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Yr 2.0 Sem 4 > Clinical Pharmacology & Prescribing > Flashcards

Clinical Pharmacology & Prescribing Flashcards

1
Q

1 How does random allocation improve the quality of data obtained? 2 marks

A

Random distribution confounding factors between groups including those which are unknown and so otherwise would not be controlled for

Prevention of allocation bias

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2
Q

1 What’s triple blinding?

A

When patient, clinician and investigator/statistician have no knowledge of group allocations

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3
Q

1 What is the basis of the placebo effect?

A

Patients get better partly due to the feeling that something is being done

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4
Q

1 What 5 things does a clinical trial need to be approved by the Research Ethics Committee?

A 
Clinical equipoise of tested intervention / treatment and alternative
Scientifically robust design of study
Ethical recruitment of participants 
Valid consent of participants 
Voluntariness of participants
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5
Q

1 What 3 groups would be considered appropriate or necessary exclusions from a clinical trial?

A

Those for whom the risk is likely to outweigh the benefit e.g. pregnant women
Communities unlikely to benefit from the results of the trial
Non-representative groups who are then likely to be excluded from the analysis

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6
Q

1 What is voluntariness?

A

Choice made free from coercion or manipulation or the perception of these

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7
Q

1 Give 3 examples of how a patients may feel coerced into participating in a clinical trial

A

May believe, or be led to believe, that not participating will result in:
Lack of access to best treatment
Lower quality of care
Disinterest from clinician

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8
Q

1 Give 3 actions that should be avoided to prevent patients feeling or being manipulated into participating in a clinical trial

A

Exploitation of emotional state
Distortion of information
Financial inducements

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9
Q

1 What 4 things do you need for consent to participate in a clinical trial to be valid?

A

Knowledgeable informant
Both verbal and written consent
Cooling off period
Freedom to opt out at any time

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10
Q

1 In which cases must you report adverse drug effects?

A

Paediatric cases
All suspected serious reactions (require or prolong hospitalisation)
Black triangle drugs and herbal remedies

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11
Q

2 In multiple dosing how long does it take to achieve steady state?

A

Depends of the drug: 3-5 half-lives

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12
Q

2 Where can an oral drug be metabolised before reaching systemic circulation? 3 locations

A

Gut lumen
Gut wall
Liver

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13
Q

2 In what 4 circumstances are changes in the protein binding of a drug particularly important?

A 
When a drug has:
High protein binding
Low volume of distribution
Narrow therapeutic window
Or is administered by IV
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14
Q

2 What’s the equation for the apparent volume of distribution (Vd)?

A

total amount of drug in the body
_____________
plasma conc of drug

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15
Q

2 Why are drugs with zero order kinetics more likely to result in toxicity? 2 marks

A

No half life is calculable so results are less predictable

Relatively small dose changes may cause large changes in plasma conc. (and thus lead to toxicity)

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16
Q

2 How do you calculate the required loading dose of a drug?

A

Calculate volume of distribution then
x multiply by x
Target drug conc

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17
Q

2 How does half life of a drug relate to a patient’s renal function?

A

Half life is inversely proportional to renal clearance or GFR

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18
Q

2 What’s the difference between specificity of a drug and selectivity of a drug?

A

Specificity - how well it targets specific receptor sub-types
Selectivity - how many sites it can act at other than the target site

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19
Q

2 What is the therapeutic index of a drug?

A

Relationship between concentration causing adverse effects and concentration causing desired effects

(EC50 adverse effects / EC50 desired effects or toxic dose/effective dose)

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20
Q

2 List 6 common drugs that are inducers of the cytochrome p450 enzyme system

A 
(PC BRAS)
Phenytoin 
Carbamazepine 
Barbiturates 
Rifampisin 
Alcohol - chronic use 
Sulphonyureas and St John's Wort
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21
Q

2 List 9 common drugs that are cytochrome p450 inhibitors

A 
(ODE VICES)
Omerprazole
Disulfiram 
Erythromycin 
Valproate
Isoniazid
Cimetidine and ciprofloxacin 
Ethanol - acutely 
Sulfonamides
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22
Q

2 List 5 categories of drugs that commonly cause drug-drug interactions

A 
(5 Aunties)
Anti-convulsants 
Antibiotics 
Anti-psychotics 
Anti-depressants 
Anti-arrythymics
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23
Q

2 What features of a patient’s medical history would confer an increased risk of adverse drug reactions? Give 4

A

Extremes of age
Co-morbidities / multiple medical problems
Poor renal and/or hepatic function
Polypharmacy

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24
Q

3 What type of arrhythmia is associated with Wolf-Parkinson-White Syndrome?

A

Supraventricular tachycardia (caused by accessory pathway known as Bundle of Kent)

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25
Q

3 What drugs would you use to control heart rate in atrial fibrillation?

A

Bisoprolol, verapamil, dilitiazem +/- digoxin

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26
Q

3 What drugs would you use for Wolf Parkinson White syndrome?

A

Flecainide, amiodarone

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27
Q

3 What drugs would you use acutely for re-entry supraventricular tachycardia?

A

IV adenosine, verapamil, flecainide

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28
Q

3 What drugs would you use to control heart rhythm in a patient with AF?

A

Sotalol, flecainide with bisoprolol, amidarone

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29
Q

3 Which ion channels do class IV antiarrhythmics act on? What action do they have?

A

Calcium channels, blocks them

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30
Q

3 Name 2 Calcium channel blockers

A

Verapamil

Diltiazem

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31
Q

3 Name 2 class III antiarrhythmics

A

Amidarone

Sotalol

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32
Q

3 Give 2 common side effects of beta blockers

A

2 of
Bronchospasm
Hypotension
Cold peripheries

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33
Q

3 List 6 side effects of Amiodarone

A 
Pulmonary fibrosis
Hepatic injury 
Increased LDL
Thyroid disease
Photosensitivity
Optic neuritis (transient blindness, rare)
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34
Q

3 How do class III anti-arrhythmics work?

A

Class III antiarrhythmics prolong the action potential and refractory period, acting primarily by potassium (K+) channel blockade.

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35
Q

9 Which types of antibacterials target DNA synthesis?

A

Quinolones (e.g. ciprofloxacin)

Folic acid antagonists (e.g. Trimethoprim)

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36
Q

9 Which classes of antibiotics inhibit production of bacterial proteins?

A

Macrolides (e.g. Erythromycin)
Aminoglycosides (e.g. Gentamicin)
Tetracyclines

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37
Q

9 Why would beta lactams and glycopeptides be ineffective against a mycoplasma infection?

A

They target cell wall synthesis so would be ineffective against mycoplasma as these don’t have a cell wall.

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38
Q

9 Give 3 types of anti-microbials that have a beta lactam ring in their chemical structure

A

Penicillins
Cephalosporins
Carbapenems

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39
Q

9 Give an example of a glycopeptide

A

Vancomycin

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40
Q

9 How can bacteria acquire resistance to an antibiotic?

A

Chromosomal gene mutation
or
Horizontal gene transfer (gain mutation via plasmids from other bacteria)

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41
Q

9 How can a genetic mutation in a bacterium prevent an antimicrobial being effective on it? (I.e. Molecular mechanism of resistance)

A

Change proteins ->
transport proteins so drug either can’t enter or is effluxed more rapidly
Binding site proteins so drug cant bind
Enzymes to deactivate
drug or to change metabolic pathways to avoid those prevented by the drug

Create new proteins which break down the antibiotic (beta-lactamase).

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42
Q

9 What are the 3 main types of intervention that can be implemented to facilitate antimicrobial stewardship?

A

Persuasive, restrictive, structural

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43
Q

3 What range of cardiac pathologies can Amiodarone be used for ?

A

Wide range, can be used for most arrythmias

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44
Q

3 What effects amiodarone and sotalol both have on the heart?

A

Slow phase 4 of cardiac action potential cycle
Slow AV (atrio-ventricular) node conduction
Slow heart rate
Increase QT interval on ECG

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45
Q

3 What are the 3 main side effects of sotalol?

A

Arrhythmia
Fatigue
Insommnia

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46
Q

3 What is vernakalant used for?

A

Convert recent onset AF to normal sinus rhythm (its an atypical class III anti-arrhythmic)

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47
Q

3 What is the main mechanism of action of class IV anti-arrhythmics?

A

Block calcium channels

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48
Q

3 In treatment of which type of arrhythmia are calcium channel blockers commonly used?

A

Supraventricular tachycardia

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49
Q

3 In the presence of which cardiovascular conditions should you be cautious about prescribing calcium channel blockers?

A

Partial AV block
Hypotension
Decreased cardiac output
Sick sinus syndrome(sinoatrial node disease)

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50
Q

3 Give 2 examples of type IV anti-arrythmics

A

Verapamil

Diltiazem

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51
Q

3 What is digoxin used for?

A

Reducing ventricular rates in atrial fibrillation and flutter
In heart failure to increase cardiac output

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52
Q

3 Why should you avoid prescribing ivabradine to women who are or may become pregnant?

A

Its teratogenicity is unknown

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53
Q

3 What is the main advantage of ivabradine’s mechanism of action?

A

As it slows sinus node by blocking the funny current it can reduce heart rate without dropping the blood pressure

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54
Q

3 How does adenosine slow the heart rate?

A

Binds to A1 receptors and activates K+ currents in AV and SA nodes. This causes hyperpolarisation which decreases action potential duration and thus heart rate.

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55
Q

3 List 3 drugs you could use to treat sinus tachycardia

A 
Amiodarone (class III / Ca channel blocker)
Lignocaine (class 1b)
Metoprolol (class II / beta blocker)
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56
Q

3 List 3 drugs you could use to treat sinus tachycardia

A

Ivabradine
Bisoprolol (beta blocker)
Verapamil (Ca+ channel blocker)

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57
Q

Yr1 Where does most cholesterol in the body come from?

A

Synthesis in the liver (some from diet)

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58
Q

Yr1 Name the 5 classes of lipoproteins

A
  • Chylomicrons
  • VLDL (Very Low Density Lipoproteins)
  • IDL (Intermediate Density Lipoproteins)
  • LDL (Low Density Lipoproteins
  • HDL (High Density Lipoproteins)
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59
Q

Yr 1 Describe the structure of a lipoprotein

A

Shell of phospholipid monolayer containing some cholesterol and apolipoprotein.
Core of triacylglycerol, cholesterol ester and fat soluble vitamins

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60
Q

Yr 1 Which lipoproteins is apoB associated with?

A

VLDL
IDL
LDL

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61
Q

Yr 1 Which apo-lipoprotein is associated with HDL?

A

apoAI

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62
Q

Yr 1 Briefly describe the causes of hyperlipoproteinaemias that are associated w/ coronary artery disease

A

Type IIa - defective LDL receptor
Types IIb, IV and V - defect unknown
Type III - defective apoE

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63
Q

Yr 1 How does raised serum LDL cause atherosclerosis?

A

Oxidised LDL recognised and engulfed by macrophages. These become foam cells and accumulate in intima of blood vessel walls to form fatty streaks. These can evolve to become atherosclerotic plaques.

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64
Q

Yr 1 How can atherosclerosis lead to thrombosis formation?

A

If plaque ruptures, released atherosclerotic activates platelets and the clotting cascade.

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65
Q

3 What are the 4 main classes of lipid lowering drugs used currently?

A

● Statins
● Cholesterol lipase inhibitors (eg ezetimibe)
● Nicotinic acid / niacin
● Fibrates (eg fenofibrate)

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66
Q

3 What are the 3 main actions statins have on lipid metabolism?

A
  • Inhibit cholesterol synthesis in hepatocytes
  • Increase clearance of IDL and LDL
  • Decrease production of VLDL and LDL
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67
Q

3 What are the 2 main indications for use of statins ?

A

Cardiovascular risk prevention (CV Disease + Diabetes)

Familial Hypercholesterolaemia

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68
Q

3 How do statins lower levels of “bad” cholesterol in the blood?

A

Block HMG CoA reductase, a key enzyme in cholesterol synthesis in the liver. Also get increased synthesis of LDL receptor

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69
Q

3 What are the 2 main possible side effects of statins?

A

Increased transaminase levels ( but rapidly reversible, no evidence of chronic liver
disease)
Myopathy
(also gastrointestinal complaints, arthralgias, and headaches )

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70
Q

3 Give 4 Secondary benefits of statin treatment

A 
(Besides lowering LDL and VLDL levels, statins:)
● Anti-inflammatory
● Plaque reduction
● Improved endothelial cell function
● Reduced thrombotic risk
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71
Q

3 How do fibric acid derivatives reduce the production of triglycerides?

A

PPARα (Peroxisome Proliferator-Activated

Receptor) agonists -> inc production of lipoprotein lipase ->

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72
Q

3 What effects do fibric acids have on the metabolism?

A

Increase fatty acid uptake and oxidation
Reduce triglyceride levels
Increases LDL particle size and HDL-C levels
Direct vascular effects

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73
Q

3 Why would you not use statins + gemfibrozil as combination therapy?

A

Higher chance of myopathy (Primarily seen when higher doses of statins are used
in combination with cyclosporine, gemfibrozil, and
occasionally erythromycin and niacin)

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74
Q

3 How does nicotinic acid reduce VLDL?

A

Inhibition of lipoprotein A synthesis

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75
Q

3 Which is the best agent for increasing plasma HDL levels?

A

Nicotinic Acid is the best agent to raise HDL-C

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76
Q

3 Why might you combine nicotinic acid with low dose aspirin?

A

Reduce adverse effects of flushing, itching, headache

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77
Q

3 Why are Active liver disease or unexplained LFT elevations contraindications for nicotinic acid?

A

It’s hepatotoxic

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78
Q

3 What effect does nicotinic acid have on the gut?

A

Can cause GI upset and reactivation of any peptic ulcers

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79
Q

3 What effect does nicotinic acid have on blood sugar?

A

Can cause hyperglycemia and reduced insulin sensitivity

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80
Q

3 Name a cholesterol lipase inhibitor

A

Ezetimibe

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81
Q

3 Give 3 adverse drug reactions caused by ezetimibe

A

Headache, abdominal pain and

diarrhoea

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82
Q

3 Why is the enterohepatic circulation of ezetimibe useful?

A

Delivers agent back to the site of action thus limiting systemic exposure. Also has an active metabolite glucuronide which can then also have an effect in the intestines.

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83
Q

3 What is Evolocumab?

A

Evolocumab (Repatha, Amgen) is a monoclonal
antibody that inhibits PCSK9 (proprotein convertase
subtilisin/kexin type 9)). allowing it to help treat 1’ hypercholesterolaemiaa and mixed dyslipidaemia.

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84
Q

3 What dietary advice would you give someone with high cholesterol?

A

Eat more oily fish and plant sterols / take a supplement.
Eat more foods that are rich in fibre and vitamins C and E.
Try to minimise intake of dietary cholesterol and fat.

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85
Q

3 How would you estimate a patient’s cardiovascular risk?

A

Desktop or internet calculator such as Qrisk2

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86
Q

3 What dose and type of statin would you ideally prescribe a patient who has cardiovascular disease? (NICE 2014)

A

Atorvastatin 80 mg (Use a lower dose of atorvastatin if
any of the following apply: potential drug interactions;
high risk of adverse effects; patient preference )

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87
Q

3 What should you offer if a patient has an estimated 10% or greater 10-year risk of
developing cardiovascular disease? (NICE 2014)

A

Atorvastatin 20 mg

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88
Q

3 List 4 side effects of fibric acid derivatives

A

GI upset, cholelithiasis (gallstones), myositis, abnormal liver function test results

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89
Q

1st yr What is the main cause of systolic heart failure?

A

Ischaemic Heart Disease

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90
Q

1st yr What is Starling’s law?

A

The relationship between cardiac output and end diastolic pressure : “The force developed in a muscle fibre depends on the degree to which the fibre is stretched”

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91
Q

1st yr What causes the thinning of the heart wall in left ventricular systolic dysfunction?

A

– Fibrosis and necrosis of myocardium

– Activity of matrix proteinases

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92
Q

1st yr What is the most frequent cause of right heart failure?

A

Secondary to left heart failure i.e. resulting in congestive / biventricular heart failure

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93
Q

Yr 1 What are the main symptoms of left heart failure?

A

Fatigue

Exertional dysponoea, orthopnoea and paroxysmal nocturnal dyspnoea

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94
Q

Renal/CPT4 How does activation of the Renin-Angiotensin-Aldosterone System increase the production of aldosterone?

A

Renin from the kidney catalyses breakdown of angiotensinogen into angiontensin I. This is then cleaved into Angiotensin II by Angiotensin-Converting-Enzyme. Angiotensin II stimulates the adrenal cortex to produce more aldosterone.

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95
Q

Renal/CPT4 What are the 3 main actions of angiontensin II?

A

Stimulates the adrenal cortex to produce more aldosterone.
Stimulates kidney tubule cells to increases salt and water retention
Vasoconstriction

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96
Q

4 Why is it important to treat high blood pressure?

A

Lowering diastolic BP (even by 10mmHg) is
associated w/ dec risk of stroke (by 58%)
and coronary heart disease (by 37%)

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97
Q

4 What is the most common aetiology of hypertension?

A

Primary/Essential hypertension - where there is no single evident cause (90% hypertensive pop)

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98
Q

4 What is the 1st Line UK

Pharmacological Therapy for hypertension?

A

ACE inhibitors / Angiotensin Receptor Blockers (ARB)

or Calcium channel blockers

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99
Q

4 Name 2 ACE inhibitors (that were mentioned in our lecture)

A

Lisinopril

Ramipril

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100
Q

4 What is the main side effect of ACE inhibitors?

A

Dry cough (occurring in 10-15%)

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101
Q

4 Why would an ACE inhibitor not be your 1st line treatment if your patient is black?

A

Typically not as effective and increased risk of angio-oedema as an adverse drug reaction

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102
Q

4 Why would you want to monitor serum creatinine, urea, potassium, sodium and eGFR for a patient on ACE inhibitors?

A

Can cause renal failure and hyperkalaemia

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103
Q

4 What 2 angiotensin receptor blockers were named in our lecture?

A

Losartan, Candesartan

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104
Q

4 What are the 3 main groups of Calcium Channel Blockers?

A
  • Dihydropyridines (eg Nifedipine, Amlodipine)
  • Benzothiazepines ( eg Diltiazem)
  • Phenylalkylamines (eg Verapamil)
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105
Q

4 How much of Dihydropyridines e.g. amlodipine would you expect to become protein bound in the body?

A

Majority (>90%)

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106
Q

4 Where are Dihydropyridines e.g. amlodipine metabolised?

A

In the liver

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107
Q

4 What are the most common side effects of Dihydropyridines e.g. amlodipine?

A

• Sympathetic nervous system activation – tachycardia
and palpitations
• Flushing, sweating, throbbing headache
• Oedema

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108
Q

4 What are the 3 main side effects of verapamil?

A

Constipation
Bradycardia
Reduced myocardial contractility

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109
Q

4 What type of calcium channel blocker is diltiazem?

A

Benzothiazepine

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110
Q

4 What is the dose-blood pressure response curve like for Thiazide and Thiazide-Like Diuretics ?

A

Flat

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111
Q

4 According to NICE guidence when should calcium channel blockers be used for hypertension?

A

As 1st line in patients >55yo or who are black
As an adjunct to ACE inhibitors or Ang II blockers where appropriate blood pressure could not be achieved with these alone

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112
Q

4 Why is combination prescribing useful for managing hypertension?

A

Can use lower doses of each drug and so limit adverse effects

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113
Q

4 What is the main contraindication for use of beta blockers?

A

Asthma

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114
Q

4 What are the most common side effects of beta-blockers?

A 
Lethargy, impaired concentration
Reduced exercise tolerance
Bradycardia
Cold hands – Raynaud’s
Impaired glucose tolerance
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115
Q

4 What are the 3 main lifestyle modifications recommended for patients with heart failure ?

A

Reduce salt intake
Drink less alcohol
Do more aerobic exercise

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116
Q

4 How do beta blockers reduce myocardial oxygen demand?

A

Reduce heart rate by antagonising cardiac beta receptors

Negative inotropic effect (lowers stroke vol & blood pressure)

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117
Q

4 How would you manage class I heart failure?

A

Reduce risk factors and treat hypertension, diabetes mellitus coronary artery disease and dyslipideamia if present. Start ACE inhibitor or angiotensin receptor blocker

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118
Q

4 Why do you need to be really careful when using beta blockers for heart failure?

A

The failing myocardium is dependent on heart rate

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119
Q

4 What 3 things are important to do if starting a heart failure patient on beta blockers?

A

Initiate on low dose and Titrate up slowly

Alter other medications if necessary e.g. diuretic

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120
Q

4 State 2 metabolic effects of beta blockers

A

Reduce mobilisation of glycogen

Negate unwanted effects of catecholamines

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121
Q

4/urinary What are the 4 categories of functions of the kidneys?

A
  • Regulatory
  • Excretory
  • Endocrine
  • Metabolism
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122
Q

4 What 4 endocrine substances do the kidneys (excl adrenal glands) secrete?

A

Renin
Erythropoetin
Prostaglandins
1-alpha calcidol (active Vitamin D)

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123
Q

4 What effects do Loop diuretics have on ion transport in the nephron?

A

(act at thick ascending limb of Loop of Henle) Inhibit NaCl reabsorption
Concurrent Ca/Mg excretion

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124
Q

4 How can kidney function affect diabetes mellitus?

A

Kidneys metabolise insulin, if their function is impaired insulin present in blood for longer

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125
Q

4 What is the main difference between ADH antagonists and other diuretic drugs?

A

ADH antgonists cause pure diuresis (water loss), other diuretics also cause naturesis (sodium loss) (and sometimes kaliuresis/K+loss too)

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126
Q

4 Why are carbonic anhydrase inhibitors that block Na+ reabsorption in proximal convoluted tubule not make very good diuretics?

A

Causes inc reabsorption of Na+ downsteam in nephron limiting its naturetic effects.
Also causes sodium bicarbonate diuresis which will cause metabolic acidosis (+ kidney stones)
Also can get hypophosphateamia.

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127
Q

4 When is mannitol used clinically?

A

For cerebral oedma / for intracerebral pressure

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128
Q

4 How does lithium affect the kidney?

A

Inhibits action of ADH so often causes polyuria (with pure water loss)

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129
Q

4 What is demeclocycline used for?

A

SIADH (antagonises ADH so can lose the excess water)

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130
Q

4 Why is amiloride a weaker diuretic than aldosterone antagonists?

A

Amiloride only blocks ENaC channels while aldosterone anatgonists prevent inserteion of ENaC AND basolateral Na+K+ATPases

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131
Q

4 What is the main advantage and main disadvantage for using Eplerenone rather than Spironolactone?

A

+ Fewer side effects (as selective to aldosterone receptor)

- More expensive

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132
Q

4 What is tolvaptan mainly used for?

A

Prevent cyst enlargement in polycystic kidney diease (also can be used for hyponatreamia)

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133
Q

4 Generically, what are the 4 main types of possible adverse drug reactions that are associated with diuretics?

A
  • Allergy - Anaphylaxis / photosensivity rash etc
  • Hypovolaemia and hypotension
  • Electrolyte Disturbance
  • Metabolic Abnormalities
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134
Q

4 How can diuretics lead to acute kidney injury?

A

Can cause hypovoleamia

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135
Q

4 What are the 5 main possible side effects of thiazide diuretics?

A
  • Gout (can cause de novo or precipitate attacks)
  • Hyperglycaemia
  • Erectile dysfunction
  • ↑LDL ↑Triglycerides
  • Hypercalcaemia
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136
Q

4 What are the 3 main side effects of spironolactone?

A

•Hyperkalaeia
• Impotence
• Painful
gynaecomastia (10-15%)

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137
Q

4 What are the 4 main side effects of frusemide?

A
  • Ototoxicity
  • Alkalosis
  • ↑LDL ↑TG
  • Gout
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138
Q

4 What is the main side effect unique to Bumetanide?

A

Myalgia (also has all side effects of frusemide)

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139
Q

4 What is the main risk of using aminoglycoside antibiotics with Loop Diuretics?

A

Hearing loss, potentially irreversible as both ototoxic

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140
Q

4 What are the 5 main drugs/categories of drugs that interact with thiazide diuretics?

A 
Digoxin
Beta Blockers
Steroids
Lithium (lithium toxicity)
Carbamazepine
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141
Q

4 What are the 4 main drugs or categories of drugs that interact with Loop diuretics?

A

Aminoglycoside antibiotics
Steroids
Digoxin
Lithium (reduced lithium levels)

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142
Q

4 What are thiazides mainly used for?

A

Hypertension (cause vasodilation as well as diuresis)

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143
Q

4 Why would you not use Loop Diuretics for hypertension?

A

Only act for a few hours (but are used in renal failure)

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144
Q

4 What is spinronolactone used for in heart failure?

A

In combi w/ loop diuretics as cardioprotective, reduces cardiac remodelling and mortality

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145
Q

4 What diuretics would you use in decompensated liver disease?

A

Spironolactone

Loop diuretics

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146
Q

4 What is the 1st line drug type for nephrotic syndrome?

A

Loop diuetcis

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147
Q

4 What type of diuretics would you use to treat the salt and water retention in chronic kidney diease?

A

Loop diuretics
+/- thiazide like
(typically AVOID K+ sparing)

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148
Q

4 Give 4 reasons why diuretics may be less effective in patients with chronic disease

A

May have:
Oedmatous gut -> poor absorption into bloodstream
Poor cardiac output so diuretics don’t reach kidney quickly
Hypoalbumineamia so less drug can bind to albumin and be delivered to kidney
Dysfunctional nephron inhibiting delivery of drug to site of action

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149
Q

4 How does furosemide get from the blood to its site of action?

A

Organic anion transporters into PCT cells, then travels in nephron lumen to Thick Ascending Limb of Loop of Henle

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150
Q

4 How would you manage a patient with refractory oedema?

A

• Check salt intake (24 hour
sodium excretion if necessary)
• Give furosemide IV if gut oedema likely
• Find minimum effective dose
• Give repeated bolus or infusion (short t1/2)

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151
Q

4 What are the 4 main conditions aldosterone antagonists are used for?

A

Heart failure, ascites,
hypertension,
hyperadrenalism

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152
Q

4 Name 4 commonly used theraputics that are potentially nephrotoxic

A
  • Aminoglycosides (e.g. gentamicin)
  • IV Vancomycin
  • Aciclovir
  • NSAIDs
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153
Q

4 Why would you not give Metformin to a patient with renal dysfunction?

A

Increased risk of metabolic acidosis

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154
Q

4 Why do NSAIDs cause problems with kidney perfusion?

A

Block prostaglandins which vasodilate afferent arteriole when BP low (ie inhibit autoregulation)

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155
Q

4 Why do ACE inhibitors and Angiotensin receptor blockers cause problems with kidney perfusion?

A

Block auto-regulatory effects of Angiotensin II: vasoconstriction of efferent arteriole when BP low

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156
Q

4 What are the 4 main things you should consider when prescribing to patients w/ chronic kindey disease?

A

Avoid nephrotoxins Avoid gentamicin / vancomycin if at all possible
Check with pharmacist! (also BNF)
Side effects may be increased eg morphine (due to accumulation of metabolites)

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157
Q

4 What are the most common causes of hyperkalaemia?

A

Muscle / tissue damage
Kidney dysfunction
Drugs that cause K+ retention
(These are often in combination)

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158
Q

4 Why should you act immediately after any ECG change in a patient with hyperkaelmia?

A

Hyperkalaemia can cause life-threatening cardiac arrhythmias and ECG changes are progressive

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159
Q

4 What is the sequence of ECG changes that occur in untreated hyperkalamiea?

A
  • Tall T waves
  • Small or absent P waves
  • Increased P-R interval
  • Wide QRS complex
  • ‘Sine wave’ pattern
  • Asystole!!
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160
Q

4 How do you treat hyperkalaemia?

A
  1. Calcium gluconate (protect heart)
  2. Insulin + dextrose
    (to lower serum K+, can use salbutamol if there’s a hospital shortage)
  3. Calcium resonium (to remove K+) + laxative
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161
Q

4 Besides treating the hyperkalaemia, what else do you need to do for a patient with high K+?

A

Identify cause

Do an ECG

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162
Q

5 What are the 4 main actions of insulin?

A
  • Stimulates uptake of glucose into liver, muscle and adipose tissue
  • Decreases hepatic glucose output via inhibition of gluconeogenesis
  • Inhibits glycogenolysis
  • Promotes uptake of fats
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163
Q

5 Which region of the insulin molecule is altered in the production of insulin analogues with different rates of absorption?

A

B26-30 region

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164
Q

5 What are the 6 main categories of insulin analogue drugs?

A
  • Ultrafast acting
  • Rapid acting
  • Short acting
  • Intermediate acting
  • Long acting
  • Very long acting
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165
Q

5 What is the physiological range of blood glucose?

A

4-7 mmol/L

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166
Q

5 What are the 5 main potential adverse effects of insulin therapy?

A 
• Hypoglycaemia
• Hyperglycaemia
• Lipodystrophy – lipohypertrophy or
lipoatrophy
• Painful injections
• Insulin allergies
167
Q

5 Name the 7 types of drugs, other than insulin that can be used for type 2 diabetes

A 
Biguanides Sulphonylureas
Thiazolidinediones
DPP4 inhibitors
α-Glucosidase inhibitors, SGLT2s
GLP1 analogues
168
Q

5 Can T2DM be treated without medications?

A

Yes, significant weight loss eg via bariatric surgery or very low calorie diets can cause remission

169
Q

5 What are the 2 main reasons that T2DM have poor adherence to pharmacological therapies?

A

Risk / perceived risk of hypoglycemia

Weight gain / fear of this

170
Q

5 What is the NICE HbA1c target range for Type 2 Diabetes Mellitus?

A

6.5 to 7.5%

171
Q

5 What are the 3 main effects of metformin that lead to its use in type 2 diabetes?

A 
Reduces:
insulin resistance 
hepatic
gluconeogenesis
CVS events 
(also limits weight gain)
172
Q

5 What is the mechanism of action of Sulphonylureas eg Gliclazide?

A

Stimulate beta cells of pancreas to release insulin (also found to decrease microvascular risk)

173
Q

5 What are the 2 main side effects of Sulphonylureas?

A

Weight gain

Hypoglycaemia

174
Q

5 What are glifozins used for?

A

Add on therapy for patients with Type 1 or 2 diabetes mellitus

175
Q

5 How does dapagliaflozin work?

A

Selectively inhibits SGLT2 in renal PCT increasing urinary excretion of glucose (NB insulin independent action)

176
Q

5 What are the main side effects of glifozins?

A

Genital candida infections and UTIs esp in women

Polyuria

177
Q

5 How do Gliptins increase insulin secretion?

A

Inhibit DPP4 -> increases postprandial active GLP1 concentrations.
GLP1 increases insulin secretion

178
Q

5 What are the main side effects of GLP1 agonists eg exenatide?

A

GI symptoms such as nausea, loose stools and diarrhoea and gastro-oesphageal reflux

179
Q

5 How are GLP1 agonists administered?

A

IM injection

180
Q

9 what are the five main types of adverse effects caused by antibiotics?

A 
Toxicities
allergic reactions
idiosyncratic reactions
ecological effects (C.diff, resistance)
drug interactions
181
Q

9 what is the MIC?

A

MIC is the minimum concentration of antibiotic that is required to inhibit growth of the bacteria in vitro

182
Q

9 what is the breakpoint of an antibiotic?

A

A breakpoint is a chosen concentration (mg/L) of an antibiotic which defines whether a species of bacteria is susceptible or resistant to the antibiotic. (If the MIC is less than or equal to the susceptibility breakpoint the bacteria is considered susceptible to the antibiotic. If the MIC is greater than this value the bacteria is considered intermediate or resistant to the antibiotic.)

183
Q

9 State 2 characteristics of a patient may affect the pharmacokinetics of an antibiotic

A

Body size and body composition

184
Q

9 When is therapeutic drug monitoring required?

A

When there is a narrow therapeutic window for the agent used, monitoring is required to ensure dose is both adequate and non-toxic. (Aminoglycosides, glycopeptides

185
Q

9 What is an XDR infection?

A

XDR infection is extensively drug-resistant, meaning there is no susceptibility to at least one agent in all but two or fewer antimicrobial categories

186
Q

9 list four ways in which a system can be structured to facilitate good antimicrobial stewardship

A

Computerised records
rapid lab tests
expert systems
quality monitoring

187
Q

6 what are the two strongest types of scientific evidence?

A

Meta analyses and systematic reviews

188
Q

6 what for features of systematic reviews make them generally unbiased and objective?

A

They have explicit assumptions
transparent methodology
and reproducible results

189
Q

6 what is the definition of a systematic review?

A

“An overview of primary studies that used explicit and reproducible methods”

190
Q

6 what is the definition of a meta-analysis?

A

Quantitative synthesis of the results of two or more primary studies that address the same hypothesis in the same way

191
Q

6 what is the most important reason for using a meta-analysis?

A

To quantify effect sizes and their uncertainty as a pooled estimate

192
Q

6 for a meta-analysis to be considered high quality what should its formal protocol specify?

A

Compilation of complete set of studies
identification of common variable category definition
standardised data extraction
analysis allowing for sources of variation

193
Q

6 how you calculate the lower confidence interval?

A

Value (odds ratio etc) divided by the error factor

194
Q

6 if the confidence interval of a odds ratio has 1 within its range what does it mean?

A

The null hypothesis is within the range of the 95% confidence interval it means the result could be due to chance

195
Q

6 which model of probability does a Forest Plot use?

A

Fixed effect model

196
Q

6 what does the size of each box in the forest plot represent?

A

Either that it was a big study or it had very low uncertainty in the odds ratio of both (The size of each box indicates the weight given to each study. Studies are weighted according to their size and the uncertainty of the odds ratio.)

197
Q

6 what’s the diamond in a forest plot for?

A

The diamond-shaped is the pooled estimate with the centre indicating the pooled odds ratio and the width representing the port 95% confidence interval

198
Q

6 what are the three main problems of performing meta-analysis?

A

Heterogeneity between studies
variable quality of the studies
publication bias in selection studies

199
Q

6 explained the two main approaches that exist for modelling for variation when calculating the pooled estimate odds ratio and its 95% confidence interval?

A

Fixed effect model – assumes that the studies are estimating exactly the same true effect size
Random effects model – assumes that studies are estimating similar, but not the same, effect size

200
Q

6 if you have high heterogeneity between studies that you are using from meta-analysis what should you do?

A

Use random effects modelling to account for the variation

Perform subgroup analysis to attempt to explain the heterogeneity

201
Q

6 describe the two types of possible subgroup analysis

A

Stratification by study characteristics.

Stratification by participant profile – fortunately data is often unavailable for this.

202
Q

6 list three ways in which variable quality of the studies within a meta-analysis can occur?

A

Poor design of studies.
Poor design protocol.
Poor protocol implementation.

203
Q

6 Which type of epidemiological study is the most prone to bias and confounding?

A

Case-control studies

204
Q

6 Explain what publication bias is

A

The phenomenon where studies were statistically significant or “favourable” results are more likely to be published and those studies with non-statistically significant or unfavourable results – this particularly applies to small studies

205
Q

6 list three ways in which publication bias in selection of studies for meta-analysis can be minimised

A

Unpublished studies should also be searched for an identified.
Should plot results identified studies against a measure of their size i.e. funnel plot.
Uses statistical test for publication bias.

206
Q

6 why are the results of a statistical test for publication bias for a meta-analysis not very useful?

A

These tend to be weak statistical tests

207
Q

6 what with the funnel plots of studies included in a meta-analysis that controlled well for publication bias look like?

A

Results spread evenly throughout the funnel, on both sides of the pooled estimate line / balanced or symmetrical

208
Q

6 what are the three main features of a meta-analysis?

A

Quantitative synthesis of primary data.
Summary of effect sizes and their uncertainty.
Forest plot to display these results

209
Q

First year what’s the difference between incidence and prevalence?

A

Incidents refers to new cases per person per year.

Prevalence refers to cases as a proportion of the population (has no units)

210
Q

First year Name the Purine DNA nucleotides

A

Adenine and guanine.

Pyramidines = cytosine and thymidine

211
Q

First year. Name the stages of the cell cycle

A 
G0 (dormant phase)
G1 (cell contents except chromsomes duplicated)
S-phase (DNA synthesis)
G2 (double check of replicated DNA, any necessary repairs)
M phase (mitosis)
212
Q
  1. Explain the fractional cell kill hypothesis of chemotherapy
A

Chemo drugs administered in pulses, allowing enough time between rounds for the cells of bone marrow to recover but not for the tumour cells to recover

213
Q
  1. Name five types of tumour that are highly sensitive to chemotherapy
A 
Lymphomas.
Germ-cell tumours.
Small-cell lung tumours.
Neuroblastoma.
Wilms' tumours (nephroblastomas)
214
Q
  1. Name four times of tumour that have low sensitivity to chemotherapy
A

Prostate
Renal cell
Brain tumours
Endometrial

215
Q
  1. What the four main types of chemotherapy agents?
A

Anti-metabolites.
Alkylating agents.
Intercalating agents.
Spindle poisons

216
Q
  1. At what point in the cell cycle do anti-metabolites act?
A

DNA synthesis/S-phase

217
Q
  1. Which type of cytotoxic agents act on DNA?
A

Alkylating agents

218
Q
  1. How do you intercalating agents kill cells?
A

Prevent DNA transcription and DNA duplication by forming a permanent bond between DNA strands

219
Q
  1. How are platinum compounds cytotoxic?
A

Because formation of platinated inter- and intra- strand adducts lean to inhibition of DNA synthesis (they are alkylating agents)

220
Q
  1. How do the taxoid class of spindle poison chemotherapy agents work?
A

Taxoids promote the assembly of spindle microtubules and prevent their disassembly, thus preventing the separation of chromatids into the two poles of the replicating cell

221
Q
  1. What do vinca alkaloids do to prevent the completion of mitosis?
A

Vinca alkaloids prevent spindle formation by inhibiting microtubule assembly.

222
Q
  1. How can cells become resistant to the action of alkylating agents?
A

Decreased entry or increased exit of agent.
Inactivation of agent within the cell.
Enhanced repair of DNA lesions produced by alkylation

223
Q
  1. How can chemotherapy drugs be administered intrathecally?
A

Drugs can be administered into the CSF via lumbar puncture or omaya reservoir (interventricular catheter)

224
Q
  1. Why is Hickman line tunnels under the skin before reaching the subclavian vein?
A

When under the skin it is protected from infection by resident macrophages

225
Q
  1. Name two types of IV pumps for chemotherapy
A

PICC line.

Hickman line

226
Q
  1. List 3 ways in which chemotherapy can adversely affect the cardiopulmonary system
A

Pulmonary fibrosis.
Cardiotoxicity.
Phlebitis.

227
Q
  1. Why are chemotherapy patients more prone to infection?
A

Chemotherapy causes myelosuppression

228
Q
  1. Describe the common GI side effects of chemotherapy
A

Nausea.
Vomiting – acutely, delayed onset (2 to 5 days), chronic phase (up to 14 days).
Diarrhoea.
(GI perforation at site of tumour has been reported in lymphoma)

229
Q
  1. Describe how chemotherapy can cause acute renal failure
A

Rapid tumour lysis can lead to hyperuriceamia leading to precipitation of urate crystals in renal tubules (agents to prevent this are now given before chemotherapy)

230
Q
  1. At what point in chemotherapy would you expect alopecia to develop?
A

Hair thins at 2 to 3 weeks

231
Q
  1. What sign may you see in the hands of a patient who has had chemotherapy?
A

Beau’s lines on the nails (horizontal lines one for each round of chemo)

232
Q
  1. How does mucositis caused by chemotherapy present?
A 
Typically worst in oropharynx 
May cause:
Sore mouth/throat
Diarrhoea
GI bleed
233
Q
  1. What effects can chemotherapy have on the heart?
A 
Chemotherapy can cause cardiomyopathy (esp doxorubicin, also high dose cyclophosamide)
or arrhythmias (cyclophosamide, etoposide)
234
Q
  1. What is the most frequent cause of death from chemotherapy toxicity?
A

Haematological toxicity e.g. neutrophils linked to sepsis, platelets leading to excessive bruising and bleeding

235
Q
  1. What blood test/s would need to be done before a specialist prescribes cisplatin chemotherapy?
A

Renal function panel – urea and electrolytes

236
Q
  1. What can cause variability in the pharmacokinetics of chemotherapy?
A

Abnormalities in:
absorption – GI problems
distribution – ascites, weight loss
elimination – liver and renal dysfunction
protein binding – low albumin, other drugs

237
Q

5 What effects may oestradiol have on a patient’s plasma lipid profile?

A

Raises HDL, lowers LDL

238
Q

5 What 6 side effects can oestrogen commonly cause?

A 
Breast tenderness
Nausea, vomiting
Water retention
Increased blood coagulability
Thromboembolism
Impaired glucose tolerance
239
Q

5 Which cancers does oestrogen increase the risk of? What cell changes are associated with these?

A

Endometrial - hyperplasia
Ovarian - metaplasia
Breast - hyperplasia

240
Q

Repro How does progesterone maintain pregnancy?

A

Keeps endometrium in secretory state

241
Q

5 What 4 psychological side effects can progesterone cause?

A

Irritability
Depression
PMS
Poor concentration

242
Q

5 Why might you avoid progesterone-only types of contraception for a women suffering from acne vulgaris?

A

Acne can be a side effect of these so may make it worse

243
Q

5 What metabolic effects does testosterone have?

A

Reduces HDL-C/LDL-C ratio

Anabolic

244
Q

5 How are oestrogens and testosterone transported in the body?

A

Bound to SHBG and albumin

245
Q

5 What is the main mechanism of action of combined oral contraceptives?

A

Suppression of ovulation by inhibiting FSH and LH (negative feedback loop)

246
Q
  1. What are the two supporting modes of action of the combined oral contraceptive pill?
A

Increased viscosity of cervical mucus

Keep endometrium in atrophic state / prevent secretory phase

247
Q
  1. What are the 4 main cardiovascular adverse effects that can be caused by the oral combined contraceptive pill?
A

Venous thromboembolism
Myocardial infarction
Hypertension
Increased risk of stroke in women w/ focal migranes

248
Q
  1. List 4 important metabolic adverse effects associated w/ the combined oral contraceptive pill?
A

Decreased glucose tolerance
Cholestatic jaundice
Increased incidence of gallstones
Precipitation of porphyria

249
Q
  1. Why is the combined oral contraceptive pills efficacy reduced by “enzyme inducing” drugs?
A

Enzyme inducing drugs increase production of hepatic cytochrome P-450, the enzyme that metabolises COCP. Faster metabolism of drug leads to faster excretion.

250
Q
  1. How do you Soya protein products effect the COCP?
A

So protein products enhance oestrogen absorption and reduces storage in adipose and muscle – >half-life reduced from 15 to 7 hours

251
Q
  1. What do you need to advise the patient to do in the case of a missed contraceptive pill?
A

If they’ve missed one pill:
take the last pill immediately even if it even if means taking 2 in 1 day
Missed 2 pills - anywhere in pack:
Same as above but use extra contraception for 7 days

+ If <7 pills left in pack after last missed pill, skip pill break (/inactive pills)

252
Q
  1. How does the progestin only pill (POP/minipill) work?
A

Thickens cervical mucous and induce premature secretory change in endometrium
(also inhibit ovulation but this is only reliable in newer formulations eg desogestrel)

253
Q
  1. What are the indications for prescribing HRT?
A

Relief of peri-menopausal and menopausal symptoms

eg hot flushes/sweats and vaginal dryness / dysparenunia

254
Q
  1. What are the 2 main types of combined HRT regimen?
A

Sequential - 28 days oestrogen + progestin for last 12-14 days
Continuous

255
Q
  1. What is the main advantage of a non-oral route of administration for HRT?
A

Only oral delivery systems for HRT have adverse effects on thromboembolism profile
(inc activated protein C resistance,
inc thrombin activation,
decreased anti-thrombin III activity and levels of protein S levels, Factor Vii and tissue factor pathway inhibitor)

256
Q
  1. What is the risk of giving oestrogen only HRT (ERT)?
A

More likely to develop endometrial and/or ovarian cancers

257
Q
  1. What are the cardiovascular risks and benefits of HRT?
A

Increased risk of stroke and ischeamic disease

But beneficial effect on lipid profile (inc HDL-C, dec oxoLDL-C, triglyceride and lipoprotein a)

258
Q
  1. What does clomiphene do?
A

Induces ovulation by inhibiting oestrogen-receptor binding thus inhibiting negative feedback resulting in inc FSH and LH.

259
Q
  1. How does Tamoxifen affect breast cancer?
A

Binds to oestrogen receptors in breast tissue to block myoepithelial cell division
(NB also causes induction of ovulation)

260
Q
  1. By what mechanism does Mifepristone cause medical termination of pregnancy?
A

Partial agonisation of progesterone receptors, inhibiting action of progesterone.
Sensitises uterus to prostatglandins
(also used for induction of labour)

261
Q
  1. Cyproterone is an anti-androgen progesterone derivative. What is its mechanism of action?
A

Partial agonist at the progesterone receptor, competing with dihydrotestosterone.
Weak progestogenic effect

262
Q
  1. What is cyproterone used for?
A

In certain combined contraceptive pills like Dianette

Can be used to treat advanced prostate cancer

263
Q
  1. What are the indications for use of finasteride, a 5-alpha reductase inhibitor?
A

Male pattern baldness
Benign prostatic inhibitor
(5 alpha reducatase catalyses breakdown of testosterone into 5alpha-dihydrotestosterone)

264
Q
  1. What methods of administration are available for testosterone replacement?
A

Implant (pure testosterone)
IM (enenthate, proprionate)
Oral (Undecanoate, Mesterolone)

265
Q
  1. What are SERMs (selective estrogen receptor modulators) e.g. Raloxifene (Evista) used for?
A

Protect against osteoporosis post menopause.
Also has beneficial effects on lipid metabolism and blood coagulation and reduced risk of breast cancer (in postmenopausal women w/ osteoporosis)

266
Q
  1. What is the main side effect of the SERM drug Raloxifene?
A

Increases hot flushes / flashes - briefly feel hot and sweaty

267
Q

1st yr What happens in the G phases of the cell cycle?

A

G1 - cellular contents except chromsomes duplicated

G2 - duplicated chromosomes double checked and any necessary repairs made

268
Q

7 What is the main ADR of microtubule poisons?

A

Glove and stocking distribution of neuropathy

269
Q

7 What are Xenon, N2O fluroxene and desflurane all used for clinically?

A

They’re all volatile general anaesthetics

270
Q

7 How would you administer propofol, barbituates or etomidate to induce general anasthesia?

A

Intravenously

271
Q

7 What do Guedel’s signs describe?

A

The stages of CNS effects produced by general anaesthesia

272
Q

7 Describe the 4 stages of CNS effects produced by general anaethesia

A

Stage 1: analgesia, conscious
Stage 2: unconscious breathing erratic +/- delirium
Stage 3: surgical anaethesia 4 levels of depth until breathing weak
Stage 4: respiratory paralysis

273
Q

7 What is the antatomical substrate for the MAC of volatile anaethetics?

A

Spinal cord

274
Q

7 What partition coefficients are anaethetics subject to?

A

Blood:gas partition
Oil:gas partition

275
Q
  1. What 5 factors INcrease MAC of an anaesthetic?
A 
Being young
Hyperthermia
Pregnancy
Alcoholism
Central stimulants
276
Q
  1. Which 3 types of drugs would DEcrease the MAC of an anaesthetic?
A

Other anaethetics eg Nitrous Oxide
Sedatives
Opioids

277
Q
  1. Which receptors do Xe, N2O and ketamine probably act on?
A

NMDA

278
Q
  1. By what mechanism do the majority of anaesthetics depress CNS activity?
A

Potentiating GABA(A) mediated Cl- conductance inducing hyperpolarisation on neurone membranes.

279
Q
  1. Why might you not form memories while under conscious sedation?
A

If hippocampus is depressed by the anaethetics

280
Q
  1. How do general anaesthetics induce analgesia?
A

Depress doral horn of spinal cord

281
Q
  1. What are the 5 main things local and regional anaesthesia are used for?
A 
Dentistry
Obstetrics
Regional surgery (where pt is awake)
Post-op for wound pain
Chronic pain managment
282
Q
  1. Name 4 local anaesthetics
A

Lidocaine
Bupivacaine
Ropivacaine
Procaine

283
Q
  1. How do general anaesthetics send you to sleep? (induce unconscious)
A

Depress reticular formation (hindbrain, midbrain and thalamus) by potentiating GABA receptors

284
Q
  1. What are the 4 very common side effects of general anaesthesia?
A

Post-op nausea and vomiting (PONV)
Post-op cognitive dysfunction (POCD)
Chest infection
Hypotension

285
Q
  1. What is usual cause of side effects of local and regional anaesthetics?
A

Systemic spread of agent/s

eg Locals are Na+ channel blockers so may cause CV toxicity

286
Q
  1. What is the aim of regional anaesthesia?
A

Selectively anaesthetising a part of a body / “blocking” a nerve so that the patient remains awake

287
Q
  1. What are the 4 main categories of immunosuppressants?
A

Steroids (prednisolone, methylprednisolone)
Biological agents (adalimumab, infliximab)
Cytokine inhibitors (cyclosporine, tacrolimus)
Antimetabolites (methotrexate, azathioprine)
(NB Janus Kinase inhibitors are also starting to be used)

288
Q
  1. What is the mechanism of action of corticosteroids?
A

Bind to intracellular cytoplasmic receptors, activated receptor then binds to nucleus (NB some pass through nuclear membrane to act on receptors there)
Either promote or inhibit gene transcription, usually to prevent IL1 and IL6 by macrophages. Also inhibit all stages of T cell activation.

289
Q
  1. What is the gold standard treatment for Rheumatoid Arthritis?
A

Methotrexate

290
Q
  1. Give 3 inflammatory disease that methotrexate is liscensed to treat
A 
eg
Psoriasis
Psoriatic arthritis
Crohn's disease
RA
291
Q
  1. What is the mechanism of action of methotrexate (in malignant disease)?
A

Competitively and irreversibly inhibits dihydrofolate reductase, an enzyme required for DNA / RNA synthesis and hence proetin production. (Dihydrofolate reductase catalyses the conversion of dihydrofolate to the active tetrahydrofolate the key carrier of one-carbon units in purine and thymidine synthesis)

292
Q
  1. What are the 3 main suggested mechanisms of action for methotrexate in non-malignant disease such as RA?
A

Inhibition of enzymes involved in purine metabolism, leading to accumulation of adenosine. Adenosine is a regulatory autocoid that interacts w/ specific GPCRs on inflamm and immune cells to regulate their function.
Inhibition of T cell activation
Suppression of intercellular adhesion molecule expression by T cells

293
Q
  1. How frequent should dosing of methotrexate be?
A

Weekly NOT DAILY

as metabolized to polyglutamates with long half lives

294
Q
  1. Why do you need to be careful if using NSAIDs with methotrexate?
A

Methotrexte is normally 50% protein bound and NSAIDs will displace it

295
Q
  1. How do patients tend to find being on methotrexate?
A

Generally well tolerated w/ pts continuing on it for longer than any disease modifying RA drugs (50% on it for >5 yrs)
Improved quality of life.

296
Q
  1. Why do female patients need reliable contraception if on methotrexate?
A

It is highly teratogenic and abortifacient (causes miscarriage)

297
Q
  1. Which 2 adverse effects of methotrexate can be relieved w/ folic acid supplementation?
A

Mucositis

Marrow suppression

298
Q
  1. What are the 6 main ADRs of methotrexate?
A 
Mucositis
Marrow suppression
Inc infection risk
Hepatitis
Cirrhosis
Pneumonitis
299
Q
  1. What are the 3 main effects of sulfasalazine on T cells?
A

Inhibition of proliferation and IL2 production

May induce T cell apoptosis

300
Q
  1. Besides its effects on T cell, how else does sulfasalazine exert its effects ?
A

Reduces chemotaxis and degranulation of neutrophils

301
Q
  1. What is sulfasalazine most useful for treating and why?
A

IBDs

as it is poorly absorbed and so its main activity is w/n the colon

302
Q
  1. How is methotrexate excreted?
A

Renally (thus must be mindful of kidney function)

303
Q
  1. What are the main 4 ADRs of sulfasalazine, that are not common to all immunosuppressants?
A

Rash
Nausea
Abdo pain
Vomiting

304
Q
  1. What are the 6 main advantages of using sulfasalazine to treat IBD?
A
  • Effective
  • Favourable toxicity
  • Long term blood monitoring not always needed
  • Very few drug interactions
  • No carcinogenic potential
  • Safe in pregnancy
305
Q
  1. What are the 5 main uses of azathioprine?
A

For maintenance tharpy in SLE/lupus vasculitis
IBD
Atopic dermatitis
Bullous skin disease
(also other uses as a steroid sparing drug)

306
Q
  1. Why is it important to test TPMT activity before prescribing azathioprine?
A

TPMT metabolises the active metabolite of the drug, 6-MP, but individuals vary markedly in its activty as its gene is highly polymorphic. If TPMT levels are low or absent there is a risk of myelosuppression.

307
Q
  1. How does azathioprine inhibit RNA/DNA synthesis?
A

Progressively cleaved into 2 active metabolites:
6MeMPN which inhibits purine synthesis
6TGN which is incorporated into DNA preventing its replication fork progressing

308
Q
  1. What are the 4 main ADRs of immunosuppressants?
A

Myelosuppression
Inc risk maligancy and infection
Hepatitis

309
Q
  1. What is the main use of mycophenolate mofetil?
A

Transplant patients
Also lupus nephritis
(but also increasingly used for inflammatory diseases)

310
Q
  1. List 3 of the most common side effects of mycophenolate mofetil
A

Nausea
Vomiting
Diarrhoea

311
Q
  1. What are the 2 mechanisms of action of mycophenolate mofetil?
A

Inhibits DNA/RNA synthesis by inhbiting inosine monophosphate dehydrogenase, an enzyme needed for guanosine synthesis
Impairs B and T cell proliferation

312
Q
  1. What are the 5 main indications for use of cyclophosphamide?
A

Lymphoma, leukaemia, solid cancers
Lupus nephritis (though mycophenolate mofetil is safer and just as effective)
ANCA vasculitis

313
Q
  1. What is the importance of p450 system in regards to cyclophosphamide?
A

Cyclophosphasmide is a pro drug, converted into its active forms by cyctochrome p450 in the liver

314
Q
  1. Why do you need to give Mesna and/or aggressively hydrate your pt when giving cyclophosphamide?
A

Cyclophosphamide is excreted renally.
One of its metabolites, arcolein, is toxic to the bladder epithelium and can lead to haemorrhagic cystitis.
Mesna and hydration prevent this

315
Q
  1. Which 3 cancers does cyclophosphamide increase the risk of?
A

Bladder cancer
Lymphoma
Leukaemia

316
Q
  1. Why might you want to avoid prescribing cyclophospahmide for a young patient who has not yet completed their family?
A

Risk of infertility which relates to cumulative dose and pt age

317
Q
  1. What is the mechanism of action of the monoclonal antibody drugs adalimumad, infliximad and gloimumab?
A

Bind to and block TNFalpha to reduce inflammation, angiogensis and joint destruction

318
Q
  1. How does TNFalpha induce inflammation?
A

TNFalpha is resposnible for cytokine cascade leading to recruitment of leukocytes to joints which then elaborate adhersion molecules and produce chemokines.

319
Q
  1. How does TNFalpha induce joint destruction?
A

TNFalpha can stimulate:
MMPs and other destructive enzymes
Bone resorption and erosion
Cartilage breakdown

320
Q
  1. How can anti-TNF therapy cause reactivation of latent TB?
A

TNFalpha released by macrophages in response to TB infection, induces development and maintenance of granulomas which contain the bacilli, protecting the body.

321
Q
  1. What is the mechanism of action of rituximab?
A

Binds specifically to CD20, a unique cell surface marker on B cells which present antigens, or produce cytokines or antibodies; to cause apoptosis.

322
Q
  1. What are the main uses of rituximab?
A

RA (v effective + good safety data)

Lupus and vasculitis - esp in young pts to preserve fertility

323
Q
  1. What are ciclosporin and tacrolimus typically used for?
A

Widely used in transplant pts

also for atopic dermatitis and psoriasis

324
Q
  1. What do you need to monitor in patients taking ciclosporin or tacrolimus?
A

BP
eGFR (due to renal toxicity)
What drugs they’re taking - multiple interactions possible via p450

325
Q
  1. What is the mechanism of action of ciclosporin and tacrolimus?
A

Bind to specific proteins; resultant complexes then bind to calcineurin, preventing its phosphatase activity on the nuclear factor of activated T cells that would normally migrate to the nucleus to start IL2 transcription.

326
Q
  1. What are the main side effects of corticosteroids?
A

hypertension, increased infection risk, osteoporosis, GI irritation, bruising/thinning of the skin, weight gain - central obesity, mood changes (psychosis/depression), increased insulin resistance (diabetes)

327
Q
  1. What are the 4 categoriesof common analgesics?
A

Non-narcotics/opiods
Narcotics/opiods
NSAIDs/non-steroidal anti-inflammatories
Neuropathic agents

328
Q
  1. What 6 types of drugs are used as adjuvants for analgesics?
A 
Antidepressants
Anticonvulsants
Antispasmodics
Muscle relaxants
Biphosphonate
Corticosteroids
329
Q
  1. What are the 2 main proposed mechanisms of action of paracetamol?
A

Indirect prostaglandin H2 synthase inhibition
Activation of serotenergic pathway - descending inhibition on pain pathway
(nobody knows for sure how paracetamol works)

330
Q
  1. What is the toxic metabolite of paracetamol and when is it produced?
A

NAPQI

produced when conjugation is saturated due to overdose

331
Q
  1. What is the principle behind using N-Acetylcysteine/NAC for paracetamol overdose?
A

Replenish liver’s supply of glutathione so that it can inactivate toxic NAPQI

332
Q
  1. What are the 3 main opioid receptors?
A

µ - mu (analgesia, euphoria)
δ - delta (analgesia, dysphoria)
Κ – kappa (analgesia, sedation)

333
Q
  1. By what mechanism do opiates induce analgesia?
A

Bind to opiate receptors (Gi protein coupled) ->
Inhibits adenyl cyclase ->
Decreases cAMP ->
Decreased influx of Ca2+ ->
Reduced neurotransmitter release ->
Reduced transmission of nociceptive impulses

334
Q
  1. What are the 3 non-analgesic indications for use of opioids?
A

Cough suppression
Manage diarrhoea
Breathlessness

335
Q
  1. What is the “antidote” drug for opioid toxicty
A

Naloxone

336
Q
  1. What are the 6 main ADRs of opiate drugs?
A 
Constipation
Reduced conscious level 
Respiratory Depression
Nausea and Vomiting
Confusion
Constricted pupils
337
Q
  1. What do you need to add to a prescription of a controlled drug?
A

Explicit statement of number and dose of tablets required - with number in words and numberals

338
Q
  1. Name 7 autacoids that signal inflammatory responses
A 
Bradykinins
Histamine
Cytokines
Leukotrienes
Nitric Oxide
Neuropeptides
Eicosanoids – Includes Prostaglandins
339
Q
  1. What do COX do?
A

synthesise prostaglandins, catalysing the production of pg’G’ from arachidonic acid and Pg’H’ from Pg’G’

340
Q
  1. What is the main role of COX1?
A

Cytoprotective - consitutively expressed by many tissues incl gastric mucosa, myocardium, renal parenchyma - ensures optimised local perfusion to reduce ischeamia

341
Q
  1. When is COX2 expressed?
A

When induced by inflammatory mediators / autacoids eg bradykinin due to injurious stimuli

342
Q
  1. Why are NSAIDs of a larger molecule size less likely to induce side effects?
A

COX1, which is responsible for most of the ADRs, has a smaller active site than COX-2 which is responsible for most of the therapeutic effects.

343
Q
  1. What type of receptors do prostaglandins bind with?
A

Prostaglandins bind with GPCRs (of different types to induce different actions)

344
Q
  1. How do prostaglandins induce vasodilation?
A

Prostaglandins have potent effects on vasodilation indirectly synergizing the effects of bradykinin/histamine.

345
Q
  1. Which prostaglandin is most important in mediating the inflammatory response?
A

Prostaglandin E

346
Q
  1. Describe the process by which prostaglandins D, E, F and I are formed
A

Cell membrane phospholipids are cleaved by phospholipase a to arachidonic acid.
This is then converted to prostaglandin G which is then converted to prostaglandin H in reactions catalysed by COX.
PG H is then converted to prostaglandin D, E, F and I the specific prostaglandin enzymes.

347
Q
  1. Exactly which type of receptor is responsible for prostaglandins’ effects on peripheral nociception?
A

EP 1 GPCRs of Gq type (of C-type neurons)

348
Q
  1. Exactly which type of receptor is responsible for prostaglandins effects on vasodilation following injury?
A

EP 2 GPCRs of Gs type

349
Q
  1. How does prostaglandin-receptor binding increase C fibre activity?
A

Increases neuronal sensitivity to bradykinin and Na+ channels sensitivity.
Inhibition of K+ channels.
(May also activate previously silent C fibres)

350
Q
  1. What effect does sustained peripheral nociceptive signalling have?
A

Increased cytokine levels in dorsal horn cell body (causing inc COX2 and ProstaglandinE2 synthesis ie local sensitisation)

351
Q
  1. How does prostaglandinE2 binding to its receptor (EP2) increase pain perception?
A

PGE2-EP2 binding, releases Gs protein (from the GPCR), increasing levels of cyclicAMP and ProteinKinaseA. This reduces glycine receptor affinity hence removing glycinergic inhibition on pain transmission. (Also inc sensitivity and discharge rate of other 2’ neurons).

352
Q
  1. What effect does ProstglandinE2 binding to EP3 receptor (a Gi type GPCR) have?
A

Results in both increased heat production and decreased heat loss -> pyrexia

353
Q
  1. How do bacterial endotoxins induce Prostaglandin2 synthesis?
A

They stimulate macrophage release of interleukin-1 which then acts within the hypothalamus to stimulate prostaglandin E2 synthesis.

354
Q
  1. How do (the vast majority of) NSAIDs achieve their pharmacological action?
A

Competitive inhibition of Cox 1 and Cox 2 (Occupation of COX-1 / 2 hydrophobic channel by NSAID competes with AA site occupation)

355
Q
  1. Why is it important to be careful of polypharmacy that includes NSAIDs?
A

Many NSAIDs heavily protein bound (up to 90-99%) so may cause competitive displacement if used w/ other highly protein bound drugs.

356
Q
  1. List 4 commonly used highly protein bound drugs
A 
NSAIDs
sulphonylureas
warfarin
methotrexate
(obviously many others see BNF/Google)
357
Q
  1. What order pharmacokinetics to NSAIDs have within the therapeutic dose ranges?
A

NSAIDs have linear pharmacokinetics within the therapeutic dose ranges.

358
Q
  1. Which patients are most likely to get renal ADRs (Na+/K+/Cl- and H20 retention, inc risk hypertension) from NSAIDs?
A

Compromised individuals w/ heart failure, renal disease, hepatic cirrhosis or hypovolaemia esp neonates and elderly. (as NSAIDs further reduce renal blood flow due to reduced Prostaglandins E2 and I2)

359
Q
  1. How common are GI ADRs from NSAID use?
A

Pretty common (around 35%) though often asymptomatic

360
Q
  1. How can NSAID use lead to stomach ulcers?
A

Inhibition of gastric COX1 which normally stimulate cytoprotective mucus secretion. reduce acid secretion and promote mucosal blood flow.

361
Q
  1. If long term NSAID use is necessary, what can you prescribe to protect the GIT?
A

PPIs or misoprostol

362
Q
  1. What are the 5 main important ADRs for NSAIDs in adults?
A

GI - pain, bleeding, ulcers etc
Renal - Na+/K+/Cl- and H20 retention -> hypertension
Vascular - inc bleeding time
Bronchial asthma in 10% asthmatics
Skin rashes, usually mild but rarely can get Steven Johnson syndrome

363
Q
  1. Why don’t we give aspirin to kids?
A

Risk of Reyes syndrome in <16s - rare and serious brain/liver injury usually in viral infections treated w/ aspirin

364
Q
  1. Why are specific COX2 inhibitors eg rofecoxib and celecoxib not used long term?
A

Inc risk CVS ADRs w/ long term use (in clinical trials)

365
Q
  1. Why do we use NSAIDs in combination w/ opiates?
A

Extends therapeutic range for treating

Reduces ADRs seen w/ opiates alone

366
Q
  1. How does unconjugated NAPQI damage the liver?
A

NAPQI is highly reactive and nucleophilic -> binds w/ cellular macromolecules / mitochondria -> loss of function primarily leads to necrotic hepatic cell death

367
Q
  1. What are the specific treatment options for paracetamol overdose?
A

If seen 0-4 hrs - oral activated charcoal to reduce uptake (50-90%)
Start N-Acetylcysteine IV if seen w/n 36 hrs, otherwise oral methionine

368
Q
  1. When do the hepatoxic effects of paracetamol OD peak?
A

72-96 hrs post ingestion

369
Q

6./1st yr How does the metabolism of paracetmol change at high doses (overdose)?

A

Becomes zero order.
Phase II conjugation into sulfate and glucuronide becomes saturated, leading to inc Phase I oxidation. This results in inc NAPQI1, detoxified by phase II conjugation w/ glutathione until glutathione becomes depleted (then NAPQI1 accumulates.)

370
Q

9./1st year. What are the 6 main stages of viral replication?

A

1 attachment (via specific host cell surface receptors
2 penetration (fusion into host cell either directly or through endocytosis and pH mediated fusion)
3 uncoating (virion disassembly)
4 replication/protein synthesis
5 assembly
6 release (via lysis of host cell or intra-or extracellular budding)

371
Q
  1. Name the 2 antivirals available for influenza a and B
A

Oseltamivir (Tamiflu) – taken orally

Zanamivir – inhaled/intranasally

372
Q
  1. What is the mechanism of action of antivirals for influenza?
A

These are neuraminidase inhibitors blocks release of newly assembled influenza virions from the host cell

373
Q
  1. What is the main drawback for use of antivirals for flu?
A

Need administeriing w/n 48 hrs of infection (will then reduced intensity & duration of symptoms, can also be used prophylactically but vaccination is preferred approach)

374
Q
  1. Name the drug used for HSV 1 or 2 and state it’s mechanism of action
A

Aciclovir (IV, oral or topical cream)

Inhibits viral DNA synthesis (by providing purine/pyramidine analogues)

375
Q
  1. What viral mutation has been attributed to aciclovir resistance?
A

Thymidine kinase enzyme mutation (prevents binding to aciclovir so it can’t act as a false substrate in DNA replication anymore)

376
Q
  1. What is ganciclovir used for?
A

Currently used for CMV retinitis in immunocompromised and CMV prophylaxis in transplant patients (administered IV)

377
Q

9 What are the 4 main side effects of ganciclovir?

A 
(action: inhibits viral DNA synthesis)
Myelosuppression
Cancer
Birth defects
Accumulation in real failure (as renally cleared)
378
Q
  1. What is lamivudine used for and what is its mechanism of action?
A

Used in HIV/Hep B Mechanism = reverse transcriptase inhibitor (acts as false substrate and chain terminator of reverse transcriptase enzyme in viral replication)

379
Q
  1. What is sofosbuvir used for and how does it work?
A

Hepatitis C

It blocks action of HCV viral polymerase to prevent production of new virus

380
Q
  1. How does interferon alpha work?
A

Immunomodulatory effect - Not directly antiviral but stimulate proteins to enhance cellular resistance to viral infection

381
Q
  1. Describe the adverse effects of interferon alpha
A

In the first hours to days : flu-like illness, fever, chills, headache, malaise, myalgia, arthralgia, nausea, vomiting, diarrhoea

382
Q
  1. What is Ribavirin used for and what are the 2 main adverse effects it causes?
A

Chronic hep C (in combo w/ interferon alpha)
Severe RSV in infants
Transient anaemia, Teratogenic

383
Q
  1. How does ribavirin work?
A

Guanosine analogue: inhibits guanosine triphosphate formation preventing viral messenger RNA capping. Essentially prevents assembly of viral genome/DNA

384
Q
  1. Name the 5 main categories of drugs used to treat HIV
A

NRTIs (Nucleoside Reverse Transcriptase Inhibitors)
NNRTIs (Non-nucleoside Reverse Transcriptase Inhibitors)
PIs (Protease inhibitors)
INIs (Integrase inhibitors)
R5 (Receptor inhibitors)

385
Q
  1. List 4 major adverse reactions that Nucleoside Reverse Transcriptase Inhibitors (e.g. zidovudine) cause
A

Hyperlactataemia
Lactic acidosis
Hepatomegaly + steatosis (possibly fatal)

386
Q
  1. What is the main indication of surgery for GORD?
A

If oesophageal cancer develops / likely to develop (metaplasia)

387
Q
  1. Why shouldn’t PPIs be used on a PRN basis?
A

Only reach max. efficiency after 2-3 days

388
Q
  1. How do alginates (eg Gaviscon) relieve GORD?
A

Viscous nature allows them to adhere to and protect damaged mucosa

389
Q
  1. What are the 2 main adverse effects of PPI drugs?
A

2 of:
Diarrhoea
Inc risk of C.diff infection
Inc risk of osteoporosis

390
Q

11/GI Which type of cell do PPIs act on?

A

Parietal / oxyntic cells

391
Q
  1. Why might you not want to prescribe a H2 antagonist to a young man?
A

Can cause gynacomastia

392
Q
  1. What is dyspepsia?
A

Combination of heart burn, acid taste in mouth

and nausea/vomiting (often caused by GORD)

393
Q
  1. How we test for H.Pylori infection?
A

Carbon-13 urea breath test

or Stool antigen test And ensure the pt hasn’t had PPIs in the past 2 wks, or antibiotics in the past 4

394
Q

11/GI What symptoms would prompt an urgent referral for endoscopy if associated w/ GORD?

A 
Haematemesis
Melaena
Weight loss
Abdominal mass
(esp if age >55yo)
395
Q
  1. What is the UHL treatment of choice for H.Pylori?
A

1 week “triple therapy” of
Clarithromycin (500mg BD)
Amoxycillin (1g BD)
and Lansoprazole (30mg BD)

396
Q 
What do the following prescription abbreviations mean:
AC
BD
PRN
(DR
EC
HS
stat
qad/qod) ?
A 
AC  - before meals (ante cibum)
BD -twice a day
PRN - as needed (pro re nata)
(DR - delayed release
EC - enteric coated
HS - bedtime [hora somni]
stat - immediately [statis]
quad/qod - every other day )
397
Q
  1. Explain what is meant by a cause-effect relationship in an epidemiological context
A

A cause is an exposure or factor that increases the probability of disease (Exposures do not have to be either necessary or sufficient to be important causes)

398
Q
  1. If there is an TRUE association between 2 factors, A and B, what explanations are there besides A causing B (i.e. a true causal association)?
A

Unknown confounding factor
Common cause
Reverse causality (B->A not A>B as assumed)

399
Q
  1. Give 4 ways that 2 factors may be observed to be associated but in fact are not
A

Confounding by known, possible or unknown factors
Selection bias (eg group not representative of study pop, comparison not fair)
Information bias (differential: recall, observation, measurement, classification)
Chance (p value >0.05 so cannot reject null hypothesis)

400
Q
  1. List Bradford Hill’s 9 criteria for inferring causality (1965)
A

Strength, Specificity and Consistency of association
Temporal sequence (factor precedes outcome: RCT and prospective cohort good for this)
Dose response (biological gradient)
Reversibility
Coherence of theory (w/ current science)
Biological plausibility Analogy (w/ other diseases, specie or settings)

401
Q
  1. What are the 3 strongest types of scientific evidence?
A

Meta-analyses
Systematic Reviews
Randomised Controlled Trials

402
Q
  1. What is the definition of statistics?
A

“Statistics is the collection, presentation, description and analysis of data (sometimes themselves called ‘statistics’) which are measurable in numerical forms.” (purpose is to generalise/infer characteristics to the population)

403
Q
  1. Define epidemiology
A

Epidemiology is the study of the distribution and determinants of health-related states or events (including disease), and the application of this study to the control of diseases and other health problem

404
Q

10./path Describe the factors which may cause abnormal blood clotting

A

Virchow’s triad:
abnormal blood, vessel or flow - i.e. Hypercoagulability
Vascular damage
Circulatory stasis

405
Q

10./path Which clotting factors are unique to the intrinsic pathway of the coagulation cascade?

A

XII
XI
IX
VIII

406
Q

10./path Which clotting factor does tissue fcator activate?

A

Factor VII

407
Q
  1. How does warfarin work?
A

Antagonism of hepatic vitamin K resulting in production of non-functional clotting factors (VII, IX, X and II) and thus reduced clotting of blood.

408
Q
  1. Why should patients on warfarin avoid excessive alcohol intake?
A

In high amounts alcohol acts as enzyme inhibitor so will reduce effects of warfarin.

409
Q
  1. What effect do most drugs that interact w/ warfarin have?
A

Most increase anti-coagulant effect of warfarin

410
Q
  1. Why is pregnancy an issue if you want to start warfarin?
A

Warfarin crosses placenta and is teratogenic in 1st trimester and can cause brain haemorrhage in 3rd trimester.

411
Q
  1. How should you change a patient’s warfarin if they are scheduled for surgery?
A

Stop warfarin 3 days prior to surgery (NB half life 48 hrs ish)

412
Q
  1. What should you do if a heparinised patient starts bleeding seriously?
A

Manage bleeding as per any other pt + Stop their heparin
Monitor APTT if unfractionated
Give protamine sulfate (dissociates heparin from anti-thrombin III)

413
Q
  1. What are the 2 main types of heparin?
A

1) Low molecular weight heparin (daily SC e.g. Dalteparin 3-4kDa)
2) Unfractionated heparin (IV bolus followed by infusion, SC for prophylaxis 20kDa)

414
Q
  1. Why can’t you give heparin PO?
A

Poor GI absorption

Yr 2.0 Sem 4 (4 decks)

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