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BDS4 > Clinical medical sciences and microbiology > Flashcards

Clinical medical sciences and microbiology Flashcards

1
Q

Clotting-
1. Name 3 stages in the formation of a clot?

A
  • Vasoconstriction
  • Platelet plug formation (temporary blockage)
  • Formation of fibrin clot (via clotting cascade)
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2
Q
  1. How do the following drugs affect clotting and at what stage- aspiring, warfarin, NOAC?
A
  • Aspirin- inhibits platelet aggregation at plug formation stage
  • Warfarin- Vitamin K antagonist so prevents formation of vitamin K dependent clotting factor 2,7,9, and 10 preventing clotting cascade and formation of fibrin clot
  • NOAC- Factor 10 inhibitor so inhibit conversion of prothrombin to thrombin stopping the coagulation cascade and so fibrin clot formation
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3
Q
  1. Why are aspirin and clopidogrel used in conjunction?
A
  • Synergistic and so potentiated effect on platelet aggregation as both work by different mechanisms; dual therapy further enhances the anti-platelet effect
  • In patients who are taking two antiplatelet drugs in combination this can affect post-extraction bleeding (one antiplatelet alone seems to have little effect) so consult doctor as may be required to stop one of the medications 7 days prior to surgery
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4
Q
  1. What is the inheritance pattern of Von Willebrand’s disease?
A
  • Autosomal dominant or recessive depending on type (but actually depends on type- type 1 and 2 and autosomal dominant and type 3 autosomal recessive)
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5
Q
  1. How does Von Willebrand’s disease affect bleeding?
A
  • Von Willebrand’s factors normally binds to factor VIII when it is inactive in circulation, when not bound to vWF factor VIII degrades rapidly
  • Therefore, Von Willebrand disease resulting in reduced VIII levels
  • It also acts to enable platelet aggregation within the blood vessel was so when reduced has an anti-platelet effect
  • Therefore, this condition may result in increased risk of haemorrhage
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6
Q
  1. What is haemophilia A?
A
  • Deficiency of clotting factor VIII (8)
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7
Q
  1. What is haemophilia B?
A
  • Deficiency of clotting factor IX (9)
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8
Q
  1. What is Von Willebrand’s Disease?
A
  • Deficiency of Von Willebrand’s Factors (results in reduced factor VIII and reduced platelet adhesion)
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9
Q
  1. How are they VWB and haemophillia A and B managed managed?
A
  • Factor replacement, use of desmopressin DDAVP (for haemophilia A and VW) and antifibrinolytics (e.g. tranexamic acid)
  • In very mild haemophilia A and VW patients only oral tranexamic acid is required
  • Majority of haemophilia A and VW patient respond to DDAVP (desmopressin) which increases factor VIII levels
  • In patient with moderate to sever haemophilia A recombinant factor VIII is require
  • Haemophilia B patient don’t response to DDAVP so prophylactic cover utilises recombinant factor IX
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10
Q
  1. What treatment would you carry out as a GDP for VWB and haemophillia A and B patients?
A
  • Non-invasive treatment- hygiene therapy, removal prosthodontics, restorative dentistry including crowns and bridges, endodontics
  • Special care and referral is required for invasive procedures- extraction, minor oral surgery, periodontal surgery, biopsies
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11
Q

Anaemia-
1. What is anaemia?

A

Anemia is a condition in which you lack enough healthy red blood cells to carry adequate oxygen to your body’s tissues.

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12
Q
  1. What are the general signs and symptoms of anaemia?
A
  • Fatigue, malaise, weakness and dizziness
  • Shortness of breath
  • Pale pallor and coldness
  • Tachycardia
  • Heart palpitations
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13
Q
  1. What are the oral sings of anaemia?
A
  • Recurrent oral ulceration
  • Candidal infections
  • Pale mucosal pallor
  • Poor wound healing

  • Recurrent oral ulceration
  • Candidal infections
  • Glossitis or smooth tongue (iron deficiency)
  • Beefy tongue (vitamin B12 or folate deficiency)
  • Oral dysesthesia
  • Pale mucosal pallor
  • Poor wound healing
  • Mucosal atrophy
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14
Q
  1. What would microcytic and macrocytic blood results show?
A
  • Microcytic- small RBC’s which are paler than normal; <80fL- due to iron deficiency or thalassemia
  • Normocytic- normal RBC’s; 80-95fL- due to internal bleeding, pregnancy, sickle cell anaemia, chronic disease (RA, diabetes, kidney disease)
  • Macrocytic- large RBC’s; >95fL due to vitamin B12 or folic acid deficiency
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15
Q
  1. What GI conditions can cause microcytic anaemia?
A
  • Coeliac disease
  • Inflammatory bowel disease- Crohn’s or ulcerative colitis
  • Haemorrhoids
  • Gastric ulcers
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16
Q
  1. What common conditions cause microcytic anaemia but require further blood tests?
A
  • Thalassemia
  • Iron deficiency
  • Sickle cell anaemia
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17
Q
  1. What 3 oral conditions are associated with microcytic anaemia?
A
  • Recurrent oral ulceration/apthae
  • Candidosis
  • Poor wound healing

  • Recurrent oral ulceration/apthae
  • Candidosis
  • Mucosal atrophy
  • Dysesthesia
  • Poor wound healing
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18
Q
  1. What treatment options for microcytic anaemia?
A
  • Replace haematinics where there is a deficiency- iron sulphate 200mg for 3 months, 5mg folic acid daily, 1mg vitamin B12 x6 then 1mg/2 months via injection (If use due to pernicious anaemia)
  • If acute or chronic blood loss diagnose and treat (e.g. menorrhagia- Tx with hormone therapy or contraceptive pill)
  • Transfusion if there is a RBC production issue or erythropoietin if production failure is due to renal disease
  • Prevention via dietary and supplement advice
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19
Q

HIV-
1. What is the rate of infection for HIV, hep C and hep B on exposure?

A
  • HIV- 0.3%
  • Hep c- 3%
  • Hep B 30%
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20
Q
  1. Name 6 oral lesions associated with HIV?

4

A
  • Hairy leucoplakia
  • Candidosis and associated lesions-
  • Periodontal disease- ANUG and ANUP
  • Others- ulceration NOS, viral infections (HSV, HPV, VZV), oral pigmentation

  • Candidosis and associated lesions- psuedeomebranous, erythematous, median rhomboid glossitis, denture induced stomatitis, angular cheilitis, hyperplastic candidosis
  • Hairy leucoplakia
  • Kaposi’s sarcoma
  • Non-Hodgki’ss lymphoma
  • Periodontal disease- ANUG and ANUP
  • Others- ulceration NOS, viral infections (HSV, HPV, VZV), oral pigmentation
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21
Q
  1. How is HIV diagnosed and treated?
A
  • Diagnosed- (venepuncture and screening assay- blood test for ELISA
  • Treatment- HAART; highly active anti-retroviral therapy

  • Diagnosed- (venepuncture and screening assay- blood test for ELISA (test for HIV antibody and p24 antigen at same time) (present about 4-6 weeks after infection) or HIV RNA testing (false positives an issue)
  • Alternatively rapid point of care test (need confirmed with serology))
  • Treatment- HAART; highly active anti-retroviral therapy which consists of 3 or more drugs; entry/fusion inhibitors, nucleoside reverse transcriptase inhibitor, non-nucleoside reverse transcriptase inhibitor, integrase inhibitors and proteinase inhibitor
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22
Q

Patient attends with facial palsy.
1. How can you differentiate between upper and lower motor neuron disease?

A
  • Upper Motor Neuron Disease (e.g. stroke)- patient still able to raise eyebrows and crinkle forehead, scrunch up eyes, increased muscle tone (muscles stiff), increased or exaggerated reflexes
  • Lower Motor Neuron Disease (e.g. facial palsy)- upper muscles also paralysed so patient cannot raise eyebrows or crinkle forehead, decreased tone (muscles flaccid), decreased reflexes

  1. How does this difference occur?
    * Upper part of the facial nuclei receives innervation from both crossed (opposite side of the brain) and uncrossed (same side of brain) fribes which corresponds to upper muscles of the face (frontalis and orbicularis oculi)
    * In upper motor neuron disease, the damage occurs before the facial nuclei (supra-nuclear) these muscles will still receive innervation from the uncrossed (same brain side) fibres
    * In lower motor neuron disease, the nerve damage occurs at or after the facial nuclei and so all innervation (from both types of fibres) stops and all the muscles, including those of the upper face, will be affected
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23
Q
  1. Give 5 possible causes for lower motor neuron disease?
A
  • Parotid tumour
  • Misplaced LA
  • Trauma
  • Motor neuron disease
  • Reactivated HSV causing bell’s palsy
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24
Q
  1. How is lower motor neuron disease managed?
A
  • Distinguish from UND and then distinguish if any underlying cause through relevant history, x-rays or blood tests
  • Reassure the patient that it will get better (80% resolve within a number of week)
  • Give patient eye patch/protecting to key the affected eye closed and protect the cornea from drying out
  • May consider prescribing prednisolone (steroid) is patient presents within 72hrs of onset to reduce swilling and initial inflammation around the facial nerve
  • Review patient and refer to specialist services if paralysis does not resolve
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25
Q
  1. Give 5 possible causes for upper motor neuron disease?
A
  • Multiple sclerosis
  • Stroke
  • TIA
  • Polio
  • Traumatic brain injury
  • Spinal cord injury
26
Q
  1. What is bell’s palsy and how does it occur?
A
  • Bell’s palsy is the name given to facial palsy of unknown cause
  • It occurs as a result of inflammation around the facial nerve which causes pressure on the next and facial paralysis on the affected side
  • Clinically the patient will present with unilateral paralysis of all of the of the muscles of the face on the affected side including those of the forehead and eye
27
Q

Patients on Steroids- Adrenal Suppression-
1. What are the signs and symptoms of adrenal suppression?

A
  • Hypoglycaemia (type 2 diabetes)
  • Osteoporosis
  • Increased infection risk
  • Oral pigmentation
  • Weakness, lethargy, dizziness and low BP
  • Postural hypotension
  • Anorexia or weight loss and dehydration
  • Loss of body hair
  • Increased cancer risk (as immune surveillance for cancer cells reduced)
  • Easy bruising
  • Cataracts and glaucoma necrtoisi
  • Peptic ulceration
28
Q
  1. What emergency can be associated with adrenal gland suppression?
A
  • Adrenal crisis (insufficient levels of cortisol)
29
Q
  1. How is an adrenal crisis treated?
A
  • Saline infusion
  • IV corticosteroids (hydrocortisone)
  • Correct hypoglycaemia if present
  • Treat precipitating event e.g. infection
30
Q
  1. What conditions may require the patients to be on long term steroids?
A
  • Severe asthma
  • COPD
  • Addison’s disease
  • Rheumatoid Arthritis
  • Crohn’s disease
  • Lupus
  • MS
31
Q

You have an asthmatic patient who takes 2 inhalers.
1. What kind of inhalers will these likely be?

A
  • Beta-agonist salbutamol inhaler- blue (short acting)
  • Corticosteroid betamethasone inhaler- brown
32
Q
  1. What is asthma?
A
  • Asthma is caused by reversible airflow obstruction characterised by a triad of inflammation (and swelling) of mucosa of the airways, increased and excessive mucous secretion and constriction of airway smooth muscle
  • It involves a bronchial hyper reactivity
33
Q
  1. What are the signs and symptoms of asthma?
A
  • Shortness of breath
  • Wheeze (exhaling sound)
  • Coughing
  • Increased sputum
  • Chest tightness or pain
  • Symptoms usually works early in the morning and possibly in the middle of the night
34
Q
  1. What are the dental effects of inhalers and what advice should be given?
A
  • Cause localised immune suppression in the mouth this can cause increased incidence of candida infection
  • Acidic so can cause erosion
  • Can cause decrease saliva flow which exacerbates likelihood of both erosion, candidal infection, caries and dry mouth
  • Patients should be advised to rinse with water after using inhalers, use inhalers as instructed and use a spacer
  • They should ensure to increase fluid intake to deal with any dry mouth symptoms and to ensure regular dental check-ups and use of fluoride to help prevent erosion and caries
35
Q
  1. What other considerations should be given for asthmatic patients when placing FV?
A

Possible associated allergy to colophony which is found in fluoride varnish
* Always enquire about asthma and allergies before placing fluoride varnish in children- do not place in patient show have been hospitalised in the last three years with an asthma attack
* Must also be aware of the risk of and therefore appropriate management of asthma attack medical emergency
* In patients have sever asthma may have to take breaks during long periods of treatment for them to take breaks

36
Q
  1. What % of people in Scotland and being treated for asthma?
A
  • Up to 7%
37
Q
  1. Why are asthmatics more prone to erosion?
A

As the brown inhaler is acidic which decreases the pH in the mouth. Coupled with dry mouth and decresed buffering capacity of the saliva causes erosive wear

38
Q
  1. What type of drug is chlorhexidine?
A
  • Biguanides (antiseptic)

Chlorhexidine is a broad-spectrum antimicrobial biguanide used as a topical antiseptic and in dental practice for the treatment of inflammatory dental conditions caused by microorganisms.

39
Q
  1. What is chlorohexidine mode of action?
A
  • Diatonic- one cation adheres to pellicle coated teeth and one adheres to the cell membrane
  • Binds to microbial cell walls (negatively charged phospholipids) causing membrane disruption (cell wall damage) and interfering with (increased) cell wall permeability (osmotic damage) causing leakage of cell cytoplasm and cell death
40
Q
  1. What is chlorohexidines substantivity?
A

12hrs

41
Q
  1. What is meant by substantivity?
A
  • Prolonged adherence of the antiseptic to the oral surface and its slow release in effective doses that guarantee the persistence of int antimicrobial activity
    How long the antiseptic effect is?
42
Q

Give a common dose of CHX

A
  • 0.2% 10ml (20mg) 2x daily
43
Q
  1. Give 4 side effects of CHX-
A
  • Staining of the teeth
  • Altered taste
  • Salivary gland enlargement
  • Dry mouth
  • Allergy

  • Staining
  • Taste disturbance
  • Salivary gland enlargement (parotid gland swelling)
  • Anaphylaxis or hypersensitivity reaction
  • Mucosal irritation or erosion
  • Interacts with SLS
  • Burning of mouth and gums
44
Q
  1. Give 4 uses of CHX?
A
  • Short term use for infection- candidosis, denture stomatitis, recurrent oral ulceration
  • As an endodontic irrigant
  • Treatment of ANUG patients
  • Maintain OH in patient with jaw fixation
  • Surgical pre-op rinse
  • Post intra-oral (periodontal or oral) surgery
  • Treatment of dry socket
45
Q

Biofilms-
1. What is a biofilm?

A
  • Aggregate of micro-organisms which adhere to each other and become embedded within a self-produced ECM which allow them to adhere to a substance
46
Q
  1. What are the stages of development of a biofilm?
A

Attachment
Cell to cell adhesion
proliferation
Maturation
Dispersion

47
Q
  1. Give 4 method of identifying organisms?
A
  • Microbiological culture- culture on a suitable agar medium
  • PCR

  • Microbiological culture- culture on a suitable agar medium, isolate bacterium and identify with API, enzyme activities, sugar fermentation testing (can also use selective agar)
  • Molecular biology- DNA probes, PCR, ELISA
48
Q
  1. What are the virulence factors for P. ginigvalis?
A
  • Capsular polysaccharides (and outer membrane vesicles)
  • Degradative enzymes (proteases)- e.g. gingipans, fibrinolysin, collagenase, MMPS which allow manipulation of host defences
  • Fimbrillar adhesions/fimbriae- allow adherence to and invasion of host cell membranes
  • Endotoxins- e.g. LPS
  • Tissue toxic metabolic by-products e.g. hydrogen sulphide and ammonia
49
Q
  1. What are the virulence factors for C. albicans?
A
  • Germ tube formation
  • Hyphae
  • Hydrolytic enzymes
  • Adhesins
  • Switching mechanisms
  • Metabolic acids
  • Extracellular enzymes)
50
Q
  1. What are the virulence factors for S. Mutans?
A
  • Glucan binding proteins- help stick and adhere to other bacteria
  • Adhesins- allow adhere to the tooth
  • Sugar modifying enzymes
  • Polysaccharides- protect organisms and provide glucose storage
  • Acid tolerance and adaptation
  • (Biofilm formation)
51
Q

Antibiotics-
1. Name 4 occasions when antibiotics are indicated for dental treatment?

A
  • Oral infection with evidence of spreading infection e.g. cellulitis, lymph node involvement, swelling) or systemic involvement (fever, malaise)
  • For the treatment for ANUG or pericorontitis where there is systemic involvement or persistent swelling despite local treatment
    (Or in either of these cases as an adjunct to surgical treatment)
  • For the treatment of dental abscess where immediate drainage cannot be achieved or prove ineffective through local measures or in cases or systemic involvement or spreading infection
  • Appropriate for sinusitis where there are persistent symptoms or purulent discharge lasting at least seven days or where symptoms are severe
  • As an adjunctive to surgical treatment in immunocompromised patients
  • In the case of an oro-antral communication
  • For the treatment of ludwig’s angina
52
Q
  1. Give 5 ways antibiotics work
A
  • Cell wall destruction
  • Protein synthesis inhibition
  • DNA synthesis inhibition
  • DNA replication inhibition
  • Cell membrane inhibition/injury
  • Inhibition of synthesis of essential metabolites
53
Q
  1. Give 3 disadvantages of antibiotics?
A
  • Antibiotic resistance
  • Interactions with other medicines
  • Can cause GI upset diahorrea
  • Can cause hypersensitivity/anaphylaxis
54
Q
  1. Name 3 antibiotics used in dental treatment and include regime example?
A

Pen V (250mg 2 tablets 4x daily for 5 days (40 pills))
Metronidazole (400mg 3x daily for 5 days (15 pills))
Amoxicillin (500mg 3x daily for 5 days (15 pills))
These are all for dental abscesses
Dosages and amount of tablets differ for ANUG and pericornitis its is same dose but only for 3 days.
Sinusitis is pen V and doxycyclin

55
Q
  1. What are the mechanisms of antibiotics resistance?
A
  • Drug inactivation- enzymatic degradation of antibacterial drugs
  • Altered target site/molecules- alteration of bacterial proteins that are antimicrobial targets
  • Blocking antibiotic entry
  • Reduced accumulation- as a result of changes in membrane permeability to antibiotics
  • Altered metabolism- again as a result of changes to membrane permeability
  • Efflux of antibiotics
56
Q

Tooth Development-
1. What are the stages of tooth development?

A
  • Initiation
  • Morphogenesis
  • Cell differentiation
  • Matrix secretion
  • Root formation
57
Q
  1. What forms the root?
A
  • Hertwig’s epithelial root sheath
58
Q
  1. How may this affect the dentition in later life?
A
  • Breaks up to form remnants know as epithelial rests/debris of Malassez which if reacted later in life can cause cyst formation
59
Q
  1. Name 4 parts of the late bell stage
A
  • Internal enamel epithelium
  • External enamel epithelium
  • Stellate reticulum
  • Stellate intermedium
60
Q

Digestion & Food Transport-
1. What is the difference between liquids and solids regarding oral seal?

A
  • Liquids require a true posterior oral seal whereas solids are ingested with the oral cavity continuous with the pharynx
61
Q
  1. Briefly describe ingestion, stage 1 transport, machinal processing, stage 2 transport and swallowing?
A
  • Ingestion – Food into mouth from external to internal environment and anterior oral seal with lips.
  • Stage 1 transport – Food is gathered up and controlled by tongue tip which them retract to move the food back onto occlusal surfaces of posterior teeth
  • Mechanical processing – solid foods broken and mixed w/saliva before swallowing, bolus squashed against palate and tongue, ood is chewed with premolars and molars
  • Stage 2 transport – Sufficiently masticator bolus moves to the oropharynx by squeeze back mechanism in which bolus is squeezes between the tongue and palate, Solid foods moved through fauces to pharyngeal surfaces of tongue while seal holds liquids at pillars of fauces.
  • Swallowing – Involuntary movements push bolus through pharynx to oesophagus, UOS opens then epiglottis closes to prevent backflow and peristalsis occurs to move bolus toward stomach

BDS4 (24 decks)

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