilles

Amphotericin

  • polyene, not absorbed by gut
  • lozenges (discontinued in U.K. 2010)

Miconazole

  • gel and denture lacquer (denture left in inc. compliance)
  • interacts w/ warfarin
806
Q

Systemic antifungals used in treatment of oral infections

A

Ketoconazole

  • imidazole
  • not used pt history liver disease or alcoholics

Fluconazole

  • triazole
  • well absorbed by mouth
  • better toxicity profile
  • v expensive
807
Q

Discuss antivirals used in treatment of oral infections

A

Acyclovir

Topical: herpes labialis; cream used @ prodromal stage
Systemic
- HCP treating immunocompromised pt
- those who present within 48h herpes infection

808
Q

Discuss 1ry hypertension

A 
Most common
Multiple factor
Genetic predisposition 
Environmental factors
Mechanism unclear
809
Q

Predisposing factors for 2ry hypertension

A

Renal diseases

  • renal parenchyma disease, pyelonephritis, polycystic renal disease, post transplant
  • Reno-vascular disease

Endocrine diseases

  • hyperaldosteronism
  • pheochromocytoma
  • Cushing Syndrome
  • congenital adrenal hyperplasia
  • hyperthyroidism

Coarctation of aorta
Excessive alcohol

Drugs

  • oral contraceptives
  • sympathomimetics, NSAIDs, corticosteroids, cocaine
810
Q

Clinical presentation of hypertension

A

Asymptomatic until complications develop

Dizziness, flushed facies, headache, fatigue, epistaxis, nervousness, retinal changes

Inc. risk

  • heart failure
  • renal failure
  • stroke
  • coronary artery disease, myocardial infarction
  • death
811
Q

Complications of hypertension

A

Generalised arteriolosclerosis; small arterioles (eyes, kidney)

Kidney: marrow arteriolar lumen; inc. total peripheral resistance -> worse hypertension

Inc. afterload: left ventricular hypertrophy; dilated cardiomyopathy -> heart failure

Thoracic aortic dissection
Abdominal aortic aneurysms

812
Q

Investigations for hypertension

A

Multiple BP measurements
Urinalysis and urinary albumin:creatinine
Blood: fasting blood glucose, Na/K, lipid profile, creatinine, thyroid function test
ECG

813
Q

Management of hypertension

A

Weight loss and exercise; regular aerobic physical activity
Smoking cessation
Diet
- inc. fruit, veg; dec. salt, alcohol
- low-fat dairy products w/ red. saturated and total fat
Medication

814
Q

Examples of antihypertensives

A 
Alpha-blocker: doxasozin, prazosin
ACE-I: captopril, enalapril, ramipril 
Angiotensinogen 2 R blocker: candesartan, losartan
Beta-blocker: atenolol, propranolol 
Ca2+-C blocker: nifedipine, verapamil 
Diuretics: furosemide, spironolactone 
Sympatholytics: clonidine, methyldopa
Vasodilators: hydralazine, minoxidil
815
Q

Dental relevance of hypertension

A

Stable: receive care in short, minimally stressful appointments

Drug side effects

  • dry mouth
  • ulcer
  • lichenoid lesion
816
Q

Discuss atherosclerosis and risk factors

A

Patchy intimal plaques encroach on lumen of medium/large arteries

Contain: lipids, inflammatory cells, smooth muscle cells, connective tissue
Initiated by endothelial injury

Risk

  • hyperlipiaemia, DM, smoking, family history
  • sedentary life, obesity, hypertension
817
Q

Compare stable and unstable plaque atherosclerosis

A

Stable: regress, remain static or grow slowly; stenosis or occlusion

Unstable: vulnerable to spontaneous rupture, erosion or fissuring

818
Q

Discuss triggering of acute thrombosis in unstable plaque atherosclerosis

A

Triggered by plaque contents
Leads to
- thrombus becomes organised and incorporated into existing plaques
- rapidly occlude vascular lumen; acute ischaemic event
- thrombus may embolise
- plaque fill w/ blood, balloon, occlude artery
- plaque contents embolise, occlude vessels downstream

819
Q

Clinical features of atherosclerosis

A

Initially asymptomatic

Stable plaque grows; red. arterial lumen by >70%
- stable angina, transient ischaemic attacks, intermittent claudication

Unstable plaque ruptures; acutely occlude major artery

  • unstable angina, ischaemic stroke, myocardial infarction
  • pain in limbs

Sudden death w/o preceding un/stable angina
Aneurysms and arterial dissection

820
Q

Investigations for atherosclerosis

A

CT angiography
Blood: fasting lipid profile; plasma glucose, HbA1C (glycated haemoglobin) levels

Cather-based imaging

  • IV ultrasonography
  • angioscopy
  • plaque thermography
  • optical coherence tomography
  • elastography/immunoscintigraphy
821
Q

Management of atherosclerosis

A

Diet: less saturated fat, no trans fat, fruit, veg, fibre, moderate alcohol
Smoking cessation, regular exercise

Drugs for diagnosed risk factors

  • statins; hyperlipiaemia
  • ACE-I (captopril), beta-blocker (atenolol); hypertension
  • metformin; DM
  • aspirin, clopidogrel, prasugrel; antiplatelet drugs
822
Q

Discuss angina pectoris

A

Precordial discomfort/pressure due to transient myocardial ischaemia w/o infarction
Cardiac workload and myocardial O2 demand exceed supply via narrowed coronary arteries
Narrowed due to atherosclerosis, spasm, embolism

823
Q

Compare unstable and stable angina

A

Stable: predictable; inc. workload leads to ischaemia

Unstable: chest pain @ rest, inc. freq./intensity of episode

824
Q

Clinical features of angina

A

Triggered by exertion or strong emotion

Persists for few min and subsidies w/ rest
Described as discomfort below sternum
Radiate: L shoulder, inside L arm, back, throat, jaw, teeth

Atypical: bloating, has, indigestion, abdominal distress
Nocturnal angina

825
Q

Investigations for angina pectoris

A

ECG
Stress testing w/ ECG/echo
Coronary artery angiography
IV sonography

826
Q

Treatment of angina pectoris

A

Relieve acute symptoms: sublingual nitroglycerin
Prevent ischaemia: antiplatelet, beta-blocker (atenolol)
Prevent future ischaemic event: Ca2+-C blocker (nifedipine), Long acting nitrates

827
Q

Discuss myocardial infarction

A

Myocardial necrosis due to acute obstruction of coronary artery

Similar pain to angina but more severe, longer-lasting and associated w/ dyspnoea, diaphoresis, nausea, vomiting

Temporary or little relief by rest or nitroglycerin

Pale clammy skin, cyanosis, threads pulse, syncope

828
Q

Investigations of myocardial infarction

A

Initial and serial ECGs
Serial cardiac markers
Coronary angiography

829
Q

Discuss treatment and management of myocardial infarction

A

Treatment
Prehospital care: O2, nitrates, aspirin, opioids (pain)
Drug
- antiplatelet, antianginal, anticoagulant
- statins, ACE-I (captopril), beta-blockers (atenolol)
Perfusion therapy
- fibrinolytics
- angiography w/ percutaneous coronary intervention
- coronary artery bypass surgery

Management

  • lifestyle; diet, weight loss, smoking cessation, exercise,
  • drugs: antiplatelets, beta-blocker, ACE-I, statins
830
Q

Discuss acute and sub-acute bacterial infective endocarditis

A

Acute

  • aggressive; 7d of bacteraemia
  • common elderly, IV drug users
  • staph aureus most common

Sub-acute

  • insidious; 2-3wks of suspected bacteraemia
  • strep viridans most common
831
Q

Clinical features infective endocarditis

A 
Fever, weight loss, night sweats, malaise, embolic phenomena, haematuria
Splinter haemorrhages 
Conjunctiva petechiae 
Osler's nodes
Janeway's lesions
832
Q

Causes of left ventricle heart failure

A 
Coronary artery disease
DM, obesity
Hypertension
Valvular heart disease
Hyperthyroid disease
Substance abuse; cocaine, smoking
833
Q

Pathogenesis of left ventricle heart failure

A

Left ventricle dysfunction ->
Dec. cardiac output ->
Compensatory mechanisms (sympathetic NS, renin-angiotensin-aldosterone system) ->
Inc. afterload ->
Further myocardial deterioration and worsening myocardial contractility ->
Cycle; progression of cardiac failure

834
Q

Clinical features of left ventricle heart failure

A

Pulmonary venous pressure inc.
Pulmonary capillary pressure exceeds oncotic
Fluid extravasates; capillaries -> interstitial space and alveoli (oedema, crackles)

Red. pulmonary compliance, inc. work of breathing (shortness of nreath’ dyspnoea)

Dec. systemic arterial oxygenation (fatigue, exertional dyspnoea)
Myocardial deterioration (central and peripheral cyanosis)
835
Q

Causes of right ventricle heart failure

A

Previous LV failure
Severe lung disorder (cor-pulmonale)
Multiple pulmonary emboli and RV infarction

836
Q

Pathogenesis of right ventricle heart failure

A

RV dysfunction ->
Systemic venous pressure inc. ->
Fluid extravasation and oedema, in dependent tissues and abdominal viscera ->
Fluid accumulation in peritoneal cavity

837
Q

Clinical features right ventricle heart failure

A 
Hepatomegaly, splenomegaly 
Abdominal distension (ascites)
Inc. jugular venous pressure
Nausea, vomiting
Chronic venous congestion in viscera; weight loss, malabsorption 
Peripheral oedema 
Nocturnal diuresis
Swelling of fingers and hands
838
Q

Investigations for heart failure

A 
FBC
Electrolyte, urea
ECG, echo
Thyroid function test
Cardiac MRI
Coronary angiography 
Chest radiograph
839
Q

Treatment of heart failure

A

Symptomatic relief

  • diuretics; furosemide (loop)
  • nitrates; isosorbide nitrate
  • digoxin

Management, inc. survival

  • ACE-I; captopril, ramipril
  • beta-blocker: atenolol, propranolol
  • diuretic (aldosterone antagonist); spironolactone
  • angiotensin 2 R blocker; losartan
840
Q

Before a medical emergency occurs, how can we prepare pt?

A

Obtain up-to-date medical and dental history
Identify risks, minimise ME occurrence
Modify treatment, refer to hospital (if req.)
Liaise w/ GP before treatment (if req.)

841
Q

In physical evaluation of pt before ME what should we observe?

A 
Posture 
Body movements 
Quality of speech
Skin: feel, colour 
Odours on breath 
Rate and pattern of respiration
842
Q

How can dental team prepare for ME?

A

Practitioners req. to be competent in managing common ME
Staff undergo training appropriate to clinical responsibility level
Training standardised and conform to resuscitation council guidelines
Training updated at least annually
Training incl. BLS, CPR, AED use, self-inflating bag and mask devices
Skills regularly practiced on site using ME scenarios

843
Q

How can the practice be prepared for a ME?

A

Availability, easy and rapid access to ME drugs and equipment
ME drugs stored together in emergency drugs container
Drugs in solution in pre-filled syringe
Process for medical risk assessment in emergency
Plan for summoning medical assistance in emergency (999)

844
Q

5 systemic classifications of ME

A 
CV
Respiratory 
Neurological 
Metabolic 
Miscellaneous
845
Q

CV MEs

A 
MI
Angina
Cardiac arrest
Syncope (vasovagal attack); fainting
Postural hypotension
846
Q

Respiratory MEs

A 
Hyperventilation 
Asthma
Respiratory arrest 
Acute respiratory obstruction 
- inhaled foreign body 
- angio-oedema
847
Q

Neurological MEs

A

Cerebrovascular accident (CVA); stroke
Seizures/epilepsy; status epilepticus
Loss of consciousness

848
Q

Metabolic MEs

A

Hyperglycaemia
Hypoglycaemia
Addisonian crisis (acute adrenal insufficiency)

849
Q

Miscellaneous MEs

A

Anaphylaxis
Drug allergy
Drug overdose
Drug interactions

850
Q

8 ME drugs

A
  1. GTN spray
  2. Salbutamol inhaler
  3. Adrenaline
  4. Aspirin
  5. Glucagon
  6. Glucose tablet/gel/solution/powder
  7. Midazolam
  8. O2
851
Q

Discuss use of glycerol trinitrate spray in ME

A

Dose: 400 microg
Route: sublingual
ME: angina
Action: vasodilator

852
Q

Salbutamol inhaler use in ME

A

Dose: 100microg
Route: inhalation
ME: asthma
Action: beta-2 agonist

853
Q

Adrenaline use in ME

A

Dose: 0.5mg
Route: IM
ME: anaphylaxis
Action: alpha and beta agonist, mast cell stabilisation, glucose elevation

854
Q

Aspirin use in ME

A

Dose: 300mg
Route: oral
ME: MI
Action: antiplatelet

855
Q

Glucagon use in ME

A

Dose: 1mg
Route: IM
ME: unconscious hypoglycaemia
Action: glycogenolysis

856
Q

Glucose use in ME

A

Dose: -
Route: oral
ME: conscious hypoglycaemia
Action: -

857
Q

Midazolam use in ME

A

Dose: 10mg/ml
Route: buccal
ME: epilepsy
Action: muscle relaxant

858
Q

O2 use in ME

A

Dose: 15L/min
Route: inhalation
ME: syncope, anaphylaxis, epilepsy, MI, Addisonian crisis, CVA
Action: -

859
Q

11 pieces of ME equipment

A
  1. Portal O2 cylinder
  2. O2 face mask w/ reservoir and tubing
  3. Pocket mask w/ O2 port
  4. Basic oropharyngeal airways (size 1-4)
  5. Self-inflating bag and mask apparatus
  6. Child and adult face masks for self-inflating bag
  7. Portable suction
  8. Single use sterile syringe, PPE, needles
  9. Spacer for inhaled bronchodilators
  10. Automated blood glucose measurement device
  11. Automated External Defibrillator (AED)
860
Q

What are DR’S ABCDE?

A

Danger: assess area
Response: does pt respond to touch and/or voice
Shout: for help, assistance

Airway
Breathing 
Circulation
Disability 
Exposure
861
Q

Assessment of airway in ME

A

Signs of airway obstruction

  • paradoxical chest and abdominal movement
  • use of accessory respiratory muscles
  • central cyanosis (late stage)
  • partial obstruction: wheeze, stridor, gurgling, snoring
  • complete: no breathing sounds

ME
- simple methods of airway clearance
— head tilt/chin lift or jaw thrust
- oropharyngeal airway adjuncts

O2 @ 15L/min

862
Q

Breathing assessment in ME

A

Look, listen, feel for signs of respiratory distress
Count respiratory rate
Assess breath depth, respiratory pattern, chest expansion normal and equal
Listen short distance from ear
Breathing depth or rate inadequate/undetectable; O2, 999
Common: hyperventilation, panic attacks; reassurance

863
Q

Circulation assessment in ME

A

Check colour hands, fingers; blue, pink, pale, mottled
Check limb temp.
Measure capillary refill time
Count pulse rate

Weak pulses + dec. consciousness + slow capillary refill = low BP

  • lie flat, legs up
  • no response, call 999

Faints/vasovagal attack most likely cause of circulation problem

  • lie flat, raise legs
  • follow ABCDE so no other cause
864
Q

Disability step in ME

A

Review and treat ABCs: exclude hypoxia and low PB
Check dug record for reversible drug induced causes of depressed consciousness
Examine pupils; size, light reaction
Rapid initial assessment of consciousness: Alert Vocal stimuli Painful stimuli Unresponsive

Measure blood glucose exclude hypoglycaemia (<3mmol/L give glucose)
Nurse unconscious pt in recovery position if airway not protected

865
Q

Exposure step in ME

A

Loosening/removal of some of pt’s clothes may be necessary for proper treatment and assessment
- rashes (anaphylaxis), defibrillation
Respect dignity, minimise heat loss

866
Q

Compare neurosis and psychosis

A

Neurosis

  • common
  • quantitatively different
  • excessive degrees of normal phenomena
  • anxiety, depression, somatisation
  • repeatedly worried and wanting checked, reassured its not

Psychosis

  • rare
  • qualitatively different
  • thought disorders
  • hallucinations, delusions
  • manic depressive illness, schizophrenia
867
Q

Discuss anxiety neuroses

A

Various combinations of psychological and physical manifestations of anxiety
Extensions of normal emotions
Signs and symptoms associated w/ sympathetic NS overactivity
Occur as panic attacks or persistent state (generalised anxiety disorder)
If due to specific trigger = phobia

868
Q

7 psychological symptoms of anxiety

A
  1. Fearful anticipation
  2. Irritability
  3. Restlessness
  4. Sensitivity to noise
  5. Subjective reports of poor memory
  6. Repetitive worrying
  7. Poor conc.
869
Q

Physical symptoms of anxiety (affecting body systems)

A

RS: difficulty inhaling, chest construction, over breathing

CVS: cardiac discomfort, palpitations

GI: excess wind, aerophagy, dysphagia, dry mouth, loose stools

GU: inc. freq. urination

Neuro: tinnitus, dizziness, blurred vision, paraesthesia

Musculoskeletal: aching, stiffness

Sleep: difficulty, night terrors, intermittent waking

870
Q

Discuss panic disorders

A

Type of anxiety neuroses

Recurrent, episodic, severe attacks lasting few mins
Unpredictable; not restricted to particular situation/set of circumstances

Psychological symptoms

  • intense fear, impending doom, impaired conc., depersonalisation
  • fear of going crazy, losing control, death

Physical symptoms

  • chest tightness, palpitations, tachycardia, paraesthesia
  • sweating, dry mouth, shortness of breath
871
Q

Discuss generalised anxiety disorder

A

Generalised, persistent, excessive anxiety about everyday circumstances >6mnth
Prolonged waxing, waning course
Exclude organic causes

872
Q

Treatment of generalised anxiety disorder

A

Psychological

  • reassurance, counselling, psychotherapy
  • behavioural therapy once avoidance behaviour established

Pharmacological

  • anxiolytic; benzodiazepines (diazepam)
  • antidepressants (anxiolytic properties); amitriptyline (TCA)
  • beta-blockers; atenolol
873
Q

Discuss simple specific phobias

A

Phobic anxiety neuroses

Childhood onset (animal phobia); early adult for specific phobias 
- animal/insect, heights, thunderstorms, darkness

Anxious thoughts occur in anticipation of event
Avoidance habits develop

Management: CBT, flooding (huge amount of phobia)

874
Q

Discuss agoraphobia

A

Fear of open spaces/situations where escape might be difficult
- crowd, outside home, bus/train/car

Condition progresses; inc. avoidance of places/situations provoke anxiety
Severe: confined to house

875
Q

Discuss social phobia

A

Anxiety provoked by social performance situations
Fear of behaving in humiliating/embarrassing way

Treatment

  • MAOI (selegiline), SSRI (fluoxetine), anxiolytics
  • exposure by systematic desensitisation
  • cognitive therapy
876
Q

Compare obsessions and compulsions

A

Obsessions: unwelcome, persistent, recurrent thoughts/ideas, impulses or images that are intrusive, senseless, recognised as absurd
- occur as thoughts, rumination, doubts, impulses, phobias

Compulsions: motor component of obsessional thought

  • repetitive, purposeful behaviours in response to obsession in stereotyped fashion
  • excessive and not connected to thought in realistic way
  • act as if to reduce distress caused by obsession
  • hand washing, cleaning, touching, checking, rearrangement
877
Q

Discuss obsessive compulsive disorder

A

Absurd, time-consuming obsessions and compulsions that interfere w/ everyday life

Management 
- CBT
— exposure and response prevention
— thought stopping, habituation training
- drug
— clomipramine (TCA)
— SSRI; fluoxetine
878
Q

Discuss CBT

A

Psychotherapeutic approach

Tackles dysfunctional emotions, maladaptive behaviours and cognitive processes and contents

Uses number of goal-orientated, explicit systematic procedures to change maladaptive thinking resulting in change in affect and behaviour

Pt challenge patterns and beliefs

Replaces errors in thinking (overgeneralising/max. -ve;min. +ve/catastrophising) w/ more realistic and effective thoughts (dec. emotional distress and self-defeating behaviour)

879
Q

Discuss somatisation

A

Neurosis

Physical symptoms where no cause can be found
- manifestation of psychological distress
Common
Reassurance and explanation may be all needed
Factitious disorders

880
Q

Discuss psychosis

A

Contact w/ reality lost
Normal mental processes suspended
Normal constraints abandoned

Features: hallucinations, delusions, thought disorder, loss of insight

Bipolar affective disorder, schizophrenia, paranoid state, organic disorder

881
Q

Compare delusion and hallucination

A

Delusion: fixed, false belief which is out of keeping w/ religious/cultural background and maintained in face of evidence to contrary

Hallucination: false sensory perception in absence of real external stimulus

882
Q

What is schizophrenia ?

A

Disintegrative psychosis involving loss of contact w/ reality
Splitting of links b/w perception, mood, thinking, behaviour, contact w/ reality

883
Q

Compare type 1 and 2 schizophrenia

A

Type 1: acute onset, +ve symptoms

  • hallucinations, delusions
  • thought disorder
  • speech

Type 2: chronic, -ve symptoms

  • lack of drive
  • poverty of speech
  • withdrawn
  • depression (common)
  • poor attention and memory
884
Q

Clinical features of schizophrenia

A

Schneider’s 1st rank symptoms

Auditory hallucinations
- 3rd person arguing about subject
- 3rd person commentary on subject's actions
- audible thoughts 
Thought withdrawal/insertion
Thought broadcasting
Somatic passivity
Delusional perception
885
Q

Management of schizophrenia

A

Antipsychotics; neuroleptic/tranquilliser

  • oral; chlorpromazine, fluphenazine, risperidol
  • IM w/ Long acting depot injection

Action

  • alter dopamine/cholinergic balance in basal ganglia
  • extrapyramidal and anticholinergic effects
  • dystonia/dyskinesia (abnormal movement)
  • akathisia (restlessness)
  • Parkinsonism, Tardive dyskinesia (involuntary movements HandN)

Psychotherapy

886
Q

Dental relevance of schizophrenia

A 
Poor OH (neglect)
Smoking: staining, oral precancer/cancer
Difficulty in communication 
Delusions symptoms 
Side effects of neuroleptics; haloperidol, clozapine; hyposalivation
887
Q

9 clinical features of depression

A
  1. Depression of mood
  2. Loss of enjoyment
  3. Red. attention and conc.
  4. Poor memory
  5. Ideas of guilt and worthlessness
  6. Hopelessness, helplessness
  7. Ideation of suicide
  8. Red. energy
  9. Low self esteem
888
Q

5 biological features of depression

A
  1. Sleep disturbance: early wakening, insomnia, unrefreshed
  2. Change: appetite, weight, psychomotor activity, menstrual cycle
  3. Loss: interest work/leisure activities, energy, libido
  4. Diurnal mood variation
  5. Constipation
889
Q

Appearance and speech of depressed pt

A

Appearance

  • dishevelled, neglected dress and grooming
  • facial: downturned corners of mouth, brow furrowed
  • red. rate blinding
  • red. gestural movements
  • shoulders bent, head inclined forward, downwards gaze

Speech

  • poverty
  • hesitant, slow
890
Q

Psychotic features of depression

A

Delusions

  • concerned w/ ideals of worthlessness, ill-health, poverty, guilt
  • persecutory; pt feels if justified

Hallucinations: 2nd person auditory confirming pt ideas of worthlessness

891
Q

Management of depression

A 
CBT
Antidepressants
- TCA: amitriptyline, dolesupin
- SSRI: fluoxetine, partoxetine, citalopram
- St Johns wort
Li/carbamazepine (mood stabilisation)
ECT
892
Q

Dental aspects of depression

A

Defer treatment until controlled

Disturbed taste
Atypical facial pain
Burning moth syndrome
TMJD
Delusions: halitosis , discharges from mouth

Adverse effects from treatment

  • xerostomia
  • altered taste
893
Q

Discuss bipolar disorders

A

Sustained episodes of elevated or agitated mood (mania)
Often alternates w/ episodes of depression
Significant effect in individuals ability to function

894
Q

Discuss bipolar affective disorder

A

Sustained period of elevated/euphoric/irritable mood

Episodes incl. brief depressive then
manic
- inc. speech, pressure of speech
- dec. need for sleep, absence of fatigue
- overspending, uninhibited sexual drive
- insight impaired
895
Q

Discuss appearance and behaviour of pt w/ bipolar affective disorder

A

Dressed in bright, gaudy colours
Untidy, dishevelled
Overactivity -> physical exhaustion
Excessive activity in risk taking pursuits, social indiscretion

896
Q

Management and dental aspect of bipolar affective disorder

A

Management

  • antipsychotics: chlorpromazine, haloperidol, respiridone, olanzapine
  • sedatives; lorazepam
  • Li/carbamazepine
  • ECT

Dental

  • Li toxicity w/ GA
  • long term potential induce hypothyroidism
897
Q

Discuss anorexia nervosa

A

Deliberate weight loss; choose not to eat -> potentially serious weight loss
Extreme avoidance fatty foods; aggravated extreme exercise, purging, vomiting

Pt has body image distortion w/ intense fear of being obese
Associated w/ OCD, anxiety, mood disorder

898
Q

Clinical features of anorexia nervosa

A 
Thin, emaciated 
Dehydration 
Hair loss from scalp
Fine, downy lanugo hair face and back
Shorter stature (early onset)
Osteoporosis, pathological #s
Hypokalaemia: muscle weakness, tetany
Amenorrhoea/loss of libido, erectile dysfunction
899
Q

Management of anorexia nervosa

A

Need for controlled weight gain agreed
Admit for feeding: severe, rapid weight loss, depression
Build relationship
Agree on weight targets
Behavioural regime
Cognitive therapy: identify, change inappropriate cognitions regarding eating, body weight/shape
Family therapy

900
Q

Dental aspects of anorexia nervosa

A

Caution during GA
Parotid enlargement
Erosion, caries
Ulcers, abrasions

901
Q

Discuss bulimia nervosa

A

Repeated bouts overeating w/ excessive preoccupation w/ control of body weight
Extreme methods to counteract fattening effects of ingested food

Clinical

  • weight normal range
  • repeated vomiting; oesophageal tears, haematemesis, hypokalaemia, depression
  • sialosis (salivary gland swelling)
  • tooth erosion
  • calluses on dorsum hand (Russell’s sign)
  • ulcers soft palate, angular cheilitis
902
Q

Aetiology of suicide

A

Psychiatric disorder (90%): depression, alcoholism, illicit drug use, personality disorder, neuroses, schizophrenia

Physical illness: chronic painful illness, epilepsy

Parasuicide: 100x risk of committing suicide following yr

903
Q

Discuss parasuicide

A

Any self-initiated act deliberately undertaken by pt which mimics act of suicide w/o fatal outcome

Argument/separation most common preceding events; trouble w/ law, physical illness

90% involve self-poisoning; paracetamol -> liver failure + death
Death not usually intended

904
Q

Factors associated w/ genuine suicide risk

A

M, inc. age, unemployed, single

Psychiatric disorders violent method (parasuicide/self harm)

905
Q

Discuss alcohol abuse

A

Regular or binge consumption of alcohol sufficient to cause social/physical damage

Alcoholic = repeated drinking leads to harm in work/social life

906
Q

Features of alcohol dependence

A 
Compulsion to drink
Preoccupation w/ alcohol
Stereotyped drinking pattern
Inc. tolerance to alcohol 
Repeated withdrawal symptoms 
Loss ability to regulate drinking 
Relief drinking to avoid withdrawal symptoms 
Persistence even after attempted withdrawal
907
Q

Discuss psychological complications and acute intoxication of alcohol

A

Psychological

  • dysphoric mood, pathological jealousy, sexual problems
  • alcoholic hallucinosis

Intoxication

  • slurred speech
  • impaired coordination
  • judgement
  • injury/accident
908
Q

Medical complications of alcohol dependence (body systems)

A

GI: gastritis, hepatitis, cirrhosis, oesophageal varices, peptic ulceration
Haematological: anaemia, thrombocytopenia
CV: cardiomyopathy, hypertension
Neuropsychiatric: Wernicke’s encephalopathy 2ry thiamine deficiency

909
Q

Discuss acute withdrawal of alcohol (delirium tremens)

A 
10-72h after last drink 
Agitation, insomnia
Tachycardia, hypotension
Pyrexia
Confusion, fits
Visual/tactile hallucinations

Management: rehydration, fits, sedation
- chlordiazepoxide, chlormethiazole

910
Q

Dental aspect of alcohol dependence

A

Poor OH
Malnutrition, anaemia
Liver disease/cirrhosis; bleeding tendency, altered drug metabolism
Problems w/ drug administration (metronidazole)
Accidents/fights -> maxillofacial trauma

911
Q

What is hepatitis?

A

Inflammation of liver w/o pinpointing specific cause

912
Q

Viruses associated w/ Hep

A 
Epstein-Barr virus (glandular fever)
Cytomegalovirus 
HSV
Congenital rubella
Mumps
ECHO viruses
Yellow fever virus
913
Q

Discuss Hep carriers

A

Evolve from acute infection; mild and anicteric (not associated w/ jaundice)
May be asymptomatic by detectable by blood testing
Freq. source infection for others
Suffer long term sequelae of persistent infection

914
Q

Discuss HepA virus

A 
Enterovirus family 
Faecal-oral contamination
- children, group homes
- shellfish, H2O/food contamination 
- oral-anal sexual activity contamination

Incubation 15-50d
Mild flu-like signs
Immunoglobulin within 2wk exposure

915
Q

Clinical features of HepA virus

A

Jaundice: <6 <10%; 6-14 40-50%; >14 70-80%
Complications
- fulminant hep; fatal form acute hep, rapidly deteriorate
- cholestatic hep; inflammation of bile ducts
- relapsing hep
No chronic sequelae
Doesn’t cause chronic liver disease

916
Q

Discuss pathogenesis of HAV

A

Replicates primarily in hepatocytes
Passes through bile duct -> intestine; shed in large quantities
Damage to liver function results inc. liver enzymes
Jaundice ~1mnth, no carrier state, no tendency for chronicity or malignancy

917
Q

Control measures for HAV

A

Passive

  • normal human Ig; 3-6mnth coverage
  • PEP HCW

Vaccination

  • 1 serotype
  • formalin inactivated vaccine prepared from HAV grown in human diploid cells

V high hygiene standards

918
Q

Discuss HBV

A

DNA virus; RNA intermediate, reverse transcriptase

Blood transmission
Skin/mucous membrane contact w/ blood/serous fluid
- lower conc. saliva, semen, vaginal fluid

Incubation 48-180d
Complications: chronic hep, cirrhosis, liver cancer

919
Q

Clinical features of HBV

A

Jaundice: <5 <10%; >5 30-50%
Acute case-fatality: 0.5-1%
Chronic infection: <5 30-90%; >5 2-10%
Premature mortality from chronic liver disease: 15-25%

920
Q

Chronic diseases associated w/ HBV

A

Chronic persistent Hep; asymptomatic
Chronic active Hep; symt9aric
Liver cirrhosis
Hepatocellular carcinoma

921
Q

Discuss transmission of HBV in community

A

Parenteral: blood; IVDU, blood transfusions

Sexual: genital fluids; sex workers and homosexuals at risk

Perinatal: @/during birth; HBeAg+ more likely to transmit

922
Q

Discuss serological markers of HBV

A

Ag

  • HBsAg; chronic and acute
  • HBeAg; chronic and acute (presence in blood = infectivity)

Viral DNA polymerase: chronic and acute

Ab

  • anti-HBs; recovery, present in convalescence
  • anti-HBe; little/no infectivity
  • anti-HBc; recent infection if in IgM form
923
Q

Community control of HBV

A

Block person-person transmission; safer sex

Widespread immunisation

924
Q

Discuss transmission, prevention and treatment of HBV in clinical setting

A

Transmission

  • breakdown; sterilisation, infection control
  • car w/ bodily fluids and PPE

Prevention: HCW vaccination/immunisation

Treatment

  • HBV vaccine (+2 boosters)
  • HepB Ig: Ab immediate, short term protection while vaccine works
925
Q

Short and long term treatment for HBV infection

A

Short (acute): no specific treatment, sometimes relieve symptoms
Long (chronic); keel virus under control
- peginterferon: stim. immune system; HBeAg+ w/ chronic active hepatitis
- entecavir
— most powerful antiviral
— chronic HBeAg + or - hep
— successful; disappearance HBsAg, HBV-DNA, seroconversion to HBeAg
- tenofovir (antiretroviral)
— nucleoside reverse transcriptase inhibitor
— usually several yrs

926
Q

Discuss HDV

A

Seen w/ HBV
Transmission: similar to HBV (blood)
Incubation 14-56d
Usually asymptomatic

927
Q

Discuss clinical features and prevention of HDV (2 types)

A 
Coinfection
- clinical
— severe acute disease
— low risk of chronic infection 
- prevention: PEP/PrEP to prevent infection 
Superinfection
- Clinical
— usually develop chronic HDV infection
— high risk severe chronic liver disease
— May present as acute hepatitis 
- prevention: educate to red. risk behaviours of pt w/ chronic HBV
928
Q

Discuss HCV

A

Transmission: skin/mucous membrane exposure w/ blood/serous fluid
Incubation 21-140d
#1 cause cirrhosis and liver cancer
Severe signs and symptoms (HepA but worse)

929
Q

Clinical features HCV

A

Clinical illness/jaundice; 30-40%/20-30%
Chronic hepatitis; 70-90%
Persistent infection 85-100%

No protective Ab response identified

930
Q

Control and treatment of HCV

A

Control
- vaccination; underdevelopment, difficult due to multiple serotypes
- general
— screening blood donors and blood products
— needle exchange schemes

Treatment
- lifestyle; prevent further liver damage, red. risk spread
- drugs
— simeprevir; protease inhibitor
— sofosbuvir; polymerase inhibitor
— daclatasvir; replication and assembly inhibitor

931
Q

Discuss HEV

A

Waterborne virus
Faecal-oral route: contaminated water 3rd world countries
Incubation 15-64d

Clinical; similar HAV but

  • longer incubation period
  • infection generally acquired adolescence/adulthood
  • late stages of pregnancy 20% mortality

Control (travellers)

  • avoid water, uncooked shellfish/fruit/veg
  • vaccine: China developed but not globally available
932
Q

Discuss HIV structure

A 
Spherical particle 100nm diameter
Lipid bilayer derived from host cell
Glycoproteins; attachment to host cell
Spherical shell p17 proteins 
Inner conical capsule p24
Virus core: RNA and reverse transcriptase
933
Q

Clinical features of AIDS

A

Unique immunosuppressive viral epidemic
Predisposes individual to life-threatening infections w/ opportunistic pathogens

Seroconversion illness: 10% pt few wks after infection, coincides w/ seroconversion
- present w/ infectious mononucleosis like illness
Months-10yr incubation period completely asymptomatic
- 8-10yr median
AIDS-related complex or persistent generalised lymphadenopathy
Full-blown AIDS

934
Q

Transmission routes of HIV

A

Mother-child
- HIV+ women before/during birth or breastfeeding

Blood: prevention of contact only respite

935
Q

6 stages of HIV infection

A
  1. Binding
    - proteins on envelope bind CD4+ surface R
    - activated other proteins on surface, envelope fuse w/ outside of cell
  2. Reverse transcription
    - viral capsid containing rival RNA, enzymes released into host cell
    - reverse transcriptase makes DNA copy of RNA
    - new DNA = proviral DNA
  3. Integration
    - Viral DNA enters nucleus
    - integrase integrates proviral DNA into cell DNA
  4. Transcription: DNA->mRNA
  5. Translation: mRNA-> viral proteins
  6. Viral assembly
936
Q

Discuss zidovudine

A

Nucleoside analogue reverse transcription inhibitor
1st licensed drug treatment HIV-1
Some strains developed resistance

Mechanism

  • selectively inhibit reverse transcriptase via DNA chain termination
  • block essential phosphodiester linkage

Adverse

  • active form accumulate in un/infected cells leading to toxicity
  • toxicity: bone marrow cells; transfusion 1/3 pt
  • immunosuppression
937
Q

Advantages and goals of antiretroviral therapy

A

Advantages

  • improve pt health
  • red. illness
  • red. hospitalisation
  • fewer deaths from AIDS

Goals

  • improved quality of life
  • red. HIV-related morbidity and mortality
  • restore and/or preserve immunologic function
  • maximally and durably suppress HIV viral load
  • prevent transmission
938
Q

Discuss PEP and PrEP

A

Post Exposure Prophylaxis

  • stop becoming infected
  • started ASAP within 24h, max. 72h

Pre-Exposure Prophylaxis

  • take drugs before sex
  • everyday or before and after sex
  • enough drug in body to block HIV if it gets into body
939
Q

HIV risk groups

A

Homosexual/men who have sex with men
IVDU
Ethnic groups: African, Hispanic
Sex workers

940
Q

Discuss Cushing’s syndrome

A

Symptoms caused by excess cortisol

  • hypothalamus produce corticotrophin releasing hormone
  • ant. pituitary release adrenocorticotrophic hormone
  • stim. adrenal cortex release cortisol

Cause: pituitary(ACTH)/adrenal(cortisol) tumour, steroids/glucocorticoids

Physical

  • moon face
  • hirsutism
  • plethora (red face)
  • weight gain; abdominal fat, DM
  • hypertension
  • immunosuppression

Dental: candidiasis

941
Q

Discuss hypothyroidism

A

Dec. activity of thyroid gland

  • hypothalamus produce thyrotropin releasing hormone
  • ant. pituitary release thyroid stimulating hormone
  • stim. thyroid release T3, T4 (thyroxine)
  • T4: metabolism, mood, hair growth, development, temp. regulation, bowl

Cause

  • radiotherapy
  • iodine deficiency
  • thyroid surgery; overactive/cancer
  • Hashimoto’s disease; autoimmune

Physical

  • coarse, mottled skin
  • peri-orbital oedema
  • loss of eyebrow (hair loss)
  • dull, listless appearance
  • constipation
  • bradycardia
  • tiredness
  • weight gain
  • muscle ache, weakness
  • cold intolerance

Dental: GA contraindicated

  • myxoedema coma
  • mental state altered
  • body into overdrive -> coma
942
Q

Briefly discuss Paget’s disease of bone (SGT)

A

Abnormal bone turnover

  • abnormal bone resorption, weaker bone formation
  • disorganised, sclerotic, enlarged
  • likely #

Unknown cause
No cure: bisphosphonates (prevent bone loss), pain killers

Dental

  • limited opening
  • hypercementosis complicate XLA
  • bone weaker; caution XLA
  • poor sight/hearing
943
Q

Discuss acromegaly

A

Overproduction of growth hormone after growth plates closed

  • hypothalamus produce growth hormone releasing hormone
  • stim. ant. pituitary release growth hormone
  • fat breakdown, gluconeogenesis (liver), protein synthesis, lipolysis, Ca2+ retention

Cause: benign tumour pituitary gland

Physical

  • tall
  • enlarged: hands, feet, jaw, nose, ear
  • macroglossia
  • joint pain
  • tiredness, weakness, headaches
  • obesity, DM, hypertension -> CV disease, cardiomyopathy

Complication: bitemporal hemianopia; tumour press on optic chiasma
Treatment: tumour excision, hormone to stop GH release

Dental: fit in chair, caries, large tongue

944
Q

Briefly discuss Parkinsonism (SGT)

A

Degeneration of dopaminergic neurons in substantia nigra
- initiation and stopping of movement

Cause: plaque build up in brain

Physical

  • resting tremor
  • bradykinesia
  • rigidity
  • dysphagia, drooling
  • postural instability, shuffling gait

Dental

  • poor OH
  • moving in chair
  • low PB
  • xerostomia, taste disturbance (medications)
945
Q

Discuss Down’s Syndrome

A

Congenital defect of trisomy 21

Physical

  • macroglossia, large jaw
  • spaced eyes, flat nose
  • round, flat face, short neck
  • dec. muscle tone
  • hyper-flexible joints
  • atrial septal defects

Dental: consent, IE, large tongue, OH

946
Q

Briefly discuss Bell’s Palsy (SGT)

A

LMN lesion
Facial nerve lesion, usually unilateral

Cause: inflammation, virus (herpes), injury

Physical

  • mouth drooping
  • hyposalivation, loss taste ant. 2/3
  • can’t: smile, close eyes, puff mouth, furrow brow
947
Q

Discuss causes of unilateral and bilateral parotid gland swelling

A

Unilateral

  • tumour
  • obstruction of gland

Bilateral

  • alcoholic/chronic liver disease
  • DM, Sjögren’s syndrome
  • infections (mumps)
948
Q

Discuss signs of peri-orbital region problems

A

Erythema, swelling; allergic reaction
Bleeding, bruising

BCC: small brown lesion
Xanthelasma: yellowing of skin around eye due to build up of cholesterol in subcutaneous layer; CV disease

949
Q

Discuss signs on eyelids of problems

A

Stye: infection of hair follicle; Staph aureus
Meibomian cyst: infection of tarsal gland (sebaceous gland underneath eyelids); fluid filled sac
BCC/rodent ulcer: necrotic tissue

950
Q

Discuss Grave’s disease and relevance to HandN examination

A

Autoimmune condition of thyroid -> hyperthyroidism (Ab against TSH R)

Physical

  • weight loss
  • tachycardia, arrhythmia
  • heat intolerance
  • diarrhoea
  • hypertension
  • enlarged thyroid gland

Orbits; exophthalmos

  • lid retraction, staring appearance (see upper sclera); inc. muscle and subcutaneous muscle growth
  • ask if have double vision
951
Q

Discuss 3 conditions that can cause abnormalities of sclera

A

Jaundice

  • excess bilirubin
  • haemolytic anaemia, liver disease, gallbladder disease, gallstones
  • yellowing of sclera

Osteogenesis imperfecta

  • abnormal bone formation due to lack of collagen production
  • blue sclera as can see choroidal veins underneath (thin sclera)
  • dental: discoloured teeth, disordered development

Conjunctivitis

  • infection/inflammation of eye
  • red sclera
952
Q

Discuss possible causes lip abnormalities in HandN examination (SGT)

A

Angular stomatitis: anaemia; folate, Fe, B12
Angular stomatitis 2ry to contact dermatitis
HSV (cold sores): crusting, bleeding lesions; antiviral before crusting
Abnormal pigmentation
- hereditary haemorrhagic telangiectasia (GIT bleeding)
- Addison’s disease; adrenal insufficiency, no cortisol
- Peutz-Jeghers Syndrome; ulcers around mouth, ulcers polyps GIT

953
Q

What drugs can cause gingival hyperplasia?

A

Phenytoin
Cyclosporine
Nifedipine (Ca2+-C blocker)

954
Q

4 possible tongue abnormalities (SGT)

A

Geographic tongue: inflammation dorsal tongue mucosa; some pain
Candida: ABs, steroids, immunocompromised (HIV, transplant, DM, cancer treatment)
Atrophic glossitis: Fe deficiency anaemia
Macroglossia: acromegaly, Down’s, hypothyroidism

955
Q

Triangles of the neck

A

Ant: below digastric, in front sternocleidomastoid
- common carotid artery, CN7 9 10-12

Post: behind sternocleidomastoid, in front trapezius, above clavicle
- external jugular vein

956
Q

Possible causes of swellings in ant. and post. triangles of neck

A

Ant.

  • lymphadenopathy
  • thyroid swellings: goitre (visible enlargement), thyroglossal cyst
  • parotid tumour
  • bronchial cyst
  • rare: carotid body tumour, laryngocoele

Post.

  • lymphadenopathy
  • rare: cystic hygroma
957
Q

Compare reactive and infiltrative lymphadenopathy

A 
Reactive
- infective
— bacterial: staph, TB, strep
— viral: EBV, HIV
- non-infective
— connective tissue disease: rheumatoid arthritis, lupus
— sarcoid (TB w/o granulomas)

Infiltrative

  • malignant: lymphomas, metastases
  • benign: histiocytosis (rare)
958
Q

Mechanism of action of benzodiazepines

A

Bind selectively to GABA-A Rs

+ allosteric modulators

  • enhance Cl- conductance caused by GABA
  • hyperpolarise cell, red. likelihood AP
959
Q

Mechanism of action of different classes of antidepressants

A

TCAs: amitriptyline (NA and T-HT), imipramine (NA>5-HT)
- inhibit 5-HT and NA uptake, prolong synaptic lifetime

SSRI: fluoxetine, paroxetine
- prolong 5-HT synaptic lifetime

MAOI: isocarboxazid (nonselective, irreversible), phenelzine (nonselective, irreversible), moclobemide (MAO-A reversible )

  • MAO-A: DA, NA, 5-HT
  • inhibit breakdown monoamine neurotransmitters (DA, Ad, NA, 5-HT)
960
Q

12 cranial nerves

A 
Olfactory - Sensory
Optic - Sensory
Oculomotor - Motor
Trochlear - Motor
Trigeminal - Both
Abducens - Motor
Facial - Both
Vestibulocochlear - Sensory
Glossopharyngeal - Both
Vagus - Both
Accessory - Motor
Hypoglossal - Motor
961
Q

Foramen of the olfactory nerve

A

Cribriform plate of ethmoid bone

962
Q

Exam and ab/normal response for olfactory nerve

A

Exam

  • test sense of smell
  • cloves ideal as preserve scent
  • pt unable to see stimulus
  • 1 nostril test @ time w/ opposite occluded

Response
Normal: perceive scent w/ either nostril
Abnormal
- unilateral: more likely be significant
— structural brain lesion affecting olfactory bulb or tract
— local causes; deviated septum, blocked nasal passage
- bilateral; rhinitis, damage to cribriform plate

963
Q

Foramen of optic nerve

A

Optic foramen

964
Q

How is visual acuity tested?

A

Snellen’s test
Pt placed 6m/20’ from test types

20/20: pt can read @ 20’ W/ same accuracy as normal pt
20/200: pt read @ 20’ what normal pt read at 200’ (poor acuity, legally blind)

965
Q

How are peripheral visual fields tested?

A

Confrontation: examiner compares pt eye to their own assuming theirs is normal

Each eye tested separately w/ test object
Place yourself 1m away from pt, pt look directly at your eye
Test object equidistant b/w examiner and pt
State no. fingers or say now when see moving target

966
Q

How are the pupils examined and what is relative afferent pupillary defect?

A

Size, shape, symmetry
Reaction to light
- direct; same eye
- consensual; opposite eye
- swinging light test; daze in to distance move light b/w eyes
- accommodation; look into distance then tip of nose

Relative afferent pupillary defect

  • 1 nerve weaker than other
  • swinging light test; moving from unaffected eye to affected pupil will dilate (respond less vigorously)
967
Q

6 extraocular muscles of eye movement

A

Sup., inf., lateral, medical rectus

Sup., inf., oblique

968
Q

What nerves supply the eye muscles?

A

LR6 SO4 R3

Oculomotor: sup., inf., medial rectus, inf. oblique

Trochlear: sup. oblique

Abducens: lateral rectus

969
Q

Exam for extra-ocular eye muscles and abnormal findings

A

1m from pt
Ask pt to look each side, up, down following H pattern
Ask pt to follow finger w/o moving head
Pause at end to check for nystagmus

Abnormal

  • ptosis: drooping of eye, weakness of levator muscle Myasthenia gravis, 3rd nerve palsy
  • strabismus: abnormal alignment; squint eye
  • nystagmus: rapid, involuntary eye movement
970
Q

Branches and foramen of trigeminal nerve

A

V1: ophthalmic; Sensory; sup. orbital fissure
V2: maxillary; Sensory; foramen rotundum
V3: mandibular; Both; foramen ovale; muscles of mastication

971
Q

Muscles of mastication

A

Masseter
Temporalis
Lat. pterygoid
Med. pterygoid

972
Q

Sensory exam of trigeminal

A

Touch cotton wisp to forehead (V1), cheek (V2), chin (V3)

Avoid angle mandible innervated by upper cervical roots

973
Q

Motor exam of trigeminal

A

Palpate temporalis, masseter either side as pt clench
Ask pt to open mouth and repeat against resistance, observe for deviation to 1 side
W/ mouth open ask to protrude to either side against resistance

974
Q

Foramen of facial nerve and branches

A

Stylomastoid foramen

Intracranial: Temporal Zygomatic Buccal Mandibular Cervical
Extracranial: Chorda tympani Greater petrosal nerve to Stapedius

975
Q

Sensory exam of facial nerve

A

Taste

Protrude tongue, held gently by examiner
Small sample solution applied 1 side of ant. 2/3 using cotton tip applicator
W/ tongue protruded point to 1 of 4 possible tastes
Given water, test repeated w/ different stimuli

976
Q

Motor exam of facial nerve and normal response

A

Muscles of facial expression

Asymmetry: widening of palpebral fissure, flattening nasolabial food
Pt wrinkle forehead (temporalis) by raising eyebrows, close eyes tightly
Asymmetry ability to bury eye lashes
Palpate differences ability to resist eye opening

Show teeth, puff cheeks (buccinator), apples lips (zygomatic)

Normal: may by asymmetries but no facial weakness

977
Q

Abnormal response to motor function of facial nerve

A

LMNL: weakness of entire side of face; equal involvement upper and lower muscles

UMNL: contralateral supranuclear pathway weakness of lower facial muscles
- U muscles less affected as facial nucleus innervating them receives partial input from ipsilateral hemisphere

978
Q

Foramen of vestibulocochlear nerve and branches

A

Foramen: internal auditory meatus

Vestibular: Sensory info from vestibular hair cells in semilunar cells
- body position and gaze stability
Cochlear: auditory info from cochlear

979
Q

Exam of vestibulocochlear nerve and ab/normal response

A

Stim. small tuning fork (high freq.)

  • rinne; place against mastoid process, say when can’t hear anymore, move beside ear
  • Weber; place in middle of head, ask which side can hear

Normal

  • Rinne: air > bone conductance; hear tuning fork beside ear
  • Weber: hear equally or unable to tell
Abnormal 
- conductive hearing loss
— Rinne: bone > air; can’t hear beside ear
— Weber: lateralises to affected ear
- sensorineural deafness
— Rinne: air > bone; similar to normal 
— Weber: lateralises to unaffected ear
980
Q

Foramen of glossopharyngeal

A

Jugular foramen

981
Q

Divisions of vagus nerve

A

Motor: voluntary muscles of pharynx and most of larynx

Autonomic: PSNS component of smooth muscle of viscera of thorax and abdomen

Sensory

  • visceral sensory info from throat and abdomen
  • chemoreceptors of aortic bodies
982
Q

Exam of glossopharyngeal and vagus and response

A

Check palatal elevation by sustaining ah
- look at palate rather than uvula
Assess gag reflex, gently stroke soft palate either side

Normal: symmetrical elevation when sustaining ah and response to stim either side

Abnormal: unilateral palatal weakness

  • fails to elevate on weak side
  • gag reflex absent on weak side
983
Q

Function and exam of accessory nerve

A

Voluntary motor to sternocleidomastoid and trapezius muscles

Exam

  • asymmetry and atrophy of muscles
  • quickness of shrug, shrug against resistance
  • turn head against resistance, watch and palpate sternocleidomastoid
  • flex head forward against resistance
984
Q

Function and exam of hypoglossal nerve

A

Motor to tongue muscles; genioglossus, hyoglossus and styloglossus (except palataloglossus CNX)

Exam

  • test tongue strength; press against cheek
  • protrude equally; no deviation to either side
985
Q

3 common causes of headaches

A

Disease: local, vascular
Referred pain (pain coming from elsewhere)
Disorder: neurological, psychogenic

986
Q

Serious causes of headaches

A 
Acute glaucoma 
Acute hypertension 
Brain tumours
Giant cell arthritis 
Meningitis 
Haemorrhage: subarachnoid, sub/epidural
987
Q

Indicators that headache may be serious

A

Abrupt, thunderclap or bilateral headache
Confusion, loss of consciousness, convulsions, fever, rash
Disrupt normal life
Follow sore throat or respiratory infection
Preceded by head trauma
Recurrence in child
Severity
Worsening on coughing, exertion, sudden movement, straining

988
Q

What is a migraine? Cause and triggers

A

Recurrent throbbing headache, unilateral accompanied by nausea, disturbed vision

Cause: intra/extracranial blood vessel dilation and inflammation
Trigger: stress, caffeine, alcohol, lack of sleep, low blood sugar

989
Q

Clinical features and management of migraines

A

Clinical

  • aura (warning symptoms); visual symptoms
  • headache: unilateral, throbbing
  • associated: nausea, vomiting, photophobia, phonophobia

Management

  • avoid triggers
  • acute: triptans (5-HT agonist)
  • recurrent: beta-blockers (atenolol, propranolol)
990
Q

Discuss migrainous neuralgia

A

Unilateral pain around eye, frontal, cheek, temporal area
Ipsilateral lacrimation, photophobia, nasal stuffiness, rhinorrhoea

Recur in separate bouts w/ daily attacks for wks/mnths
Management: O2 (15L/min), triptans, verapamil (Ca2+-C blocker)

991
Q

Discuss stroke and the common causes

A

Syndrome consisting of rapidly developing symptoms of loss of focal CNS function
- last >24h or lead to death

Mechanism: ischaemic (embolic, thrombotic,); haemorrhagic

Common: atherosclerosis in carotid or intracerebral arteries (consequent thromboembolism)
Other: embolism from heart
- atrial fibrillation
- valvular disease
- recent MI
Atherosclerosis risk: DM, hypertension, obesity, hyperlipidaemia

992
Q

Clinical features and investigations of stroke

A

Clinical; depend on vascular territory affected

  • sudden visual deterioration
  • speech disturbance
  • hemiplegia (unilateral paralysis)
Investigations
- risk factors 
- cranial CT
— distinguish ischaemic or haemorrhagic 
— eliminate differentials; tumour, haematoma
993
Q

Diagnosis, treatment and prognosis of stroke

A

Diagnosis: clinical and history

Treatment
- aspirin 300mg; best within 48h
- admission stroke unit for rapid clinical assessment
- thombolysis (IV tissue plasminogen activator)
— not for haemorrhagic as risk haemorrhage

Prognosis: dependent on timing of treatment; best within 1st 4h onset of symptoms

994
Q

Dental relevance of stroke

A

Recognise

  • ME
  • impaired mobility, communication; speak slowly, clearly, simply
  • OH deterioration paralysed side; electric brush, adapted holders
  • modifications; sit upright, good suction

Monitor BP, anticoagulation status
Treatment mid-morning, short, stress free

995
Q

Discuss transient ischaemic attack

A

Cause: thromboembolism from atheroma in carotid vessels
Manifests as sudden loss of focal CNS function
- last mins, not hrs (longer = stroke)

Risk

  • alcohol/smoking
  • hypercholesterolaemia
  • atrial fibrillation/valvular disease
  • hypertension
  • DM
996
Q

Discuss Parkinson’s disease

A

Degenerative condition 1rily affecting substantia nigra of basal ganglia (dopaminergic neurons)
- gradual and progressive death of neurons

Loss of DA -> less motor cortex stim. and slower onset of movement
Symptoms manifest when 80% DA neurons lost

997
Q

Discuss 3 main symptoms of Parkinson’s

A

Akinesia

  • bradykinesia
  • poverty of facial expression
  • difficulty changing position
  • quiet, monotonous speech

Gait

  • flexed/stopped posture
  • red. arm swing on walking
  • postural instability

Tremor/rigidity

998
Q

Parkinson’s treatment

A

Enhance DA pathway

DA replacement: L-dopa + carbidopa = co-carelopa
DA agonist: bromocriptine, pergolide
Block DA metabolism: selegiline (irreversible MAOB-I)
Block DA, l-dopa breakdown: entacapone (COMT inhibitor)

Anticholinergics: benzotropine, procyclidine

999
Q

Dental relevance of Parkinson’s

A

Blackness, unresponsiveness not lack of reaction/intelligence
Difficulty changing position
Min. anxiety as inc. tremor
Compromised restorative care; drooling, movements
Anticholinergics; dry mouth, hallucinations

Avoid LA w/ Ad interacts w/ L-dopa, dopa decarboxylase inhibitor , COMT inhibitor

  • tachycardia
  • arrhythmia
  • hypertension
1000
Q

What is multiple sclerosis?

A

Chronic relapsing neurological condition affecting young adult
Autoimmune disease in genetically susceptible individuals

Affects white matter brain, spinal cord, optic nerves

  • multiple foci of inflammatory demyelination (plaques)
  • scarring (sclerosis)

Results

  • red. conduction velocity
  • loss of info. conveyed by impulse traffic along various pathways
1001
Q

Treatment of multiple sclerosis

A

No cure

Management of acute relapse
- high dose corticosteroids; methylprednisolone

Modification of disease course

  • azathioprine, methotrexate, cyclophosphamide (immunosuppressor)
  • beta-interferons, glatiramer, natalizumab, mitoxantrone

Control of symptoms

  • depression: SSRI (fluoxetine), TCA (amitriptyline
  • spasms: muscle relaxants (benzodiazepines)
  • bladder dysfunction: anticholinergics
1002
Q

Oral manifestations of multiple sclerosis

A

No specific manifestations
Suggestive of advanced MS
- trigeminal neuralgia; often bilateral
- facial para/anaesthesia; numbness lower lip, chin
- facial palsy
- abnormal facial/IO pain and discomfort
- dysphagia
- higher incidence caries, stomatitis, ulceration, candidiasis
- Lhermitte phenomenon (tingling arms/legs on neck flexion)

1003
Q

Dental relevance of multiple sclerosis

A

Short appointments; unable keep mouth open
Morning appointment; fatigue less pronounced
Limited mobility; assistance wheelchair -> chair
Treat semi-supine; respiratory problems
V severe: GA hospital setting
Emphasis on preventative care

1004
Q

Discuss epilepsy

A

Recurrent occasional, sudden, excessive, rapid and local discharges of nerve cells in grey matter
Paroxysmal disorder
- intermittent, stereotyped attacks of altered consciousness, Motor/sensory function, behaviour or emotion

Idiopathic or symptomatic of underlying pathology
Focal (partial) or generalised
- grand-mal or tonic clonic seizures (adult)
- petit-mal or absence seizures (child)

1005
Q

What is status epilepticus ?

A

Uncontrolled series of seizures w/ no regain of consciousness in b/w attacks

1006
Q

Causes of seizures

A

Infection: meningitis, encephalitis, brain abscess

Inflammation: MS

Metabolic abnormalities

  • electrolyte imbalance
  • renal failure
  • nutritional deficiency
1007
Q

Drugs used to treat different types of seizures

A

Tonic-clonic

  • carbamazepine
  • phenytoin
  • sodium valproate
  • gabapentin

Absence

  • sodium valproate
  • ethosuximide

Partial

  • carbamazepine
  • sodium valproate
1008
Q

Dental relevance of epilepsy

A 
Treatment coincide w/ good phase 
Precautions
- strong mouth props
- keep mouth free of debris
- minimal equipment around pt

Phenytoin: gingival hyperplasia, folic acid/macrocytic anaemia
Sodium valproate: thrombocytopenia, inhibit platelet aggregation
NSAIDs, aspirin, azole antifungals, metronidazole potentiate anticonvulsant activity

Must prevent injury during tonic, clonic, flaccid phases
Flaccid: recovery potion, clear airways, monitor signs
O2 (15L/min)
Status epilepticus; call ambulance
Midazolam: Buccal/intranasal during flaccid state to stop constant seizure activity

1009
Q

Discuss palsies of nerves controlling eye movement

A

R CN3: R eye downward, outward gaze, dilated pupil, ptosis; L normal

L CN4: gaze to right

L CN6: R normal; L does not abduct

1010
Q

Discuss Bell’s Palsy

A

Acute paralysis of facial nerve near stylomastoid foramen (LMNL)
Unilateral, may be recurrent
2ry to virus (HZV, VZV) or autoimmune

Clinical

  • pain jaw/ear prior to paralysis
  • unilateral facial paralysis
  • hyperacusis, loss taste ant. 2/3, changes in salivation

Management

  • high dose prednisolone
  • antiviral (acyclovir)
  • protect exposed cornea

Spontaneously recover

1011
Q

Discuss trigeminal neuralgia

A

Unilateral, brief electric shock, lighting fast pain limited to distribution of 1/+ divisions
Each bout few secs/mins
Paroxysms May occur in quick succession
Associated w/ trigger zones within trigeminal area

Mild stimuli
- shaving, breeze, touch, movement, smiling, chewing

Treatment

  • prophylactic carbamazepine
  • gabapentin, lamotrigine
1012
Q

Discuss shingles

A

VZV dormant in dorsal root ganglia cells after chickenpox
Reactivation
- localised pain and swelling
- unilateral vesicular rash affecting single dermatome

Post-herpetic neuralgia: persistent pain post eruption and healing of zoster

Self-limiting, treat w/ acyclovir

1013
Q

Complications of shingles

A

Zoster ophthalmicus: risk corneal damage

Ramsay Hunt Syndrome

  • VZV infection of facial nerve
  • lower motor neuron facial palsy
  • vesicles in external auditory meatus
  • severe ear pain
1014
Q

4 main ways in which infection can be diagnosed

A

History
Clinical exam
Lab investigations: haematological, biochemical, microbiology/virology
Other: X-rays, scans

1015
Q

Important information to ascertain when taking history from pt w/ infection

A 
Symptoms and duration: acute v chronic
Travel
- risk of tropical/imported infection
- vaccination history 
Contact w/ animals: zoonotic infection
Contact w/ infected person: TB/meningitis 
Food
Drugs: AB treatment
1016
Q

5 factors contributing to good quality sample

A

Collect @ optimal time
Collect appropriate specimen
Taking specimen well and w/ minimal contamination
Getting samples to lab w/ min. delay
Providing relevant clinical data on request form

1017
Q

Explain optimal time for taking specimen sample

A

Taken before commencing antimicrobial therapy
Serology
- trying to show rise in Ab titre
- acute and convalescent samples
Some pathogens don’t survive long @ RT, others proliferate
- misleading results if left @ RT before being processed

1018
Q

Tests to identify and classify bacteria

A 
Culture: gold standard
Initial identification: few simple tests
- microscopy
- growth characteristics 
Further
- biochemical tests
- Ag detection 
- toxin demonstration 
Indirect: organism can’t be grown
- immunofluorescence
- nucleic acid amplification (PCR)
- serological: 4 fold rise IgM
1019
Q

Discuss use of microscopy for identifying bacteria

A 
Gram stain commonly used
Relies on differences in cell wall
- +: purple
- -: pink
Shows morphology 
- rods/cocci
- pairs/clusters/chain
Special stains
- Ziehl-Nielsen: mycobacteria 
- cotton blue: fungi
- dark field microscopy: spirochetes
1020
Q

Discuss cytochrome oxidase as means to classify bacteria

A

Bacteria w/ oxidative metabolism possess cytochrome oxidase which activate cytochrome c oxidase in ETC
Bacteria using O2 as terminal electron acceptor; red. O2 to H2O

Oxidase +

  • pseudomonas, neisseria, campylobacter
  • aerobes, facultative anaerobes

Oxidase -

  • enterobacteriaceae: O2 terminal electron acceptor, no cytochrome c
  • most gram+, anaerobes
1021
Q

Discuss fermentation as means to classify bacteria

A

Bacteria differ in ability to produce acid from monosaccharides, polysaccharides, alcohols by fermentation

Monosaccharides: arabinose, ribose; fructose, galactose, mannose
Disaccharides: sucrose, fructose, lactose

Useful in determining species level, may req. up to 20 reactions

1022
Q

For an ECG what lead is analysed and why?

A

Lead II

Follows same direction as flow of current in heart

1023
Q

What are P, QRS and T waves on ECG?

A

P: atrial contraction; small depolarisation

QRS: ventricular complex; large peak (ventricles thicker)

T: ventricular re-polarisation; small

1024
Q

Discuss PR, QRS, ST, RR intervals on ECG

A

PR: T for activation to pass SAN -> AVN to ventricle
- 0.12-0.2s (3-5 small sq.)

QRS: ventricular depolarisation
- <0.12s (<3 small sq. (0.04s))

ST: ventricular depolarisation; isoelectric (appears flat)

RR: b/w peaks, HR

1025
Q

Sinus rhythm requirements

A

Fixed relationship b/w P and QRS
PR interval 0.12-0.2s
QRS <0.2s

‘Sinus tachycardia/bradycardia’

1026
Q

How is HR/pulse calculated from ECG?

A

300/no. large sq. in RR interval

1027
Q

Cutoffs for bradycardia and tachycardia in ECG analysis

A

Bradycardia <60bpm

Tachycardia >100bpm

1028
Q

How can ECG determine if HR is regular or irregular?

A

P wave before each QRS

RR interval consistent

1029
Q

Discuss abnormal findings in P, QRS, ST, T waves and possible causes

A

P

  • should be 0.12-0.2s
  • inverted/absent in atrial fibrillation

QRS

  • should be <0.12s
  • wide: ventricular rhythm
  • wide, regular, rapid: ventricular tachycardia
  • wide, irregular rapid: ventricular fibrillation

ST

  • should be isoelectric (flat)
  • elevated: infarct
  • depressed: ischameia

T
- inverted: ischaemia

1030
Q

Discuss 6 liver function test domains and possible abnormal findings

A

Bilirubin
Aspartate transaminase (AST): inc. in hepatocellular damage
Alanine transaminase (ALT): inc. in hepatocellular damage and bile obstruction
Alkaline phosphatase (ALP): inc. in bile obstruction
Gamma-glutamyl transpeptidase
Album: dec. in liver failure

1031
Q

Discuss findings for 1ry and 2ry hyperthyroidism and hypothyroidism

A 
Hyperthyroidism 
- 1ry: Graves' disease
— T3 and 4 inc.
— TSH dec. (-ve feedback)
- 2ry: pituitary tumour secreting TSH
— T3 and 4 inc. 
— TSH N/inc. 
Hypothyroidism 
- 1ry: Hashimoto's thyroiditis (defective gland)
— T3 and 4 dec.
— TSH inc. 
- 2ry: destructive pituitary tumour 
— T3 and 4 dec. 
— TSH dec.
1032
Q

Discuss findings in 1ry and 2ry hypercotisolism and hypocortisolism

A 
Hypercortisolism
- 1ry
— cortisol inc. 
— ACTH dec.
- 2ry: pituitary tumour
— cortisol inc. 
— ACTH N/inc.
Hypocortisolism
- 1ry: Addison's disease
— cortisol dec., Na dec., K inc.
— ACTH inc. 
- 2ry: pituitary adenoma 
— cortisol dec., Na dec., K inc.
— ACTH dec.
1033
Q

What are cystic lesions?

A

Sacks filled w/ gas/pus/fluid/blood

1034
Q

Aetiology, clinical and description of dermis cyst

A

Aetiology: proliferation of epithelial rests
Clinical: young adults, asymptomatic, un-inflamed
Site: floor of mouth above mylohyoid; middle of neck
Surface: smooth, globular, tense
Consistency: soft or fluctuant

1035
Q

Aetiology, clinical and description of thyroglossal cyst

A

Aetiology: failure of complete descent of thyroid tissue from foramen caecum w/ subsequent cystification
Clinical: noticed middle/old age
Site: midline swelling above thyroid
- in thyroid region; swelling pushed to 1 side (L)
- moves up on tongue protrusion or swallowing

1036
Q

Aetiology, clinical and description of branchial cyst

A

Aetiology: proliferation of epithelial remnants from 2nd branchial cleft within lymph nodes
Clinical: child/adolescent; asymptomatic, un-inflamed
Site: upper part lat. neck beneath ant. border SCM
Surface: smooth, globular, tense
Consistency: soft or fluctuant

1037
Q

Aetiology, clinical and description of lymphangioma/cystic hygroma

A

Filled w/ lymph fluid

Aetiology: proliferation of sequestrated lymphatic endothelium of the jugular sac
Clinical: present at birth or manifest during infancy/childhood
- asymptomatic, un-inflamed
Site: lower 1/3 neck
Surface: smooth, diffuse, tense
Consistency: spongy, soft, translucent
Colour: lighter than surrounding tissue

1038
Q

Reasons for lymph node enlargement

A

Inc. no. cells: benign lymphocytes and macrophages in response to Ag

Infiltration w/ malignant cells

  • inflammatory cells in infection (lymphadenitis)
  • in situ proliferation of malignant lymphocytes and macrophages
  • metastatic malignant cells
  • metabolite laden macrophages (lipid storage disease)
1039
Q

Aetiology, clinical and description of pyogenic lymphadenopathy

A

Aetiology: oral inflammatory condition esp. abscess
Clinical: present as single or multiple painful nodes
Site: depends on site of infection
Surface: smooth, diffuse, tense
Consistency: soft (acute), not fixed to surrounding

1040
Q

Aetiology, clinical and diagnosis viral lymphadenopathy

A

Aetiology: EBV
Clinical
- young adults
- fever, malaise, sore throat
- lymph nodes: discrete, mobile, tender, firm
- purpura or petechiae on palate
Diagnosis: +ve Paul-Bunnell or Monospot slide test

1041
Q

Aetiology, clinical, diagnosis of tuberculous lymphadenopathy

A

Aetiology: M. tuberculosis transmitted via sputum droplets
Clinical
- single/multiple swellings lat. neck
- indurated, asymptomatic, firm
- fever, malaise, might sweat, weight loss
- undergoes caseous necrosis form collar-stud abscess
- ulcer dorsum tongue

Diagnosis: Ziehl-Neelsen stain, Mantoux, biopsy, X-ray

1042
Q

Aetiology, clinical, diagnosis of malignant lymphadenopathy

A

Aetiology

  • unknown; Hodgkin’s
  • EBV; Burkitt’s
  • HIV; lymphoma

Clinical

  • middle age/elderly; Burkitt’s child/young adult
  • single or bilateral swelling lat. neck
  • asymptomatic, slowly enlarging, firm, rubbery matted lymph nodes
  • fever, malaise, night sweat, weight loss

Diagnosis
- Reed-Sternberg cells (Hodgkin’s)

1043
Q

Aetiology, clinical, diagnosis of malignant lymphadenopathy - metastatic carcinoma

A

Aetiology: metastatic oral cancer/nasopharyngeal leasion
Clinical
- usually single swelling, may be multiple, rarely bilateral
- middle aged/elderly
- progressive inc. size
- indurated, fixed, rocky hard, painless
- affects submandibular and jugulodigastric nodes

Diagnosis
- biopsy show metastatic cells (advanced disease; poor prognosis)

1044
Q

Discuss cervical rib

A

Non-lymphatic/Non-cystic HandN swelling

Clinical

  • arises 7th cervical vertebra
  • feels like bony swelling in neck

Symptoms

  • vascular: excessive pulsation and thrill subclavian artery
  • neurological: pain, paraesthesia, anaesthesia forearm, hands
1045
Q

Clinical and diagnosis of lipoma

A

Non-lymphatic/non-cystic HandN swelling

Clinical

  • rare
  • slow-growing
  • soft, semi-fluctuant, lobulated tumour, varying size
  • painless, asymptomatic
  • IO appears yellowish

Diagnosis: biopsy

1046
Q

5 parotid lesions

A

Appear as neck swelling when fail of parotid affected

Neoplasm
- indurated, asymptomatic, unilateral

Sjogren’s
- bilateral, diffuse, soft, sicca complex (dry)

Sialadenitis (parotitis)

  • unilateral, diffuse, soft, painful, pus extruding duct orifice
  • IO: pus at papilla; diffuse erythematous tender swelling

Metabolic (sialosis)
- bilateral, symmetrical, painless, soft

Acute viral sialadenitis (mumps)
- bilateral, painful, systemic (fever, malaise)

1047
Q

Discuss thyroid nodule

A

Non-lymphatic/non-cystic HandN swelling

Aetiology unknown 
Clinical
- uncommon
- firm
- painless, asymptomatic  
- midline swelling neck thyroid gland region
1048
Q

Aetiology and clinical of carotid body tumour

A

Non-lymphatic/non-cystic swelling HandN

Aetiology: neoplastic transformation of carotid body cells
Clinical
- rare, adult
- painless, asymptomatic
- firm, moveable mass at carotid bifurcation
- bruit and thrill single or bilateral swelling lat. neck
- can cause compression effects

1049
Q

Structure of herpes virus

A

Envelope

  • fragile; damaged not infectious
  • sensitive to drying, acids, detergents, organic solvents

Tegument

  • space b/w envelope and capsid
  • contain virally-encoded proteins and enzymes (initiation replication)

Capsid: doughnut shaped capsomere w/ icosahedral nucleocapsid

Genome: dsDNA, variable size

1050
Q

Main viruses of herpes family

A 
HHV1 HSV1
HHV2 HSV2
HHV3 VZV
HHV4 EBV
HHV5 CMV
HHV 6/7
HHV8
1051
Q

Discuss HSV1/2

A

Very large, genome encode at least 80 proteins
Enzymes
- DNA-dependent DNA polymerase
- thymidine kinase

Genome encodes surface glycoproteins

  • attachment
  • immune escape
  • fusion membrane w/ host
1052
Q

HSV1/2 pathogenesis

A

Infect humans and animals
Infect mucoepithelial cells or enter through wounds
Freq. set up latent infection in neuronal cells
Persistently infect macrophages, lymphocytes
Replication around lesion, enter innervating neuron

1053
Q

Discuss oral herpes

A

Cold sores
HSV1 or 2

1ry herpetic gingivostomatitis
- typical clear lesion develop then ulcers w/ white appearance

Initially on lips spread all of mouth and pharynx

  • move to trigeminal ganglion remain latent
  • reactive: return to original site cause cold cores
1054
Q

Discuss latency, reactivation and recurrence of HSV

A

Infect epithelial mucosal cells/lymphocytes, travel up peripheral nerves to nucleated neuron

Reactivation: travel down nerve axon
- triggered by UV, fever, immunocompromised

Lesion in dermatome; reddened area give rise to macula, crusts -> papula
- fluid filled; filled w/ virus (moist = infectious)

Recurrence; prodromal burning sensation in area will erupt

1055
Q

Immune response to HSV

A

Innate: interferon and NK limit initial infection
Humoral: Ab against surface glycoproteins -> neutralisation
Cellular: cytotoxic T and macrophages

1056
Q

Diagnosis of HSV

A

Cells obtained from base of lesion (Tzank smear), histochemistry performed
Isolated from biopsy specimen, cultured; characteristic cytopathic effects (plaque) incl. multinucleated cells
Anti-HSV Ab (1ry infection); recurrence not accompanied by Ab rise

1057
Q

Discuss herpes whitlow and eczema herpeticum

A

Herpes whitlow

  • manual contact w/ body secretions
  • enters via small wounds on hands/wrists

Eczema Herpeticum

  • child w/ eczema/preexisting atopic dermatitis, virus spread over skin @ lesions
  • virus spread to organs; liver, adrenals
1058
Q

Discuss genital herpes and proctitis

A 
Genital herpes 
- usually HSV2 (10% HSV1)
- 1ry infection asymptomatic; painful lesions can develop
— M glans/shaft
— F vulva, vagina, cervix, perianal 
— urethra both sexes 
- fever, myalgia, glandular inflammation Groin
- 2ry episodes: less severe, shorter

Proctitis: inflammation rectum and anus

1059
Q

Discuss neonatal HSV infections

A

HSV2: often fatal, rare
Usually if mother shedding virus at delivery
- active genital herpes during delivery; c-section
- obtained in utero or during birth (more common)
Underdeveloped immune system; spread rapidly to peripheral organs (liver, lungs)

1060
Q

Discuss HSV encephalitis and meningitis

A

Encephalitis

  • HSV1: most common sporadic viral encephalitis
  • febrile disease
  • may result in damage to 1 of temporal lobes
  • blood in spinal fluid and neurological symptoms

Meningitis: HSV2

  • M homosexuals
  • resolve spontaneously
1061
Q

Discuss chemotherapy of HSV infection

A

Nucleoside analog drugs used; high specificity as depend on thymidine kinase
Only activated in infected cells; few side effects
Acyclovir; famciclovir, valacyclovir

Only act against active virus; ineffective against latent virus
- competitive inhibition DNA polymerase

1062
Q

Discuss chicken pox

A

HHV3: VZV

Highly infectious
Spread by respiratory aerosols or direct contact w/ skin lesions
- infection via mucosa

Complications

  • pneumonia
  • fulminant encephalitis
  • aseptic meningitis
  • traverse myelitis
  • cerebellar ataxia
  • Guillian Barre Syndrome
1063
Q

Discuss shingles

A

HHV3: VZV

Reactivation, usually later in life

Severe pain in nerve latent infection has occurred
Chicken-pox like lesions occur only in immediately affected area
- not widespread like chicken pox

1064
Q

Diagnosis, treatment and vaccine for HHV3

A

VZV

Diagnosis

  • characteristic appearance
  • definitive: culture; specific Ag

Treatment

  • acyclovir: present dissemination immunocompromised pt
  • varicella Ig
  • normally only supportive care

Vaccine

  • PEP
  • live attenuated virus; Ab production, cellular immunity
1065
Q

Discuss HHV4 symptoms and infections in child and adult

A

EBV

Clinical: fever, fatigue, swollen lymph nodes, inflamed throat, enlarged spleen, swollen liver, rash

Child: asymptomatic, like other illnesses
Adult: glandular fever (swollen glands, tonsils, liver, spleen)

Can cause infectious mononucleosis

1066
Q

Complications and treatment of HHV4 infection

A

Complications

  • further infections: brain, liver, lungs
  • severe anaemia: lack RBC
  • breathing difficulties; swollen tonsils
  • ruptured spleen

Treatment: no drugs

1067
Q

Discuss HHV5

A

CMV
Largest genome

High proportion popn.; mostly harmless/asymptomatic
May develop; fever, sore throat, fatigue, swollen gland

Complications
- serious disease immunocompromised
- congenital CMV infecting
— 1 in 5 develop permanent problem; hearing loss, developmental disability

No treatment

1068
Q

What is endocarditis?

A

Infection of membrane layer of endothelial cells lining heart that is continuous w/ artery and vein lining (endocardium)

1069
Q

Main etiological agents of IE

A

Streptococci esp. viridans (oral) group 40-60%
Enterococci
Staph aureus, coagulase -ve staph 20-40%

HACEK
Haemophilus
Aggregatibacter
Cardiobacterium
Eikenella
Kingella
1070
Q

Discuss oral strep and staph aureus virulence factors associated w/ IE

A

Strep

  • ability bind fibronectin: protein on surface host cells incl. heart endothelium
  • production EC polysaccharides
  • ability bind platelets; Platelet Aggregation Associated Protein (prod. by strep.)
Staph
- Microbial Surface Components Recognising Adhesion Matrix molecules 
— surface exposed staph. protein A
— fibrinogen-binding protein 
- evasion/defence against immune system
— leukocidin subunit
— superantigen-like protein
1071
Q

Pathogenesis of IE

A

Bacteraemia occurrence -> bacteria deposited, adhere, multiple on endothelial breach which has developed platelet thrombus
Become encased in layers of fibrin and platelets -> vegetation
- helps protect from phagocytic cells (evade immune response)
Vegetations characteristic lesion of IE
- usually occur on heart valve leaflets and when blood flow high->low pressure chamber
- may involve septal defect or mural endocardium in L ventricular aneurysms
- complicate cardiac abnormalities: arteriovenous shunts, aorta coarctation (narrowing), developmental defect

1072
Q

4 types of IE

A

Affecting previously normal valve
Affecting previously abnormal native valve
Affecting prosthetic valve
Iatrogenic

1073
Q

How can IE affect previously normal valve?

A

Bacteraemia due to

  • Staph aureus
  • coagulase -ve aureus
  • enterococci
  • strep. pneumoniae
1074
Q

Predisposing factors for IE

A

Rheumatic fever/degenerative (calcific) disease
Congenital heart defects; turbulent flow
Mitral valve prolapse
Degenerative valve disease
IVDU
Prosthetic valve/valve replacement surgery

1075
Q

Discuss predisposition to IE of previously abnormal valve and likely pathogens

A

Rheumatic fever/degenerative (calcific) disease
Congenital defects; turbulent flow
Mitral valve prolapse; 5-10x risk
Degenerative valve disease

Pathogen: usually oral/gut/urinary tract

  • strep sanguinis, mitis, mutans
  • enterococcus spp.
1076
Q

Discuss prosthetic valve IE

A

Greatest risk 1st few months post surgery

  • staph aureus
  • coagulase -ve staph: epidermidis, haemolyticus

Late onset: >1yr post surgery; usually present as native IE

1077
Q

How may iatrogenic IE occur?

A

Cannulae

IVDU

1078
Q

Need for cross-speciality liaison in diagnosis and treatment of IE

A

Diagnosis: req. both lab and clinical findings

Treatment

  • AB prescription
  • surgical intervention
1079
Q

Major criteria in Duke criteria for IE diagnosis

A

Blood culture

  • typical bacteria for endocarditis from 2 separate blood cultures
  • persistently +ve cultures for any microbe
  • all of 3 OR most of 4 blood cultures

Evidence of endocardial involvement

  • echocardiogram +ve for IE, vegetation or abscess
  • new artificial valve damage
  • new valvular regurgitation
1080
Q

Discuss minor criteria in Duke criteria for IE diagnosis

A

Predisposition: heart condition, IVDU
Fever
Vascular phenomena: arterial embolism, septic pulmonary infarcts
Immunological phenomena: glomerulonephritis
Echo: consistent w/ IE doesn’t meet major criteria
Microbiological
- +ve blood culture doesn’t meet major criteria
- Ab response indicating active infection w/ typical bacteria

1081
Q

Treatment of IE

A

Bactericidal AB: floxacillin, penicillin, amoxicillin, vancomycin
- synergistic combination
- IV min. 2 weeks
Min. inhibitory concentration of microorganism essential
Isolation of microorganism essential
Surgical backup essential

1082
Q

Define atrophy

A

Wasting/dec. in size of organ/tissue/part of tissue due to disease/injury/lack of use

1083
Q

Examples of atrophy

A 
Physiological: remnants structures during development: thyroglossal cyst
Wasting of muscles after stopping weight training 
Alzheimer’s 
Pathological
- cardiac
- nutritional 
- hair follicles 
- ageing in general
1084
Q

Define and give examples of hypertrophy

A

Inc. size of organ due to inc. cell size
- cells don’t divide; stimulus to cytoplasmic inc.
Athletes heart and muscles
Pathological: cardiomyopathy
Complications: obstruction and infarction

1085
Q

Define hyperplasia, give examples

A

Inc. no. cell but not cell size
- cells dividing; stimulus to cellular division
Occurs in organs w/ capacity to proliferate and stem cells

Physiological
- endometrium: mucous membrane lining uterus
— proliferating and secretory phases
- thyroid

Pathological

  • lymph node reaction to viral infection
  • prostate
1086
Q

Possible consequences of hyperplasia

A

Obstruction: prostate hyperplasia -> bladder obstruction
Infarction
Over secretion of hormone

1087
Q

Define metaplasia and give examples

A

Change from 1 fully mature tissue type to another fully mature tissue type
Not pre-neoplastic but changes which cause metaplasia may go on to cause dysplasia

Squamous -> glandular: Barrett’s oesophagus
Glandular -> squamous: bronchi
Stomach -> intestinal

1088
Q

Define oncogene

A

Genes that have potential to cause cancer

May be abnormally turned on/off due to mutations, translocations or effects of another gene

1089
Q

Discuss oncogenes

A

Normal if not inappropriately turned on
Normal state: proto-oncogene; abnormal state: oncogene
Ras: GTPase protein; mutated in 1 in 4 cancers

1090
Q

Discuss tumour suppressor genes

A

By being switched off (due to mutation or other mechanism) makes cancer more likely

Tumour suppressor gene
P53: triggers apoptosis if DNA damage in cell

1091
Q

Define carcinogenesis

A

Formation of cancer

Normal cells transformed to cancer cells

1092
Q

Classes of carcinogens

A

Chemical
Radiation
Viral

1093
Q

Examples of chemical carcinogens

A 
Aromatic hydrocarbons (benzene): lung
Naphthalene dyes: bladder cancer
Cigarette smoke: lung/bladder cancer
Asbestos: lung, mesothelioma
Dietary: colonic cancer 
Nitrosamines, amides: gastric
1094
Q

How does ionising radiation cause cancer, give examples

A

Damage to cellular genes = mutations
More exposure = greater chance mutation w/ resultant tumour

Occupational: space crew, airline crew, miners, US Capitol (granite), radiographer
Accidental: Chernobyl: thyroid cancer, leukaemia, lymphoma

UV radiation: melanoma, skin cancer

1095
Q

Discuss DNA and retroviruses as carcinogens

A 
DNA
- HPV
— introduces DNA into cell; interferes w/ gene function
— inactivates P53
— cervical cancer
- HBV
— long term liver cirrhosis
— hepatocellular carcinoma 
- EBV
— Burkitt’s lymphoma
— Nasopharyngeal cancer
— B-cell lymphomas

Retrovirus
- HIV1: immune suppression
— no immune surveillance to kill cancer cells
- HCV: RNA flavivirus

1096
Q

Define neoplasm

A

Abnormal mass of tissue; growth of which is virtually autonomous and exceeds that of normal tissue

  • growth continues after cessation of stimuli that initiated changed
  • benign and malignant
1097
Q

Clinical features of colon cancer

A

R side

  • bleeding/mucus pr
  • altered bowel habit
  • obstruction
  • tenesmus: feeling of incomplete bowl emptying
  • mass on pr

L

  • red. weight
  • anaemia
  • abdominal pain
  • obstruction

Both

  • abdominal pain
  • perforation
  • haemorrhage
  • fistula
1098
Q

Cancer screening methods

A 
Chest X-ray (lung)
Positron emission tomography
Genetic analysis: breast (BRCA1/2), 
Cytology
Biopsy
Tumour markers

Self exam: breast, testes

1099
Q

Risk factors of OSCC

A 
Old M
Alcohol, tobacco, paan
Sun/ionising radiation
LP
HPV, Candida
1100
Q

Clinical features of OSCC

A

Granular ulcer w/ fissuring or raised exophytic margins
Erythroplakia/Leukoplakia/speckled lesion
Indurated ulcer: attached underlying tissue or overlying skin/mucosa
Lump

Non-healing XLA socket
Pain or numbness
Lymph node enlargement
Loose tooth
Dysphagia 
Weight loss
1101
Q

Common locations of OSCC

A

Lips, lat border tongue, floor of mouth
Paan chewer: B mucosa, commissure region
Reverse smokers: palate

1102
Q

Diagnosis of OSCC

A

History +

Exam identify

  • high suspicion lesion: non-healing ulcer persisting >3wks
  • potentially precancerous

Investigations

  • lesional biopsy
  • fine needle aspiration enlarged lymph’s
  • imaging: jaw/chest X-ray, MRI/CT HandN, bronchoscopy, endoscopy
1103
Q

Discuss TNM tumour classification system

A

Tumour size

  • 1-4 inc. size
  • Tis carcinoma in situ

Lymph node involvement

  • 1 single node, <3cm
  • 2 single/multiple nodes <6cm
  • 3 any node >6

Metastases
- 0-1 evidence of metastasis

x: not available/not measured
0: no evidence

1104
Q

Discuss management of cancers

A

Local

  • curative surgery
  • radiotherapy

Regional spread

  • debulking surgery
  • radiotherapy

Distant metastases

  • palliative surgery: don’t cure; lessen symptoms/prolong life
  • radiotherapy
  • chemotherapy
1105
Q

Possible side effects of radiotherapy

A

Week 1: Nausea, vomiting
Week 2: mucositis, taste changes
Week 3: dry mouth

Later

  • infections
  • caries
  • pulp pain and necrosis
  • hypersensitivity
  • trismus
  • craniofacial defects
1106
Q

Discuss the genetic basis of cancer and how some cancers are inherited

A

Genetic

  • all cancers have somatic mutation
  • rare change in DNA sequence from that found in normal tissue of same pt
  • polymorphisms: changes in DNA sequence commonly occur in popn.

Inheritance

  • some people carry rare germ line mutations inc. risk particular cancers
  • distinct from common polymorphisms
  • retinoblastoma, multiple endocrine tumour, colon, breast cancer
1107
Q

Discuss proto/oncogenes

A

Oncogene: gain of function or inc. function associated w/ cancer
- in tumour cells; often mutated or expressed at high levels

Proto-oncogene

  • normal gene become oncogene through inc. expression or mutations
  • code proteins that regulate growth and differentiation
  • often involved in signal transduction and execution of mitogenic signals
1108
Q

Give examples oncogene activation

A

MYC gene Burkitt’s lymphoma

  • translocation moves enhancer sequence in vicinity of MYC
  • encodes widely used transcription factors
  • produced at higher rates -> over expression

BCR-ABL gene Chronic Myeloid Leukaemia

  • translocation of pieces of chromosomes 9 and 22 forming Philadelphia chromosome
  • encodes R tyrosine kinase, constitutively active -> uncontrolled proliferation
1109
Q

Discuss caretaker genes

A

DNA repair genes or genes that protect genome from acquiring/retaining DNA damage

Smaller inc. in cancer risk as up to 3 further mutations req. to initiate neoplasia

Nucleotide excision repair genes (xeroserma pigmentosum); skin cancer
BRCA1/2: recombinational repair; breast, ovarian

1110
Q

Discuss gatekeeper genes

A

Genes that regulate tumour growth by controlling proliferation or promote apoptosis

Inactivation leads to v large inc. cancer risk as only 1 further mutation req. to imitate neoplasia

RB1: control of restriction point; retinoblastoma, carcinoma
P53: cell cycle, apoptosis; breast
APC: cell cycle, apoptosis, differentiation; colon

1111
Q

Discuss viral oncogenes

A

Several human viruses known to cause cancer

HPV encodes proteins E6/7 that inactive key tumour suppressor genes (RB1, P53) cause cervical cancer

1112
Q

Classification of malignant neoplasms w/ examples

A

Epithelial: carcinoma

  • squamous: SCC
  • transitional: transitional cell carcinoma
  • glandular: adenocarcinoma

Connective: sarcoma

  • fat: liposarcoma
  • smooth muscle: leiomyosarcoma
  • nerve: neurofibrosarcoma
  • striated muscle: rhabdomyosarcoma
  • endothelium: haemangiosarcoma

Embryonic: blastoma

  • kidney: nephroblastoma
  • neural: neuroblastoma
  • retina: retinoblastoma
1113
Q

What are teratomas?

A

Germ cell neoplasms
Found in ovaries and testis
Differentiate along more than 1 germ cell line

1114
Q

Compare macroscopic and microscopic features of benign and malignant neoplasms

A

Benign

  • macro: well defined, smooth-surface
  • micro: blunt, pushing margin

Malignant

  • macro: ill-defined, craggy surfaced
  • micro: infiltrative, invasive
1115
Q

Compare the features of benign and malignant neoplasms

A 
Nuclear:cytoplasm: normal; high
Nuclear pleomorphism: uncommon; common
Necrosis: rare; common
Mitotic rate: normal/low; high, abnormal mitoses 
Metastases: none; common
1116
Q

Define metastasis and discuss spread

A

2ry growth of neoplasm at 1/+ locates distant from 1ry site

Spread

  • lymphatics
  • blood vessels (haematogenous)
  • transcoelomic (through body cavities)
  • CSF
1117
Q

Discuss the mechanism of metastasis

A

Detachment of tumour cells from each other
Attachment to ECM via specific Rs
Degradation ECM via collagenases, proteases
Locomotion through ECM via secreted motility factors
Vascular intravasation
Interaction tumour cells w/ host lymphocytes
Formation tumour embolus
Adhesion to endothelium (distant site) via adhesion molecules
Vascular extravasation
Regrowth of metastatic clone

1118
Q

Discuss why cancers may cause anaemia and cachexia

A

Anaemia

  • haemorrhage due to neoplasm
  • dec. life span RBC
  • Auto-Ab against RBC
  • replacement bone marrow by metastatic tumour

Cachexia

  • weight loss, fever, weakness
  • due to cytokines secreted by tumour or reactive host cell
  • underlying metabolic changes obscure
1119
Q

How can cancers result in death?

A 
Widespread disease in multiple organs
Metastatic disease in vital sites
Immunosuppression -> opportunistic infections 
Organ failure
Haemorrhage 
Late stage 2nd malignancies
1120
Q

What are the geriatric giants? What is there importance?

A

Incontinence
Immobility
Instability: falls, syncope
Intellectual impairment: delirium, dementia

Several different diseases can present as 1/+ of them

1121
Q

Discuss red. homeostatic reserve as a challenge of treating elderly

A

Ageing associated w/ red. organ function and ability to compensate
- CV responses in severe illness red.
- renal function dec.; renal failure (medication, illness) more likely
— NSAIDs: constrict vessels supplying kidney -> failure
- thermoregulation impaired

1122
Q

Discuss impaired immunity as challenge of treating elderly

A

Less effective
Shingles: reactivation of HZV
May not have inc. WCC or pyrexia in infection; hypothermia

1123
Q

Discuss rehabilitation as challenge to treating elderly

A

Take longer to recover
Time to recuperate: early, poorly planned discharge = failure
Input from social services and physiotherapy vital to regaining independence and ADLs
- in intermediate care facilities or home

1124
Q

Define fragility #

A

sustained when falling from standing height/less

1125
Q

What is osteoporosis? Aetiology

A

Slowly progressive dam asymptomatic reduction in bone mass causing fragility and inc. risk #

F: postmenopausal; oestrogen deficiency
M: hypogonadism, glucocorticoid treatment, alcoholism

1126
Q

Risk factors and 2ry causes of osteoporosis

A

Risk

  • F >65
  • family history
  • low BMI
  • smoking, alcohol
  • low Ca intake, VitD deficiency
  • drugs: glucocorticoids, anticonvulsants, cytotoxic therapy

2ry

  • rheumatoid arthritis
  • hyperthyroidism
  • 1ry hyperparathyroidism
  • malabsorption
  • chronic liver disease
  • immobilisation
  • anorexia
1127
Q

How is osteoporosis diagnosed?

A

Marked osteopenia on X-ray
Previous fragility #
Risk factors

Standard: bone mineral density by DEXA scan

1128
Q

Discuss the lifestyle changes and medications for treatment of osteoporosis

A

Lifestyle

  • smoking cessation, alcohol moderation
  • balanced diet: Ca intake, low Na
  • appropriate sun exposure

Medications

  • Ca, VitD supplements
  • bisphosphonates: alendronate, risedronate
  • raloxifene
  • teriparatide
  • calcitonin
  • strontium ranelate
1129
Q

Discuss BRONJ

A 
Bisphosphonate-associated osteonecrosis of the jaw 
Clinical
- delayed healing post-XLA
- pain, soft tissue infection, swelling
- numbness, paraesthesia
- non/exposed bone

Management

  • education
  • atraumatic surgical intervention
  • stop BSP; ABs, chlorhexidine, supplements, hyperbaric O2
1130
Q

Pathophysiology of transient ischaemic attack/stroke

A

Sudden disruption to brain blood supply due to:
Cerebral infarction
- blockage of arterial blood supply due to
— small vessel occlusion
— atherothromboembolism (from carotids)
— embolisation (a fib, MI)

Intracerebral haemorrhage
- rupture of blood vessels in brain tissue -> direct neuronal injury and cerebral oedema

1131
Q

Risk factors of TIA

A 
Hypertension, hyperlipidaemia
Smoking, alcoholism 
DM
Heart disease: valvular, ischaemic, a fib
Peripheral vascular disease
Past TIA
Polycythaemia
1132
Q

Clinical features of TIA and stroke

A

Sudden onset of focal neurological deficit
Ensuing disability relates to distribution of affected artery
Difficult to distinguish ischaemic and haemorrhagic stroke clinically
- haemorrhagic: meningism, severe headaches, coma (within hrs)

1133
Q

Management of TIA/stroke

A

Maintain airway
Monitor blood glucose, BP
Urgent CT/MRI
Antiplatelet once haemorrhagic stroke ruled out

1134
Q

Prevention of TIA/stroke

A

Antiplatelet: aspirin, clopidogrel, dipyridamole
Anticoagulant: warfarin
Risk factor management: smoking, alcohol, hypertension

1135
Q

Discuss dementia and how pt may present

A

Acquired, global, progressive impairment of mental function

Memory loss over months/yrs
Later: non-cognitive symptoms; agitation, aggression, apathy
Wandering, hallucinations, slow repetitive speech, mood disturbance

1136
Q

Presentation of Alzheimer’s

A

Impaired visuospatial skill, memory/verbal abilities, planning abilities, lack of insight

Later: irritability, mood disturbance, behavioural change (aggression, hallucination), agnosia

Finally: sedentary, apathy

1137
Q

Cause of Alzheimer’s

A

Accumulation of beta amyloid peptide (degradation product of amyloid precursor protein)
Results in progressive neuronal damage, neurofibrillary tangles, amyloid plaques, loss of ACh

1138
Q

Management of Alzheimer’s

A

Exacerbated by unfamiliar environments, peo0e
Develop routines
AChE inhibitors: rivastigmine (beneficial in mild AD)
BP control
Support for carers

1139
Q

What are the 2 types of DM?

A

T1: complete lack/inadequate production of insulin from beta pancreatic cells

T2: insulin resistance @ R level in peripheries

1140
Q

Clinical presentation of DM

A

Osmotic symptoms: polyuria, polydipsia (thirst), nocturia, weight loss
Recurrent infections: oral/genital candidiasis
Lethargy
Visual blurring

1141
Q

Discuss 2 types of diabetic emergency

A

Diabetic ketoacidosis (DKA)

  • T1(>T2): insulin deficiency; fat -> ketones -> acids
  • osmotic, weight loss, confusion, abdominal pain, sweet smelling breath

Hyperosmolar hyperglycaemic Syndrome (HHS)

  • T2: sugar high; lose H2O -> loss fluid
  • osmotic, dry mouth, confusion, hallucinations, red. consciousness, coma
1142
Q

Vascular complications of DM? How do these occur?

A

Long term, poorly controlled DM

Microvascular

  • retinopathy
  • nephropathy
  • neuropathy

Macrovascular atherosclerosis leading to

  • angina pectoris, MI
  • TIA, strokes
  • peripheral vascular disease: acute limb ischaemia, gangrene, amputation
1143
Q

Discuss types of neuropathy complications seen in DM

A

Symmetric polyneuropathy

  • D feet, hands
  • paraesthesia, dysesthesia OR
  • painless loss of touch, vibration, proprioception, temp.

Autonomic neuropathy
- gastroparesis, erectile dysfunction, orthostatic hypotension, neuropathic bladder

Mononeuropathy

  • diplopia, ptosis (CN3), Motor palsies (CN4/6)
  • finger weakness, numbness; foot drop; carpal tunnel syndrome
1144
Q

Discuss inc. risk of infections and poor healing due to DM

A

Adverse effects hyperglycaemia on granulocytes and T-cell function
Fungal and bacterial: mucocutaneous candidiasis, foot infections

1145
Q

Diagnostic criteria for DM

A

Random glucose: >11.1mmol/L
Fasting glucose: >7.0mmol/L
Oral glucose tolerance test (2h): >11.1mmol/L (75g glucose)

1146
Q

Discuss HbA1c DM test

A

Glycated Hb
Average plasma glucose conc. past 8-12 wks
Contraindicated: haemoglopinopathy; fructoasmine used
<53mmol/mol cutoff for retinopathy
<48mmol/mol on metformin alone

Normal: <42
Pre-DM: 42-47
DM: 48

1147
Q

Treatment of DM

A 
Control hyperglycaemia: alleviate symptoms 
Prevent complications
Address risks
Lifestyle
Medications
1148
Q

Discuss lifestyle changes used for treatment of DM

A

Diet
- low saturated fat and cholesterol
— red. carb intake; whole grain sources w/ high fibre
- caloric intake balanced w/ activity
- ideal body weight; meals at regular intervals

Weight loss
Exercise
Smoking cessation

1149
Q

Basics of medications prescribed in DM and when

A

T1: insulin
T2
- lifestyle changes insufficient: single oral hypoglycaemic
- combination therapy (2/+)
- + insulin: glycaemic control inadequate >3 agents

1150
Q

Discuss 4 main oral hypoglycaemics

A

Biguanides: metformin

  • red. tissue resistance
  • no risk of hypoglycaemia

Sulphonylureas: gliclazide

  • stim. insulin release
  • risk hypoglycaemia

DDP-4 inhibitor: sitaliptin

  • stim. insulin prod. GLP-1 pathway
  • promote weight loss, improves glycaemic control

SGLT-2 inhibitor: dapagliflozin

  • excrete glucose through urine
  • UTI, vaginal thrush, dehydration
1151
Q

Discuss non-insulin and insulin injectables

A

Non-insulin: GLP-1 analogue
- inc. weight loss, improve glycaemic control

Insulin
Novorapid: short acting
- @ mealtime control postprandial glucose spike
Detemir: Long acting
- steady basal glucose 24h
Novomix 30: combination 
- short and intermediate insulin 
- 30% short acting
1152
Q

Principles of DM management

A 
Education: self monitoring, target glucose
Lifestyle changes
Oral hypoglycaemics w or w/o insulin 
Risks: lipids, BP, alcohol
Assess complications
1153
Q

Dental aspect of DM

A

Chronic/aggressive periodontitis: poor glycaemic control
Severe dentoalveolar abscess: poorly controlled
Dry mouth: 2ry dehydration
Oral lichenoid reaction: oral hypoglycaemics
Inc. salivary flow (parotid): autonomic neuropathy
Oral candidiasis, angular stomatitis, mucormycosis

1154
Q

Discuss thyroid gland

A

-ve feedback mechanism from hypothalamus and pituitary
Produce thyroxine hormones T3 and T4
Target: brain, bone, heart, gut, skin, metabolism

1155
Q

Causes of thyroid disorders

A

Hyper

  • Graves’ disease
  • toxic adenoma
  • toxic multinodular goitre
  • exogenous thyroxine
  • 2ry to pituitary dysfunction: TSHoma
  • drugs: amiodarone
  • thyroiditis: post-partum, viral

Hypo

  • autoimmune
  • Hashimoto’s disease
  • post thyroidectomy/radioactive iodine
  • congenital
  • 2ry to pituitary dysfunction
  • drugs: lithium, chemotherapy, amiodarone
  • iodine deficiency

Other

  • non-functioning thyroid nodule
  • multinodular goitre
  • thyroid carcinoma
  • infiltration: lymphoma, TB
1156
Q

Compare clinical features of hyperthyroidism and hypothyroidism

A

CV: tachy; brady
Metabolism: weight loss, hunger; weight gain
GI: diarrhoea; constipation
Skin: palmar sweating; dry, loss hair
Neurological: anxiety, insomnia, restlessness; poor conc./memory
Temp: heat intolerance; cold intolerance

1157
Q

How can amiodarone cause both hyper and hypothyroidism?

A

Amiodarone causes release of T3/T4 (hyper) but then hormones become depleted (hypo)

1158
Q

Investigations into hyper and hypothyroidism

A

T3/4: inc.; dec.
TSH: dec.; inc,
Ab: +ve thyroperoxidase Ab, TSH R Ab (Graves’); +ve thyroperoxidase Ab

1159
Q

Management of hyper and hypothyroidism

A

Drugs: beta-blockers (atenolol) slow HR, antithyroid (carbimazole, propylthiouracil); thyroxine replacement
Others: radioactive iodine, thyroidectomy

1160
Q

Dental aspects of hyper and hypothyroidism

A

Hyper

  • inc. susceptibility caries, PD disease
  • burning mouth syndrome
  • accelerated eruption
  • osteoporosis jaw
  • ulcers (carbimazole)
Hypo
- congenital
— delayed eruption 
— macroglossia
— micrognathia
— malocclusion 
- glossitis
- dysgeusia
1161
Q

Discuss the adrenal gland

A

Cortex: produce androgens
Medulla: cortisol, aldosterone, adrenaline

1162
Q

Causes of adrenal insufficiency

A

Lack of cortisol and aldosterone

1ry

  • autoimmune (Addison’s)
  • infiltration: TB, sarcoidosis, malignancy

2ry: pituitary/hypothalamus impairment
- pituitary adenoma
- exogenous steroids

1163
Q

Action of cortisol

A

Anti-inflammatory and immunosuppressive

Physiological actions

  • hepatic gluconeogenesis
  • proteolysis
  • Na retention, K loss
  • dyslipidaemia, hypertension, insulin resistance (hypercortisolaemia)
1164
Q

Clinical features Addison’s disease

A 
Hypotension 
Hypoglycaemia 
Weight loss
Lethargy 
Abdominal pain 
Skin, oral pigmentation: inc. MSH and ACTH
1165
Q

Dental aspects of adrenal insufficiency

A

Infections managed aggressively (risk acute adrenal insufficiency)
Steroid cover
- major procedure: IM hydrocortisone 100mg QDS
- minor: 2x steroid dose for 24h

Precautions

  • steroid bracelet/card
  • emergency IM hydrocortisone
  • sick day rules
1166
Q

Causes of hyperparathyroidism

A

1ry

  • parathyroid adenoma
  • parathyroid hyperplasia: genetic familial hyperparathyroidism, multiple endocrine neoplasia
  • parathyroid carcinoma

2ry

  • VitD deficiency
  • chronic renal failure
1167
Q

Clinical features hyperparathyroidism

A 
Abdominal pain, constipation
Renal stones
Bone pain, osteopaenia, osteoporosis 
Lethargy, fatigue
Confusion, memory impairment, depression, hallucinations 
Polyuria, polydipsia, urinary freq,
1168
Q

Diagnostic investigations for 1ry and 2ry hyperparathyroidism

A 
Serum phosphate: dec.;inc. 
1,25-dihydroxycholecalciferol: inc.; dec.
ALP: inc.; inc. 
Serum Ca: inc.; dec. 
Serum PTH: inc.; inc.
1169
Q

Treatment of hyperparathyroidism

A

1ry

  • adenoma: para-thyroidectomy
  • hyperplasia: drug; cinacalcet

2ry: treat underlying cause

1170
Q

Dental aspect of hyperparathyroidism

A 
Malocclusion 
PDL widening 
Spacing 
Brown tumour
- benign 
- radiolucent 
- abnormal bone metabolism 
- extensive bone resorption; replaced by fibrovascular tissue and giant cells
1171
Q

What is acromegaly? Clinical features

A

Excess growth due to excess GH

Jaws: enlargement, teeth spacing
Macroglossia 
Coarse facial features; broad nose
Large hands
Cardiomyopathy 
Osteoarthritis 
Goitre
DM
Bitemporal visual field loss
1172
Q

Investigations and treatment of acromegaly

A

Investigations

  • raised insulin growth factor 1
  • OGTT
  • MRI pituitary
  • visual field assessment

Treatment

  • surgery (transphenoidal)
  • radiotherapy
  • drugs: dopamine agonist, somatostatin (GHIH) analogue, pegvisomant (GH R antagonist)
1173
Q

What is Cushing’s syndrome? Aetiology

A

Excess cortisol

Adrenal Cushing’s syndrome (cortisol)
Pituitary Cushing’s disease (ACTH)
Ectopic ACTH production

1174
Q

Investigations for Cushing’s syndrome

A

Midnight cortisol (diurnal variation; lowest at night), cortisol day curve (static)
Low dose dexamethasone suppression test (can’t suppress)
MRI adrenal/pituitary
Pituitary catheter

1175
Q

Treatment of Cushing’s syndrome

A

Surgery: transnasal transsphenoidal (TSS), adrenalectomy
Drugs: metyrapone, ketoconazole
Radiotherapy

1176
Q

Dental aspects of Cushing’s/excess cortisol

A

Peptic ulcers: avoid NSAIDs, aspirin
DM: PD health
Osteoporosis, myopathy: dentures adjustment, mobility
Immunosuppression: opportunistic infections
Pour wound healing

1177
Q

What are pheochromocytoma and paraganglioma? Dental relevance

A

Excess catecholamine
Pheochromocytoma (adrenal), paraganglioma (extra-adrenal)

Dental

  • alpha blocker (treatment) risk bleeding
  • avoid opiates, MAOI
  • hypertension
1178
Q

Define benign and malignant neoplasm

A

Benign: usually harmless; may be harmful due to

  • site: meningioma; inc. intracranial pressure
  • produce hormone: insulinoma

Malignant: usually harmful

1178
Q

Discuss differentiation of neoplasms and define anaplasia

A

Differentiation: degree to which neoplasm resembles its normal cell of origin

  • well differentiated: closely resembles
  • poorly: little resemblance

Anaplasia: complete lack of differentiation in a neoplasm

1178
Q

Classification of benign neoplasms w/ examples

A

Origin tissue, differentiation

Epithelial

  • squamous (skin): squamous cell papilloma
  • transitional (UT): transitional papilloma
  • glandular (GIT): adenoma

Connective

  • fat: lipoma
  • smooth muscle: leiomyoma
  • nerve: neurofibroma
  • striated muscle: rhabdomyoma
  • endothelium: haemangioma
1179
Q

General indications for GA

A 
Child req. multiple. XLA
Special needs pt
Oral and max fax
Inability to anaesthetise w/ LA
True LA allergy
1180
Q

Considerations for pt w/ CVD receiving GA

A

Chronic conditions optimised pre-op
IHD
- MI greater risk reinfarction shorter T b/w infarct and GA
Hypertension
- avoid ACEI on day, hospitalisation/intubation inc. BP
Artificial valve: anticoagulant altered (short acting) depending on surgery and INR
- AB prophylaxis

1181
Q

Considerations for pt w/ respiratory disease receiving GA

A

Recent URTI: risk URTI post-op, excess secretions
COPD: delay until chest physio, bronchodilators, ABs
Asthma: free from attacks, chest clear not contraindicated
Major trauma: risk rib #s/pneumothorax, pleural effusion

1182
Q

Considerations for pt w/ haematological disease receiving GA

A

Red. Hb = red. O2 carrying capacity of blood

Anaemia: defer until Hb >10g/dl; transfusions, Fe tablets
Sickle cell
- SS: risk haemolysis, multiple infarcts following minor hypoxia/hypercapnia
- AS: severe hypoxia to induce sickling
Thalassaemia syndromes

1183
Q

Considerations for pt w/ endocrine disorder receiving GA

A

DM: maintain glucose while fasting; any surgery may upset control
Thyroid
- uncontrolled hyper: provoke thyroid crisis
- myxoedema: delayed recovery, hypothermia, cardiac failure
- goitre: narrow/deviated trachea; intubation difficult

1184
Q

Considerations for pt w/ hepatitis receiving GA

A

Bleeding tendencies
Drug metabolism
Infection risk

1185
Q

Considerations for pt w/ renal disease receiving GA

A

Often marked anaemia
Dialysis: circulating volume and cause CV problems during anaesthesia
Serum electrolytes altered

1186
Q

Considerations for pt w/ musculoskeletal problems receiving GA

A

LMN disease: altered response to suxamethonium
Myasthenia gravis: sensitivity to non-depolarising muscle relaxants
Malignant hyperthermia: hyper-metabolic state -> hyperthermia, electrolyte derangement
Arthritis: limited neck movement

1187
Q

Problems associated w/ obese pt receiving GA

A

Intubation, airway maintenance, ventilation difficult
Moving pt difficult
Difficulty finding veins
Drug doses difficult to calculate

1188
Q

Discuss aspirin

A

NSAID

Analgesic, anti-inflammatory, anti-thrombotic
Hepatic metabolism, renal excretion
Contradicted: severe liver disease, on dialysis

Permanently affects platelet cohesiveness for lifespan (10-14d)
Affects 1ry homeostasis; prolong bleeding
No effect: INR/PT, APTT

1189
Q

Discuss non-selective NSAIDs

A

Ibuprofen, naproxen, diclofenac

Analgesic, anti-inflammatory, antipyretic
Inhibit
- COX1: side effects, toxicity
- COX2: anti-inflammatory

Adverse
- gastric irritability
- reversible platelet dysfunction; cohesiveness regain once cleared (48-72h)
- acute renal failure: low dose, short time won’t cause
- bronchoconstriction
— leukotriene overproduction due to 5-LOX pathway
— asthmatics contraindicated

1190
Q

Discuss selective NSAID

A

COX2 inhibitors: celecoxib, etiricoxib

Don’t affect gastric mucosa
Promote platelet aggregation
- contraindicated pt w/ history atherosclerosis

Hepatic metabolism, renal excretion
Similar renal affects to non-selective NSAIDs

1191
Q

Indications of immunosuppressives

A

Arthritis: psoriatic, rheumatoid, ankylosing spondylitis, acute gouty
Psoriasis, Behçet’s disease, LP
Ulcerative colitis, Crohn’s, Coeliac
Organ transplant

1192
Q

Discuss mechanism, indications and screening for steroidal immunosuppressives

A

Corticosteroids: prednisolone
Anti-inflammatory/immunosuppressive action
- limit capillary dilation, vascular permeability
- restrict granulocytes, macrophages accumulation; red. release vasoactive kinins

Indications

  • 1/2ry adrenocortical insufficiency
  • SLE, pemphigus, acute rheumatic fever
  • bursitis, liver disorders
  • leukaemia, lymphoma, thrombocytopenia purpura, autoimmune HA

Pre-treatment

  • BP, weight, height
  • Hb1Ac, triglycerides, K+
  • glaucoma, cataract
1193
Q

How to minimise adverse effects of corticosteroids?

A 
Lowest effect dose, min. T possible 
Take in morning, alternate days
Steroid treatment card
PPI for GI protection in pt w/ high risk GI bleed
Gradual withdrawal
1194
Q

Discuss antimitotics

A

Azathioprine: cyclophosphamide, chlorambucil

Immunosuppressive, antimetabolite
Converted into 6-mercaptopurine

Inhibit purine and DNA synthesis necessary for cell proliferation
- esp. lymphocytes, leukocytes

Pretreatment: serum thiopurine methyl transferase assay; high = inc. dose

Adverse
- myelopsuppresion, hepatotoxicity, lymphoproliferative disorders, thrombocytopenia
Signs: rash, oral ulcers, abnormal bruising, severe sore throat
Post-treatment: FBC, U+E, LFT

1195
Q

Discuss cyclosporine

A

Calcineurin inhibitor: tacrolimus

Immunosuppressive: specific action T lymphocytes
Binds immunophilins, inhibits calcineruin (activate transcription interleukin 2)
- inhibit lymphokine production, interleukin 2 release
- preferentially inhibit T helper and killer cells

Hepatic metabolism

1196
Q

Adverse effects and drug interactions of cyclosporine

A

Adverse

  • hypertension
  • nephrotoxicity, neurotoxicity
  • malignancies
  • gingival hyperplasia
  • lymphoproliferative disorders
  • teratogenicity

Interactions

  • inc. toxicity: macrolide AB (clarithromycin, erythromycin); antifungals (fluconazole, miconazole)
  • NSAID promote nephrotoxicity
1197
Q

Post-treatment monitoring of cyclosporine

A

FBC
LFT
U+E

1198
Q

Discuss mycophenolate mofteil

A

Immunosuppressive

Antibiotic substance derived from penicillium stoloniferum (mould)
Block de novo biosynthesis purine by inhibiting inosine monophosphate dehydrogenase
- prevent proliferation T cells, lymphocytes
- Ab formation from B cells

Adverse

  • fever, chills
  • bruising, bleeding
  • Black tarry stool
  • abdominal pain, nausea, vomiting
  • dyspepsia, diarrhoea, oesophagitis, gastritis, GI bleed
1199
Q

Discuss biological response modifiers

A

Adalimumab, infliximab

Block inflammation and immune response
Act directly to neutralise specific target immune components
Less immunosuppressive

Indicated

  • not responded to conventional therapy
  • convention contraindicated

Commonly TNF-alpha (promotes inflammation) inhibitors

Monitoring: LFT, FBC, HIV testing, hepatitis screening

1200
Q

Discuss Behçet’s disease

A

Multisystem disease

Recurrent orogenital ulcers; indistinguishable from RAS
Ocular lesions: ant. uveitis, recurrent hypopyon, iritis, choriorentinitis
Skin: erythema nodosum, thrombophlebitis

BDS 2 (4 decks)

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