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PED2007 Flashcards

1
Q

What is hypertension

A

high blood pressure
leads to heart attacks and leading cause of death

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2
Q

what are the impact of cardiovascular disease

A
  • heart attacks
  • strokes
  • heart failure
  • chronic kidney disease
  • peripheral arterial disease
  • vascular dementia
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3
Q

what are the risk factors of CVD

A
  • obesity
  • physical inactivity
  • smoking
  • drinking
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4
Q

what are the treatments of CVD

A
  • antihypertensives
  • statins
  • anticoagulants
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5
Q

what can be used to detect CVD

A
  • hypertension
  • high cholesterol
  • atrial fibrillation
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6
Q

what is atrial fibrillation

A
  • rapid, irregular heartbeat
  • heart rhythm irregularity
  • can cause blood clot
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7
Q

what is high cholesterol

A
  • build up of fatty deposits in arteries
  • can cause ischaemic heart disease
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8
Q

how to lower cholesterol levels

A
  • diet
  • stop smoking
  • reducing weight
  • use of statins
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9
Q

what is the range of blood pressure for stage 1 hypertension

A
  • 140/90 mmHg to 159/99 mmHg and subsequent ABPM daytime average
  • HBPM average blood pressure ranging from 135/85 mmHg to 149/94 mmHg
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10
Q

what is stage 2 mechanism for diagnosing hypertension

A
  • blood pressure of 160/100 mmHg or higher but less than 180/120 mmHg and subsequent ABPM daytime avergae
  • HBPM average blood pressure of 150/95 mmHg or higher
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11
Q

what mechanism should prevent sustained elevations in arterial blood pressure

A
  • baroreceptor reflex
  • in hypertension, its reset itself to a higher level. nerve activity reduces with high blood pressures
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12
Q

what is essential hypertensions and how does this differ from secondary hypertension

A
  • high blood pressure that doesn’t have a known cause is called essential hypertension.
  • secondary hypertension has a known cause
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13
Q

what is essential hypertension

A
  • develops overtime
  • haemodynamic characteristics change over time with patients younger than 40 the cause is mainly associated with high cardiac output with normal total peripheral resistance
  • older patients tend to have normal/reduced cardiac output but high total peripheral resistance
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14
Q

what is linked to secondary hypertensions

A
  • sleep apnoea
  • kidney disease
  • thyroid disease
  • diabetes
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15
Q

what is secondary hypertension

A
  • caused by an underlying condition
  • appear suddenly and cause high blood pressure
  • linked to kidney problems, adrenal gland tumours, thyroid tumours, medications
  • malignant hypertension is a severe, often acute form of hypertension which carries a significant risk of cardiovascular events. this should be managed as a matter of urgency
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16
Q

briefly describe the renin-angiotensin-aldosterone system

A

sympathetic nerves switch on renin release from kidney. this converts angiotensinogen I (inactive) ACE enzyme converts angiotensin I to angiotensin II (active)

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17
Q

angiotensin II effects

A
  • stimulates adrenal cortex to release aldosterone
  • causes release of ADH
  • stimulates thirst
  • causes vasoconstriction
  • cardiac and vascular hypertrophy
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18
Q

what happens when the adrenal cortex is stimulated

A
  • aldosterone released
  • promotes sodium and fluid retention in the kidney
  • fluid volume increases
  • blood volume increases and blood pressure rises
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19
Q

implications of ADH release from pituitary

A
  • promotes water reabsorption in the kidneys
  • fluid volume increase
  • blood volume increases and blood pressure increases
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20
Q

implications of vasoconstriction

A
  • increases blood pressure
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21
Q

what are the implications of cardiac vascular hypertrophy

A
  • more muscle mass
  • in heart increases cardiac output and thus blood pressure
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22
Q

what is the biggest risk factor of hypertension

A

left sided heart failure

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23
Q

which drug/drug class would you initially prescribe to a 46 year old Caucasian man recently diagnosed with hypertension

A
  • too old for beta blocker (under 40 appropriate) - the younger the patient the more likely it is driven by cardiac output
  • ACE inhibitor or angiotensin 2 receptor blocker
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24
Q

what are the endings for different classes of drugs

A
  • ACE inhibitor = end in pril
  • beta blockers = end in ol
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25
Q

side effects of ACE inhibitors

A
  • alopecia
  • angina
  • angioedema
  • chest pains
  • constipation
  • dizziness
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26
Q

which drug/drug class would you initially prescribe to a 51 year old man of African Caribbean origin recently diagnosed with hypertension and who does not have type 2 diabetes

A

calcium channel blocker because ACE inhibitors don’t work as well

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27
Q

which drug/drug class would you initially prescribe to a 65 year old woman of caucasian origin recently diagnosed with hypertension who does not have diabetes

A

calcium channel blocker

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28
Q

what are the side effects if amlodipine

A
  • cariogenic shock
  • constipation
  • drowsiness
  • gastrointestinal disorders
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29
Q

side effects of ca blockers

A
  • dizziness
  • flushing
  • headache
  • nausea
  • palpitations
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30
Q

the 46 year old caucasians origin following use of an ACE inhibitor does not show a significant improvement towards his target blood pressure and it is decided to change his treatment. what would you of next

A
  • check mediation is taken correctly
  • keep him on ACE inhibitor but add in either a calcium channel blocker or thiazide like diuretic
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31
Q

the 51 year old man of African Caribbean origin following use of calcium channel blocker does not show a significant improvement towards his target blood pressure and it is decided to change his treatment. what would you do next

A
  • check medicine is taken correctly
  • keep him on the calcium channel blocker but either add in ARB, or thiazide-like diuretics
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32
Q

which patients are more susceptible to problems due to excessive fluid loss due to diuretics (increases loss of urine)

A

diabetes
elderly

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33
Q

what are the effects of thiazides

A
  • hypokalaemia can occur and is dangerous in severe cardiovascular disease and in patients also being treated with cardiac glycosides
  • constipation
  • electrolyte imbalance
  • headache
  • postural hypotension
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34
Q

what are the effects of indapamide

A
  • hypersensitivity
  • skin rashes
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35
Q

what drugs could be considered for patients still not responding to step 3 of treatment

A
  • consider low dose spironolactone diuretic, if the serum potassium level is not elevates
  • if contraindicated or ineffective, consider alpha or beta blockers
  • if still not responding to the combination of drug, see expert advice
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36
Q

what is an example of a calcium channel blocker

A

amlodipine

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37
Q

what do calcium channels blockers act on

A

myocardial muscle
myocardial conducting system
vascular smooth muscle

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38
Q

what is the effect of a calcium channel blocker on myocardial muscle

A

inhibit contractability

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39
Q

what is the effect of a calcium channel blocker on mycardial conducting system

A

inhibit formation and propagation of depolarisation

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40
Q

what is the effect of calcium channel blockers on vascular smooth muscle

A

coronary or systemic vascular tone reduced - vasodilation

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41
Q

what are the the pharmacokinetics of amlodipine

A
  • oral route - bioavailability 60%
  • half life 30-50hrs
  • steady state plasma concentrations 7 to 8 days
  • liver CYP450 - slowly metabolised
  • poor renal elimination
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42
Q

what is an example of an ACE inhibitor

A

lisinoprile

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43
Q

what is the mechanism of ACE inhibitors

A

inhibits the angiotensin - converting enzyme in the renin angiotensin system

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44
Q

what are the pharmacokinetics of lisinopril

A
  • oral administration - 25% bioavailability
  • peak plasma concentration 4-8hrs - half life 12 hrs
  • water soluble - not metabolised in liver and undergoes renal excretion unchanged
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45
Q

what is an example of ARBs

A

losartan

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46
Q

what is the mechanism of action of ARBs

A

selective competitive blockers of angiotensin II at the AT1 receptors

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47
Q

what are the pharmacokinetics of losartan

A
  • oral administration - 32% bioavailability
  • first pass metabolism 14% to active metabolite which is more potent, non-competitive and longer acting
  • cytochrome p450 metabolism - half life of 2h and 3-9h for metabolite
  • extensive plasma protein binding
  • excreted in urine and bile
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48
Q

what are the contraindication of ARBs

A

combination with renin inhibitor in patients with reduced eGFR and in patients with diabetes mellitus

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49
Q

what are the cautions of ARBs

A

use in African-carribean patients - particularly those with left ventricular hypertrophy; elderly patients

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50
Q

what are the contraindications of losartan

A

severe cardiac failure, pregnancy, severe hepatic impairment

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51
Q

what are the side effects of losartan

A

anaemia; hypoglycaemia; postural disorders

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52
Q

what are the side effects of ARBs

A

abdominal pain, diarrhoea, dizziness; headache; hyperkalaemia

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53
Q

what is an example of thiazide-like diuretics

A

indapamide

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54
Q

what is the mechanism of action of thiazide-like diuretics

A

inhibition of Na+ and cl- reabsorption from the distal convoluted tubules by blocking the Na+ - Cl- symporter. at lower doses vasodilation is more prominent than diuresis

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55
Q

what is the site of action of thiazide-like diuretics

A

act on the reabsorptive process in the distal convolute tubule

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56
Q

when is indapamide useful

A
  • low dose thiazide such as indapamide sufficient for therapeutic effect
  • higher doses - marked changes in plasma K+, Na+, uric acid, glucose and lipid
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57
Q

what are the pharmacokinetics of indapamide

A
  • oral administration act within 1 to 2hrs
  • administered early in the day doe diuresis does not interfere with sleep
  • duration of action 12 to 24hrs
  • 75% plasma protein bound
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58
Q

what are the contraindications of thiazides

A

Addisons disease
electrolyte imbalance

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59
Q

what are the cautions associated with thiazide-like diuretics

A
  • diabetes; gout; hyperaldosteronism; malnourishment; nephrotic syndrome
  • history of hypersensivity to sulphonamides
  • avoid in severe liver disease
  • thiazides are ineffective if renal function is low
  • indapamide acute porphyria
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60
Q

what are the side effects of indapamide

A
  • hypokalaemia can occur and is dangerous in severe cardiovascular disease and in patients also being treated with cardiac glycoside
  • constipation; electrolyte imbalance; headache; postural hypotension
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61
Q

what are the side effects of indapamide

A

hypersensitivity
skin rashes

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62
Q

what is spironolactone

A
  • anti-hypertensive in patients with resistance hypertension
  • blocks aldosterone-induced Na reabsorption - causes Na+ and H2O loss, K+ retention
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63
Q

what is the mechanism of action off spironolactone

A

K-sparing diuretics inhibit the action of aldosterone on the collecting ducts. by themselves are weak diuretics but are important for the sparing of K . Often used in conjugation with other more potent diuretics

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64
Q

what is an example of an alpha blocker

A

doxazosin

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65
Q

what is the job of alpha blockers

A
  • blocker arterial alpha 1 receptors
  • postural hypertension
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66
Q

when are beta blockers used

A
  • not a preferred initial therapy for hypertension
  • may be considered in younger children
  • women of child bearing potential
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67
Q

what are the cautions of beta blockers

A

intolerance or contraindication to ACE inhibitors and ARBs

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68
Q

what the the types of heart failure

A
  • acute or chronic
  • left sided
  • right sided
  • biventricular failure
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69
Q

what is left sided failure

A

commonest - due to hypertension

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70
Q

what is right sided failure

A

cor pulmonale - chronic lung disease

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71
Q

what is biventricular failure

A
  • both chamber often affected
  • left ventricular causes pulmonary congestion which can then lead to right sided failure
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72
Q

what is class 1 heart failure

A

no symptoms during normal physical activity

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72
Q

what is class 2 heart failure

A
  • comfortable at rest
  • normal physical activity triggers symptoms
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72
Q

what is class 3 heart failure

A
  • comfortable at rest
  • minor physical activity triggers symptoms
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72
Q

what are the clinical features of heart failure

A
  • reduced ejection fraction <40% in echocardiogram - stroke volume reduced
  • hypotension - tiredness and dizziness
  • reduced urine flow
  • cold periperpheris
  • breathlessness
  • oedema
  • atrial fibrillation
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73
Q

what is class 4 heart failure

A
  • unable to carry out physical activity without discomfort
  • many have symptoms even when resting
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73
Q

what are the symptoms of systolic left sided heart failure

A
  • increase in volume of blood left in the left ventricle at the end of contraction
  • end systolic volume increases
  • as more venous return refills the left ventricle during diastole the reduced systolic emptying leads to end diastolic volume increasing
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74
Q

what are the symptoms of left sided heart failure

A
  • reduced ventricular compliance may lead to diastolic dysfunction resulting in left sided heart failure
  • pressure in the ventricle during diastole is increased because of stiffness of the ventricular wall
  • end diastolic volume reduces due to reduced filling of the ventricle
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75
Q

how do you initially treat heart failure

A

HF with reduced cardiac function (ejection fraction <40%)
first line treatment - ACE inhibit plus beta blocker

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76
Q

stages of treating heart failure with reduced ejection fraction - spironolactone

A
  • aldosterone antagonist - spironolactone as add-on therapy
  • improves survival in chronic heart failure
  • contraindicated if hyperkalaemia or renal impairment
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76
Q

what is the action of canrenone

A
  • blocks aldosterone-induced production of sodium transport proteins in the DCT
  • causes Na+ and H2Oloss
  • K+ retention
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76
Q

what is the second line of treatment of chronic heart failure

A

mineralocorticoid receptor antagonist - spironolactone

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77
Q

what drugs used to treat chronic heart failure

A
  • ivabradine
  • digoxin
  • SGLT2 inhibitors - dapagliflozin
  • sacubitril valsartant
  • hydralazine with nitrate
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78
Q

when is ivabradine used to treat heart failure

A
  • used for treatment of angina and mild to severe chronic heart failure
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79
Q

what is the action of ivabradine

A
  • inhibit if current reducing cardiac pacemaker activity
  • slows heart rate
  • alternative to beta blockers
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80
Q

what are the contraindications of ivabradine

A

mi
cariogenic shock
heart block
slow heart rates

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81
Q

what are the cautions associated with ivabradine

A
  • ineffective if atrial fibrillation present
  • elderly
  • angina
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82
Q

what are the side effects of ivabradine

A

arrhythmias
AV block
dizziness
headache

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83
Q

how can sacubitril valsartan be used to treat heart failure

A
  • sascubritil inhibits the breakdown of natriuretic peptides increased diuresis, natriuresis and vasodilation
  • may be used in patients not currently taking an ACE inhibitor or ARB
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84
Q
A
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85
Q

what is the contra-indication of sacubitril valsartan

A

systolic blood pressure <100 mmHg

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86
Q

what are the side effects of sacubitril valsartan

A

anaemia
cough
diarrhoea
dizziness
electrolyte imbalance
headache
hypoglycaemia
hypotension
nausea
renal impairments
syncope
vertigo

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87
Q

when is hydralazine with nitrate used to treat heart failure

A

patients intolerant of both ACE inhibitors and ARBs

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88
Q

what is the use of venodilators

A
  • reduced pre-load
  • reduce the risk of pulmonary congestion
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89
Q

what is the use of arterial vasodilators

A
  • reduce after load
  • increase stroke volume
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90
Q

what are the contraindications of hydralazine with nitrate

A

acute prophyrias
cor pulmonale
dissecting aortic aneurysm
poor cardiac function
tachycardia

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91
Q

what are the side effects of hydralazine with nitrate

A

angina
headaches
tachycardia
diarrhoea
dizziness
flushing
gastrointestinal disorders

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92
Q

what are the cautions of hydralazine with nitrate

A

cerebrovascular or coronary artery disease

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93
Q

why is digoxin

A
  • antiarrhythmic drug - increases vagal tone to heart
  • positive inotrope - increases intracellular Ca2+
94
Q

what are the indication for use of digoxin

A
  • chronic heart failure - improves symptoms but not mortality rates
  • supra ventricular arrhythmias
  • chronic atrial fibrillation
95
Q

what are the pharmacokinetics of digoxin

A
  • oral administration bioavailability 75%
  • onset of action 30mins
  • peak effect - 1-5hrs
  • half life 36h
  • elimination 70% renal, GFR
  • VD 640L/70kg - binds to skeletal muscle
96
Q

what is the contraindication of digoxin

A

heart block

97
Q

what are the cautions of digoxin

A

risks of digitalis toxicity with electrolyte imbalances,

98
Q

what are the side effects of digoxin

A

arrhythmias
cardiac conduction problems
cerebral impairment
diarrhoea
dizziness
skin reactions
vision disorders

99
Q

when are SGLT2 inhibitors such as dapagliflozin used to treat heart failure

A

treatment for type 2 diabetes and heart failure

100
Q

what is the action of SGLT2 inhibitors

A

blocks the SGLT2 glucose transporter in the renal PCT glycosuria and fluid loss

101
Q

what are the haemodynamic changes associated with SGLT2 inhibitors

A
  • reduced pre load and after load
  • cardiac function improves
102
Q

what is an example of endothelial cell damage

A
  • atherosclerosis
  • vasculitis of any cause
  • high levels of homocysteine
  • turbulent blood flow at arterial bifurcation
  • oxidised LDL
  • cigarette smoke
  • cytokines
102
Q

what is thrombosis

A

pathological formation of an intravascular blood clot
can occur in a vein or an artery

102
Q

what are the contra-indication of dapagliflozin

A

diabetic ketoacidosis

102
Q

what are the adverse effects of dapagliflozin

A

rare severe ketoacidosis

102
Q

what are the cautions associated with dapagliflozin

A

elderly
hypotension
risk of volume depletion

103
Q

what is a hypercoaguable states

A
  • due to excessive procoagulant factors or defective anticoagulant
  • may be inherited (AT3 deficiency)
  • classic presentation is recurrent DVTs or DVTs at a young age
103
Q

describe thrombosis

A

characterised by the lines of Zahn (if large vessel) and attachment to a vessel wall (both features can be used to distinguish thrombus from postpartum)

103
Q

what are the 3 components of Virchows triad

A

disruption to blood flow
endothelial cell damage
hypercoaguable stress

103
Q

what are the examples of disruption to blood flow

A
  • immobilisation
  • cardiac wall dysfunction
  • aneurysm
  • atrial fibrillation
  • left atrial dilation due to mitral stenosis
104
Q

what causes venous thrombosis

A

stasis of blood most commonly in deep vein of lower limb

105
Q

what are the symptoms of venous thrombosis

A

red
swollen
painful leg
skin discolouration

106
Q

what are the risks associated with venous thrombosis

A

can dislodge to the lungs causing a pulmonary embolism

107
Q

what drugs can be used to treat venous thrombosis

A

warfarin, or other anticoagulants e.g. rivaroxaban, apixaban
these do not dissolve clot they prevent further formation
the fibrinolytic systems break down the clot

108
Q

what is the cause of arterial thrombosis

A
  • most commonly due to endothelial damage related to turbulent blood flow at bifurcation or over atherosclerotic plaques in high velocity vessels
  • in some cases they are mixed thrombi composed of platelets and with RBCs held together by fibrin - lines of Zahn
  • hyper coagulability and stasis are rare causes of arterial thrombosis
109
Q

what are the signs of arterial thrombosis

A

grey/white fibrin clot primarily composed of platelets

110
Q

how can arterial thrombosis be inhibited

A

inhibitors of platelet aggregation prevent their formation e.g. aspirin

111
Q

what are the examples of arterial thrombosis

A

MI
small bowel infarction
stroke

112
Q

what are the stages of platelet activation

A

adhesion
release reaction
aggregation

113
Q

how is a platelet plug formed

A
  • platelets undergo shape change and degranulate
  • release mediators ADP (from dense core granules)
  • thromboxane A2 (TXA2) - a derivative of platelet cyclooxygenase
  • calcium
  • ADP induces the expression of GP2b/3a (another essential receptor for aggregation of platelets) and fibrinogen which acts as a linker molecules in the developing cloth
114
Q

what are the functions of thrombin

A
  • acts on fibrinogen to produce fibrin molecules
  • activates fibrin stabilising factor 13 which converts these monomers to cross linked fibrin and strengthens blood clot
  • acts in a feedback loop to activate several other coagulation factors therefore pivotal in the amplification system
  • thrombin itself is switched off by the natural anticoagulant antithrombin limits clot formation
115
Q

what are the functions of plasmin

A
  • breaks down clot
  • cleaves fibrin and fibrinogen into fibrinogen degradation products form fragment known as D-dimers
  • degrades some clotting factors
  • blocks platelet aggregation
116
Q

what are the 3 main drug classes than prevent and/or reverse thrombus formation

A

anticoagulants
anti platelet agents
fibrinolytic agents

117
Q

what are anticoagulants

A

factor Xa inhibitors
antithrombins
heparin and vit k antagonists - modify blood clotting mechanisms

118
Q

what are anti platelet agents

A

aspirin - inhibit COX-1 activity to inhibit platelet aggregation

119
Q

what are fibrinolytic agents

A

alteplase - breaks down fibrin

120
Q

a 78 year old female has a very swollen, red painful left leg and is struggling to catch her breath. what would be the most appropriate immediate drug class to administer

A

anticoagulant

121
Q

what are the classes of anticoagulant drugs

A
  • selective factor Xa inhibitors - apixaban
  • direct thrombin inhibitors - dabigatran
  • heparin and low molecular weight heparins
  • vitamin K antagonists - warfarin
122
Q

what is the target of anticoagulants

A

target various factors in the coagulation cascade preventing formation of a stable fibrin framework

123
Q

what is the treatment for venous thromboembolism

A

apixaban or rivaroxaban

124
Q

how would you treat a venous thromboembolism if apixaban or rivaroxaban are contraindicated

A
  • low molecular weight heparin, followed by dapigatran extexilate or edoxaban
  • LMWH given with a vit K antagonism for at least 5 days or target INR achieved followed by a vitamin k antagonist on its own
125
Q

what are the examples of drug which are direct-acting oral anticoagulants

A

apixaban
dabigatran extexilate
edoxaban
rivaroxaban

126
Q

what is the mechanism of action of dabigatran extexilate

A
  • reversible inhibitor of thrombin
  • idarucizumab reversal agent
127
Q

what is the mechanism of action of apixaban, edoxaban and rivaroxaban

A
  • reversible inhibitor of activated X (factor Xa) - andexanet alfa reversal agent
  • prevents thrombin generation
  • prevents thrombus development
128
Q

what are the indications of apixaban, dabigatran extexilate, edoxaban and rivaroxaban

A
  • prevention of stroke
  • secondary prevention of DVT and/or PE
129
Q

what are the indications of apixaban, dabigatran extexilate and rivaroxaban

A

prevention of venous thromboembolism following surgery

130
Q

what are the indications of rivaroxaban

A

prevention of atherothrombotic events in patients with coronary or peripheral artery disease following an acute myocardial infarction

131
Q

what are the contra-indications of apixaban

A

avoid in conditions with significant risk of bleeding such as gastrointestinal ulceration, malignant neoplasms with high risk of bleeding or oesophageal varices

132
Q

what are risks of apixaban with the elderly

A

prescription can potentially be inappropriate - STOPP criteria
risk of bleeding e.g. severe hypertension

133
Q

what are the side effects of apixaban

A

anaemia
haemorrhage

134
Q

what are the pharmacodynamics of heparin

A
  • family of sulphates mucopolysaccharides, found in the secretory granules of mast cells
  • inhibits coagulation by activation antithrombin III
135
Q

how does heparin inhibit coagulation by activation. antithrombin III

A
  • AT III is a naturally occurring inhibitor of thrombin and clotting factors IX, Xa, XI and XII
  • in the presence of heparin, AT III become 1000x more active and inhibition of clotting factors is instantaneous
136
Q

what are the examples of LMWHs

A

dalteparin sodium
enoxaparin sodium
tinzaparin sodium

137
Q

what are the pharmacodynamics of LMWHs

A
  • more consistent activity - enoxaparin
  • inactivate factor Xa (and thrombin)
  • have immediate onset
138
Q

what are the pharmacokinetics of heparin and LMWH

A
  • inactive given orally
  • administered IV or SC
  • eliminated mainly by renal excretion
  • overdose treated by IV protamine
139
Q

what is the pharmacokinetic of heparin

A
  • short half lifer (<1hr, 2h large dose)
  • given frequently or as continuous infusion)
140
Q

what is the pharmacokinetic of LMWH

A
  • longer duration of actions (half lifer of 4-5hr)
  • allows once daily dosing
141
Q

what are the side effects of heparin and LMWH

A

bleeding and hypersensitivity

142
Q

what are the examples of vitamin k antagonists

A

warfarin
acenocoumarol
phenindone

143
Q

what is the function of vitamin k antagonists

A

inhibits the action of vitamin K1 dependent clotting factors II, VII, IX and X

144
Q

how long does it take for vitamin K antagonists to work

A

at least 48-72hrs for there anticoagulant effect to develop

145
Q

what are the side effects of vitamin k antagonists

A

haemorrhage and skin necrosis

146
Q

what is warfarin

A
  • warfarin targets INR
  • A small population of patients are genetically resistant to warfarin, due to reduced binding to vitamin K reductases
147
Q

what are the pharmacokinetics of warfarin

A
  • absorption - rapidly and almost totally absorbed from the GI tract. levels peak in blood 0.5-4h after administration
  • distribution - low volume of distribution as 99% plasma protein bound
  • metabolism - action is terminated by metabolism in the liver by CYP450 enzymes
  • excretion - metabolites are conjugated to glucuronide and excreted in urine and faeces
  • half life of 15-80hrs
  • dose is highly variable
148
Q

what are anti platelet drugs

A
  • inhibition of platelet function is useful prophylactic and therapeutic strategy against MI and stroke caused by thrombosis
149
Q

a 82 year old man is found slumped in his kitchen. he is weak on his left side and has a left sided facial droop. he has chronic arterial fibrillation for which he takes warfarin with a target INR of 2-3. he takes no other medication except amlodipine. a CT scan is performed. briefly describe the most likely cause of this mans stroke

A

history of hypertension (a risk of thromboembolic and haemorrhage stroke)

150
Q

a 76 year old male experiences severe crushing central chest pain going down his left arm. he is taken to hospital where blood tests and an ECG confirm an acute myocardial infarction. what would be the most appropriate immediate treatment

A

anti platelet drug such as aspirin

151
Q

what is the action of platelets

A
  • activated platelets cover and adhere to exposed sub endothelial surface of damaged endothelium
  • activated platelets release chemical mediators
  • chemical mediators released by platelets
  • thromboxane A2, ADP, serotonin, PAF
  • platelets are recruited into the platelet plug
  • thromboxane, ADP, serotonin, PAF
152
Q

what is the mechanism of action of aspirin

A
  • aspirin irreversibly inhibits COX1, therefore inhibits the synthesis of TXA2
  • because platelets do not contain DNA or RNA they cannot synthesis new COX1
  • the inhibition is irreversible and effective for the life of the circulating platelet
153
Q

what is the clinical use of aspirin

A
  • used prophylactically to prevent arterial thrombosis leading to:
  • transient ischemic attack
  • stroke
  • myocardial infarction
154
Q

give two examples of fibrinolytic drugs

A

streptokinase
alteplase

155
Q

what are thrombolytic drugs

A
  • thrombolytic drugs potentiate the effects of the fibrinolytic system
  • they activate conversion of plasminogen to plasmin which breaks down fibrin, thus dissolves clots
156
Q

a 58 year old man collapsed at work 2 hours ago and is taken to AnE. his work colleagues told the paramedic at the scene that he has complained of his face feeling weird and numbness in his hand before he fell to the ground. he is found to have weakness down his left side and a left sided facial dropping. a CT scan shows normal results. he is diagnosed as experiencing an acute ischaemic stroke. which drug is most appropriate

A
  • CT scan rules out bleed
  • acute ischaemic stroke cause by thrombus
  • alteplase is recommended in the treatment of acute ischaemic stroke if it can be administered within 4.5h of symptom onset; it should be given by medical staff experienced in the administration of thrombolytics and the treatment of acute stroke, preferably within a specialist stroke centre. treatment with aspirin should be initiated 24 hours after thrombolysis
157
Q

what are the pharmacokinetics of thrombolytic drugs

A
  • administered IV; immediate effect
  • short half lives
  • main hazard is bleeding
158
Q

what are the main uses of fibrinolytic (thrombolytic) drugs

A
  • restoring catheter and shunt function, by lysing clots causing occlusions
  • to dissolve clots that result in stroke
159
Q

aspirin is a cox-2 inhibitor and irreversibly blocks conversion of arachidonic acid to prostaglandin endoperoxide H2 in platelets resulting in inhibition of TXA2 synthesis. select the option that best describes an action of TXA2

A

constricts vascular smooth muscle

160
Q

select the option that is correct regarding the action of aspirin

A
  • TXA2 synthesis is blocked for the lifespan of the platelets exposed to the drug
  • aspirin is an irreversible blocker of platelets
161
Q

select the option that is not a contra-indication for use of aspirin

A

following coronary by-pass surgery

162
Q

clopidogrel inhibits platelet aggregation and used in the prevention of atherothrombotic events. what is its mechanism of action

A

irreversible blocker of P2Y12 receptors

163
Q

clopidogrel may be administered orally as a prodrug and undergoes CYP2C19 metabolism by the liver to its active form. a patient is prescribed clopidogrel alongside omeprazole, which they were already taking (also metabolised by CYP2C19). select the correct response from the options below

A

the risk of thrombus formation is increased compared to when clopidogrel is taken alone

164
Q

glycoprotein IIB/IIIA receptor antagonists such as tirofiban or the monoclonal antibody fragment abciximab inhibit platelet GPIIb/IIIa receptors and may be used in high risk patients who require angioplasty. what is most appropriate route of administration

A

intra-venous

165
Q

vitamin K deficiency may lead to excessive bleeding (e.g. haemorrhage disease of the newborn. which drug, if used excessively may lead to excessive bleeding due to inactivation of vitamin K dependent clotting factors

166
Q

which one of the following does not enhance the effect of the vitamin k antagonist warfarin. enhancing the effects of warfarin increases the risk of haemorrhage

167
Q

which one of the following enhances the effects of the vitamin K antagonist warfarin. enhancing the effects of warfarin increases the risk of haemorrhage

A

liver disease

168
Q

how is atherosclerosis developed

A
  • circulating LDL gains access to sub endothelial space
  • where it is oxidised
  • cytokines IL-1 and MCP-1 attract circulating monocytes
  • that cross intimate to become macrophages
  • smooth muscle cells migrate and proliferate under the influence of smooth muscle mitogens
  • a primitive plaque is formed of foam cells, smooth muscle, lipid and necrotic cells
  • the plaque enlarges, develops a fibrous capsule and protrudes a vessel lumen
169
Q

which is a cause of primary dyslipaemia

A

familial hypercholesterolaemia

170
Q

what is the prevalence of familial hypercholesterolaemia

171
Q

select the incorrect statement regarding cholesterol

A

it is found in low levels in the gall bladder

172
Q

an average male synthesises ~1000mg cholesterol per day. what is the average daily dietary intake of cholesterol

173
Q

LMWHs are preferred for use clinically to unfarctionated heparin as they may be given subcutaneously and have longer half-lives. all heparins do have a risk of a heparin-induced thrombocytopenia and in some patients this may lead to thrombosis. why may a heparin-induced thrombocytopenia cause a thrombosis?

A

heparin may induce antibody synthesis targeting platelets and platelet factors

174
Q

a patient receiving warfarin is not maintaining a consistent INR and the decision is made to switch to the DOAC drug rivaroxaban. when the patient stops taking warfarin their INR is too high which means the blood is taking too long to clot. select the most appropriate statement regarding the introduction of the rivaroxaban treatment

A

there should be a delay in starting the rivaroxaban until the INR value returns to its target value

175
Q

which one of the below is not true for plasminogen

A

plasminogen is inactivated once inside a formed thrombus

176
Q

select the incorrect response from below

A

alteplase is more effective against plasma plasminogen compared to fibrin bound plasminogen

177
Q

select the best description for a clinical use of alterplase

A

thrombotic stroke

178
Q

select the best option for a caution for clinical use of alteplase

A

atrial fibrillation

179
Q

what is the definition of ischaemia

A

is a condition in which blood flow is restricted or reduced in a part of the body. cardiac ischaemia is decreased blood flow and oxygen to the heart muscle

180
Q

what is the definition of infarction

A

infarction is an obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus causing local death

181
Q

list 4 things that can cause a blockage of artery

A

build up of fat, cholesterol or calcium in the arteries
blood clot
thrombus
plaque

182
Q

list what factors determine myocardial oxygen supply

A
  • oxygen carrying capacity
  • coronary artery flow
  • coronary perfusion pressure
  • coronary vascular resistance
183
Q

list what factors determine myocardial oxygen demand

A
  • heart rate
  • contractility
  • ventricular wall tension
184
Q

how is stable angina treated with nitrates

A
  • GTN short acting - isosorbide mononitrate longer acting
  • nitrates are vasodilators
185
Q

what are the clinical benefits of GTN

A
  • relax vascular smooth muscle - some reduction of after load
  • relax veins - reduction in central venous pressure, reduced preloads
186
Q

what is the mechanism of action of GTN

A
  • nitrates are metabolised release NO
  • activates guanylyl cyclase - increases cGMP
  • dephosphorylation of myosin light chain
  • reduced cytoplasmic Ca2+
  • relaxation of smooth muscle
187
Q

what are the adverse effects of GTN

A
  • postural effects
  • headache
188
Q

what are the pharmacokinetics of GTN

A
  • sublingual administration - effects in minutes
  • rapidly inactivated by hepatic metabolism
189
Q

state one named drug to relieve hypoxia in the immediate drug treatment of MI

A

only given oxygen if oxygen saturation reduced

190
Q

state one named drug and provide ration for pain relief in the immediate drug treatment of MI

A
  • morphine/diamorphine with an antiemetic
  • relieves pain and nausea
  • ventilation
191
Q

state one named drug and provide rationale for reduced cardiac workload in the immediate drug treatment of MIU

A

nitrates - GTN
- vasodilator
- reduced cardiac work

192
Q

state one names drug and provide rationale for reduced risk of another infarction in the immediate drug treatment of MI

A
  • anti-platelet
  • aspiring, clopidogrel - prevent further clot formation
193
Q

name 4 subsequent drug treatments used to treat MI

A
  • beta blockers - to improve myocardial perfusion and reduce risk of arrhythmias
  • captopril (ACE inhibitor) - improves survival and useful is risk of heart failure/left ventricular dysfunction
  • heparin (anticoagulants) - protection from thrombus in a risk patient
  • other useful drugs - nitrates, antiarrhthmics, statin - lipid lowering
194
Q

what is the primary prevention for statin treatment

A

offer atorvastatin 20mg for the primary prevention of cardiovascular disease to people who have a 10% greater 10-year risk of developing cardiovascular disease
- for people 85 years or older consider atrovastatin 20mg as statins may be of benefit in reducing the risk of non-fatal myocardial infarction

195
Q

what causes primary dyslipidaemia

A

combination of dietary and genetic factors
familial hypercholesterolaemia high risk of CHD

196
Q

what are the causes of dyslipidaemia

A

consequence of other conditions
diabetes mellitus, alcoholism, renal disease

197
Q

what are the non-pharmacological treatments of dyslipideamia

A

cardioprotective diet
weight loss
physical activity
reduce alcohol consumption
smoking cessation

198
Q

what are the pharmacological treatments of dyslipidaemia

A

anti-hyperlipideamic drugs

199
Q

what are lipid lowering drugs

A

HMG-CoA reductase inhibitors
fibrates
cholesterol absorption inhibitors e.g. ezetimibe, bile-acid binding resins
omega fatty acids

200
Q

what are some of the HMG CoA reductase inhibitors

A

simvastatin, pravastatin, lovastatin, atrovastatin, rosuvastatin, fluvastatin

201
Q

what are the pharmacokinetics of HMG CoA reductase inhibitors

A

short acting
oral, night
well absorbed
liver cytochrome P450 metabolism - not rosuvastatin

202
Q

what is the importance of blocking HMG CoA reductase enzyme

A

rate limiting step in cholesterol synthesis
blocks conversion HMG CoA to mevalonic acid

203
Q

which of the statins are short acting, specific, reversible inhibitors

A

simavastatin
lovastatin

204
Q

which of the statins are longer lasting inhibitors

A

atorvastatin

205
Q

what is the benefit of blocking cholesterol synthesis

A

unregulated LDL receptor synthesis
increases LDL clearance by liver

206
Q

what is the clinical use of primary hyperlipidaemia

A

reduce LDL by 30%
raise HDL by 20%

207
Q

what are the adverse effects of HMG CoA reductase inhibitors

A

well tolerated but may have muscle pain, GI disturbance, insomnia, rash
rarely myositis and angio-oedema

208
Q

how do HMG CoA reductase inhibitors increase life expectancy

A
  • serum LDL reduced by 35%
  • death reduced by 30%
  • death by CHD reduced by 42%
209
Q

what are the beneficial physiological effects of HMG CoA reductase inhibitors

A
  • endothelial function improves
  • improve vascularisation of ischaemic tissue
  • atherosclerotic plaque stabilisation
  • reduces vascular inflammatory response
  • reduced platelet activation
  • enhanced fibrinolysis
  • antithrombotic
210
Q

what are the examples of fibrates

A

gemofibrozil
fenofibrate
bezafibrate

211
Q

what is the mechanism of action of fibrates

A
  • agonist at peroxisomes proliferator-activated receptors (PPAR-alpha) nuclear receptor that regulates lipid metabolism
212
Q

how do fibrates regulate lipid metabolism

A

increase synthesis of lipoprotein lipase by adipose tissue
stimulated fatty acid oxidation in the liver
increases expression of apia-I and apoA5
increases hepatic LDL uptake

213
Q

what are the causes of increases lipid

A

marked reduction circulating VLDL and TG
modest reduction in LDL
increase LDL uptake by liver

214
Q

what are the pharmacokinetics of fibrates

A

well absorbed from the gastrointestinal tract
high degree of binding to albumin
metabolised by the cytochromes P450
primarily excreted via the kidneys

214
Q

what are the clinical uses of fibrates

A

hypertriclycerideamia
mixed hyperlipidaemia
TG levels reduced by 20-30%
cholesterol reduced by 10-15% associated
rise in HDL

215
Q

what are the adverse effects of fibrates

A

rash, GI disturbance
rhabdomyolysis causing renal failure
clofibrate may cause gall stones

216
Q

what are the drug examples of cholesterol absorption inhibitors

A

ezetimibe, colestipol, cholestyramine

217
Q

what is the mechanism of action of ezetimibe

A

inhibits intestinal absorption of cholesterol by interfering with Neimann-pick C1-like 1 transport protein
decreases LDL and VLDL

218
Q

what are the pharmacokinetics of ezetimibe

A

administered orally
absorbed into intestinal epithelial
extensively metabolised into active metabolite
enterohepatic recycling slows elimination

219
Q

what is the clinical use of ezetimibe

A

treatment of hyperlipidaemia in combination with statins

220
Q

what are the adverse effects of ezetimibe

A

mild - diarrhoea, abdominal pain, headache
rash and angioedema
secreted in breast milk, contraindicated in breastfeeding

221
Q

what is the mechanism of action of colestipol, cholestyramine

A

binds bile acid in gut
prevent reabsorption
diverting hepatic cholesterol to BA synthesis
upregulates LDL receptors increases LDL removal from the blood

222
Q

what are the pharmacokinetics of colestipol and cholestyramine

A

administered by mouth (stays in the GIT)

223
Q

what are the clinical uses of colestipol and cholestyramine

A

primary hypercholesterolemia when statin is contraindicated
pruritus associated with biliary obstruction
bile acid diarrhoea

224
Q

what are the adverse effects of colestipol and cholestyramine

A

constipation, bloating
malabsorption of vitamin K, folic acid, ascorbic acid
disrupts absorption of digitalis, thiazides, warfarin, iron

225
Q

what is the mechanism of action of niacin in the liver

A

reduced VLDL synthesis
reduced VLDL and LDL

226
Q

what is the mechanism of action of niacin in the adipose tissue

A

reduced hormone-sensitive lipase activity
reduced TG

227
Q

what is the general mechanism of action of niacin

A

reduced catabolic rate for HDL, increases HDL
increased clearance of VLDL by activating lipoprotein lipase

228
Q

what are the pharmacokinetics of niacin

A

readily absorbed in GIT following oral administration
metabolised in the liver
excreted via kidneys

229
Q

what are the clinical uses of niacin

A

hypercholesterolemia
hypertriglycerideamia with low levels of HDL

230
Q

what are the adverse effects of niacin

A

cutaneous flushing
associated with pruritus and palpitations
reduced with pre-treatment of aspiring or other NSAIDs
dose-dependent nausea and abdominal discomfort
moderate elevation of liver enzymes to severe hepatotoxicity
hyperuricemia in 20% of the patients

CM2001 (13 decks)

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