BDS5002: HHD

Question 1

Define macule, papule, nodule

Answer 1

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

Question 2

Describe finger clubbing

Answer 2

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

Question 3

Describe nail pitting

Answer 3

Small indents/depressions in surface of nail

Caused by:
Psoriasis
Lichen planus
Alopecia areata

Question 4

Describe koilonychia

Answer 4

Spoon shaped nail

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

Question 5

Describe Beau’s lines

Answer 5

Transverse depressions in nail usually reflect poor growth

Caused by
Raynaud’s phenomenon
Trauma

Question 6

Describe splinter haemorrhages

Answer 6

Tiny blood clots, tend to run vertically

Caused by
Trauma
IE 
Lupus
Rheumatoid disease 
Psoriasis

Question 7

Describe herpetic whitlow

Answer 7

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

Question 8

Describe paronychia

Answer 8

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

Question 9

What are the most common cutaneous malignancies?

Answer 9

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

Question 10

What are the common predisposing factors of B/SCC?

Answer 10

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

Question 11

What is BCC?

Answer 11

Locally invasive cancer of epidermal basaloid cells

Question 12

Describe the presentation of BCC

Answer 12

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

Question 13

What is the prognosis of BCC?

Answer 13

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

Question 14

What is SCC?

Answer 14

Malignant tumour of keratinocytes

Question 15

Where is SCC most common?

Answer 15

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

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

Question 16

What are malignant melanomas?

Answer 16

Malignant tumours of melanocytes

Question 17

What are the common predisposing factors for malignant melanomas?

Answer 17

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

Question 18

How is malignant melanoma diagnosed?

Answer 18

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

Question 19

Describe the prognosis of malignant melanoma

Answer 19

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

Question 20

What is the primary treatment for malignant melanomas?

Answer 20

Surgical excision w/ adequate clearance margin

Question 21

What is psoriasis?

Answer 21

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

Question 22

What are the predisposing factors of psoriasis?

Answer 22

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

Question 23

Describe the presentation of psoriasis

Answer 23

Well demarcated red scaly patches topped w/ silvery scales

Pitting or onycholysis of nails

Question 24

What is psoriatic arthropathy/arthritis?

Answer 24

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)

Question 25

What are the treatments for psoriasis?

Answer 25

``` Coal tar Corticosteroids Retinoids VitD Ciclosporin Monoclonal AB ```

Question 26

What are the dental aspects of psoriasis?

Answer 26

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

Question 27

What is eczema?

Answer 27

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

Question 28

Name endogenous eczema types

Answer 28

Atopic Seborrhoeic Venous

Question 29

Describe seborrhoeic eczema/dermatitis

Answer 29

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

Question 30

Describe the treatment of seborrhoeic eczema

Answer 30

Topical combinations of anitfungals w/ weak corticosteroids

Question 31

What are the types of exogenous eczema?

Answer 31

Contact irritant Contact allergic Infective

Question 32

Describe contact dermatitis/eczema

Answer 32

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

Question 33

What is the treatment plan for eczema?

Answer 33

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

Question 34

What are the dental aspects of eczema?

Answer 34

Association w/ atopy Perioral dermatitis Exfoliative cheilitis Oral allergy syndrome

Question 35

What is atopy?

Answer 35

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

Question 36

Define Ag and immunogen

Answer 36

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

Question 37

Define adjuvant

Answer 37

Substance that enhances Ab response

Question 38

Define vaccine and toxoid

Answer 38

Vaccine: antigenic substance that provides immunity against 1/+ disease Toxoid: toxin from pathogen that is no longer toxic but still antigenic

Question 39

Define Ab titre

Answer 39

Amount Ab in blood

Question 40

Discuss passive immunisation and give examples of vaccines given

Answer 40

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

Question 41

Discuss how active immunisation works

Answer 41

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

Question 42

Discuss the characteristics of an ideal vaccine

Answer 42

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

Question 43

Discuss the 3 different types of active vaccine

Answer 43

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

Question 44

Compare the primary and secondary immune response

Answer 44

Primary: slow, primarily IgM, levels rapidly return to normal, Ab titre small Secondary: rapid, IgG, Ab titre much higher

Question 45

Discuss different administration routes of vaccines w/ examples

Answer 45

Mouth: colonise gut, promote local and humoral Abs; oral polio vaccine Subcutaneous, intramuscular: anterolateral thigh, upper arm; all except BCG Intradermal: BCG

Question 46

Discuss the possible complications of vaccines

Answer 46

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

Question 47

What are the 5 main contraindications for vaccines?

Answer 47

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

Question 48

Define sterilisation, disinfection, antiseptic, asepsis

Answer 48

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

Question 49

What are the 4 main methods of sterilisation?

Answer 49

1. Heat 2. Irradiation 3. Gas 4. Filtration

Question 50

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

Answer 50

Higher temp., hold time dec. to achieve sterilisation | Indirect

Question 51

Discuss moist heat sterilisation

Answer 51

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)

Question 52

Discuss dry heat sterilisation

Answer 52

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

Question 53

Discuss irradiation sterilisation

Answer 53

Ionising radiation incl. gamma, X-ray, accelerated electrons | Commercial sterilisation single use items; plastic syringes

Question 54

Discuss gas and filtration sterilisation

Answer 54

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

Question 55

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

Answer 55

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

Question 56

3 main sources of infection and 3 main transmission routes

Answer 56

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

Question 57

Define anaemia

Answer 57

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

Question 58

What is mean corpuscular vol?

Answer 58

MCV is av. vol. RBCs

Question 59

What are the predisposing factors for anaemia?

Answer 59

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

Question 60

What are the main classifications of anaemia?

Answer 60

Microcytic: MCV < 76 - Fe deficiency, thalassaemia Normocytic: MCV 76-96 - cancer - chronic disease Macrocytic: MCV >96 - VitB12, folate deficiency - alcohol, drugs, liver disease

Question 61

Explain how Fe deficiency can cause anaemia

Answer 61

Fe in haem; no haem = no Hb | Defective Hb synthesis causes red. RBC maturation so RBCs small and red. Hb

Question 62

How must an Fe deficiency be confirmed?

Answer 62

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

Question 63

Causes of Fe deficiency and treatments

Answer 63

Causes - pre-menopausal F: menorrhagia - M/post-menopause: GIT bleeding; ulcer, cancer Treatment: replace Fe - diet - oral Fe (best) - avoid blood transfusion

Question 64

Discuss nomocytic anaemia

Answer 64

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 ```

Question 65

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

Answer 65

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

Question 66

Causes of B12 deficiency

Answer 66

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

Question 67

Discuss pernicious anaemia

Answer 67

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

Question 68

Discuss causes and features of folate deficiency

Answer 68

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

Question 69

Discuss haemolytic anaemia

Answer 69

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

Question 70

Discuss lab findings for haemolytic anaemia

Answer 70

``` 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 ```

Question 71

Discuss heredity spherocytosis

Answer 71

Congenital: autosomal dominant Disorder RBC membrane Chronic HA Spherocytes in peripheral blood

Question 72

Discuss sickle cell disease

Answer 72

``` 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 ```

Question 73

Discuss glucose-6-phosphate dehydrogenase deficiency

Answer 73

``` 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 ```

Question 74

Discuss acquired haemolytic anaemia

Answer 74

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

Question 75

What is haemostasis?

Answer 75

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

Question 76

Describe the 2 mechanisms of haemostasis

Answer 76

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

Question 77

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

Answer 77

Primary - vascular disorders - vWF disease (can be secondary) - platelet disorders Secondary - clotting factor disorders

Question 78

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

Answer 78

Congenital - vWD (1/2) - Haemophilia A and B (2) Acquired - thrombocytopenia (1) - platelet dysfunction associated w/ drugs (1) - antiplatelet (1) - anticoagulants (2)

Question 79

Discuss vascular disorders in relation to haemorrhagic disorders

Answer 79

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

Question 80

What is the function of Von williebrand factor?

Answer 80

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

Question 81

Discuss vWD

Answer 81

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

Question 82

Discuss dental relevance of vWD

Answer 82

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

Question 83

Discuss platelet deficiency disorders

Answer 83

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

Question 84

What is the dental relevance of platelet deficiency disorders?

Answer 84

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

Question 85

Discuss platelet dysfunction disorders

Answer 85

Antiplatelets: aspirin, NSAIDs, clopidogrel, dipyridamole - all except NSAIDs act irreversibly, permanently on lifespan of RBC - NSAIDs reversible and cleared in 1/2d vWD

Question 86

Discuss the dental relevance of platelet dysfunction disorders

Answer 86

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

Question 87

Describe clinical features of platelet disorders

Answer 87

Easy bruising and bleeding - petechiae - purpura - ecchymosis

Question 88

Discuss haemophilia A and B

Answer 88

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

Question 89

Discuss dental relevance of haemophilia A and B

Answer 89

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

Question 90

Discuss anticoagulant therapy

Answer 90

Thrombosis or significant risk of thrombosis | Indications: atrial fibrillation, cardiac valvular disease, ischaemic heart disease

Question 91

Discuss use of warfarin

Answer 91

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

Question 92

Discuss dental relevance of warfarin

Answer 92

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

Question 93

Discuss herparin

Answer 93

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

Question 94

Define determinant, receptor and specificity

Answer 94

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

Question 95

Describe non-immunological defences

Answer 95

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

Question 96

Describe activation of innate immune system

Answer 96

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

Question 97

Discuss molecules of innate immune system

Answer 97

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

Question 98

Discuss circulation of lymphocytes

Answer 98

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

Question 99

Discuss activation of adaptive immune response

Answer 99

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.

Question 100

Discuss memory and tolerance in active immunity

Answer 100

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

Question 101

Distinguish b/w Ab, cytokines, complement

Answer 101

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)

Question 102

Discuss myeloid derived immune system cells

Answer 102

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

Question 103

Discuss natural killer cells

Answer 103

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

Question 104

Discuss clonal selection

Answer 104

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

Question 105

Discuss histamine

Answer 105

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

Question 106

Discuss leukotrienes

Answer 106

Lipid mediators of inflammation derived from arachidonic acid Produced by macrophages and mast cells Smooth muscle contraction Inc. vascular permeability Stim. mucous secretion

Question 107

Discuss prostaglandins

Answer 107

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

Question 108

Discuss chemokines

Answer 108

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

Question 109

Discuss interferons

Answer 109

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

Question 110

Discuss tumour necrosis factor (TNF)

Answer 110

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

Question 111

Discuss interleukins

Answer 111

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

Question 112

Discuss erythropoiesis

Answer 112

Production of RBCs ``` Controlled by -ve feedback Stim. by - hypoxia - high altitude - inc. exercise - loss lung tissue due to emphysema ```

Question 113

What is polycythaemia?

Answer 113

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

Question 114

Discuss general aetiology if anaemia

Answer 114

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

Question 115

Discuss Fe deficiency anaemia

Answer 115

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

Question 116

Discuss B12 deficiency anaemia

Answer 116

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

Question 117

Discuss folate deficiency anaemia

Answer 117

Causes - chronic alcoholism - drugs; cytotoxic, phenytoin, HIV/AIDS Symptoms: same as B12 w/o neurological Treatment: daily oral intake folic acid

Question 118

Discuss sickle cell anaemia

Answer 118

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

Question 119

Discuss aplastic anaemia

Answer 119

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

Question 120

Discuss general management of anaemia

Answer 120

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

Question 121

General symptoms of respiratory diseases

Answer 121

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

Question 122

General signs of respiratory disease

Answer 122

``` 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 ```

Question 123

Define asthma

Answer 123

Common chronic inflammatory condition of airways | Airway hyper responsiveness causes reversible (spontaneous or w/ therapy) airflow obstruction

Question 124

2 classifications of asthma

Answer 124

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

Question 125

Compare extrinsic and intrinsic asthma

Answer 125

``` 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 ```

Question 126

Pathogenesis of asthma

Answer 126

``` 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 ```

Question 127

Discuss clinical features asthma

Answer 127

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

Question 128

Discuss investigations into diagnosing asthma

Answer 128

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

Question 129

Discuss management of asthma

Answer 129

``` 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) ```

Question 130

Discuss dental relevance of asthma

Answer 130

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

Question 131

Define and discuss risk of COPD

Answer 131

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

Question 132

Discuss chronic bronchitis

Answer 132

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

Question 133

Discuss emphysema

Answer 133

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

Question 134

Discuss diagnosis and management of COPD

Answer 134

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

Question 135

Discuss clinical features of COPD

Answer 135

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

Question 136

Discuss dental relevance of COPD

Answer 136

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

Question 137

What is pneumonia?

Answer 137

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

Question 138

Risk factors of pneumonia

Answer 138

Smoking Chronic lung/heart disease Alcohol Immunosuppression

Question 139

Clinical features and complications of pneumonia

Answer 139

Clinical - cough, sputum - fever - chest pain - lung abscess - dyspnoea - pyrexia - tachypnoea - tachycardia - empyema - red. lung expansion - plural rub Complications - lung abscess - empyema - respiratory failure

Question 140

Management and dental relevance of pneumonia

Answer 140

Management - alcohol, tobacco avoidance - analgesics and antipyretic relieve symptoms - broad spectrum antimicrobial - prophylaxis: smoking cessation, influenza immunisation Dental - defer all treatment - GA contraindicated

Question 141

What is tuberculosis?

Answer 141

Chronic granulomatous infection caused by M. tuberculosis

Question 142

Risk factors of TB

Answer 142

``` Homeless Prison HIV Alcoholism IV drug use Migrants, asylum seekers ```

Question 143

Clinical features TB

Answer 143

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 ```

Question 144

Discuss diagnosis and treatment of TB

Answer 144

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

Question 145

Discuss dental relevance of TB

Answer 145

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

Question 146

Lung cancer aetiology

Answer 146

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

Question 147

Clinical features lung cancer

Answer 147

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

Question 148

Discuss lung cancer investigations and management

Answer 148

Investigations - chest X-ray - CT and PET scan - bronchoscopy - sputum cytology - biopsy Management - TNM tumour staging - surgery - radiotherapy; palliative care, chemotherapy

Question 149

Prognosis of lung cancer

Answer 149

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

Question 150

Dental relevance of lung cancer

Answer 150

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

Question 151

What is cystic fibrosis?

Answer 151

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

Question 152

Discuss clinical features and complications of CF

Answer 152

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

Question 153

How is CF diagnosed?

Answer 153

Na, Cl in sweat >60mmol/L

Question 154

Management of CF

Answer 154

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

Question 155

Dental relevance of CF

Answer 155

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

Question 156

Main types of mucocutaneous lesions

Answer 156

Lichen planus - vulvovaginal-gingival syndrome Lichenoid reaction Lupus erythematous

Question 157

What is lichen planus?

Answer 157

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

Question 158

Discuss natural history of L.P.

Answer 158

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

Question 159

Oral presentation of LP

Answer 159

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

Question 160

Variants of LP

Answer 160

``` Papular Reticular Plaque-like Atrophic Erosive (ulcerative) Bullous ```

Question 161

Discuss extra-oral presentation of LP

Answer 161

Cutaneous, purple polygonal pruritic papules Dystrophic nails Lichen planopilaris (hair) -> scarring alopecia Ocular, nasal, laryngeal, oesophageal, gastric, bladder

Question 162

Discuss cutaneous LP

Answer 162

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

Question 163

Discuss other sites of LP

Answer 163

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

Question 164

Discuss vulvovaginal-gingival syndrome

Answer 164

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

Question 165

Discuss lichenoid drug reaction

Answer 165

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

Question 166

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

Answer 166

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

Question 167

Discuss clinical features of lichenoid reaction

Answer 167

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

Question 168

Discuss oral contact hypersensitivity reactions

Answer 168

``` 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 ```

Question 169

Discuss systemic lupus erythematosus

Answer 169

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

Question 170

Discuss discoid lupus erthematosus

Answer 170

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

Question 171

Define vesicle and bulla

Answer 171

Vesicle: small, fluid-filled blister <5mm | Bulla;p: large, fluid-filled blister >5mm

Question 172

Discuss varicella zoster virus

Answer 172

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

Question 173

Discuss chickenpox

Answer 173

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

Question 174

Discuss shingles and post herpetic neuralgia

Answer 174

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

Question 175

What is dermatitis herpetiformis?

Answer 175

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

Question 176

Oral presentation of dermatitis herpetiformis

Answer 176

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

Question 177

Discuss clinical features of dermatitis herpetiformis

Answer 177

Smaller bullae and vesicles | Associated w/ Coeliac disease

Question 178

Treatment of dermatitis herpetiformis

Answer 178

Gluten free diet and dapsone

Question 179

Aetiology of erythema multiforme

Answer 179

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

Question 180

What is erythema multiform?

Answer 180

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

Question 181

Clinical features of erythema multiforme

Answer 181

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

Question 182

Discuss pemphigus vulgaris

Answer 182

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

Question 183

Discuss oral presentation of pemphigus vulgaris

Answer 183

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

Question 184

Discuss cutaneous pemphigus

Answer 184

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

Question 185

Discuss mucous membrane pemphigoid

Answer 185

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

Question 186

Management of mucous membrane pemphigoid

Answer 186

``` Topical corticosteroids Oral - prednisolone - dapsone - tetracyclines - azathioprine - cyclophosphamide ```

Question 187

Discuss bullous pemphigoid

Answer 187

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

Question 188

Management of bullous pemphigoid

Answer 188

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

Question 189

Corticosteroid side effects CUSHINGOID

Answer 189

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

Question 190

Define acute inflammation

Answer 190

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

Question 191

Exogenous and endogenous causes of acute inflammation

Answer 191

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

Question 192

5 Cardinal Signs of Acute inflammation (macroscopic changes)

Answer 192

``` Redness Swelling Heat Pain Loss of function ```

Question 193

Discuss the microscopic changes seen during acute inflammation

Answer 193

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

Question 194

Discuss impact of inc. permeability in acute inflammation

Answer 194

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

Question 195

Mechanisms involved in migration of WBCs from blood to tissue

Answer 195

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

Question 196

Discuss neutrophil polymorphs

Answer 196

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

Question 197

Discuss eosinophils and basophils/mast cells

Answer 197

Eosinophils - esp. allergy and helminth infections - bilobed nucleus, red granules Basophils/mast cells - esp. early - blue/purple cytoplasm - degranulate w/ release vasoactive amines

Question 198

Discuss monocytes/macrophages

Answer 198

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 ```

Question 199

Discuss neutrophil chemotaxis

Answer 199

Conc. gradient neutrophil is drawn up due to - bacteria - fungi - immune complexes - toxins - complement components - lipoxygenase products - WBC breakdown products

Question 200

Discuss phagocytosis

Answer 200

Recognition and attachment - mechanical contact - opsonisation Engulfment - pseudopods - phagosomes Killing and degradation - lysosomal contents

Question 201

Discuss clinical features of acute inflammation

Answer 201

``` Pyrexia Drowsiness Lethargy Leukocytosis Dec. appetite Acute phase proteins ```

Question 202

Discuss resolution of acute inflammation

Answer 202

Clearance of injury Clearance of any inflammatory cells and mediators Replacement of injured cells Normal function resumed Can be spontaneous or w/ treatment

Question 203

Discuss repair outcome of acute inflammation

Answer 203

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

Question 204

Discuss chronic inflammation

Answer 204

If Acute inflammation injury can’t be dealt w/ | Or repeated episodes

Question 205

Discuss suppurative inflammation

Answer 205

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

Question 206

Discuss septicaemia

Answer 206

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

Question 207

Possible outcomes of tissue loss and destruction

Answer 207

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

Question 208

Define regeneration and repair

Answer 208

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

Question 209

Discuss general features of wound healing

Answer 209

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

Question 210

Discuss haemostasis role in tissue repair

Answer 210

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

Question 211

3 groups cells can be divided into

Answer 211

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

Question 212

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

Answer 212

Architecture structure may be lost | Intact basement membrane req. for regeneration of most tissues

Question 213

3 tissues capable of regenerating all constituents

Answer 213

Liver Bone Bone marrow

Question 214

Discuss the granulation tissue

Answer 214

``` 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 ```

Question 215

Discuss angiogenesis

Answer 215

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)

Question 216

Discuss remodelling of wound after repair/regeneration

Answer 216

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

Question 217

Compare 1ry and 2ry intention healing

Answer 217

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)

Question 218

Discuss fracture healing

Answer 218

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

Question 219

What is special about fracture healing ?

Answer 219

Only situation where granulation tissue leads to regeneration

Question 220

Control of repair

Answer 220

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

Question 221

Factors affecting healing

Answer 221

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

Question 222

Discuss mycobacterium

Answer 222

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

Question 223

Distinguishing factors of mycobacterium tuberculosis

Answer 223

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

Question 224

What is TB and it’s aetiology?

Answer 224

Chronic granulomatous disease Aetiology - M. tuberculosis: human - M. bovis: human and mammal - M. africanum: human, equatorial Africa - M. microti: vole (seldom)

Question 225

Discuss pathogenesis of TB

Answer 225

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)

Question 226

Significance of immunocompromised pt and TB

Answer 226

Bacteria much more likely to reactivate | Cavity formation rare as lack immune response to 1ry infection

Question 227

Discuss transmission of TB

Answer 227

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

Question 228

How can the spread of TB be controlled?

Answer 228

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

Question 229

Discuss vaccination for TB

Answer 229

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 ```

Question 230

How is TB diagnosed?

Answer 230

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

Question 231

Treatment of TB

Answer 231

Long, drawn out, compliance problems Intensive phase; 2/12 - rifampicin - isoniazid - pyrazinamide (and/or ethambutol) Continuous phase 9/12 - rifampicin - isoniazid

Question 232

Discuss upper respiratory tract infections

Answer 232

Involve - nose - paranasal sinuses - middle ear - laryngeal, epiglottal tissues - post. pharynx - tonsils Mainly bacteria and viruses Colds, sore throats economic burden

Question 233

Discuss lower respiratory infections

Answer 233

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

Question 234

Discuss respiratory infections below larynx

Answer 234

Bronchitis - acute: mycoplasma pneumoniae - chronic: H. influenzae, S. pneumoniae Bronchiectasis - H. influenzae - Ps. aeruginosa Whooping cough: B. pertussis

Question 235

Discuss 2ry pneumonia

Answer 235

Predisposing - chronic bronchial disease - compromised pt - CF Pathogens - S. pneumoniae - Haemophilus influenzae - Branhamella catarrhalis - fungal infections

Question 236

Discuss Haemophilus species

Answer 236

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

Question 237

Discuss the carriage and pathogenesis of haemophilus influenzae

Answer 237

Carriage - URT, nasopharynx/throat Pathogenesis - possibly penetration of submucosa of nasopharynx Otitis media (inflammation ear): pathogenesis unclear, caused by non-typable strains

Question 238

Discuss the virulence and diagnosis of haemophilus influenzae

Answer 238

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)

Question 239

Discuss non-invasive haemophilus influenzae disease

Answer 239

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

Question 240

Discuss treatment of haemophilus influenzae

Answer 240

Ampicillin resistance; use cefotaxime (cephalosporin) | Vaccine: capsular polysaccharide preparations used

Question 241

Discuss general features of Corynebacterium diphtheriae

Answer 241

Cause diphtheria Aerobic/facultative anaerobic Gram +ve rods; diphtheroids or coryneforms Strains: gravis, intermedius, mitis

Question 242

Discuss epidemiology and pathogenesis of corynebacterium diphtheriae

Answer 242

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

Question 243

Discuss the Elek test

Answer 243

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

Question 244

Discuss treatment and vaccination for corynebacterium diphtheriae

Answer 244

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

Question 245

Causative species and risk of bacterial sialadenitis

Answer 245

Sialadenitis: inflammation salivary gland Causative - S. aureus - alpha-haemolytic strep. - anaerobes Risk - dehydration - red. salivary flow - anaerobes

Question 246

Clinical features and diagnosis of bacterial sialadenitis

Answer 246

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

Question 247

Management of bacterial sialadenitis

Answer 247

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

Question 248

Causative species and risk of acute necrotising ulcerative gingivitis

Answer 248

Causative: strict anaerobic bacteria Risk - poor OH - smoking - stress - malnutrition - vit deficiency - immunodeficiency

Question 249

Clinical features and diagnosis of acute necrotising ulcerative gingivitis

Answer 249

Clinical - rapid development - painful ulceration - gingival margin and inter-dental papillae - halitosis - widespread Diagnosis - clinical - gram-stained smear; fusobacteria, medium sized sprochetes, acute inflammation

Question 250

Management of acute necrotising ulcerative gingivitis

Answer 250

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

Question 251

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

Answer 251

Gangrene of face and mouth

Question 252

Causative species and risk of noma

Answer 252

Causative - fusobacterium necrophorum - prevotella intermedia - alpha-haemolytic strep. - pseudomonas Risk - ANUG - malnutrition - poor OH - debilitation after severe illness - immunosuppression

Question 253

How is noma spread?

Answer 253

Through muscle and bone | NOT through anatomic spaces of head and neck

Question 254

Causative species and risk of actinomycosis

Answer 254

Causative: actinomyces Risk - caries and XLA - gingivitis and gingival trauma - poor OH - immunocompromised

Question 255

Clinical features of actinomycosis

Answer 255

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

Question 256

Diagnosis and treatment actinomycosis

Answer 256

Diagnosis - aspirated pus w/ aggregates actinomyces forming yellow particles (sulphur granules) Treatment - surgical tissue + removal dead tissue - + Long course penicillin or erythromycin

Question 257

Discuss staphylococcus mucositis

Answer 257

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

Question 258

Discuss TB

Answer 258

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

Question 259

Causative species, spread and treatment of syphilis

Answer 259

Causative: treponema pallidum Transmission: sexual contact, vertical, blood transfusion Treatment: penicillin

Question 260

Discuss 1ry syphilis

Answer 260

Highly infectious firm nodule @ site of inoculation Breakdown after few days leaving painless ulcer w/ indurated margins Usually on genitals Lymphadenopathy Resolves 3-12wks

Question 261

Discuss 2ry syphilis

Answer 261

Highly infectious maculopapular rash Mucosal ulcers Condylomata lata (warts on genitals) Lymphadenopathy Febrile illness Malaise 6wk post-1ry infection Resolves 2-6wks

Question 262

Discuss 3ry syphilis

Answer 262

3-15yr after infection Gummatous, CV, neuro-syphilis Oral lesions - gumma (necrotic, painless ulcer) on palate - leukoplakia of dorsum tongue

Question 263

Discuss congenital syphilis

Answer 263

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 ```

Question 264

What is ischaemic heart disease?

Answer 264

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

Question 265

Aetiology of IHD

Answer 265

95% caused by atheroma of coronary arteries | Remainder by vasculitides (inflammation vessel) and arterial vasospasm

Question 266

What is atheroma?

Answer 266

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

Question 267

IHD risk factors

Answer 267

``` Hypertension Hyperlipidaemia Smoking DM Age Gender Familial predisposition Obesity Insufficient exercise ```

Question 268

Pathogenesis of IHD

Answer 268

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

Question 269

Complications of IHD

Answer 269

Ulceration Fissuring Haemorrhage Thrombosis

Question 270

Epidemiology of IHD

Answer 270

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

Question 271

4 Clinical syndromes of IHD

Answer 271

Sudden death; unexpected death within 1h cardiac symptoms Myocardial infarct Angina Chronic IHD

Question 272

Discuss sudden death in IHD

Answer 272

Atheroma w/ complicated plaque | Death due to arrhythmias

Question 273

Compare stable and unstable angina

Answer 273

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

Question 274

4 types of atheroma plaque

Answer 274

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

Question 275

3 types of myocardial infarct

Answer 275

Regional, transmural Regional, subendocardial Circumferential, subendocardial

Question 276

Discuss regional, transmural MI

Answer 276

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

Question 277

Discuss regional, subendocardial MI

Answer 277

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

Question 278

Discuss circumferential, subendocardial MI

Answer 278

Caused by general under-perfusion due to - moderate hypotension on background of triple vessel disease - severe hypotension and normal vessels - other factors; severe anaemia

Question 279

Macroscopic changes seen in IHD

Answer 279

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

Question 280

Short term complications IHD

Answer 280

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

Question 281

Long term complications IHD

Answer 281

``` LVF Sudden death/arrhythmia Aneurysm Dressler's syndrome Recurrent infarction ```

Question 282

Discuss valvular HD

Answer 282

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

Question 283

Describe infective endocarditis

Answer 283

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

Question 284

Epidemiology of IE

Answer 284

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

Question 285

Discuss subacute IE

Answer 285

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

Question 286

Discuss acute IE

Answer 286

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

Question 287

Morphology of IE

Answer 287

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

Question 288

Cardiac complications of IE.

Answer 288

``` Valvular insufficiency or stenosis Myocardial abscess Suppurative pericarditis Dehiscence of artificial valve Emboli of coronary arteries ```

Question 289

Systemic embolic complications of IE

Answer 289

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

Question 290

Renal complications IE

Answer 290

Renal infarction or emboli (2ry abscess)

Question 291

Discuss acute rheumatic fever

Answer 291

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

Question 292

Symptoms and pathology of acute rheumatic fever

Answer 292

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)

Question 293

Discuss chronic rheumatic fever

Answer 293

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

Question 294

Discuss congenital HD

Answer 294

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

Question 295

4 steps of immune system

Answer 295

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

Question 296

Discuss Ag presenting cells (APC)

Answer 296

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

Question 297

3 main APCs

Answer 297

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)

Question 298

Compare exogenous and endogenous Ag

Answer 298

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

Question 299

Steps in Ag processing and presentation

Answer 299

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 ```

Question 300

Discuss role of MHC molecules in Ag recognition

Answer 300

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+)

Question 301

Role of CD4 and 8 T-lymphocytes in Ag recognition

Answer 301

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

Question 302

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

Answer 302

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

Question 303

Structure of Ab

Answer 303

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

Question 304

General functions of Ab (4)

Answer 304

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

Question 305

Isotypes of Ab

Answer 305

IgG: complement activation, placental Ig IgM: macroglobulin, form pentamers, complement IgA: dimers, high MWt secreted forms IgD IgE: mast cell activation

Question 306

Compare T in/dependent Ag

Answer 306

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)

Question 307

Discuss B cell activation signals

Answer 307

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

Question 308

Discuss possible fates of activated B cells

Answer 308

``` 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

Question 309

Define chronic inflammation

Answer 309

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

Question 310

When does chronic inflammation arise?

Answer 310

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

Question 311

Etiological agents of chronic inflammation

Answer 311

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

Question 312

4 effector cells of chronic inflammation

Answer 312

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

Question 313

What is granulomatous inflammation?

Answer 313

Distinctive chronic inflammation reaction w/ predominant cell activated macrophage Granuloma: collection of epithelioid macrophages surrounded by lymphocytes and occasionally plasma cells

Question 314

Describe appearance of granulomatous inflammation

Answer 314

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

Question 315

Examples of granulomatous inflammation

Answer 315

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

Question 316

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

Answer 316

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

Question 317

Discuss hypersensitivity in relation to chronic inflammation

Answer 317

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

Question 318

Possible outcomes of chronic inflammation

Answer 318

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

Question 319

Discuss herpes simplex virus and the different types

Answer 319

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

Question 320

Causative virus and clinical features primary herpetic gingivostomatitis

Answer 320

Causative: HSV1/2 Clinical - intraepithelial vesicles rupture; blood, crusted lip, widespread painful ulcers - gingiva swollen and erythematous - pyrexia, headache - cervical lymphadenopathy

Question 321

Diagnosis and treatment of primary herpetic gingivostomatitis

Answer 321

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

Question 322

Discuss herpes labiallis

Answer 322

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

Question 323

3 other common HSV viruses

Answer 323

Eczema herpeticum Erythema multiforme Herpetic whitlow

Question 324

Discuss chicken pox

Answer 324

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

Question 325

What is shingles? Clinical features, diagnosis, treatment

Answer 325

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

Question 326

Complication of shingles

Answer 326

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

Question 327

Discuss Ramsay Hunt Syndrome

Answer 327

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

Question 328

What is infectious mononucleosis? Pathogenesis and clinical features

Answer 328

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

Question 329

Diagnosis and management infectious mononucleosis

Answer 329

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

Question 330

3 other diseases caused by Epstein-Barr virus

Answer 330

``` 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 ```

Question 331

Discuss hand, foot and mouth disease

Answer 331

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

Question 332

Discuss herpangina

Answer 332

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

Question 333

Discuss causative species and clinical features mumps

Answer 333

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

Question 334

Complications, diagnosis, management of mumps

Answer 334

Complications - meningitis - encephalitis - transient deafness - epididymo-orchitis - oophoritis - pancreatitis - nephritis Diagnosis; clinical + - detection IgM - virus culture Management; rest, fluid, analgesic

Question 335

Compare verruca vulgaris and condyloma acuminatum

Answer 335

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

Question 336

Diagnosis and management of papillomavirus

Answer 336

Diagnosis; clinical + - histopathology - immunostaining detect HPV Management - excision

Question 337

Predisposing, clinical features, diagnosis and management pseudomembranous candidosis

Answer 337

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

Question 338

Discuss chronic hyperplastic candidosis

Answer 338

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

Question 339

Compare acute and chronic erythematous candidosis

Answer 339

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

Question 340

Discuss median rhomboid glossitis

Answer 340

Clinical; smooth, well demarcated erythematous area b/w ant. 2/3 and post. 1/3 tongue Diagnosis; microscopy and culture Management - predisposing, antifungal

Question 341

Discuss angular cheilitis

Answer 341

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

Question 342

Discuss chronic mucocutaneous candidiasis

Answer 342

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

Question 343

Anatomy of lower GIT

Answer 343

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

Question 344

Common diseases of small intestine

Answer 344

Coeliac | Crohn's

Question 345

Features of malabsorption

Answer 345

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

Question 346

Clinical features and causes steatorrhoea

Answer 346

Clinical - bulky stool - float - greasy/fatty/frothy - foul smell - difficult to flush Causes - Coeliac/Crohn's - CF - pancreatitis/cancer - liver disease

Question 347

What is Coeliac disease?

Answer 347

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

Question 348

Clinical findings of coeliac disease

Answer 348

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

Question 349

Investigations for Coeliac disease

Answer 349

``` 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

Question 350

Associated diseases of Coeliac disease

Answer 350

Dermatitis herpetiformis Linear IgA disease Selective IgA deficiency

Question 351

Discuss management of Coeliac disease

Answer 351

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

Question 352

Dental relevance Coeliac disease

Answer 352

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

Question 353

Clinical features of Crohn’s on mouth region

Answer 353

``` 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 ```

Question 354

Clinical features Crohn’s of SI area

Answer 354

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

Question 355

Clinical feature Crohn’s of LI

Answer 355

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

Question 356

Clinical features Crohn’s disease of perianal area

Answer 356

Anal tags Anal fistulae, fissure Anal abscess formation

Question 357

Extra-intestinal feature Crohn’s disease

Answer 357

Musculoskeletal - arthritis - ankylosing spondylitis Skin - erythema nodosum - psoriasis - pyoderma gangrenosum

Question 358

Investigation for Crohn’s disease

Answer 358

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

Question 359

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

Answer 359

1ry: refer adult pt <40 w/ - diarrhoea >6wk - abdominal pain w/ weight loss - raised faecal calprotectin - unexplained vit B12, folate deficiencies 2ry: individualised

Question 360

Management of Crohn’s

Answer 360

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

Question 361

Dental relevance of Crohn’s

Answer 361

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

Question 362

What is ulcerative colitis?

Answer 362

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

Question 363

Clinical features ulcerative colitis

Answer 363

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 ```

Question 364

Investigations and management ulcerative colitis, complications

Answer 364

Investigations and management - similar to Crohn’s, focus on colon Complications - carcinoma of colon - inc. risk if early onset or chronic disease (>10y)

Question 365

Discuss pseudomembranous colitis

Answer 365

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

Question 366

What is IBS? Discuss aetiology and clinical findings

Answer 366

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

Question 367

Discuss management and dental aspect IBS

Answer 367

Management - reassurance - stress relieve - high fibre diet - anti-spasmodics; mebeverine - CBT - antidepressants Dental; psychogenic oral symptoms - burning mouth - persistent idiopathic facial pain - sore tongue

Question 368

Discuss Peutz-Jegher's Syndrome

Answer 368

``` 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

Question 369

Define antimicrobial, antibiotic, bactericidal, bacteriostatic

Answer 369

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

Question 370

8 features of idea antimicrobial

Answer 370

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

Question 371

Discuss mechanisms of action and resistance of antimicrobials

Answer 371

``` 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 ```

Question 372

4 principles of antimicrobial stewardship

Answer 372

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

Question 373

5 common groups of antibacterials in dentistry

Answer 373

1. Penicillins 2. Macrolides 3. Lincosamides 4. Tetracyclines 5. Nitroimidazoles

Question 374

6 groups of penicillin

Answer 374

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

Question 375

Mechanism of action and resistance of penicillins

Answer 375

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

Question 376

Discuss side effects penicillins

Answer 376

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

Question 377

Common macrolides

Answer 377

Erythromycin Clarithromycin Azithromycin

Question 378

Mechanism of action and resistance, activity of macrolides

Answer 378

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

Question 379

Side effects macrolides

Answer 379

``` GIT symptoms Skin rash Fever Eosinophilia Cholestatic jaundice Transient hearing loss ```

Question 380

Mechanism of action and resistance, activity of lincosamides

Answer 380

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

Question 381

Common lincosamides

Answer 381

Clindamycin

Question 382

Side effect lincosamides

Answer 382

C. difficile colitis Allergic reaction Transient hepatitis Neutropenia, thrombocytopenia

Question 383

Common tetracyclines

Answer 383

1st gen - tetracycline - chlortetracycline - oxytetracycline 2nd - doxycycline 3rd - tigecycline

Question 384

Mechanism of action and resistance, activity of tetracyclines

Answer 384

Action - inhibit bacterial protein synthesis (30S) - bacteriostatic Resistance - efflux - ribosomal protection protein - enzymatic inactivation Activity; broad spectrum; gram+/-, IC organisms

Question 385

Side effects tetracyclines

Answer 385

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

Question 386

Common nitroimidazoles

Answer 386

Metronidazole

Question 387

Mechanism of action and resistance, activity metronidazole

Answer 387

Action - interact w/ nuclei acids and proteins causing breakage, destabilisation, cell death Resistance: rare Activity: anaerobes, facultative anaerobes, Protozoa

Question 388

Side effect nitroimidazoles

Answer 388

``` 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 ```

Question 389

2 families of common antifungals

Answer 389

Polyenes | Azoles

Question 390

Common polyenes

Answer 390

Amphotericin (IV) | Nystatin (oral)

Question 391

Discuss polyenes

Answer 391

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

Question 392

2 groups of azoles

Answer 392

Imidazoles - ketoconazole - miconazole - clotimazole Tiazoles - itraconazole - fluconazole - voriconazole - posaconazole - ravuconazole

Question 393

Discuss azoles

Answer 393

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

Question 394

5 targets for antivirals

Answer 394

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

Question 395

Discuss acyclovir

Answer 395

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 ```

Question 396

General characteristics of staphylococcus genus

Answer 396

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

Question 397

Classification of staphylococci

Answer 397

Coagulase+ - aureus - aureus var. anaerobius - delphini - intermedius Coagulase- - epidermidis - haemolyticus - lugdunensis - saprophyticus

Question 398

4 main diagnostic features of S. aureus

Answer 398

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

Question 399

Common infections caused by S. aureus

Answer 399

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

Question 400

Pathogenesis of S. aureus

Answer 400

Opportunistic pathogen - lowered host resistance - damaged skin/mucous membranes

Question 401

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

Answer 401

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

Question 402

Discuss toxic shock syndrome toxin in relation S. aureus

Answer 402

TSST-1 Causes toxic shock syndrome Associated w/ highly absorbent tampons Vaginal colonisation w/ S. aureus; multiplication and toxin production

Question 403

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

Answer 403

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

Question 404

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

Answer 404

Hyaluronidase (spreading factor) - break down IC ground substance (hyaluronic acid) of tissues Other - lipases - proteases - coagulases - DNase - phosphatases

Question 405

Discuss the other virulence factors of S. aureus

Answer 405

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

Question 406

Discuss epidemiology of Staphylococcal infections

Answer 406

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

Question 407

Discuss diagnosis of staphylococcal infections

Answer 407

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

Question 408

Discuss AB resistance in staphylococcus and methods to over come

Answer 408

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

Question 409

Discuss methicillin resistant S. aureus (MRSA)

Answer 409

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

Question 410

Characteristics of coagulase- staphylococci

Answer 410

``` 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 ```

Question 411

Infections caused by coagulase- staph.

Answer 411

``` Infected prostheses, implants Ventriculitis; shunt associated Peritonitis Septicaemia Endocarditis; prosthetic valve ```

Question 412

Discuss pathogenesis and treatment of coagulase- staph.

Answer 412

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

Question 413

Discuss fungi and mycoses

Answer 413

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

Question 414

3 types of mycoses

Answer 414

1. Superficial mycoses 2. Subcutaneous 3. Systemic

Question 415

Discuss superficial mycoses

Answer 415

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

Question 416

Discuss subcutaneous and systemic mycoses

Answer 416

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

Question 417

Discuss diagnosis and treatment of mycoses

Answer 417

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

Question 418

Discuss ringworm

Answer 418

Superficial mycoses ``` Scalp and feet 3 genera dermatophytes - Trichoohyton - Microsporum - Epidermophyton ``` Peeling/trauma epidermis probably necessary for infections - irritation, erythema, oedema, some vesiculation

Question 419

Discuss superficial candidiasis

Answer 419

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

Question 420

Discuss acute pseudomembranous and chronic mucocutaneous candidiasis

Answer 420

Acute pseudomembranous - new-born, elderly/debilitated, immunocompromised - white plaques become confluent to form pseudomembrane Chronic mucocutaneous - rare condition esp. children and elderly

Question 421

Discuss acute atrophic and chronic atrophic candidiasis

Answer 421

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

Question 422

Discuss chronic hyperplastic candidiasis and angular cheilitis

Answer 422

Chronic hyperplastic candidiasis - leukoplakia — thickened epithelium penetrated by C. albicans hyphae Angular cheilitis - eroded condition of angle(s) of mouth

Question 423

6 predisposing factors for oral candidiasis

Answer 423

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

Question 424

Discuss vaginal candidiasis and skin infections

Answer 424

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

Question 425

Discuss systemic candidiasis

Answer 425

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

Question 426

Discuss actinomyces

Answer 426

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

Question 427

Clinical features actinomycosis

Answer 427

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-

Question 428

Discuss diagnosis and treatment actinomycosis

Answer 428

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 ```

Question 429

Discuss the mucosal immune system

Answer 429

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

Question 430

Compare systemic and mucosal immune system

Answer 430

Systemic: largely sterile environment, vigorous reposts to microbial invasion Mucosal: constant exposure

Question 431

5 factors that contribute to OC health (Immunology)

Answer 431

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

Question 432

Discuss non-specific defence mechanisms in OC

Answer 432

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)

Question 433

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

Answer 433

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

Question 434

Discuss innate cells of OC immunity

Answer 434

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

Question 435

Discuss 7 innate molecules of OC immunity

Answer 435

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

Question 436

7 antimicrobial substances of saliva

Answer 436

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

Question 437

Discuss mechanism of action of OC Ab

Answer 437

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

Question 438

Briefly outline non/specific factors of OC immunity

Answer 438

Non-specific - mucosal barrier - innate cells (macrophages, neutrophils, NK, DC) - innate molecules; histatins, lysozyme, cystatins, peroxidases, lactoferrin Specific - SIgA - IgG, IgM - effector T cells

Question 439

4 functions of kidneys

Answer 439

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

Question 440

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

Answer 440

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

Question 441

Discuss chronic renal disease

Answer 441

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)

Question 442

Discuss common and rare causes of chronic renal disease

Answer 442

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

Question 443

When do symptoms of CRD manifest?

Answer 443

Kidney function <25%

Question 444

Discuss blood and immune symptoms of CRD

Answer 444

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

Question 445

Discuss the GI and metabolic symptoms of CRD

Answer 445

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

Question 446

Discuss neuromuscular symptoms of CRD

Answer 446

``` Headaches Confusion Sensory disturbances Tremors Peripheral neuropathy ```

Question 447

Discuss CV symptoms CRD

Answer 447

Hypertension Congestive heart disease Atheroma Peripheral vascular disease

Question 448

Discuss skin features of CRD

Answer 448

Pruritus Bruising Infection

Question 449

Discuss special investigations for diagnosing CRD

Answer 449

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

Question 450

Discuss general management of CRD

Answer 450

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 ```

Question 451

Discuss peritoneal dialysis and haemodialysis

Answer 451

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

Question 452

Discuss renal transplantation

Answer 452

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

Question 453

Dental relevance of general renal disease pt

Answer 453

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

Question 454

Dental relevance of haemodialysis CRD pt

Answer 454

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

Question 455

Discuss dental relevance of renal osteodystrophy

Answer 455

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

Question 456

Dental relevance of kidney transplant pt

Answer 456

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)

Question 457

Discuss symptoms and clinical feature of nephrotic syndrome

Answer 457

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

Question 458

General characteristics of streptococci

Answer 458

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

Question 459

Discuss serological classification of strep.

Answer 459

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

Question 460

Discuss 3 different types of haemolysis seen in strep

Answer 460

``` 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)

Question 461

Main diseases associated w/ S. pyogenes

Answer 461

URT: Acute tonsillitis, pharyngitis Skin: impetigo, erysipelas Toxin mediated: scarlet fever Systemic: septicaemia, toxic shock Post streptococcal infection: rheumatic fever, acute glomerulonephritis

Question 462

Discuss virulence factors of S. pyogenes

Answer 462

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

Question 463

Discuss the 7 toxins produced by S. pyogenes

Answer 463

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

Question 464

Discuss upper respiratory tract S. pyogenes infection

Answer 464

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

Question 465

Discuss erysipelas and impetigo

Answer 465

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

Question 466

Discuss scarlet fever

Answer 466

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

Question 467

Discuss rheumatic fever

Answer 467

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

Question 468

Discuss acute glomerulonephritis

Answer 468

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

Question 469

Discuss main diseases caused by S. agalactiae

Answer 469

``` 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

Question 470

Main diseases associated w/ S. pneumoniae

Answer 470

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

Question 471

Discuss characteristics of viridans strep

Answer 471

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

Question 472

Discuss strep mutans group

Answer 472

Isolated from carious lesions, IE Mutans Sobrinus

Question 473

Characteristics of S. mutans important to dental caries

Answer 473

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

Question 474

Discuss S. mutans anti-caries therapy

Answer 474

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

Question 475

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

Answer 475

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

Question 476

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

Answer 476

Caries vaccinations | Production of monoclonal Abs for prevention of S. mutans tooth colonisation

Question 477

Discuss members of S. mitis group

Answer 477

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

Question 478

Discuss strep salivarius group

Answer 478

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 ```

Question 479

Discuss strep anginosus group

Answer 479

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

Question 480

Discuss strep virulence factors in relation to IE

Answer 480

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

Question 481

Define commensal, carriage, pathogen, opportunistic pathogen, virulence

Answer 481

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

Question 482

Define endemic, epidemic, outbreak and pandemic

Answer 482

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

Question 483

4 common instances when opportunistic pathogens arise

Answer 483

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

Question 484

Discuss the sources of infections

Answer 484

Endogenous: within; normal flora invade Exogenous: from outside - contact w/ other human - zoonoses: animal pathogen - organisms in environment; H2O, soil - fomites: inanimate environment

Question 485

2 types of ways in which infections are spread

Answer 485

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

Question 486

Discuss vertical transmission

Answer 486

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

Question 487

Discuss attachment and invasion of bacteria

Answer 487

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

Question 488

3 main ways in which pathogens evade the immune system

Answer 488

Overcome immune defence Avoid destruction by phagocytes Motility

Question 489

Discuss how pathogens overcome immune defence

Answer 489

Respiratory bacteria secrete IgA protease which degrades Ig | S. pyogenes express protein A which binds Ig preventing opsonisation and activation of complement

Question 490

Discuss how bacteria avoid phagocytosis

Answer 490

S. pneumoniae has a polysaccharide capsule which inhibits uptake by polymorphs Some bacteria (mycobacterium tuberculosis) survive inside host macrophages

Question 491

Discuss motility as a means to evade immune defence

Answer 491

Ability to move enhances pathogenicity | - flagellae of S. typhimurium

Question 492

Discuss bacterial enzymes used to damage host cells

Answer 492

Coagulase: walling off of staph lesions (S. aureus) Proteases: porphyromonas gingivalis Bacteria express proteases, nucleases, lipases, glycosidases

Question 493

Discuss exotoxins used by bacteria to damage host

Answer 493

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

Question 494

Discuss endotoxins used by bacteria to damage host cell

Answer 494

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

Question 495

Discuss some of the lab investigations used to identify bacterial infections

Answer 495

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

Question 496

6 factors affecting transmissibility of bacteria

Answer 496

``` Ability to survive Ability to find alternative host Shedding capacity Infectivity Virulence Ability to evade immune response ```

Question 497

Discuss bacterial ability to survive in relation to transmissibility

Answer 497

Resist drying, UV: enterovirus H2O: Legionella, Giardia Soil: Clostridium tetanii

Question 498

Discuss shedding capacity in relation to bacterial transmissibility

Answer 498

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

Question 499

Compare active and carrier infection

Answer 499

Active: clinically unwell Carrier: looks well but chronically infected - may not be aware infected - HBV

Question 500

Common modes of infection transmission

Answer 500

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

Question 501

Discuss skin/mucous membrane spread of infection

Answer 501

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

Question 502

Discuss salivary spread of infection

Answer 502

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

Question 503

Discuss sexual transmission of infection

Answer 503

Usually b/w sexual partners - neisseria gonorrhoea (gonorrhoea) - treponema pallidum (syphilis) Infant @ birth via birth canal - congenital syphilis - GrpB strep

Question 504

Discuss respiratory spread of infections

Answer 504

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)

Question 505

Discuss faecal-oral route of transmission

Answer 505

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

Question 506

Discuss blood-borne transmission of infection

Answer 506

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

Question 507

Discuss zoonotic transmission of infection

Answer 507

Animal-human Animals that have natural reservoirs to humans Zoonotic diseases; salmonella, rabies

Question 508

Discuss insect spread of infection

Answer 508

Winged insects vectors for many infections; malaria Fleas: wingless insects - jump long distances; bubonic plague

Question 509

Discuss fomite spread of infection

Answer 509

Fomites; inanimate objects that can carry, transmit infection Soft toys, shared towels, handkerchiefs

Question 510

What are nosocomial infections?

Answer 510

Hospital acquired infections

Question 511

Common nosocomial infections

Answer 511

UTI Wound/skin and soft tissue infections Respiratory tract infections

Question 512

Discuss how nosocomial infections can be prevented

Answer 512

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

Question 513

Clinical features lobar pneumonia

Answer 513

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

Question 514

Discuss pathology of lobar pneumonia

Answer 514

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

Question 515

Complications of lobar pneumonia

Answer 515

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

Question 516

4 typical clinical settings of bronchopneumonia

Answer 516

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

Question 517

Causative species of bronchopneumonia

Answer 517

Low virulence bacteria - staph - S. viridans - H influenzae - coliforms

Question 518

Pathology of bronchopneumonia

Answer 518

Bilateral, basal, patchy Grey or grey-red spots of consolidation Microscopically: Acute inflammatory infiltrate in bronchioles and alveoli

Question 519

Complications of bronchopneumonia

Answer 519

Death; usually terminal event/complicating event in other debilitating illness or old age Resolution Scarring Abscess/empyema (rare)

Question 520

Discuss interstitial/atypical pneumonia

Answer 520

``` 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 ```

Question 521

Discuss pulmonary TB

Answer 521

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

Question 522

Discuss 1ry TB

Answer 522

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

Question 523

Discuss 2ry TB

Answer 523

Reinfection or reactivation | Usually apical, about 3cm at clinical presentation

Question 524

Discuss microscopic findings of TB

Answer 524

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

Question 525

Complications of pulmonary TB

Answer 525

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

Question 526

Discuss chronic obstructive pulmonary diseases

Answer 526

Group of diseases characterised by obstruction to airflow - intermittent, reversible, irreversible Cf restrictive diseases; no obstruction but inhibition to lung expansion

Question 527

Discuss chronic bronchitis

Answer 527

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

Question 528

Discuss emphysema

Answer 528

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

Question 529

Discuss bronchial asthma

Answer 529

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

Question 530

Discuss bronchiectasis

Answer 530

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

Question 531

Aetiology of lung (bronchogenic) cancer

Answer 531

``` Directly caused by cigarette smoking Other factors - asbestos - mineral dusts - radiation - pollution - scarring ```

Question 532

Classifications of lung cancers

Answer 532

Histological - squamous cell carcinoma - adenocarcinoma - small cell (oat cell) carcinoma - large cell carcinoma Clinical - small cell - non-small cell

Question 533

Compare small cell and non-small cell lung carcinoma

Answer 533

Small cell - not treatable surgically; usually widely disseminated @ diagnosis - chemotherapy Non-small cell - surgically treatable

Question 534

Clinical features of lung cancer

Answer 534

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

Question 535

Lung cancer prognosis

Answer 535

Depends on staging | 5yr survival <10%

Question 536

Discuss occupational lung disease

Answer 536

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

Question 537

2 mechanisms by which occupational lung diseases occur

Answer 537

1. Scarring from chronic irritation; inert substances - coal workers' pneumoconiosis 2. Hypersensitivity - organic dusts

Question 538

Examples of occupational lung disease

Answer 538

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

Question 539

Discuss pulmonary oedema

Answer 539

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)

Question 540

Discuss diffuse alveolar damage

Answer 540

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

Question 541

Discuss emboli and infarction

Answer 541

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

Question 542

Discuss pulmonary hypertension

Answer 542

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

Question 543

3 main groups of WBCs and members of groups

Answer 543

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)

Question 544

2 types of WBC disorders

Answer 544

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

Question 545

What is leukaemia? What are the 2 types?

Answer 545

Leukaemia: malignant proliferation of WBCs Acute; proliferation of immature blast cells Chronic; proliferation of mature cells

Question 546

Discuss ALL, AML and CML, CLL

Answer 546

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)

Question 547

Discuss acute leukaemia and clinical presentation

Answer 547

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

Question 548

Discuss chronic leukaemia and clinical presentation

Answer 548

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

Question 549

Discuss management of leukaemias

Answer 549

Adjunct supportive therapy; compensate for lack of functioning cells - red cell transfusion - platelet transfusion - granulocyte colony stimulating factor Specific - chemotherapy - radiotherapy - bone marrow transplantation

Question 550

Dental relevance of leukaemia

Answer 550

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

Question 551

Types of lymphomas

Answer 551

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

Question 552

What is a lymphoma?

Answer 552

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

Question 553

What is Hodgkin’s lymphoma?

Answer 553

Dysfunctional B cell resulting in accumulation of abnormal B cell Characterised by presence of Reed-Sternberg cells in biopsy (mutated B cells, huge)

Question 554

Risk factors of Hodgkin's lymphoma

Answer 554

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

Question 555

Clinical features of Hodgkin's lymphoma

Answer 555

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

Question 556

Special investigations for diagnosing Hodgkin's lymphoma

Answer 556

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

Question 557

Discuss the staging of Hodgkin's lymphoma

Answer 557

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

Question 558

Discuss treatment options for Hodgkin's lymphoma

Answer 558

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

Question 559

Dental relevance of Hodgkin's lymphoma

Answer 559

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

Question 560

Discuss non-Hodgkin's lymphoma

Answer 560

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

Question 561

Discuss Burkitt's lymphoma

Answer 561

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

Question 562

What is multiple myeloma?

Answer 562

Proliferation of malignant plasma cell

Question 563

Discuss malignant myeloma

Answer 563

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

Question 564

Clinical features of multiple myeloma

Answer 564

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

Question 565

Special investigations for diagnosing multiple myeloma

Answer 565

``` 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 ```

Question 566

Dental relevance of multiple myeloma

Answer 566

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

Question 567

Discuss reactive leucocytosis

Answer 567

Causes - disease - infection - neoplastic condition Evaluate w/ WBC differential count Changes to WBC differential - establish differential diagnosis - guide treatment

Question 568

Discuss WBC differential count patterns

Answer 568

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

Question 569

Briefly outline functions of liver

Answer 569

Metabolic: detoxification and breakdown of toxins, hormones, drugs Synthesis - bile - protein - carb - lipid - RBCs - clotting factors Storage

Question 570

Outline responses of liver to injury

Answer 570

``` Hepatocyte degeneration and IC accumulations Hepatocyte necrosis and apoptosis Inflammation Regeneration Fibrosis ```

Question 571

4 common symptoms of liver disease

Answer 571

Jaundice Oedema Ascites Cerebral dysfunction

Question 572

What is jaundice?

Answer 572

Raised serum bilirubin w/ bilirubin deposited in tissues Characterised by yellowing of skin and eyes

Question 573

5 stages in bilirubin metabolism

Answer 573

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

Question 574

Classification of causes of jaundice

Answer 574

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

Question 575

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

Answer 575

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

Question 576

Discuss oedema/ascites and cerebral dysfunction symptoms of jaundice

Answer 576

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 ```

Question 577

What is hepatitis?

Answer 577

Inflammation of liver following injury

Question 578

4 common causes of hepatitis

Answer 578

Viral Alcohol Drugs/toxin Autoimmune

Question 579

Discuss the 5 types of viral hepatitis

Answer 579

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

Question 580

Discuss acute hepatitis

Answer 580

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

Question 581

What is chronic hepatitis?

Answer 581

Necroinflammatory disease in which hepatocytes are target of attack

Question 582

Discuss chronic hepatitis

Answer 582

May be asymptomatic or non-specific Lab evaluation Extensive damage may lead to cirrhosis, portal hypertension Clinically - symptomatic, biomedical, histological evidence of disease >6mnth

Question 583

Causes of chronic hepatitis

Answer 583

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

Question 584

Histology of chronic hepatitis

Answer 584

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

Question 585

What is cirrhosis?

Answer 585

Irreversible end stage liver disease

Question 586

Histology of cirrhosis

Answer 586

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

Question 587

Causes of cirrhosis

Answer 587

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

Question 588

Complications of cirrhosis

Answer 588

Hepatic failure Hepatic encephalopathy Portal hypertension Oesophageal varices; massive haemorrhage

Question 589

Discuss hepatic encephalopathy as complication of cirrhosis

Answer 589

Mechanism - portal blood bypasses liver - toxic or metabolic effect on brain - ammonia, bacteria, altered GABA level Clinically - ranges from subtle psychiatric disturbances to coma

Question 590

Possible effects of portal hypertension

Answer 590

Ascites Portal-systemic venous shunts Splenomegaly (congestive)

Question 591

Discuss ascites as result of portal hypertension

Answer 591

Mechanisms - high intra-sinusoidal pressure - leakage from hepatic lymphatics - hypoalbuminaemia - Na, H2O retention

Question 592

Discuss portal-systemic venous shunts as result of portal hypertension

Answer 592

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

Question 593

Discuss alcoholic liver disease

Answer 593

Alcoholic steatosis - fatty change; soft, yellow liver - fibrosis Alcoholic hepatitis - fatty change - fibrosis - hepatocyte necrosis - inflammation - +/- Mallory's hyaline; Fe deposition Alcoholic cirrhosis

Question 594

Discuss 1ry and 2ry liver tumours

Answer 594

``` 1ry - benign; liver cell adenoma - malignant — hepatocellular carcinoma — cholangiocarcinoma — angiosarcoma — hepatoblastoma ``` 2ry (metastatic) - source — carcinoma; colorectal, stomach, pancreas, breast — malignant melanoma

Question 595

Discuss liver metastases

Answer 595

Sources - carcinoma - multiple melanoma Morphology - hepatomegaly - typically multiple nodules

Question 596

Aetiology of hepatocellular carcinoma

Answer 596

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

Question 597

Discuss clinical presentation of hepatocellular carcinoma

Answer 597

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

Question 598

Discuss the macroscopy and microscopy of hepatocellular carcinoma

Answer 598

``` 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

Question 599

What is dysphagia?

Answer 599

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

Question 600

Causes of dysphagia

Answer 600

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)

Question 601

What is Patterson-Kelly Syndrome?

Answer 601

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

Question 602

Discuss achalasia

Answer 602

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

Question 603

What is Gastro-oesophageal reflux (GORD)?

Answer 603

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

Question 604

Predisposing factors of GORD

Answer 604

``` 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 ```

Question 605

Discuss oesophageal and extra-oesophageal symptoms of GORD

Answer 605

Oesophageal - heartburn - belching - acid brash - water brash - odynophagia Extra-oesophageal - nocturnal asthma - chronic cough - laryngitis - sinusitis

Question 606

Complications of GORD

Answer 606

``` Oesophaitis Ulcers Benign strictures Oesophageal adenocarcinoma Fe deficiency anaemia ```

Question 607

Discuss some of the treatments for GORD

Answer 607

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

Question 608

Dental relevance of GORD

Answer 608

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

Question 609

What is hiatus hernia?

Answer 609

Condition in which proximal stomach herniates into thorax 50% symptomatic GORD 30% >50 More common obese women

Question 610

What are the 2 types of hiatus hernia?

Answer 610

Sliding | Rolling

Question 611

Compare sliding and rolling hiatus hernia

Answer 611

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

Question 612

2 investigations to diagnose hiatus hernia

Answer 612

Ba swallow | Upper GI endoscopy

Question 613

Discuss treatment of hiatus hernia

Answer 613

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

Question 614

Discuss Barrett's oesophagus

Answer 614

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

Question 615

Risk factors of oesophageal carcinoma

Answer 615

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

Question 616

Clinical presentation of oesophageal carcinoma

Answer 616

``` Hoarseness, cough Dysphagia Weight loss Retrosternal pain Lymphadenopathy (occ) ```

Question 617

Dental relevance of oesophageal carcinoma

Answer 617

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

Question 618

What is dyspepsia?

Answer 618

Indigestion Nonspecific group of symptoms related to upper GIT

Question 619

Symptoms of dyspepsia

Answer 619

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 ```

Question 620

What is peptic ulceration and risk factors

Answer 620

Ulcer + break in continuity of epithelial surface Risk - H pylori - drugs; aspirin, NSAID, corticosteroid - smoking, stress

Question 621

Compare gastric and duodenal ulceration

Answer 621

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 ```

Question 622

Risk factors for gastric cancer

Answer 622

``` Alcohol, smoking H pylori Dietary salt and preservatives Dietary fruit and veg Pernicious anaemia ```

Question 623

Presentation of gastric cancer

Answer 623

Vague and nonspecific Dysphagia Nausea Malaena Anaemia

Question 624

Discuss investigations for gastric cancer

Answer 624

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

Question 625

What are haematemesis and malaena? Causes of both

Answer 625

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

Question 626

Discuss oesophageal varices

Answer 626

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

Question 627

What is Mallory-Weiss tear/Syndrome?

Answer 627

Forceful or long term vomiting or coughing resulting in bleeding via oesophageal tear Tear involved mucosa and submucosa but not underlying muscular layer

Question 628

Associations of Mallory-Weiss tear

Answer 628

``` Alcoholism Eating disorder Hyperemesis Gravidarum (prolonged vomiting) Epileptic convulsion NSAID abuse ```

Question 629

Discuss the healing and treatment of Mallory-Weiss tear

Answer 629

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)

Question 630

Discuss initial management of upper GI bleed

Answer 630

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

Question 631

Define obligate and facultative anaerobes and anaerobiosis

Answer 631

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

Question 632

List methods of anaerobic cultivation

Answer 632

``` Anaerobic jars Gas-generating sachets Anaerobic cabinets Roll-tube/Hungate Robertons Cooked meat medium ```

Question 633

Discuss anaerobic jars

Answer 633

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

Question 634

Discuss gas-generating sachets

Answer 634

Anaerogen sachets O2 absorbed CO2 produced No catalyst or H2O

Question 635

Discuss anaerobic cabinets

Answer 635

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

Question 636

List important gram+ anaerobes

Answer 636

Cocci: peptostreptococci Spore forming rods: clostridium Non-spore forms:g - propionibacterium - eubacterium - actinomyces - bifidobacterium

Question 637

List important gram- anaerobes

Answer 637

Cocci: veillonella Rods and filaments - bacteriodes - fusobacterium - porphyromonas - prevotella - campylobacter Spirochaetes - spirochaeta - treponema

Question 638

Discuss dentoalveolar/PA abscess

Answer 638

Abscess develop around apices of teeth w/ necrotic and infected root canals Oral strep, many anaerobes (predominately obligate)

Question 639

Discuss osteomyelitis

Answer 639

Rare disease Inflammation of jaw bone cavity Gram- anaerobes, streptococcus spp.

Question 640

Discuss chronic marginal and acute ulcerative gingivitis

Answer 640

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.

Question 641

Discuss periodontitis

Answer 641

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

Question 642

Discuss pericoronitis

Answer 642

Inflammation of soft tissues surrounding crown of PE tooth Prevotella intermedia, fuscobacterium nucleatum

Question 643

Discuss peri-implantis

Answer 643

Inflammation around implant systems replacing missing teeth Prevotella intermedia Porphyromonas gingivalis

Question 644

Discuss actinomycosis and sialadenitis

Answer 644

Actinomycosis - formation chronic granuloma w/ swelling - chronic; multiple discharging sinuses observed - actinomyces israelii Sialadenitis - infection salivary glands - strep spp., Staph aureus, gram- anaerobes

Question 645

Discuss general features of Clostridium spp.

Answer 645

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

Question 646

List important diseases and which clostridium causes them

Answer 646

Botulism; C. botulinum Gas gangrene; perfringens, novyi, septicum Food poisoning; perfringens Tetanus; tetani Pseudomembranous colitis; difficle

Question 647

Discuss tetanus

Answer 647

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

Question 648

Discuss botulism

Answer 648

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

Question 649

Discuss gas gangrene

Answer 649

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

Question 650

Discuss benefits of normal gut flora

Answer 650

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

Question 651

Outline composition of normal gut flora

Answer 651

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 ```

Question 652

Discuss diarrhoeal diseases

Answer 652

``` 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

Question 653

Discuss general features of escherichia spp. and conditions caused by E. coli

Answer 653

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

Question 654

4 pathotypes of E. Coli

Answer 654

Enterooathogenic (EPEC) Entertoxigenic (ETEC) Entero-invasive (EIEC) Vero enterocytoxigenic (VTEC)

Question 655

Discuss enteropathogenic E. Coli

Answer 655

Adherence and effacing lesions of intestine Acute enteritis in infants High mortality Non-invasive Virulence: adherence to epithelium, cytoskeletal rearrangement; Ca2+ and electrolyte loss

Question 656

Discuss entertoxigenic E. Coli

Answer 656

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

Question 657

Discuss entero-invasive E. coli

Answer 657

Causes dysentery-like disease Invasive w/ bacteria entering LI epithelial and multiplying Virulence: epithelial invasion; destruction and spread

Question 658

Discuss vero cytotoxigenic E. coli

Answer 658

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

Question 659

Discuss general features and pathogenesis of salmonella genus

Answer 659

Gram- bacilli, non-lactose fermenter Inhabit animal intestine Pathogenesis - ingestion; infectious dose varies - bacteria attach to epithelium of ileum mucosa, invade and multiply

Question 660

Discuss enteric fevers and outline pathogenesis

Answer 660

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

Question 661

Discuss gastroenteritis

Answer 661

Caused by salmonella From: meat, eggs, human/animal carrier (S. enteritidis) Symptoms - cramps - diarrhoea - fever - vomiting - dehydration - renal failure; young/elderly

Question 662

Discuss shigella and condition caused by spp.

Answer 662

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

Question 663

Discuss Klebsiella bacteria

Answer 663

Gram- rods, lactose fermenter Large mucoid colonies Infections - UTI - severe bronchopneumonia and lung abscess - serious cause nosocomial infections; surgical wounds

Question 664

Discuss proteus bacteria

Answer 664

Gram-, non-lactose fermenter Causes - UTI infants - wound infections - surgical infections

Question 665

Discuss general features of Vibrio spp.

Answer 665

Gram- rods Comma shaped Motile-polar flagellum

Question 666

Discuss Vibrio cholerae

Answer 666

``` 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

Question 667

Discuss Vibrio parahaemolyticus

Answer 667

Causes explosive diarrhoea Common Japan, Singapore (raw seafood) Symptoms abate ~3d

Question 668

Discuss pseudomonas aeruginosa

Answer 668

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

Question 669

Discuss campylobacter spp and infections caused

Answer 669

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 ```

Question 670

Discuss helicobacter pylori

Answer 670

Gram- rod Colonises stomach in gastric mucosa - can cause gastritis ~25% popn. thought to be carriers Important in peptic ulceration V high urease producer

Question 671

Outline some of the underlying causes of STIs in the UK

Answer 671

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

Question 672

Discuses the causative agent of gonorrhoea

Answer 672

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

Question 673

Discuss clinical presentation of gonorrhoea

Answer 673

Purulent infection of mucous membranes of urethra, cervix (rectal, pharyngeal) Purulent discharge, dysuria Microscopy; bacteria inside polymorphonuclear cells of inflammatory exudate

Question 674

Complications of gonorrhoea

Answer 674

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

Question 675

Discuss treatment and control of gonorrhoea

Answer 675

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

Question 676

Discuss the causative agent of syphilis

Answer 676

Treponema pallidum Spirochaete; spiral shaped, rigid cell Motile; polar flagella enclosed in outer membrane Visible through dark ground microscopy

Question 677

Discuss the pathogenesis of syphilis

Answer 677

Treponema pallidum enter by penetration of intact mucosa or abraded skin Has 1, 2, 3ry stages

Question 678

Discuss 1ry, 2ry, 3ry syphilis

Answer 678

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

Question 679

Discuss latent and congenital syphilis

Answer 679

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)

Question 680

Discuss the diagnosis of syphilis

Answer 680

``` 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

Question 681

Discuss treatment and control of syphilis

Answer 681

Treatment - penicillin — tetracycline, erythromycin, chloramphenicol Control - incidence dec. since ABs - barrier contraception - indexing cases/contacts and treatment of them

Question 682

Discuss causative agent of chlamydia

Answer 682

Chlamydia trachomatis Obligate intracellular parasites Elementary bodies: live outside host, initiate infection Attachment, entry Reticulate bodies: intracellular multiplication, new EB produced infect adjacent cells

Question 683

Discuss clinical manifestations of chlamydia

Answer 683

``` Urethritis Cervicitis Proctitis Epididymitis Conjunctivitis ```

Question 684

Discuss diagnosis and treatment of chlamydia

Answer 684

Diagnosis - cell culture growth - immunofluorescent staining - direct Ab detection Treatment: tetracycline

Question 685

Briefly discuss viral STIs

Answer 685

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

Question 686

Discuss aetiology of UTIs

Answer 686

Usually ascending bacterial infection Urethra -> bladder -> kidney -> urinary tract -> bloodstream (septicaemia) Less commonly reach kidney through haematogenous route

Question 687

Outline some predisposing factors of UTIs

Answer 687

``` Disruption of urine flow; catheter, pregnancy, prostatic hypertrophy F; shorter urethra Sexually active Prevention of complete bladder emptying Reflux of urine DM ```

Question 688

Discuss the virulence factors of some common UTI agents

Answer 688

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

Question 689

Discuss clinical features of UTIs

Answer 689

``` 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

Question 690

Discuss the diagnosis of UTI

Answer 690

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

Question 691

Treatment of UTI

Answer 691

Trimethoprim, ampicillin 5d | If resistant; cephaloxin

Question 692

Define hypersensitivity, autoreactivity, autoimmunity

Answer 692

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

Question 693

Define atopy and allergy

Answer 693

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

Question 694

Discuss immunodeficiency

Answer 694

Loss of function 1ry; rare; congenital or inherited 2ry; common - acquired as consequence of disease and treatment - mainly affecting phagocyte and lymphocyte function

Question 695

Contributing factors to 2ry immunodeficiency

Answer 695

``` Ageing Malnutrition Tumours Cancer chemotherapy Trauma Infection ```

Question 696

Discuss ageing as contributing factor to 2ry immunodeficiency

Answer 696

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

Question 697

Discuss malnutrition as contributing factor to 2ry immunodeficiency

Answer 697

Calorie malnutrition; body protects important organs, immune system less important Lack certain dietary elements (Fe, Zn); immune system not supported

Question 698

Discuss and cytotoxic therapy as contributing factor to 2ry immunodeficiency

Answer 698

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)

Question 699

Discuss trauma and infection as contributing factors to 2ry immunodeficiency

Answer 699

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

Question 700

Outline types of hypersensitivity reaction

Answer 700

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

Question 701

Discuss type I hypersensitivity reaction

Answer 701

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

Question 702

Effect of mast cell activation

Answer 702

GIT: inc. fluid secretion, peristalsis Airways: dec. diameter, inc. mucus secretion Blood vessels: inc. blood flow, permeability

Question 703

Discuss molecules released by mast cells

Answer 703

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

Question 704

Discuss molecules released by eosinophils

Answer 704

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

Question 705

Discuss type II hypersensitivity

Answer 705

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

Question 706

Discuss type V hypersensitivity

Answer 706

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

Question 707

Discuss type III hypersensitivity

Answer 707

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)

Question 708

Discuss type IV hypersensitivity

Answer 708

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

Question 709

List non-autoimmune bone disorders by inherited and acquired

Answer 709

Inherited - osteogenesis imperfecta - cleidocranial dysplasia - osteopetrosis Acquired - osteomalacia, rickets - osteoporosis - osteomyelitis - Paget's disease of bone - Reiter's Syndrome - osteoarthritis - fibrous dysplasia

Question 710

Discuss general features of osteogenesis imperfecta

Answer 710

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

Question 711

Clinical features of osteogenesis imperfecta

Answer 711

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

Question 712

Discuss diagnosis and management of osteogenesis imperfecta

Answer 712

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

Question 713

Discuss dental relevance of osteogenesis imperfecta

Answer 713

Handle pt carefully Don’t confuse w/ physical abuse Min. force, support jaw, ensure haemostasis Chest deformities may contraindicate surgery Dentinogenesis imperfecta Bisphosphonates

Question 714

Discuss cleidocranial dysplasia

Answer 714

Rare, autosomal dominant trait on chromosome 6 | Defect of membrane bone formation; skull, clavicle

Question 715

Clinical features of cleidocranial dysplasia

Answer 715

Absent/defective clavicle Prognathic mandible due to maxillary hypoplasia Depressed nasal bridge Parietal, frontal, occipital bossing Kyphoscoliosis, pelvic abnormalities may be associated

Question 716

Diagnosis and dental relevance of cleidocranial dysplasia

Answer 716

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

Question 717

General features of osteopetrosis

Answer 717

Rare genetic disorder characterised by excessive bone density Defective osteoclastic activity and remodelling Dense but weak, fragile bones; heal normally Severity varies

Question 718

Clinical features of osteopetrosis

Answer 718

None (mild) Bone pain, #s, osteomyelitis (severe) Infection, anaemia Cranial neuropathies Epilepsy, learning disability (rare)

Question 719

Discuss investigations for osteopetrosis

Answer 719

X-ray: dense (marble-like) bone appearance Ca, PO usually normal

Question 720

Dental relevance of osteopetrosis

Answer 720

``` Frontal bossing, hypertelorism Trigeminal or facial neuropathies Jaw # Delayed eruption Osteomyelitis ```

Question 721

What are osteomalacia and rickets? Discuss common risk factors

Answer 721

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

Question 722

Clinical features and investigations of osteomalacia and rickets

Answer 722

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 ```

Question 723

Management and dental relevance of osteomalacia and rickets

Answer 723

Management - treat underlying cause - VitD, Ca2+ supplements Dental - delayed eruption (severe) - if associated w/ malabsorption Syndrome — May cause VitK deficiency, 2ry hyperparathyroidism

Question 724

Discuss osteoporosis

Answer 724

Common condition usually in elderly Diminished bone mass; fragility, inc. risk # Inadequate peak bone mass and/or ongoing bone loss Usually spine, forearm, hips

Question 725

Modifiable and non-modifiable risk factors of osteoporosis

Answer 725

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

Question 726

Clinical features and investigations for osteoporosis

Answer 726

Clinical - #: thoracic and Lu bar vertebrae, head of femur, D radius - kyphosis and height shrinkage Investigations - bone density by DEXA;

Question 727

Management and dental relevance of osteoporosis

Answer 727

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

Question 728

What is osteomyelitis? Distinguish b/w haematogenous and direct/contiguous source

Answer 728

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

Question 729

Clinical features osteomyelitis

Answer 729

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

Question 730

Diagnosis and treatment osteomyelitis

Answer 730

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

Question 731

Dental relevance of osteomyelitis

Answer 731

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

Question 732

Discuss Paget's disease of bones

Answer 732

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

Question 733

Clinical features of Paget’s disease

Answer 733

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)

Question 734

Discuss diagnosis and treatment of Paget’s disease

Answer 734

Diagnosis - X-ray - radionuclide bone scans - raised ALP; normal Ca, PO Treatment: bisphosphonates

Question 735

Dental relevance of Paget's disease

Answer 735

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)

Question 736

Discuss osteoarthritis and risk factors for it

Answer 736

``` 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

Question 737

Clinical features of osteoarthritis

Answer 737

``` Joint pain; worse on movement Joint stiffness Deformity Loss of function Herberden's nodes (hard/bony swellings in distal interphalangeal joints) ```

Question 738

Management of osteoarthritis

Answer 738

``` Refuser exercise Weight control Good footwear Walking stick Heat/cold ``` Drugs: NSAID, antidepressant, intra-articular injections Surgery

Question 739

Dental relevance of osteoarthritis

Answer 739

Access complicated by age and immobility Bleeding tendency due to aspirin Red. manual dexterity; poor OH TMJ involvement

Question 740

Discuss Reiter's Syndrome

Answer 740

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

Question 741

Discuss fibrous dysplasia and compare monostotic and polyostotic

Answer 741

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

Question 742

Diagnosis and management of fibrous dysplasia

Answer 742

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

Question 743

Dental relevance of fibrous dysplasia

Answer 743

Facial bones freq. involved monostotic type - 25% polyostotic Hyperthyroidism and DM may be associated w/ polyostotic type

Question 744

Discuss autoimmunity/autoimmune disease

Answer 744

``` 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 ```

Question 745

Discuss rheumatoid arthritis

Answer 745

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 ```

Question 746

Joints commonly involved in rheumatoid arthritis

Answer 746

Wrists, elbow, shoulder Hips, knees, ankles Upper cervical spine Index and middle metacarpophalangeal joints Proximal interphalangeal joints Metatarsophalangeal

Question 747

Clinical features of acute rheumatoid arthritis

Answer 747

``` 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

Question 748

Clinical features chronic rheumatoid arthritis

Answer 748

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

Question 749

Extra-articular clinical features rheumatoid arthritis

Answer 749

Pulmonary fibrosis, pleurisy Pericarditis, myocarditis, vasculitis, valvulitis Atlantoaxial subluxation, spinal cord compression Lymphadenopathy Uveitis Anaemia

Question 750

Investigations for rheumatoid arthritis

Answer 750

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

Question 751

Management of rheumatoid arthritis

Answer 751

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

Question 752

Dental relevance of rheumatoid arthritis

Answer 752

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

Question 753

Discuss ankylosing spondylitis

Answer 753

Seronegative spondyloarthropathy Genetic predisposition, environmental factors may play role Affects axial skeleton (spine) and large peripheral joints

Question 754

Clinical features of ankylosing spondylitis

Answer 754

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

Question 755

Investigations for ankylosing spondylitis

Answer 755

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

Question 756

Treatment of ankylosing spondylitis

Answer 756

Goal - pain relief - maintain joint range of motion - prevent end-organ damage

Question 757

Dental relevance of ankylosing spondylitis

Answer 757

Avoid GA: restricted mouth opening, respiratory and cardiac complications TMJ involvement Pt difficulty placing neck on headrest

Question 758

Discuss psoriatic arthritis

Answer 758

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

Question 759

Discuss Sjögren’s syndrome

Answer 759

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

Question 760

Investigations and dental relevance of Sjorgen's syndrome

Answer 760

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

Question 761

Causes and histological features of oesophagitis

Answer 761

Causes - GORD - other chemical stimuli - infection: Candida, HSV, cytomegalovirus (CMV) - eosinophilic oesophagitis Histology - ulceration - inflammatory cells - epithelial hyperplasia

Question 762

Discuss Barrett's oesophagus

Answer 762

Columnar metaplasia: stratified squamous epithelium replaced by gastric/intestinal type columnar epithelium Prolonged reflux increases risk M>F Prevalence rising

Question 763

Types of oesophageal tumours

Answer 763

Benign - squamous papilloma - leiomyoma Malignant - adenocarcinoma - SCC

Question 764

Symptoms and clinical features of oesophageal carcinoma

Answer 764

Symptoms - dysphagia - weight loss Clinical - aspiration pneumonia - fistulas

Question 765

Macroscopic features and microscopic types of oesophageal carcinoma

Answer 765

Macroscopic - polyp/exophytic - central ulcer - infiltrating Microscopic - adenocarcinoma 60% - SCC 35% - other 5%

Question 766

Aetiology and general features of oesophageal adenocarcinoma

Answer 766

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%

Question 767

Risk factors and general features of oesophageal SCC

Answer 767

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%

Question 768

What is chronic gastritis?

Answer 768

Chronic inflammation of gastric mucosa Common Often asymptomatic Classified by histology, aetiology, distribution

Question 769

Histological features and complications of H pylori associated chronic gastritis

Answer 769

Histology - chronic inflammatory cells - neutrophils - H pylori visible - atrophy and intestinal metaplasia w/ T Complications - peptic ulceration - gastric carcinoma - gastric lymphoma

Question 770

4 other types of chronic gastritis

Answer 770

Autoimmune - fundus > antrum - atrophy common Granulomatous: TB, Crohn's, sarcoidosis Chemical: NSAID, alcohol, Nike reflux Radiation

Question 771

Common sites of peptic ulceration

Answer 771

Stomach | Duodenum

Question 772

Predisposing factors and complications of peptic ulceration

Answer 772

Predisposing - NSAID - H pylori - alcohol - Zollinger-Ellison syndrome (gastric acid hypersecretion) Complications - bleeding - perforation - obstruction

Question 773

Types of stomach polyps and tumours

Answer 773

Non-malignant - polyps: fundic gland polyp, hyperplastic polyp - adenoma: potentially malignant Potentially/Malignant - adenocarcinoma - lymphoma - GI stromal tumour - carcinoid/endocrine tumour

Question 774

Risk factors for gastric carcinoma

Answer 774

Chronic gastritis, intestinal metaplasia - H pylori - autoimmune Diet: nitrates, nitrosamines, lack fruit/veg Smoking Hereditary: early gastric cancer Adenoma

Question 775

Clinical features and spread of gastric carcinoma

Answer 775

Clinical - weight loss - vomiting - abdominal pain Spread - local: pancreas - metastasis; lymph noises, liver, lungs - peritoneal seeding - transcoelomic; to ovaries 5yr survival 5-15%

Question 776

Discuss Coeliac disease

Answer 776

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

Question 777

Types of small intestine tumour

Answer 777

Benign: hamartomas, hyperplastic polyps Potentially/malignant - carcinoid/endocrine tumour - GIST - Lymphoma - adenocarcinoma

Question 778

Discuss small intestine carcinoid/endocrine tumour

Answer 778

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

Question 779

Discuss acute appendicitis

Answer 779

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

Question 780

Discuss Crohn’s disease

Answer 780

Chronic inflammatory disorder Characterised by crampy abdominal pain w/ diarrhoea Can occur anywhere in GIT

Question 781

Macroscopic features of Crohn’s

Answer 781

``` Discontinuous involvement; 'skip' lesions Thickening of wall Strictures Linear ulcers Fistulas w/ bowel, skin, other organs Perianal fissures, fistulas ```

Question 782

Extra-intestinal complications of Crohn’s

Answer 782

Polyarthritis/sacroilitis/ankylosing spondylitis Uveitis Erythema nodosum

Question 783

Histology of Crohn’s disease

Answer 783

Transmural chronic inflammation Non-necrotising granulomas Ulcers

Question 784

Discuss ulcerative colitis

Answer 784

Chronic inflammatory disorder Affects large bowel Characterised by bloody and freq. diarrhoea

Question 785

Macroscopic appearance and histology of ulcerative colitis

Answer 785

Macroscopic - continuous; starts distally, spreads proximal - erythema, granularity, ulceration of mucosa, pseudopolyps Histology - diffuse chronic inflammation of mucosa - mucosal architectural distortion

Question 786

Complications of ulcerative colitis

Answer 786

Extra-intestinal - arthritides - 1ry sclerosing cholangitis - cholangiocarcinoma Intestinal - toxic megacolon - dysplasia and colorectal carcinoma — proportional to extent, duration of disease

Question 787

Discuss diverticular disease

Answer 787

Large intestine disease Most common >60, sigmoid colon Outpouchings of mucosa through walk @ weak points Associated w/ low fibre diet

Question 788

Complications of diverticular disease

Answer 788

Peri-diverticular abscess Stricture Perforation, peritonitis

Question 789

Discuss colorectal carcinoma

Answer 789

60-70yo Clinical - rectal bleeding - change in bowel habit - weight loss, malaise Macroscopic - polypoid - ulcerated Histology - well/moderately/poorly differentiated

Question 790

Common bacterial agents detected in oral cavity

Answer 790

``` Cocci Gram+ - enterococcus - peptostreptococcus - streptococcus Gram- - branhamella - neisseria - veillonella ``` ``` Rods Gram+ - actinomyces - bifidobacterium - corynebacterium - lactobacillus Gram- - porphyromonas - prevotella - aggregatibacter - fusobacterium ```

Question 791

Discuss common fungal and viral agents found in oral cavity

Answer 791

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

Question 792

How are oral infections classified?

Answer 792

1. Bacterial, fungal, viral 2. Endo/exogenous 3. Hard/soft tissue

Question 793

Discuss endogenous and exogenous classification of oral infections

Answer 793

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

Question 794

4 examples of bacterial hard tissue oral infections

Answer 794

Caries: S. mutans, lactobacilli Abscesses: oral strep., gram- anaerobes (prevotella, porphyromonas, fusobacterium, treponema) Dry socket: various incl. actinomyces spp. Osteomyelitis: staph aureus, others

Question 795

5 examples endogenous soft tissue oral infections

Answer 795

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

Question 796

3 examples exogenous soft tissue oral infections

Answer 796

Gonorrhoea: neisseria gonorrhoeae Syphilis: treponema pallidum Tuberculosis: mycobacterium tuberculosis

Question 797

Example of fungal soft tissue oral infection

Answer 797

Candidiasis: C. albicans, Candida spp.

Question 798

Examples of 1ry and 2ry viral soft tissue oral infections

Answer 798

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

Question 799

How do disturbances to oral microflora allow for oral infection to arise?

Answer 799

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

Question 800

Physiological predisposing factors for oral infection

Answer 800

Old age, infancy: dec. Abs, saliva flow; candidiasis, root caries Pregnancy: unknown mechanism; gingivitis

Question 801

How is trauma a predisposing factor for oral infections ?

Answer 801

Local: loss of tissue integrity; various opportunistic infections General: general debilitation, dehydration; candidiasis

Question 802

Malnutrition, endocrine disorders and AIDs as predisposing factors to oral infections

Answer 802

Malnutrition: Fe/folate deficiency; candidiasis Endocrine disorder: unknown mechanisms; fungal infections AIDs: red. host immune defence; opportunistic, candidiasis

Question 803

AB therapy, chemotherapy, oral malignancies as predisposing factors to oral infections

Answer 803

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

Question 804

Discuss antibiotics used in treatment of oral infections

Answer 804

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

Question 805

Discuss topical antifungals used in treatment of oral infections

Answer 805

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

Question 806

Systemic antifungals used in treatment of oral infections

Answer 806

Ketoconazole - imidazole - not used pt history liver disease or alcoholics Fluconazole - triazole - well absorbed by mouth - better toxicity profile - v expensive

Question 807

Discuss antivirals used in treatment of oral infections

Answer 807

Acyclovir Topical: herpes labialis; cream used @ prodromal stage Systemic - HCP treating immunocompromised pt - those who present within 48h herpes infection

Question 808

Discuss 1ry hypertension

Answer 808

``` Most common Multiple factor Genetic predisposition Environmental factors Mechanism unclear ```

Question 809

Predisposing factors for 2ry hypertension

Answer 809

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

Question 810

Clinical presentation of hypertension

Answer 810

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

Question 811

Complications of hypertension

Answer 811

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

Question 812

Investigations for hypertension

Answer 812

Multiple BP measurements Urinalysis and urinary albumin:creatinine Blood: fasting blood glucose, Na/K, lipid profile, creatinine, thyroid function test ECG

Question 813

Management of hypertension

Answer 813

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

Question 814

Examples of antihypertensives

Answer 814

``` 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 ```

Question 815

Dental relevance of hypertension

Answer 815

Stable: receive care in short, minimally stressful appointments Drug side effects - dry mouth - ulcer - lichenoid lesion

Question 816

Discuss atherosclerosis and risk factors

Answer 816

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

Question 817

Compare stable and unstable plaque atherosclerosis

Answer 817

Stable: regress, remain static or grow slowly; stenosis or occlusion Unstable: vulnerable to spontaneous rupture, erosion or fissuring

Question 818

Discuss triggering of acute thrombosis in unstable plaque atherosclerosis

Answer 818

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

Question 819

Clinical features of atherosclerosis

Answer 819

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

Question 820

Investigations for atherosclerosis

Answer 820

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

Question 821

Management of atherosclerosis

Answer 821

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

Question 822

Discuss angina pectoris

Answer 822

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

Question 823

Compare unstable and stable angina

Answer 823

Stable: predictable; inc. workload leads to ischaemia Unstable: chest pain @ rest, inc. freq./intensity of episode

Question 824

Clinical features of angina

Answer 824

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

Question 825

Investigations for angina pectoris

Answer 825

ECG Stress testing w/ ECG/echo Coronary artery angiography IV sonography

Question 826

Treatment of angina pectoris

Answer 826

Relieve acute symptoms: sublingual nitroglycerin Prevent ischaemia: antiplatelet, beta-blocker (atenolol) Prevent future ischaemic event: Ca2+-C blocker (nifedipine), Long acting nitrates

Question 827

Discuss myocardial infarction

Answer 827

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

Question 828

Investigations of myocardial infarction

Answer 828

Initial and serial ECGs Serial cardiac markers Coronary angiography

Question 829

Discuss treatment and management of myocardial infarction

Answer 829

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

Question 830

Discuss acute and sub-acute bacterial infective endocarditis

Answer 830

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

Question 831

Clinical features infective endocarditis

Answer 831

``` Fever, weight loss, night sweats, malaise, embolic phenomena, haematuria Splinter haemorrhages Conjunctiva petechiae Osler's nodes Janeway's lesions ```

Question 832

Causes of left ventricle heart failure

Answer 832

``` Coronary artery disease DM, obesity Hypertension Valvular heart disease Hyperthyroid disease Substance abuse; cocaine, smoking ```

Question 833

Pathogenesis of left ventricle heart failure

Answer 833

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

Question 834

Clinical features of left ventricle heart failure

Answer 834

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) ```

Question 835

Causes of right ventricle heart failure

Answer 835

Previous LV failure Severe lung disorder (cor-pulmonale) Multiple pulmonary emboli and RV infarction

Question 836

Pathogenesis of right ventricle heart failure

Answer 836

RV dysfunction -> Systemic venous pressure inc. -> Fluid extravasation and oedema, in dependent tissues and abdominal viscera -> Fluid accumulation in peritoneal cavity

Question 837

Clinical features right ventricle heart failure

Answer 837

``` 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 ```

Question 838

Investigations for heart failure

Answer 838

``` FBC Electrolyte, urea ECG, echo Thyroid function test Cardiac MRI Coronary angiography Chest radiograph ```

Question 839

Treatment of heart failure

Answer 839

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

Question 840

Before a medical emergency occurs, how can we prepare pt?

Answer 840

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.)

Question 841

In physical evaluation of pt before ME what should we observe?

Answer 841

``` Posture Body movements Quality of speech Skin: feel, colour Odours on breath Rate and pattern of respiration ```

Question 842

How can dental team prepare for ME?

Answer 842

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

Question 843

How can the practice be prepared for a ME?

Answer 843

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)

Question 844

5 systemic classifications of ME

Answer 844

``` CV Respiratory Neurological Metabolic Miscellaneous ```

Question 845

CV MEs

Answer 845

``` MI Angina Cardiac arrest Syncope (vasovagal attack); fainting Postural hypotension ```

Question 846

Respiratory MEs

Answer 846

``` Hyperventilation Asthma Respiratory arrest Acute respiratory obstruction - inhaled foreign body - angio-oedema ```

Question 847

Neurological MEs

Answer 847

Cerebrovascular accident (CVA); stroke Seizures/epilepsy; status epilepticus Loss of consciousness

Question 848

Metabolic MEs

Answer 848

Hyperglycaemia Hypoglycaemia Addisonian crisis (acute adrenal insufficiency)

Question 849

Miscellaneous MEs

Answer 849

Anaphylaxis Drug allergy Drug overdose Drug interactions

Question 850

8 ME drugs

Answer 850

1. GTN spray 2. Salbutamol inhaler 3. Adrenaline 4. Aspirin 5. Glucagon 6. Glucose tablet/gel/solution/powder 7. Midazolam 8. O2

Question 851

Discuss use of glycerol trinitrate spray in ME

Answer 851

Dose: 400 microg Route: sublingual ME: angina Action: vasodilator

Question 852

Salbutamol inhaler use in ME

Answer 852

Dose: 100microg Route: inhalation ME: asthma Action: beta-2 agonist

Question 853

Adrenaline use in ME

Answer 853

Dose: 0.5mg Route: IM ME: anaphylaxis Action: alpha and beta agonist, mast cell stabilisation, glucose elevation

Question 854

Aspirin use in ME

Answer 854

Dose: 300mg Route: oral ME: MI Action: antiplatelet

Question 855

Glucagon use in ME

Answer 855

Dose: 1mg Route: IM ME: unconscious hypoglycaemia Action: glycogenolysis

Question 856

Glucose use in ME

Answer 856

Dose: - Route: oral ME: conscious hypoglycaemia Action: -

Question 857

Midazolam use in ME

Answer 857

Dose: 10mg/ml Route: buccal ME: epilepsy Action: muscle relaxant

Question 858

O2 use in ME

Answer 858

Dose: 15L/min Route: inhalation ME: syncope, anaphylaxis, epilepsy, MI, Addisonian crisis, CVA Action: -

Question 859

11 pieces of ME equipment

Answer 859

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)

Question 860

What are DR'S ABCDE?

Answer 860

Danger: assess area Response: does pt respond to touch and/or voice Shout: for help, assistance ``` Airway Breathing Circulation Disability Exposure ```

Question 861

Assessment of airway in ME

Answer 861

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

Question 862

Breathing assessment in ME

Answer 862

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

Question 863

Circulation assessment in ME

Answer 863

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

Question 864

Disability step in ME

Answer 864

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

Question 865

Exposure step in ME

Answer 865

Loosening/removal of some of pt's clothes may be necessary for proper treatment and assessment - rashes (anaphylaxis), defibrillation Respect dignity, minimise heat loss

Question 866

Compare neurosis and psychosis

Answer 866

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

Question 867

Discuss anxiety neuroses

Answer 867

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

Question 868

7 psychological symptoms of anxiety

Answer 868

1. Fearful anticipation 2. Irritability 3. Restlessness 4. Sensitivity to noise 5. Subjective reports of poor memory 6. Repetitive worrying 7. Poor conc.

Question 869

Physical symptoms of anxiety (affecting body systems)

Answer 869

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

Question 870

Discuss panic disorders

Answer 870

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

Question 871

Discuss generalised anxiety disorder

Answer 871

Generalised, persistent, excessive anxiety about everyday circumstances >6mnth Prolonged waxing, waning course Exclude organic causes

Question 872

Treatment of generalised anxiety disorder

Answer 872

Psychological - reassurance, counselling, psychotherapy - behavioural therapy once avoidance behaviour established Pharmacological - anxiolytic; benzodiazepines (diazepam) - antidepressants (anxiolytic properties); amitriptyline (TCA) - beta-blockers; atenolol

Question 873

Discuss simple specific phobias

Answer 873

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)

Question 874

Discuss agoraphobia

Answer 874

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

Question 875

Discuss social phobia

Answer 875

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

Question 876

Compare obsessions and compulsions

Answer 876

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

Question 877

Discuss obsessive compulsive disorder

Answer 877

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 ```

Question 878

Discuss CBT

Answer 878

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)

Question 879

Discuss somatisation

Answer 879

Neurosis Physical symptoms where no cause can be found - manifestation of psychological distress Common Reassurance and explanation may be all needed Factitious disorders

Question 880

Discuss psychosis

Answer 880

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

Question 881

Compare delusion and hallucination

Answer 881

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

Question 882

What is schizophrenia ?

Answer 882

Disintegrative psychosis involving loss of contact w/ reality Splitting of links b/w perception, mood, thinking, behaviour, contact w/ reality

Question 883

Compare type 1 and 2 schizophrenia

Answer 883

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

Question 884

Clinical features of schizophrenia

Answer 884

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 ```

Question 885

Management of schizophrenia

Answer 885

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

Question 886

Dental relevance of schizophrenia

Answer 886

``` Poor OH (neglect) Smoking: staining, oral precancer/cancer Difficulty in communication Delusions symptoms Side effects of neuroleptics; haloperidol, clozapine; hyposalivation ```

Question 887

9 clinical features of depression

Answer 887

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

Question 888

5 biological features of depression

Answer 888

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

Question 889

Appearance and speech of depressed pt

Answer 889

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

Question 890

Psychotic features of depression

Answer 890

Delusions - concerned w/ ideals of worthlessness, ill-health, poverty, guilt - persecutory; pt feels if justified Hallucinations: 2nd person auditory confirming pt ideas of worthlessness

Question 891

Management of depression

Answer 891

``` CBT Antidepressants - TCA: amitriptyline, dolesupin - SSRI: fluoxetine, partoxetine, citalopram - St Johns wort Li/carbamazepine (mood stabilisation) ECT ```

Question 892

Dental aspects of depression

Answer 892

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

Question 893

Discuss bipolar disorders

Answer 893

Sustained episodes of elevated or agitated mood (mania) Often alternates w/ episodes of depression Significant effect in individuals ability to function

Question 894

Discuss bipolar affective disorder

Answer 894

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 ```

Question 895

Discuss appearance and behaviour of pt w/ bipolar affective disorder

Answer 895

Dressed in bright, gaudy colours Untidy, dishevelled Overactivity -> physical exhaustion Excessive activity in risk taking pursuits, social indiscretion

Question 896

Management and dental aspect of bipolar affective disorder

Answer 896

Management - antipsychotics: chlorpromazine, haloperidol, respiridone, olanzapine - sedatives; lorazepam - Li/carbamazepine - ECT Dental - Li toxicity w/ GA - long term potential induce hypothyroidism

Question 897

Discuss anorexia nervosa

Answer 897

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

Question 898

Clinical features of anorexia nervosa

Answer 898

``` 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 ```

Question 899

Management of anorexia nervosa

Answer 899

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

Question 900

Dental aspects of anorexia nervosa

Answer 900

Caution during GA Parotid enlargement Erosion, caries Ulcers, abrasions

Question 901

Discuss bulimia nervosa

Answer 901

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

Question 902

Aetiology of suicide

Answer 902

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

Question 903

Discuss parasuicide

Answer 903

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

Question 904

Factors associated w/ genuine suicide risk

Answer 904

M, inc. age, unemployed, single | Psychiatric disorders violent method (parasuicide/self harm)

Question 905

Discuss alcohol abuse

Answer 905

Regular or binge consumption of alcohol sufficient to cause social/physical damage Alcoholic = repeated drinking leads to harm in work/social life

Question 906

Features of alcohol dependence

Answer 906

``` 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 ```

Question 907

Discuss psychological complications and acute intoxication of alcohol

Answer 907

Psychological - dysphoric mood, pathological jealousy, sexual problems - alcoholic hallucinosis Intoxication - slurred speech - impaired coordination - judgement - injury/accident

Question 908

Medical complications of alcohol dependence (body systems)

Answer 908

GI: gastritis, hepatitis, cirrhosis, oesophageal varices, peptic ulceration Haematological: anaemia, thrombocytopenia CV: cardiomyopathy, hypertension Neuropsychiatric: Wernicke's encephalopathy 2ry thiamine deficiency

Question 909

Discuss acute withdrawal of alcohol (delirium tremens)

Answer 909

``` 10-72h after last drink Agitation, insomnia Tachycardia, hypotension Pyrexia Confusion, fits Visual/tactile hallucinations ``` Management: rehydration, fits, sedation - chlordiazepoxide, chlormethiazole

Question 910

Dental aspect of alcohol dependence

Answer 910

Poor OH Malnutrition, anaemia Liver disease/cirrhosis; bleeding tendency, altered drug metabolism Problems w/ drug administration (metronidazole) Accidents/fights -> maxillofacial trauma

Question 911

What is hepatitis?

Answer 911

Inflammation of liver w/o pinpointing specific cause

Question 912

Viruses associated w/ Hep

Answer 912

``` Epstein-Barr virus (glandular fever) Cytomegalovirus HSV Congenital rubella Mumps ECHO viruses Yellow fever virus ```

Question 913

Discuss Hep carriers

Answer 913

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

Question 914

Discuss HepA virus

Answer 914

``` 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

Question 915

Clinical features of HepA virus

Answer 915

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

Question 916

Discuss pathogenesis of HAV

Answer 916

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

Question 917

Control measures for HAV

Answer 917

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

Question 918

Discuss HBV

Answer 918

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

Question 919

Clinical features of HBV

Answer 919

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%

Question 920

Chronic diseases associated w/ HBV

Answer 920

Chronic persistent Hep; asymptomatic Chronic active Hep; symt9aric Liver cirrhosis Hepatocellular carcinoma

Question 921

Discuss transmission of HBV in community

Answer 921

Parenteral: blood; IVDU, blood transfusions Sexual: genital fluids; sex workers and homosexuals at risk Perinatal: @/during birth; HBeAg+ more likely to transmit

Question 922

Discuss serological markers of HBV

Answer 922

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

Question 923

Community control of HBV

Answer 923

Block person-person transmission; safer sex | Widespread immunisation

Question 924

Discuss transmission, prevention and treatment of HBV in clinical setting

Answer 924

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

Question 925

Short and long term treatment for HBV infection

Answer 925

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

Question 926

Discuss HDV

Answer 926

Seen w/ HBV Transmission: similar to HBV (blood) Incubation 14-56d Usually asymptomatic

Question 927

Discuss clinical features and prevention of HDV (2 types)

Answer 927

``` 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 ```

Question 928

Discuss HCV

Answer 928

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)

Question 929

Clinical features HCV

Answer 929

Clinical illness/jaundice; 30-40%/20-30% Chronic hepatitis; 70-90% Persistent infection 85-100% No protective Ab response identified

Question 930

Control and treatment of HCV

Answer 930

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

Question 931

Discuss HEV

Answer 931

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

Question 932

Discuss HIV structure

Answer 932

``` 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 ```

Question 933

Clinical features of AIDS

Answer 933

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

Question 934

Transmission routes of HIV

Answer 934

Mother-child - HIV+ women before/during birth or breastfeeding Blood: prevention of contact only respite

Question 935

6 stages of HIV infection

Answer 935

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

Question 936

Discuss zidovudine

Answer 936

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

Question 937

Advantages and goals of antiretroviral therapy

Answer 937

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

Question 938

Discuss PEP and PrEP

Answer 938

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

Question 939

HIV risk groups

Answer 939

Homosexual/men who have sex with men IVDU Ethnic groups: African, Hispanic Sex workers

Question 940

Discuss Cushing's syndrome

Answer 940

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

Question 941

Discuss hypothyroidism

Answer 941

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

Question 942

Briefly discuss Paget's disease of bone (SGT)

Answer 942

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

Question 943

Discuss acromegaly

Answer 943

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

Question 944

Briefly discuss Parkinsonism (SGT)

Answer 944

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)

Question 945

Discuss Down's Syndrome

Answer 945

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

Question 946

Briefly discuss Bell's Palsy (SGT)

Answer 946

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

Question 947

Discuss causes of unilateral and bilateral parotid gland swelling

Answer 947

Unilateral - tumour - obstruction of gland Bilateral - alcoholic/chronic liver disease - DM, Sjögren’s syndrome - infections (mumps)

Question 948

Discuss signs of peri-orbital region problems

Answer 948

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

Question 949

Discuss signs on eyelids of problems

Answer 949

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

Question 950

Discuss Grave's disease and relevance to HandN examination

Answer 950

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

Question 951

Discuss 3 conditions that can cause abnormalities of sclera

Answer 951

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

Question 952

Discuss possible causes lip abnormalities in HandN examination (SGT)

Answer 952

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

Question 953

What drugs can cause gingival hyperplasia?

Answer 953

Phenytoin Cyclosporine Nifedipine (Ca2+-C blocker)

Question 954

4 possible tongue abnormalities (SGT)

Answer 954

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

Question 955

Triangles of the neck

Answer 955

Ant: below digastric, in front sternocleidomastoid - common carotid artery, CN7 9 10-12 Post: behind sternocleidomastoid, in front trapezius, above clavicle - external jugular vein

Question 956

Possible causes of swellings in ant. and post. triangles of neck

Answer 956

Ant. - lymphadenopathy - thyroid swellings: goitre (visible enlargement), thyroglossal cyst - parotid tumour - bronchial cyst - rare: carotid body tumour, laryngocoele Post. - lymphadenopathy - rare: cystic hygroma

Question 957

Compare reactive and infiltrative lymphadenopathy

Answer 957

``` 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)

Question 958

Mechanism of action of benzodiazepines

Answer 958

Bind selectively to GABA-A Rs + allosteric modulators - enhance Cl- conductance caused by GABA - hyperpolarise cell, red. likelihood AP

Question 959

Mechanism of action of different classes of antidepressants

Answer 959

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)

Question 960

12 cranial nerves

Answer 960

``` Olfactory - Sensory Optic - Sensory Oculomotor - Motor Trochlear - Motor Trigeminal - Both Abducens - Motor Facial - Both Vestibulocochlear - Sensory Glossopharyngeal - Both Vagus - Both Accessory - Motor Hypoglossal - Motor ```

Question 961

Foramen of the olfactory nerve

Answer 961

Cribriform plate of ethmoid bone

Question 962

Exam and ab/normal response for olfactory nerve

Answer 962

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

Question 963

Foramen of optic nerve

Answer 963

Optic foramen

Question 964

How is visual acuity tested?

Answer 964

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)

Question 965

How are peripheral visual fields tested?

Answer 965

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

Question 966

How are the pupils examined and what is relative afferent pupillary defect?

Answer 966

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)

Question 967

6 extraocular muscles of eye movement

Answer 967

Sup., inf., lateral, medical rectus | Sup., inf., oblique

Question 968

What nerves supply the eye muscles?

Answer 968

LR6 SO4 R3 Oculomotor: sup., inf., medial rectus, inf. oblique Trochlear: sup. oblique Abducens: lateral rectus

Question 969

Exam for extra-ocular eye muscles and abnormal findings

Answer 969

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

Question 970

Branches and foramen of trigeminal nerve

Answer 970

V1: ophthalmic; Sensory; sup. orbital fissure V2: maxillary; Sensory; foramen rotundum V3: mandibular; Both; foramen ovale; muscles of mastication

Question 971

Muscles of mastication

Answer 971

Masseter Temporalis Lat. pterygoid Med. pterygoid

Question 972

Sensory exam of trigeminal

Answer 972

Touch cotton wisp to forehead (V1), cheek (V2), chin (V3) | Avoid angle mandible innervated by upper cervical roots

Question 973

Motor exam of trigeminal

Answer 973

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

Question 974

Foramen of facial nerve and branches

Answer 974

Stylomastoid foramen Intracranial: Temporal Zygomatic Buccal Mandibular Cervical Extracranial: Chorda tympani Greater petrosal nerve to Stapedius

Question 975

Sensory exam of facial nerve

Answer 975

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

Question 976

Motor exam of facial nerve and normal response

Answer 976

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

Question 977

Abnormal response to motor function of facial nerve

Answer 977

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

Question 978

Foramen of vestibulocochlear nerve and branches

Answer 978

Foramen: internal auditory meatus Vestibular: Sensory info from vestibular hair cells in semilunar cells - body position and gaze stability Cochlear: auditory info from cochlear

Question 979

Exam of vestibulocochlear nerve and ab/normal response

Answer 979

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 ```

Question 980

Foramen of glossopharyngeal

Answer 980

Jugular foramen

Question 981

Divisions of vagus nerve

Answer 981

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

Question 982

Exam of glossopharyngeal and vagus and response

Answer 982

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

Question 983

Function and exam of accessory nerve

Answer 983

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

Question 984

Function and exam of hypoglossal nerve

Answer 984

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

Question 985

3 common causes of headaches

Answer 985

Disease: local, vascular Referred pain (pain coming from elsewhere) Disorder: neurological, psychogenic

Question 986

Serious causes of headaches

Answer 986

``` Acute glaucoma Acute hypertension Brain tumours Giant cell arthritis Meningitis Haemorrhage: subarachnoid, sub/epidural ```

Question 987

Indicators that headache may be serious

Answer 987

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

Question 988

What is a migraine? Cause and triggers

Answer 988

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

Question 989

Clinical features and management of migraines

Answer 989

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)

Question 990

Discuss migrainous neuralgia

Answer 990

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)

Question 991

Discuss stroke and the common causes

Answer 991

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

Question 992

Clinical features and investigations of stroke

Answer 992

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 ```

Question 993

Diagnosis, treatment and prognosis of stroke

Answer 993

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

Question 994

Dental relevance of stroke

Answer 994

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

Question 995

Discuss transient ischaemic attack

Answer 995

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

Question 996

Discuss Parkinson’s disease

Answer 996

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

Question 997

Discuss 3 main symptoms of Parkinson’s

Answer 997

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

Question 998

Parkinson’s treatment

Answer 998

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

Question 999

Dental relevance of Parkinson’s

Answer 999

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

Question 1000

What is multiple sclerosis?

Answer 1000

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

Question 1001

Treatment of multiple sclerosis

Answer 1001

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

Question 1002

Oral manifestations of multiple sclerosis

Answer 1002

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)

Question 1003

Dental relevance of multiple sclerosis

Answer 1003

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

Question 1004

Discuss epilepsy

Answer 1004

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)

Question 1005

What is status epilepticus ?

Answer 1005

Uncontrolled series of seizures w/ no regain of consciousness in b/w attacks

Question 1006

Causes of seizures

Answer 1006

Infection: meningitis, encephalitis, brain abscess Inflammation: MS Metabolic abnormalities - electrolyte imbalance - renal failure - nutritional deficiency

Question 1007

Drugs used to treat different types of seizures

Answer 1007

Tonic-clonic - carbamazepine - phenytoin - sodium valproate - gabapentin Absence - sodium valproate - ethosuximide Partial - carbamazepine - sodium valproate

Question 1008

Dental relevance of epilepsy

Answer 1008

``` 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

Question 1009

Discuss palsies of nerves controlling eye movement

Answer 1009

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

Question 1010

Discuss Bell’s Palsy

Answer 1010

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

Question 1011

Discuss trigeminal neuralgia

Answer 1011

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

Question 1012

Discuss shingles

Answer 1012

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

Question 1013

Complications of shingles

Answer 1013

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

Question 1014

4 main ways in which infection can be diagnosed

Answer 1014

History Clinical exam Lab investigations: haematological, biochemical, microbiology/virology Other: X-rays, scans

Question 1015

Important information to ascertain when taking history from pt w/ infection

Answer 1015

``` 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 ```

Question 1016

5 factors contributing to good quality sample

Answer 1016

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

Question 1017

Explain optimal time for taking specimen sample

Answer 1017

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

Question 1018

Tests to identify and classify bacteria

Answer 1018

``` 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 ```

Question 1019

Discuss use of microscopy for identifying bacteria

Answer 1019

``` 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 ```

Question 1020

Discuss cytochrome oxidase as means to classify bacteria

Answer 1020

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

Question 1021

Discuss fermentation as means to classify bacteria

Answer 1021

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

Question 1022

For an ECG what lead is analysed and why?

Answer 1022

Lead II | Follows same direction as flow of current in heart

Question 1023

What are P, QRS and T waves on ECG?

Answer 1023

P: atrial contraction; small depolarisation QRS: ventricular complex; large peak (ventricles thicker) T: ventricular re-polarisation; small

Question 1024

Discuss PR, QRS, ST, RR intervals on ECG

Answer 1024

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

Question 1025

Sinus rhythm requirements

Answer 1025

Fixed relationship b/w P and QRS PR interval 0.12-0.2s QRS <0.2s 'Sinus tachycardia/bradycardia'

Question 1026

How is HR/pulse calculated from ECG?

Answer 1026

300/no. large sq. in RR interval

Question 1027

Cutoffs for bradycardia and tachycardia in ECG analysis

Answer 1027

Bradycardia <60bpm | Tachycardia >100bpm

Question 1028

How can ECG determine if HR is regular or irregular?

Answer 1028

P wave before each QRS | RR interval consistent

Question 1029

Discuss abnormal findings in P, QRS, ST, T waves and possible causes

Answer 1029

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

Question 1030

Discuss 6 liver function test domains and possible abnormal findings

Answer 1030

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

Question 1031

Discuss findings for 1ry and 2ry hyperthyroidism and hypothyroidism

Answer 1031

``` 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. ```

Question 1032

Discuss findings in 1ry and 2ry hypercotisolism and hypocortisolism

Answer 1032

``` 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. ```

Question 1033

What are cystic lesions?

Answer 1033

Sacks filled w/ gas/pus/fluid/blood

Question 1034

Aetiology, clinical and description of dermis cyst

Answer 1034

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

Question 1035

Aetiology, clinical and description of thyroglossal cyst

Answer 1035

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

Question 1036

Aetiology, clinical and description of branchial cyst

Answer 1036

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

Question 1037

Aetiology, clinical and description of lymphangioma/cystic hygroma

Answer 1037

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

Question 1038

Reasons for lymph node enlargement

Answer 1038

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)

Question 1039

Aetiology, clinical and description of pyogenic lymphadenopathy

Answer 1039

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

Question 1040

Aetiology, clinical and diagnosis viral lymphadenopathy

Answer 1040

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

Question 1041

Aetiology, clinical, diagnosis of tuberculous lymphadenopathy

Answer 1041

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

Question 1042

Aetiology, clinical, diagnosis of malignant lymphadenopathy

Answer 1042

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)

Question 1043

Aetiology, clinical, diagnosis of malignant lymphadenopathy - metastatic carcinoma

Answer 1043

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)

Question 1044

Discuss cervical rib

Answer 1044

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

Question 1045

Clinical and diagnosis of lipoma

Answer 1045

Non-lymphatic/non-cystic HandN swelling Clinical - rare - slow-growing - soft, semi-fluctuant, lobulated tumour, varying size - painless, asymptomatic - IO appears yellowish Diagnosis: biopsy

Question 1046

5 parotid lesions

Answer 1046

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)

Question 1047

Discuss thyroid nodule

Answer 1047

Non-lymphatic/non-cystic HandN swelling ``` Aetiology unknown Clinical - uncommon - firm - painless, asymptomatic - midline swelling neck thyroid gland region ```

Question 1048

Aetiology and clinical of carotid body tumour

Answer 1048

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

Question 1049

Structure of herpes virus

Answer 1049

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

Question 1050

Main viruses of herpes family

Answer 1050

``` HHV1 HSV1 HHV2 HSV2 HHV3 VZV HHV4 EBV HHV5 CMV HHV 6/7 HHV8 ```

Question 1051

Discuss HSV1/2

Answer 1051

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

Question 1052

HSV1/2 pathogenesis

Answer 1052

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

Question 1053

Discuss oral herpes

Answer 1053

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

Question 1054

Discuss latency, reactivation and recurrence of HSV

Answer 1054

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

Question 1055

Immune response to HSV

Answer 1055

Innate: interferon and NK limit initial infection Humoral: Ab against surface glycoproteins -> neutralisation Cellular: cytotoxic T and macrophages

Question 1056

Diagnosis of HSV

Answer 1056

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

Question 1057

Discuss herpes whitlow and eczema herpeticum

Answer 1057

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

Question 1058

Discuss genital herpes and proctitis

Answer 1058

``` 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

Question 1059

Discuss neonatal HSV infections

Answer 1059

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)

Question 1060

Discuss HSV encephalitis and meningitis

Answer 1060

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

Question 1061

Discuss chemotherapy of HSV infection

Answer 1061

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

Question 1062

Discuss chicken pox

Answer 1062

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

Question 1063

Discuss shingles

Answer 1063

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

Question 1064

Diagnosis, treatment and vaccine for HHV3

Answer 1064

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

Question 1065

Discuss HHV4 symptoms and infections in child and adult

Answer 1065

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

Question 1066

Complications and treatment of HHV4 infection

Answer 1066

Complications - further infections: brain, liver, lungs - severe anaemia: lack RBC - breathing difficulties; swollen tonsils - ruptured spleen Treatment: no drugs

Question 1067

Discuss HHV5

Answer 1067

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

Question 1068

What is endocarditis?

Answer 1068

Infection of membrane layer of endothelial cells lining heart that is continuous w/ artery and vein lining (endocardium)

Question 1069

Main etiological agents of IE

Answer 1069

Streptococci esp. viridans (oral) group 40-60% Enterococci Staph aureus, coagulase -ve staph 20-40% ``` HACEK Haemophilus Aggregatibacter Cardiobacterium Eikenella Kingella ```

Question 1070

Discuss oral strep and staph aureus virulence factors associated w/ IE

Answer 1070

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 ```

Question 1071

Pathogenesis of IE

Answer 1071

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

Question 1072

4 types of IE

Answer 1072

Affecting previously normal valve Affecting previously abnormal native valve Affecting prosthetic valve Iatrogenic

Question 1073

How can IE affect previously normal valve?

Answer 1073

Bacteraemia due to - Staph aureus - coagulase -ve aureus - enterococci - strep. pneumoniae

Question 1074

Predisposing factors for IE

Answer 1074

Rheumatic fever/degenerative (calcific) disease Congenital heart defects; turbulent flow Mitral valve prolapse Degenerative valve disease IVDU Prosthetic valve/valve replacement surgery

Question 1075

Discuss predisposition to IE of previously abnormal valve and likely pathogens

Answer 1075

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.

Question 1076

Discuss prosthetic valve IE

Answer 1076

Greatest risk 1st few months post surgery - staph aureus - coagulase -ve staph: epidermidis, haemolyticus Late onset: >1yr post surgery; usually present as native IE

Question 1077

How may iatrogenic IE occur?

Answer 1077

Cannulae | IVDU

Question 1078

Need for cross-speciality liaison in diagnosis and treatment of IE

Answer 1078

Diagnosis: req. both lab and clinical findings Treatment - AB prescription - surgical intervention

Question 1079

Major criteria in Duke criteria for IE diagnosis

Answer 1079

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

Question 1080

Discuss minor criteria in Duke criteria for IE diagnosis

Answer 1080

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

Question 1081

Treatment of IE

Answer 1081

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

Question 1082

Define atrophy

Answer 1082

Wasting/dec. in size of organ/tissue/part of tissue due to disease/injury/lack of use

Question 1083

Examples of atrophy

Answer 1083

``` Physiological: remnants structures during development: thyroglossal cyst Wasting of muscles after stopping weight training Alzheimer’s Pathological - cardiac - nutritional - hair follicles - ageing in general ```

Question 1084

Define and give examples of hypertrophy

Answer 1084

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

Question 1085

Define hyperplasia, give examples

Answer 1085

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

Question 1086

Possible consequences of hyperplasia

Answer 1086

Obstruction: prostate hyperplasia -> bladder obstruction Infarction Over secretion of hormone

Question 1087

Define metaplasia and give examples

Answer 1087

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

Question 1088

Define oncogene

Answer 1088

Genes that have potential to cause cancer | May be abnormally turned on/off due to mutations, translocations or effects of another gene

Question 1089

Discuss oncogenes

Answer 1089

Normal if not inappropriately turned on Normal state: proto-oncogene; abnormal state: oncogene Ras: GTPase protein; mutated in 1 in 4 cancers

Question 1090

Discuss tumour suppressor genes

Answer 1090

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

Question 1091

Define carcinogenesis

Answer 1091

Formation of cancer | Normal cells transformed to cancer cells

Question 1092

Classes of carcinogens

Answer 1092

Chemical Radiation Viral

Question 1093

Examples of chemical carcinogens

Answer 1093

``` Aromatic hydrocarbons (benzene): lung Naphthalene dyes: bladder cancer Cigarette smoke: lung/bladder cancer Asbestos: lung, mesothelioma Dietary: colonic cancer Nitrosamines, amides: gastric ```

Question 1094

How does ionising radiation cause cancer, give examples

Answer 1094

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

Question 1095

Discuss DNA and retroviruses as carcinogens

Answer 1095

``` 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

Question 1096

Define neoplasm

Answer 1096

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

Question 1097

Clinical features of colon cancer

Answer 1097

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

Question 1098

Cancer screening methods

Answer 1098

``` Chest X-ray (lung) Positron emission tomography Genetic analysis: breast (BRCA1/2), Cytology Biopsy Tumour markers ``` Self exam: breast, testes

Question 1099

Risk factors of OSCC

Answer 1099

``` Old M Alcohol, tobacco, paan Sun/ionising radiation LP HPV, Candida ```

Question 1100

Clinical features of OSCC

Answer 1100

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 ```

Question 1101

Common locations of OSCC

Answer 1101

Lips, lat border tongue, floor of mouth Paan chewer: B mucosa, commissure region Reverse smokers: palate

Question 1102

Diagnosis of OSCC

Answer 1102

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

Question 1103

Discuss TNM tumour classification system

Answer 1103

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

Question 1104

Discuss management of cancers

Answer 1104

Local - curative surgery - radiotherapy Regional spread - debulking surgery - radiotherapy Distant metastases - palliative surgery: don’t cure; lessen symptoms/prolong life - radiotherapy - chemotherapy

Question 1105

Possible side effects of radiotherapy

Answer 1105

Week 1: Nausea, vomiting Week 2: mucositis, taste changes Week 3: dry mouth Later - infections - caries - pulp pain and necrosis - hypersensitivity - trismus - craniofacial defects

Question 1106

Discuss the genetic basis of cancer and how some cancers are inherited

Answer 1106

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

Question 1107

Discuss proto/oncogenes

Answer 1107

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

Question 1108

Give examples oncogene activation

Answer 1108

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

Question 1109

Discuss caretaker genes

Answer 1109

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

Question 1110

Discuss gatekeeper genes

Answer 1110

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

Question 1111

Discuss viral oncogenes

Answer 1111

Several human viruses known to cause cancer HPV encodes proteins E6/7 that inactive key tumour suppressor genes (RB1, P53) cause cervical cancer

Question 1112

Classification of malignant neoplasms w/ examples

Answer 1112

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

Question 1113

What are teratomas?

Answer 1113

Germ cell neoplasms Found in ovaries and testis Differentiate along more than 1 germ cell line

Question 1114

Compare macroscopic and microscopic features of benign and malignant neoplasms

Answer 1114

Benign - macro: well defined, smooth-surface - micro: blunt, pushing margin Malignant - macro: ill-defined, craggy surfaced - micro: infiltrative, invasive

Question 1115

Compare the features of benign and malignant neoplasms

Answer 1115

``` Nuclear:cytoplasm: normal; high Nuclear pleomorphism: uncommon; common Necrosis: rare; common Mitotic rate: normal/low; high, abnormal mitoses Metastases: none; common ```

Question 1116

Define metastasis and discuss spread

Answer 1116

2ry growth of neoplasm at 1/+ locates distant from 1ry site Spread - lymphatics - blood vessels (haematogenous) - transcoelomic (through body cavities) - CSF

Question 1117

Discuss the mechanism of metastasis

Answer 1117

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

Question 1118

Discuss why cancers may cause anaemia and cachexia

Answer 1118

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

Question 1119

How can cancers result in death?

Answer 1119

``` Widespread disease in multiple organs Metastatic disease in vital sites Immunosuppression -> opportunistic infections Organ failure Haemorrhage Late stage 2nd malignancies ```

Question 1120

What are the geriatric giants? What is there importance?

Answer 1120

Incontinence Immobility Instability: falls, syncope Intellectual impairment: delirium, dementia Several different diseases can present as 1/+ of them

Question 1121

Discuss red. homeostatic reserve as a challenge of treating elderly

Answer 1121

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

Question 1122

Discuss impaired immunity as challenge of treating elderly

Answer 1122

Less effective Shingles: reactivation of HZV May not have inc. WCC or pyrexia in infection; hypothermia

Question 1123

Discuss rehabilitation as challenge to treating elderly

Answer 1123

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

Question 1124

Define fragility #

Answer 1124

sustained when falling from standing height/less

Question 1125

What is osteoporosis? Aetiology

Answer 1125

Slowly progressive dam asymptomatic reduction in bone mass causing fragility and inc. risk # F: postmenopausal; oestrogen deficiency M: hypogonadism, glucocorticoid treatment, alcoholism

Question 1126

Risk factors and 2ry causes of osteoporosis

Answer 1126

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

Question 1127

How is osteoporosis diagnosed?

Answer 1127

Marked osteopenia on X-ray Previous fragility # Risk factors Standard: bone mineral density by DEXA scan

Question 1128

Discuss the lifestyle changes and medications for treatment of osteoporosis

Answer 1128

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

Question 1129

Discuss BRONJ

Answer 1129

``` 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

Question 1130

Pathophysiology of transient ischaemic attack/stroke

Answer 1130

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

Question 1131

Risk factors of TIA

Answer 1131

``` Hypertension, hyperlipidaemia Smoking, alcoholism DM Heart disease: valvular, ischaemic, a fib Peripheral vascular disease Past TIA Polycythaemia ```

Question 1132

Clinical features of TIA and stroke

Answer 1132

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)

Question 1133

Management of TIA/stroke

Answer 1133

Maintain airway Monitor blood glucose, BP Urgent CT/MRI Antiplatelet once haemorrhagic stroke ruled out

Question 1134

Prevention of TIA/stroke

Answer 1134

Antiplatelet: aspirin, clopidogrel, dipyridamole Anticoagulant: warfarin Risk factor management: smoking, alcohol, hypertension

Question 1135

Discuss dementia and how pt may present

Answer 1135

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

Question 1136

Presentation of Alzheimer’s

Answer 1136

Impaired visuospatial skill, memory/verbal abilities, planning abilities, lack of insight Later: irritability, mood disturbance, behavioural change (aggression, hallucination), agnosia Finally: sedentary, apathy

Question 1137

Cause of Alzheimer’s

Answer 1137

Accumulation of beta amyloid peptide (degradation product of amyloid precursor protein) Results in progressive neuronal damage, neurofibrillary tangles, amyloid plaques, loss of ACh

Question 1138

Management of Alzheimer’s

Answer 1138

Exacerbated by unfamiliar environments, peo0e Develop routines AChE inhibitors: rivastigmine (beneficial in mild AD) BP control Support for carers

Question 1139

What are the 2 types of DM?

Answer 1139

T1: complete lack/inadequate production of insulin from beta pancreatic cells T2: insulin resistance @ R level in peripheries

Question 1140

Clinical presentation of DM

Answer 1140

Osmotic symptoms: polyuria, polydipsia (thirst), nocturia, weight loss Recurrent infections: oral/genital candidiasis Lethargy Visual blurring

Question 1141

Discuss 2 types of diabetic emergency

Answer 1141

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

Question 1142

Vascular complications of DM? How do these occur?

Answer 1142

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

Question 1143

Discuss types of neuropathy complications seen in DM

Answer 1143

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

Question 1144

Discuss inc. risk of infections and poor healing due to DM

Answer 1144

Adverse effects hyperglycaemia on granulocytes and T-cell function Fungal and bacterial: mucocutaneous candidiasis, foot infections

Question 1145

Diagnostic criteria for DM

Answer 1145

Random glucose: >11.1mmol/L Fasting glucose: >7.0mmol/L Oral glucose tolerance test (2h): >11.1mmol/L (75g glucose)

Question 1146

Discuss HbA1c DM test

Answer 1146

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

Question 1147

Treatment of DM

Answer 1147

``` Control hyperglycaemia: alleviate symptoms Prevent complications Address risks Lifestyle Medications ```

Question 1148

Discuss lifestyle changes used for treatment of DM

Answer 1148

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

Question 1149

Basics of medications prescribed in DM and when

Answer 1149

T1: insulin T2 - lifestyle changes insufficient: single oral hypoglycaemic - combination therapy (2/+) - + insulin: glycaemic control inadequate >3 agents

Question 1150

Discuss 4 main oral hypoglycaemics

Answer 1150

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

Question 1151

Discuss non-insulin and insulin injectables

Answer 1151

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 ```

Question 1152

Principles of DM management

Answer 1152

``` Education: self monitoring, target glucose Lifestyle changes Oral hypoglycaemics w or w/o insulin Risks: lipids, BP, alcohol Assess complications ```

Question 1153

Dental aspect of DM

Answer 1153

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

Question 1154

Discuss thyroid gland

Answer 1154

-ve feedback mechanism from hypothalamus and pituitary Produce thyroxine hormones T3 and T4 Target: brain, bone, heart, gut, skin, metabolism

Question 1155

Causes of thyroid disorders

Answer 1155

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

Question 1156

Compare clinical features of hyperthyroidism and hypothyroidism

Answer 1156

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

Question 1157

How can amiodarone cause both hyper and hypothyroidism?

Answer 1157

Amiodarone causes release of T3/T4 (hyper) but then hormones become depleted (hypo)

Question 1158

Investigations into hyper and hypothyroidism

Answer 1158

T3/4: inc.; dec. TSH: dec.; inc, Ab: +ve thyroperoxidase Ab, TSH R Ab (Graves'); +ve thyroperoxidase Ab

Question 1159

Management of hyper and hypothyroidism

Answer 1159

Drugs: beta-blockers (atenolol) slow HR, antithyroid (carbimazole, propylthiouracil); thyroxine replacement Others: radioactive iodine, thyroidectomy

Question 1160

Dental aspects of hyper and hypothyroidism

Answer 1160

Hyper - inc. susceptibility caries, PD disease - burning mouth syndrome - accelerated eruption - osteoporosis jaw - ulcers (carbimazole) ``` Hypo - congenital — delayed eruption — macroglossia — micrognathia — malocclusion - glossitis - dysgeusia ```

Question 1161

Discuss the adrenal gland

Answer 1161

Cortex: produce androgens Medulla: cortisol, aldosterone, adrenaline

Question 1162

Causes of adrenal insufficiency

Answer 1162

Lack of cortisol and aldosterone 1ry - autoimmune (Addison's) - infiltration: TB, sarcoidosis, malignancy 2ry: pituitary/hypothalamus impairment - pituitary adenoma - exogenous steroids

Question 1163

Action of cortisol

Answer 1163

Anti-inflammatory and immunosuppressive Physiological actions - hepatic gluconeogenesis - proteolysis - Na retention, K loss - dyslipidaemia, hypertension, insulin resistance (hypercortisolaemia)

Question 1164

Clinical features Addison's disease

Answer 1164

``` Hypotension Hypoglycaemia Weight loss Lethargy Abdominal pain Skin, oral pigmentation: inc. MSH and ACTH ```

Question 1165

Dental aspects of adrenal insufficiency

Answer 1165

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

Question 1166

Causes of hyperparathyroidism

Answer 1166

1ry - parathyroid adenoma - parathyroid hyperplasia: genetic familial hyperparathyroidism, multiple endocrine neoplasia - parathyroid carcinoma 2ry - VitD deficiency - chronic renal failure

Question 1167

Clinical features hyperparathyroidism

Answer 1167

``` Abdominal pain, constipation Renal stones Bone pain, osteopaenia, osteoporosis Lethargy, fatigue Confusion, memory impairment, depression, hallucinations Polyuria, polydipsia, urinary freq, ```

Question 1168

Diagnostic investigations for 1ry and 2ry hyperparathyroidism

Answer 1168

``` Serum phosphate: dec.;inc. 1,25-dihydroxycholecalciferol: inc.; dec. ALP: inc.; inc. Serum Ca: inc.; dec. Serum PTH: inc.; inc. ```

Question 1169

Treatment of hyperparathyroidism

Answer 1169

1ry - adenoma: para-thyroidectomy - hyperplasia: drug; cinacalcet 2ry: treat underlying cause

Question 1170

Dental aspect of hyperparathyroidism

Answer 1170

``` Malocclusion PDL widening Spacing Brown tumour - benign - radiolucent - abnormal bone metabolism - extensive bone resorption; replaced by fibrovascular tissue and giant cells ```

Question 1171

What is acromegaly? Clinical features

Answer 1171

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 ```

Question 1172

Investigations and treatment of acromegaly

Answer 1172

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)

Question 1173

What is Cushing's syndrome? Aetiology

Answer 1173

Excess cortisol Adrenal Cushing’s syndrome (cortisol) Pituitary Cushing's disease (ACTH) Ectopic ACTH production

Question 1174

Investigations for Cushing's syndrome

Answer 1174

Midnight cortisol (diurnal variation; lowest at night), cortisol day curve (static) Low dose dexamethasone suppression test (can’t suppress) MRI adrenal/pituitary Pituitary catheter

Question 1175

Treatment of Cushing's syndrome

Answer 1175

Surgery: transnasal transsphenoidal (TSS), adrenalectomy Drugs: metyrapone, ketoconazole Radiotherapy

Question 1176

Dental aspects of Cushing's/excess cortisol

Answer 1176

Peptic ulcers: avoid NSAIDs, aspirin DM: PD health Osteoporosis, myopathy: dentures adjustment, mobility Immunosuppression: opportunistic infections Pour wound healing

Question 1177

What are pheochromocytoma and paraganglioma? Dental relevance

Answer 1177

Excess catecholamine Pheochromocytoma (adrenal), paraganglioma (extra-adrenal) Dental - alpha blocker (treatment) risk bleeding - avoid opiates, MAOI - hypertension

Question 1178

Define benign and malignant neoplasm

Answer 1178

Benign: usually harmless; may be harmful due to - site: meningioma; inc. intracranial pressure - produce hormone: insulinoma Malignant: usually harmful

Question 1178

Discuss differentiation of neoplasms and define anaplasia

Answer 1178

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

Question 1178

Classification of benign neoplasms w/ examples

Answer 1178

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

Question 1179

General indications for GA

Answer 1179

``` Child req. multiple. XLA Special needs pt Oral and max fax Inability to anaesthetise w/ LA True LA allergy ```

Question 1180

Considerations for pt w/ CVD receiving GA

Answer 1180

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

Question 1181

Considerations for pt w/ respiratory disease receiving GA

Answer 1181

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

Question 1182

Considerations for pt w/ haematological disease receiving GA

Answer 1182

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

Question 1183

Considerations for pt w/ endocrine disorder receiving GA

Answer 1183

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

Question 1184

Considerations for pt w/ hepatitis receiving GA

Answer 1184

Bleeding tendencies Drug metabolism Infection risk

Question 1185

Considerations for pt w/ renal disease receiving GA

Answer 1185

Often marked anaemia Dialysis: circulating volume and cause CV problems during anaesthesia Serum electrolytes altered

Question 1186

Considerations for pt w/ musculoskeletal problems receiving GA

Answer 1186

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

Question 1187

Problems associated w/ obese pt receiving GA

Answer 1187

Intubation, airway maintenance, ventilation difficult Moving pt difficult Difficulty finding veins Drug doses difficult to calculate

Question 1188

Discuss aspirin

Answer 1188

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

Question 1189

Discuss non-selective NSAIDs

Answer 1189

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

Question 1190

Discuss selective NSAID

Answer 1190

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

Question 1191

Indications of immunosuppressives

Answer 1191

Arthritis: psoriatic, rheumatoid, ankylosing spondylitis, acute gouty Psoriasis, Behçet’s disease, LP Ulcerative colitis, Crohn’s, Coeliac Organ transplant

Question 1192

Discuss mechanism, indications and screening for steroidal immunosuppressives

Answer 1192

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

Question 1193

How to minimise adverse effects of corticosteroids?

Answer 1193

``` 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 ```

Question 1194

Discuss antimitotics

Answer 1194

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

Question 1195

Discuss cyclosporine

Answer 1195

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

Question 1196

Adverse effects and drug interactions of cyclosporine

Answer 1196

Adverse - hypertension - nephrotoxicity, neurotoxicity - malignancies - gingival hyperplasia - lymphoproliferative disorders - teratogenicity Interactions - inc. toxicity: macrolide AB (clarithromycin, erythromycin); antifungals (fluconazole, miconazole) - NSAID promote nephrotoxicity

Question 1197

Post-treatment monitoring of cyclosporine

Answer 1197

FBC LFT U+E

Question 1198

Discuss mycophenolate mofteil

Answer 1198

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

Question 1199

Discuss biological response modifiers

Answer 1199

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

Question 1200

Discuss Behçet’s disease

Answer 1200

Multisystem disease Recurrent orogenital ulcers; indistinguishable from RAS Ocular lesions: ant. uveitis, recurrent hypopyon, iritis, choriorentinitis Skin: erythema nodosum, thrombophlebitis