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Pharmacology 201 > pharm logbook interview > Flashcards

pharm logbook interview Flashcards

1
Q

Common examples of ACEI

A

ramipril
enalapril

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2
Q

MoA of ACEI

A

ACEI competitively block ACE, which is necessary for conversion of angiotensin I into angiotensin II.
Angiotensin II is a vasoconstrictor that raises blood p and causes aldosterone release (more Na and H2O retention)
–> overall inhibits production of angiotensin II, so less Na and H2O retention, and limits aldo release –> reduce systemic vascular resistance

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3
Q

effects of ACEI

A
  • Decrease vascular tone (vasoconstriction) (directly lowers BP)
  • Inhibits aldo release (less sodium and water reabsorption, slight elevation in serum K+) –> decreased BP
  • Increase plasma renin activity (due to loss of negative feedback loop on renin release)
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4
Q

metabolism of ramipril and enalapril

A

hepatic

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5
Q

excretion of ramipril and enalapril

A

mostly renal

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5
Q

administration of ramipril and enalapril

A

oral, once or twice daily

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6
Q

indication of ramipril and enalapril

A

HTN

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7
Q

contraindication of ramipril and enalapril

A
  • hypersensitivity
  • angioedema
  • hyperkalaemia
  • preg
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8
Q

adverse effects of ramipril and enalapril

A
  • Dry cough: due to inhibited degradation of bradykinin, leading to increased bradykinin levels
  • Dizziness
  • Angioedema
  • Hypotension (orthostatic/postural hypotension): due to vasodilation, which reduces afterload and TPR
  • Hyperkalaemia: reduced aldo release due to reduced angiotensin II will reduce sodium and water reabsorption, potassium excretion, causing increased serum potassium levels
  • Hypersensitivity
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9
Q

monitoring for ramipril?

A
  • Renal function
  • Signs of postural hypotension, angioedema, hyperkalaemia
  • Serum potassium
  • Serum creatinine
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10
Q

monitoring for enalapril?

A
  • Renal function
  • Vital signs
  • Cardiac activity
  • Serum potassium
  • Serum creatinine
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11
Q

common examples of AT1 receptor antagonists?

A

candesartan
irbesartan

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12
Q

MoA of AT1 receptor antagonists

A
  • Decreased vasoconstriction
  • Decreased aldo secretion (which decrease sodium and water retention, and decrease K+ excretion, ad decrease blood blood volume) – causing overall decreased BP
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13
Q

metabolism of candesartan and irbesartan?

A

hepatic

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14
Q

excretion of candesartan?

A

mainly renal

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15
Q

excretion of irbesartan?

A

mainly biliary

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16
Q

administration of candesartan/irbesartan?

A

oral once daily

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17
Q

indication for candesartan/ irbesartan?

A

HTN

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18
Q

contraindication for candesartan and irbesartan?

A
  • Hypersensitivity
  • Angioedema
  • Hyperkalaemia
  • Pregnancy
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19
Q

adverse effects of candesartan and irbesartan?

A
  • Dizziness
  • Angioedema
  • Hypotension (orthostatic/postural hypotension): due to vasodilation, which reduces afterload and TPR
  • Hyperkalaemia: reduced aldo release due to reduced angiotensin II will reduce sodium and water reabsorption, potassium excretion, causing increased serum potassium levels
  • Hypersensitivity
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20
Q

monitoring for candesartan and irbesartan?

A
  • Routine BP measurement
  • Adverse effects of symptomatic hypotension – syncope, nausea, fatigue, lightheadedness, dizziness
  • serum potassium
  • renal function
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21
Q

which are the first line antihypertensives?

A
  • ACEI
  • ARBs
  • thiazide diuretics if > 65
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22
Q

common example of thiazide diuretic?

A

hydrochlorothiazide

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23
Q

MoA of thiazide

A

Directly inhibits Na+/Cl- co-transporter in distal convoluted tubule of kidneys, which then prevents sodium reabsorption, and induces natriuresis and diuresis effects – loss of sodium, chloride, and water  reduce systemic vascular resistance

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24
Q

effects of thiazide

A
  • Reduced reabsorption of sodium, chloride and water
  • Vasodilation (through an unknown mechanism)
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25
Q

is thiazide metabolised?

A

no

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26
Q

excretion of thiazides?

A

renal

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27
Q

administration of thiazides?

A

oral, once/twice daily

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28
Q

indication of thiazides?

A

HTN

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29
Q

contraindications of thiazides

A
  • Glucose intolerance
  • DM
  • Gout
  • Pregnancy
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30
Q

adverse effects of thiazides?

A
  • Postural hypotension
  • Dizziness
  • Hypokalaemia
  • Hyperuricaemia  gout
  • Hyperglycaemia  diabetes
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31
Q

monitoring for thiazides

A
  • Electrolyte imbalances (sodium, potassium, calcium, magnesium)
  • Acute gout flare in pt with family or personal history of gout
  • BP monitoring
  • Blood glucose levels in pt with impaired glucose metabolism
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32
Q

3 classes of CCB and their common examples?

A
  • phenylalkylamaines - verapamil
  • benzothiazepines - diltiazem
    dihydroppyridines - amlodipine
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33
Q

MoA of CCBs?

A

Blocks L-type calcium channel in cardiac and smooth muscle, which causes smooth muscle relaxation since Ca2+ is needed for contraction

  • Vascular-selective: reduce systemic vascular resistance
  • Cardio-selective: reduce CO
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34
Q

effects of CCBs?

A
  • Cardiac-selective CCBs will decrease HR, AV conduction, contractility, and thus CO
     causes an overall reduction in BP
  • Vascular selective CCBs will decrease vascular smooth muscle contraction, vascular tone (vasodilation), which cause a decrease in vascular resistance and an overall reduction in BP
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35
Q

metabolism of CCBs?

A

hepatic

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36
Q

excretion of CCBs?

A

renal

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37
Q

administration of verapamil (phenylalkylamine)?

A

oral, q8-12h
IV

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38
Q

administration of diltiazem (benzothiazepine)?

A

oral, once daily
IV

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39
Q

administration of amlodipine (dihydropyridine)?

A

oral once daily

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40
Q

indication of verapamil (phenylalkylamine)?

A
  • HTN
  • angina
  • arrhythmias (a-fib)
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41
Q

indication of diltiazem (benzothiazepine)?

A
  • HTN
  • angina
  • arrhythmias (a-fib)
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42
Q

indication of amlodipine (dihydropyridine)?

A
  • HTN
  • angina
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43
Q

adverse effects of verapamil (phenylalkylamine)?

A
  • Bradycardia
  • AV block
  • Constipation
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44
Q

adverse effects of diltiazem (benzothiazepine)?

A
  • Bradycardia
  • AV block
  • Constipation
  • Reflex tachycardia
  • Peripheral oedema
  • Headache
  • Flushing
  • Hypotension
  • Dizziness
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45
Q

adverse effects of amlodipine (dihydropyridine)?

A
  • Reflex tachycardia
  • Peripheral oedema
  • Headache
  • Flushing
  • Hypotension
  • Dizziness
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46
Q

contraindication of CCB?

A

Vascular selective:
* Tachyarrhythmias
* Heart failure
* Hypersensitivity
Cardio-selective:
* Heart failure
* Bradycardia
* AV block

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47
Q

monitoring for CCBs?

A
  • Routine BP measurement
  • Adverse effects such as peripheral oedema, dizziness and flushing
  • ECG
  • HR
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48
Q

common examples of beta blockers

A

atenolol
metoprolol

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49
Q

MoA of beta blockers

A
  • Block beta1 receptors in cardiac muscle – which then inhibits noradrenaline
  • Inhibits SNS action on cardiac muscle:
  • decreased HR
  • decreased AV conduction
  • decreased contractility
  • decreased automacity (spontaneous AP generation)
  • less O2 consumption by myocardium
  • Negative inotropic and chronotropic (contractility and rate)
  • decreased CO and arterial P
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50
Q

effects of beta blockers

A
  • Activation of beta 1 receptors normally increases intracellular Ca2+ (via increased cAMP and PKA) – so inhibition of this will cause decreased intracellular Ca2+
  • Opposing action of SNS - decreased HR, AV conduction, contractility
  • decreased CO, thus decreased arterial BP
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51
Q

metabolism of atenolol

A

very little portion metabolised by liver

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52
Q

metabolism of metoprolol

A

hepatic

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53
Q

excretion of atenolol and metoprolol?

A

renal

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54
Q

administration of atenolol

A

oral once daily

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55
Q

administration of metoprolol

A

oral once/twice daily

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56
Q

indications for beta blockers

A
  • HTN
  • HF
  • tachyarrhythmia (a-fib)
  • angina
  • post-AMI
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57
Q

contraindications for beta blockers

A
  • Asthma, COPD
  • Bradycardia
  • Peripheral vascular disease
  • DM
  • AV block
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58
Q

adverse effects of beta blockers

A
  • Bradycardia
  • Fatigue
  • Cold extremities
  • Bronchoconstriction
  • Nightmares
  • Hypoglycaemia
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59
Q

monitoring of beta blockers

A
  • Blood glucose monitoring
  • Routine BP measurement
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60
Q

common examples of alpha1 antagonists

A

prazosin
terazosin

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61
Q

MOA of alpha 1 antagonists

A
  • Blocks alpha1 receptors in vascular smooth muscle
    -> at postsynaptic receptors on peripheral blood vessels, NA binds to alpha1 receptors –> increased phosphalipase C –> increased IP3 and DAG –> increased intracellular Ca2+ and vasoconstriction –> blockade of alpha1 receptor causes vasodilation –> reduce systemic vascular resistance
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62
Q

effects of alpha 1 antagonists

A

Vasodilation -> decreased TPR and BP

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63
Q

metabolism of alpha 1 antagonists

A

hepatic

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64
Q

excretion of prazosin

A

mainly biliary

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65
Q

excretion of terozosin

A

mainly biliary, some renal

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66
Q

administration of prazosin

A

oral, 2-3 times daily

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67
Q

administration of terazosin

A

oral, once daily or q12h

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68
Q

indication for alpha 1 antagonists

A

HTN

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69
Q

contraindication/ caution for alpha 1 antagonist

A

elderly

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70
Q

adverse effects of alpha 1 antagonist

A
  • Postural hypotension
  • Dizziness
  • Headache
  • Oedema
  • Nasal congestion – due to peripheral vasoconstriction
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71
Q

monitoring for alpha 1 antagonist

A
  • For adverse effects like dizziness, oedema
  • Routine BP measurement
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72
Q

what are the second line antihypertensives?

A
  • CCBs
  • beta blockers
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73
Q

third line antihypertensives?

A

alpha 1 antagonists

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74
Q

last line antihypertensives?

A

alpha 2 agonists (except use of methyldopa in pregnancy)

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75
Q

common examples of alpha 2 agonists

A

clonidine
methyldopa

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76
Q

effects of alpha 2 agonist

A
  • Mimics autoinhibitory response in CNS -> less SNS outflow
    > less NA effects
    > less vasoconstriction
    > less SNS effects on heart
    > less CO
    > less BP
  • Constant reduction of SNS outflow -> up-rego of SNS receptors -> increased sensitivity to sympathomimetics (avoid sudden drug cessation and drug interactions like alpha1 agonists – can cause sudden and dangerous increase in BP)
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76
Q

MOA of alpha 2 agonist

A
  • Inhibit further NA release through negative-feedback (autoinhibitory) control by NA at pre-synaptic 2 receptors
  • 2 receptor agonists activate 2 receotors in CNS and inhibit NA release, and thus SNS outflow
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77
Q

metabolism of clonidine and methyldopa

A

hepatic

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78
Q

excretion of clonidine and methyldopa

A

mainly renal

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79
Q

indication of clonidine and methyldopa

A

HTN

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80
Q

administration of clonidine

A

oral q12h

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81
Q

administration of methyldopa

A

oral q6-12h

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82
Q

contraindications of methyldopa and clonidine

A
  • Bradycardia
  • AV block
  • Peripheral vascular disease
  • Depression
  • Diabetes
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83
Q

adverse effects of methyldopa and clonidine

A
  • Drowsiness
  • Fatigue
  • Bradycardia
  • Dizziness
    -> all due to SNS activity
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84
Q

monitoring for methyldopa and clonidine

A
  • For adverse effects like dizziness, bradycardia
  • Routine BP measurement
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85
Q

common examples of statins

A

atorvastatin
simvastatin

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86
Q

MOA of statin

A
  • Competitively inhibit HMG-CoA reductase (normally HMG-CoA converts into mevalonic acid through HMG-CoA reductase, which mevalonic acid turns into cholesterol)
  • Inhibition of HMG-CoA reductase -> decreased hepatic cholesterol synthesis -> increased demand for cholesterol -> increased expression of LDL receptors -> increased LDL clearance from plasma (due to decreased hepatic cholesterol and increased demand) -> decrease plasma LDL cholesterol
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87
Q

effects of stains

A
  • Decrease plasma LDL cholesterol
  • Other actions:
  • Decreased plasma TG
  • Increased plasma HDL
  • Improved endothelial function (reduces % of atherosclerotic plaque forming)
  • Reduced vascular inflammation (reduces % of atherosclerotic plaque forming)
  • Reduced platelet aggregability (which can limit pathogenesis of atherosclerotic plaque)
  • Increased neovascularisation of ischaemic tissue
  • Stabilisation of atherosclerotic plaque
  • Antithrombotic actions
  • Enhanced fibrinolysis
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88
Q

metabolism of statins

A

hepatic

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89
Q

excretion of statins

A

mainly biliary

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90
Q

administration of atorvastatin

A

oral once daily

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91
Q

administration of simvastatin

A

oral once daily (at night - due to shorter half life so take at night when cholesterol metabolism is highest)

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92
Q

contraindications of statins

A
  • Drugs that inhibit CYP450 enzymes
  • Acute liver disease
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93
Q

indications of statins

A
  • Hypercholesterolaemia
  • High risk of coronary heart disease (e.g., patients post-acute MI), with or without hypercholesterolaemia
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94
Q

adverse effects of statins

A
  • Myalgia
  • Mild GI disturbances – nausea, stomach pain
  • Elevated aminotransferase actions
  • Rhabdomyolysis (rare)
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95
Q

monitoring of statins

A
  • Liver function?
  • Blood lipid levels
  • Protein kinase levels
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96
Q

MOA of ezetimibe

A
  • Decreases absorption of exogenous cholesterol by blocking transport protein (NPC1L1) in small intestine absorptive enterocytes > increase demand for cholesterol > increase LDL receptor expression > increase plasma LDL clearance > reduced plasma concentration of LDL
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97
Q

effects of ezetimibe

A
  • Reduce plasma LDL cholesterol
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98
Q

metabolism of ezetimibe

A

enterohepatic circulation

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99
Q

administration of ezetimibe

A

oral once daily

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100
Q

indication of ezetimibe

A
  • Hypercholesterolaemia (when statins are not tolerated/ added to statins)
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101
Q

contraindication of ezetimibe

A
  • Hypersensitivity
  • Acute liver disease
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102
Q

adverse effects of ezetimibe

A
  • Headache
  • Abdominal pain
  • Diarrhoea
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103
Q

monitoring for ezetimibe

A
  • Blood lipid levels
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104
Q

common example of bile acid binding resin

A

cholestyramine

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105
Q

MOA of cholestyramine

A

Bind bile acids in intestinal lumen, which prevents their reabsorption through enterohepatic circulation, which then increases bile acid excretion in faeces > decreased absorption of exogenous cholesterol and increased metabolism of endogenous cholesterol into bile acids > increased demand for cholesterol (since exogenous absorption of cholesterol decreased) > increase LDL receptor expression > increase plasma LDL clearance > decrease plasma concentration of LDL-cholesterol

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106
Q

effects of cholestyramine

A
  • Decrease plasma LDL levels
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107
Q

is cholestyramine metabolised

A

no

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108
Q

excretion of cholestyramine

A

biliary

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109
Q

administration of cholestryamine

A

oral q12-24h

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110
Q

indication of cholestyramine

A

Combination treatment for hyperlipidaemia when statin alone is inadequate

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111
Q

contraindication of cholestyramine

A
  • hypertriglyceridemia
  • Pt with complete biliary obstruction
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112
Q

adverse effects of cholestyramine

A
  • GI disturbances – constipation, abdominal pain, flatulence, dyspepsia, nausea, vomiting, diarrhoea, anorexia
  • Can increase TG levels
  • Decrease fat soluble vitamins levels (vit A D E K) – due to interference with absorption of dietary lipids
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113
Q

monitoring for cholestyramine

A
  • Blood lipid levels, esp. TG?
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114
Q

common example of PCSK9 inhibitors

A

evolucumab

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115
Q

MOA of evolucumab

A
  • Monoclonal Ab – they have monovalent affinity – they bind to the same epitope
  • PCSK9: crucial role in cholesterol homeostasis – binds to LDL receptors and promotes lysosomal degradation > which then decreases hepatic LDL uptake, and increases plasma LDL
  • Evolocumab specifically bind to PCSK9 > increase LDL receptor (and inhibition of lysosomal degradation of LDL rcts > increases hepatic LDL uptake) > decreased plasma LDL concentration
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116
Q

effects of evolucumab

A
  • Decrease plasma LDL concentration by 55-75%
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117
Q

metabolism of evolucumab

A

mainly through saturable binding to PCSK9

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118
Q

administration of evolucumab

A

subcutaneous injection every 2 weeks or once monthly

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119
Q

indication of evolucumab

A

Combination therapy with statin in familial hypercholesterolaemia, or primary hypercholesterolaemia after inadequate response or intolerance of statins

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120
Q

contraindication of evolucumab

A

hypersensitivity

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121
Q

adverse effects of evolucumab

A
  • injection site reactions
  • infections
  • angioedema
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122
Q

monitoring for evolucumab

A
  • for angioedema
  • for infections
  • blood lipid levels
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123
Q

common examples of fibrates

A

fenofibrate
gemfibrozil

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124
Q

MOA of fibrates

A
  • Agonists at PPARa w nuclear receptors which is usually located in cytoplasm of cell
  • Increase transcription of genes for lipoprotein lipase
  • Enhanced lipoprotein lipase results in increased TG uptake by VLDL and chylomicrons > increased removal of plasma TG
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125
Q

effects of fibrates

A
  • Decrease TG by 40-80%
  • Decrease LDL by 5-15%
  • Increase HDL by 10-30%
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126
Q

metabolism of fenofibrate

A

hepatic CYP450

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127
Q

metabolism of gemfibrozil

A

enterohepatic circulation

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128
Q

excretion of fibrates

A

mainly renal

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129
Q

administration of fenofibrate

A

oral once daily

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130
Q

administration of gemfibrozil

A

oral q12h

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131
Q

indication of fibrates

A
  • Severe hypertriglyceridemia
  • Combination therapy with statin for mixed hyperlipidaemia with predominant hypertriglyceridemia
  • Second-line option when statins are not tolerated or are contraindicated
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132
Q

contraindication of fibrates

A

Severe renal and hepatic impairment – primary biliary cirrhosis, gallstones, gall bladder disease, photosensitivity due to fibrates

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133
Q

adverse effects of fibrates

A
  • GI disturbances
  • LDL levels can increase in pure hypertriglyceridemia (rather than mixed hyperlipidaemia)
  • Rhabdomyolysis (rare, but high risk if used in combination with statins)
  • Headache
  • Dry mouth
  • Myalgia
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134
Q

monitoring for fibrates

A
  • protein kinase levels
  • blood lipid levels
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135
Q

MOA of nicotinic acid

A
  • Exact MoA unknown, but is thought to decrease release of free fatty acids from adipose tissue > decreases hepatic synthesis of TG > decreased hepatic VLDL secretion > decreased plasma TG and LDL
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136
Q

effects of nicotinic acid

A
  • Reduced TG by 25-40%
  • Reduced LDL by 15-30%
  • Increases HDL by 20-35%
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137
Q

metabolism of nicotinic acid

A

hepatic

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138
Q

excretion of nicotinic acid

A

renal

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139
Q

administration of nicotinic acid

A

oral, once daily

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140
Q

indication of nicotinic acid

A
  • Use is limited by its poor tolerability
  • May be used for hypertriglyceridaemia
  • Combination therapy for mixed hyperlipidaemia if tolerated
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141
Q

contraindication of nicotinic acid

A
  • Recent MI
  • Gout
  • Hyperuricaemia
  • Hepatic or renal impairment
  • DM
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142
Q

adverse effects of nicotinic acid

A
  • Vasodilation effects – flushing, hypertension, headache
  • Nausea
  • Vomiting
  • Diarrhoea
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143
Q

monitoring of nicotinic acid

A
  • Blood lipid levels
  • For adverse effects like hypotension and nausea
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144
Q

common examples of nitrates

A
  • GTN: IV/ sublingual/ transdermal
  • isosorbide mononitrate (tablet)
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145
Q

MOA of nitrates

A

In endothelial cells, nitrates react with tissue sulfhydryl groups to release NO – NO diffuses into smooth muscle cell and activates guanylate cyclase > increased cGMP > increased protein kinase G – PKG induces smooth muscle relaxation by decreasing intracellular calcium and K, and increasing MLC phosphatase activity

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146
Q

effects of nitrates

A
  • Therapeutic effects are dose-related
  • At low doses:
  • Venorelaxation, with little effect on arterial resistance vessels
    > venorelaxation > peroopheral pooling > decreased venous return > decreased preload and VEDP > increased coronary perfusion (perfusion window) > decrease cardiac workload anad O2 demand
  • At higher doses:
  • Dilation of arteries:
    > coronary arterial vasodilation > increased cardiac perfusion
    > systemic arterial vasodilation > decreased afterload > decreased cardiac workload and O2 demand
  • Nitrates also diverts blood from normal to ischaemic areas of myocardium – due to the dilatation of collateral vessels that bypass narrowed coronary artery
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147
Q

metabolism of GTN

A

hepatic

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148
Q

excretion of GTN

A

renal

149
Q

excretion of isosorbide mononitrate

A

mainly renal

150
Q

metabolism of isosorbide mononitrate

A

not subject to first pass metabolism in liver - hepatic via conjugation

151
Q

administration of GTN

A
  • IV: for acute treatment
  • Sublingual: every 5 minutes up to 3 times
  • Transdermal: once daily for no more than 12 hours
152
Q

administration of isosorbide mononitrate

A

Oral, twice daily (immediate release); once daily (extended release)

153
Q

indication of GTN

A
  • Angina
    > prophylactic (transdermal) and acute (sublingual tablets and sprays)
154
Q

indication of isosorbide mononitrate

A

angina > prophylactic

155
Q

contraindications for GTN

A
  • Hypotension
  • Inferior and posterior MI/ RV infarct
  • Fixed cardiac output – aortic stenosis, tamponade
  • Significant tachycardia or bradycardia
  • Hypersensitivity
156
Q

adverse effects of GTN + isosorbide mononitrate

A

Vasodilatory effects:
* Headache
* Postural hypotension
* Reflex tachycardia
* Flushing
* Fainting
* Palpitations
* Peripheral oedema

157
Q

monitoring for GTN and isosorbide mononitrate

A
  • for adverse effects like peripheral oedema
158
Q

contraindication for isosorbide mononitrate

A
  • Do not administer with PDE5 inhibitors (sildenafil, vardenafil, tadalafil) – increase nitrate effects – systemic vasodilation and severe hypotension
  • Hypersensitivity to nitrates
159
Q

MOA of aspirin

A
  • Irreversibly and non-selectively inhibits cyclo-oxygenase enzyme (COX) – thus inhibits the production of prostanoids > inhibits production of prostacyclin and thromboxane A2
  • COX-1: present in most cells as a constitutive enzyme, regardless of needs – produced prostanoids that function as homeostatic regulators (e.g., gastric protection, renal blood flow, platelet function)
  • COX-2: not normally present, inducible – induced during inflammation and tissue repair and has physiological roles to play in reproduction and renal function
  • Irreversible inhibition of COX reduces both TXA2 synthesis in platelets and PGI2 synthesis in endothelium – vascular endothelial cells can continue to synthesise new COX-1 because these cells are nucleated, but platelets are not so they cannot continue to synthesise COX-1, so once it is irreversibly inhibited by aspirin, they cannot continue to produce TXA2
160
Q

effects of aspirin

A
  • Inhibition of TXA2 synthesis and inhibition of platelet aggregation and activation
    ** after administration of aspirin TXA2 synthesis does not recover until more platelets are produced (turnover, which is 7-10day)
161
Q

metabolism of aspirin

A

hepatic

162
Q

excretion of aspirin

A

mainly renal

163
Q

administration of aspirin

A

oral, 75-300mg daily

164
Q

indication of aspirin

A
  • ACS
  • Thrombosis prevention
  • Post-AMI
  • History of symptomatic atherosclerosis
165
Q

contraindication of aspirin

A
  • Hypersensitivity - especially people with pre-existing allergies like asthma
  • Bleeding GI ulcers
166
Q

adverse effects of aspirin

A
  • Bleeding
  • GI disturbances – discomfort, dyspepsia, ulceration – due to direct irritation and COX-1 inhibition
  • Allergic reactions – urticaria, bronchoconstriction
167
Q

monitoring for aspirin

A

monitor for adverse effects like allergic reactions and bleeding

168
Q

common example of P2Y12 antagonists

A

clopidogrel

169
Q

MOA of clopidogrel

A

Irreversibly inhibits P2Y12 platelet (which usually acts as a chemoreceptor for ADP) – this prevents ADP-mediated activation of GP iib/iiia complex and thus inhibit platelet aggregation

170
Q

effects of clopidogrel

A

anti-platelet effects via inhibition of platelet aggregation

171
Q

metabolism of clopidogrel

A

hepatic CYP450

172
Q

excretion of clopidogrel

A

mainly renal

173
Q

administration of clopidogrel

A

oral once daily - loading dose for pt >75y

174
Q

indication of clopidogrel

A

-ACS
-thrombosis prevention

175
Q

contraindications of clopidogrel

A
  • Hypersensitivity
  • Active pathologic bleeding – peptic ulcer, intracranial haemorrhage
176
Q

adverse effects of clopidogrel

A
  • Bleeding
  • GI disturbances (upset stomach/ pain, diarrhoea, constipation)
177
Q

monitoring of clopidogrel

A

for adverse effects

178
Q

MOA of dipyridamole

A
  • Inhibits the phosphodiesterase enzymes (PDE3) that break down cAMP > increased cAMP > activation of PKA > phosphorylation of IP3 receptors > decreased Ca2+ release from ER > decreased release of granules
  • Block of adenosine uptake into RBC (adenosine then binds to A2 receptors, which increases platelet cAMP)
179
Q

effects of dipyridamole

A

Decrease platelet aggregation via decreased activation of platelets

180
Q

metabolism of dipyridamole

A

hepatic

181
Q

excretion of dipyridamole

A

feces

182
Q

administration of dipyridamole

A

oral twice daily w aspirin

183
Q

indication of dipyridamole

A

Thrombosis prevention/ ischaemic stroke, TIA prevention

184
Q

contraindication of dipyridamole

A
  • Hypersensitivity
  • Thrombocytopenia
185
Q

adverse effects of dipyridamole

A

Vasodilatory effects:
* Headache
* Flushing
* Dizziness

186
Q

monitoring of dipyridamole

A

for adverse effects

187
Q

common example of Glycoprotein IIb/IIIa inhibitors

A

tirofiban

188
Q

MOA of tirofiban

A
  • Block GPIIb/IIIa receptors > prevents fibrinogen from binding to the GP IIb//IIIa receotors > prevents linkage of adjacent platelets
  • Block all pathways to platelet aggregation since GP IIa/IIIb receptors constitute at a point at which the pathways converge
189
Q

effects of tirofiban

A
  • Decrease platelet aggregation due to inhibition of fibrinogen crosslinking
190
Q

metabolism of tirofban

A

negligible

191
Q

excretion of tirofiban

A

mainly renal

192
Q

administration of tirofiban

A

IV – loading dose with 5 minutes, then post loading dose for up to 18h

193
Q

indication of tirofiban

A

thrombosis
high risk unstable angina

194
Q

contraindication for tirofiban

A
  • Hypersensitivity
  • Thrombocytopenia
  • Active internal bleeding or history of bleeding diathesis
  • Major surgical procedure or severe physical trauma within previous month
195
Q

adverse effects for tirofiban

A
  • Dizziness
  • Allergic reaction
  • Nausea
  • Headache
  • Bleeding
196
Q

monitoring for tirofiban

A

adverse effects

197
Q

common example of thrombolytics

A

alteplase

198
Q

MOA of alteplase

A
  • Convert plasminogen to plasmin, which catalyses fibrin breakdown
    > plasminogen deposition on fibrin strand within thrombus – exogenous plasminogen activators then diffuse into thrombus and cleave plasminogen to release plasmin – plasmin breaks down the thrombus
199
Q

metabolism of alteplase

A

hepatic

199
Q

effects of alteplase

A
  • Dissolves clots through plasmin-mediated fibrinolysis
200
Q

excretion of alteplase

A

mainly renal

201
Q

administration of alteplase

A

IV – initial bolus over 1 minute (10% of total dose), then remainder over 60 minutes

202
Q

indication of alteplase

A
  • STEMI
  • Ischaemic stroke
203
Q

contraindication of alteplase

A
  • Active internal bleeding
  • Stroke or serious trauma within 3 months
  • Severe uncontrolled hypertension
  • Bleeding diathesis
204
Q

adverse effects of alteplase

A
  • Bleeding
  • Angioedema
  • Anaphylaxis
  • Unusual bleeding
  • Headache
  • Dizziness
205
Q

monitoring of alteplase

A
  • For adverse effects like angioedema, bleeding, anaphylaxis
206
Q

example of neprilysin inhibitor

A

ARNI - sacubitril with valsartan

207
Q

MOA of ARNI

A
  • Valsartan: decreased vasoconstriction > decreased aldo secretion > decreased sodium and water retention > decreased potassium secretion > decreased blood volume and pressure > decreased venous pooling and oedema
  • Sacubitril:
    Inhibits the degradation of natriuretic peptides, which causes more vasodilation, natriuresis and diuresis
208
Q

effects of ARNI

A
  • Help maintain sodium and fluid balance, and protect CVS from effects of fluid overload
    (sacubitril acts to raise NP levels and results in vasodilation, natriuresis, and diuresis
209
Q

metabolism of ARNI

A

hepatic

210
Q

excretion of ARNI

A

Sacubitril: mainly renal
Valsartan: faeces

211
Q

administration of ARNI

A

oral twice daily

212
Q

indication of ARNI

A

heart failure with reduced ejection fraction

213
Q

contraindication of ARNI

A
  • Elderly
  • Renal and hepatic impairment
  • Hyperkalaemia
  • Angioedema
  • Hypotension
214
Q

adverse effects of ARNI

A
  • Hypotension
  • Hyperkalaemia
  • Dizziness
  • Angioedema
215
Q

monitoring for ARNI

A
  • Monitor hypotension, hyperkalaemia, renal impairment, angioedema
216
Q

common effect of aldosterone antagonist

A

spironolactone

217
Q

MOA of spironolactone

A
  • Antagonises aldosterone
  • Inhibits aldosterone-induced increase in sodium channels in luminal membrane, and Na/K ATPase pumps in basolateral membrane of collecting tubules
  • increased loss of sodium and water, and decreased excretion of potassium in urine
218
Q

effects of spironolactone

A

decreased aldosterone effects helps with pathophysiology of heart failure and improve outcomes

219
Q

metabolism of spironolactone

A

hepatic and renal

220
Q

excretion of spironolactone

A

renal

221
Q

administration of spironolactone

A

Oral, once daily initial dose, if not tolerated, then once every other day

222
Q

indication of spironolactone

A

HFrEF

223
Q

contraindication of spironolactone

A
  • Hypersensitivity
  • Conditions associated with hyperkalaemia
224
Q

adverse effects of spironolactone

A
  • Hyperkalaemia
  • Gynaecomastia
  • Menstrual disorders
  • Testicular atrophy
225
Q

monitoring of spironolactone

A

monitor adverse effects like hyperkalaemia - K levels

226
Q

common examples of SGLT2 inhibitors

A

dapagliflozin
empagliflozin

227
Q

MOA of SGLT2 inhibitors

A
  • Inhibit sodium-glucose co-transporter 2 (SGLT2), which reduce glucose reabsorption in the kidney, and increase its secretion in urine
  • Inhibiting SGLT2 produces glycosuria and osmotic diuresis, reducing fluid load
228
Q

effects of SGLT2 inhibitors

A

Reduces fluid load through glycosuria and osmotic diuresis

229
Q

metabolism of dapagliflozin

A

hepatic

230
Q

metabolism of empagliflozin

A

minimally metabolised - primarily metabolised via glucuronidation

231
Q

metabolism of SGLT2 inhibitors

A

renal

232
Q

administration of SGLT2 inhibitors

A

oral daily

233
Q

indication of SGLT2 inhibitors

A

heart failure with preserved ejection fraction

234
Q

contraindication of SGLT2 inhibitors

A

hypersensitivity
pt on dialysis

235
Q

adverse effects of SGLT2 inhibitors

A
  • Urinary and genital tract infection
  • Thirst
236
Q

monitoring of SGLT2 inhibitors

A

monitor adverse effects

237
Q

common example of loop diuretics

A

furosemide

238
Q

MOA of furosemide

A
  • Inhibit Na/K/2Cl symporter in luminal membrane of thick ascending limb of loop of Henle
  • Increases loss of Na, K, Cl, and water in urine
  • Decreases venous return and venous pooling
239
Q

effects of furosemide

A
  • Reduces fluid load through glycosuria and osmotic diuresis
  • Decreases venous return and venous pooling due to reduced sodium chloride reabsorption
    > aims to reduce signs and symptoms of congestion, and improve exercise tolerance
240
Q

metabolism of furosemide

A

renal and hepatic - glucuronidation

241
Q

excretion of furosemide

A

mainly renal

242
Q

administration of furosemide

A

oral once or twice daily

243
Q

indication of furosemide

A

heart failure with reduced ejection fraction

244
Q

contraindications of furosemide

A

hypersensitivity
anuria

245
Q

adverse effects of furosemide

A
  • Hyperuricaemia
  • Hypokalaemia
  • Dizziness
  • Orthostatic hypotension
246
Q

monitoring for furosemide

A
  • for adverse effects
  • uric acid levels
247
Q

MOA of crystalloids (saline)

A
  • after arriving at vascular space, it will diffuse into interstitial space
  • the sodium does not enter intracellular space due to active sodium extrusion
  • which then causes immediate expansion of intravascular volume, and equilibration between vascular and interstitial spaces (these two spaces have higher osmolarity than that of intracellular space)
  • which then ultimately results in water movement from intracellular space in order to equalise osmolarity throughout intracellular, interstitial, and intravascular space.
248
Q

effects of crystalloid saline

A
  • Immediate expansioin of intravascular volume – corrects hypovolaemia
249
Q

fluids to resuscitation?

A
  • crystalloid: normal saline
  • colloids: albumin
250
Q

administration of fluids of resuscitation

A

IV

251
Q

indication of fluids of resuscitation

A

hypovolaemic shock

252
Q

contraindications of normal saline

A
  • Oedema
  • Heart disease
  • Cardiac decompensation
  • Hyperchloremic metabolic acidosis
253
Q

adverse effects of normal saline

A

injection site infection

254
Q

monitoring of normal saline

A
  • clinical and laboratory findings of patient – electrolyte concentrations, volume status, acid-base disturbances
  • evaluation for dehydration/ fluid overload
255
Q

MOA of colloids albumin

A
  • expansion of intravascular compartment  the fluid does not leave across the blood vessel walls and other compartments are unaffected
256
Q

effects of colloids albumin

A
  • more blood volume – restoration of hypovolaemia
257
Q

metabolism of albumin

A

liver

258
Q

excretion of albumin

A

intestinal mucosa

259
Q

contraindication of albumin

A

hypersensitivity
severe anaemia
HF

260
Q

indication of albumin

A

hypovolaemic shock

261
Q

adverse effects of albumin

A
  • Hypersensitivity
  • Flushing
  • Urticaria
  • Fever
  • Chills
  • Nausea
  • Vomiting
  • Tachycardia
  • Hypotension
262
Q

monitoring of albumin

A
  • Monitor for any adverse effects
  • Patient’s fluid status
263
Q

types of vasopressors?

A

noradrenaline
adrenaline
vasopressin
dopamine

264
Q

MOA of dopamine?

A
  • Preferentially activates alpha-1 receptors in the vasculature, causing vasoconstriction and increased peripheral resistance
  • Some activation of beta-1 receptor in the heart, but since increased TPR is coupled with compensatory baroreceptor reflexes, there is either no change or HR and CO
265
Q

effects of dopamine

A
  • Vasoconstriction and INCREASED TPR helps raise BP and establishes a more adequate circulation
266
Q

metabolism of noradrenaline

A

monoamine oxidase in adrenergic neuron

267
Q

excretion of noradrenaline

A

renal

268
Q

administration of noradrenaline

A

IV

269
Q

indication of noradrenaline

A

hypovolaemic shock

270
Q

contraindication of noradrenaline

A

hypersensitivity

271
Q

adverse effects of noradrenaline

A
  • Headache
  • Dizziness
  • Reflex bradycardia
  • Blurred vision
  • Chest pain/ discomfort
  • Nervousness
  • unusual tiredness or weakness
272
Q

monitoring of noradrenaline and adrenaline

A

adverse effects
pt fluid status

273
Q

MOA of adrenaline

A
  • at low doses, beta 1 and 2 receptors are activated – beta 1: increased HR and contractility; beta 2: decreased TPR
  • at higher doses, alpha 1 receptors are activated, which increases peripheral resistance
274
Q

effects of adrenaline

A
  • Alpha 1 and beta 2 effects helps raise BP and establishes a more adequate circulation
275
Q

metabolism of adrenaline

A

hepatic

276
Q

excretion of adrenaline

A

renal

277
Q

administration of adrenaline

A

IV

278
Q

indication of adrenaline

A

hypovolaemic shock

279
Q

contraindication of adrenaline

A
  • Non-anaphylactic shock
  • Thyrotoxicosis
  • Diabetes
280
Q

adverse effects of adrenaline

A
  • Tachyarrhythmia
  • Ischaemia
  • Headache
  • Flushing
  • Dizziness
  • Palpitations
  • Hypertension
281
Q

monitoring of adrenaline

A

fluid status
electrolyte levels
ECG
BP

282
Q

MOA of vasopressin

A
  • Causes vasoconstriction by acting on V1 (Gq GPCR) receptors
  • This activation in vascular smooth muscle causes increased phospholipase C and IP3
  • V2 receptors in kidneys are also activated to increase water reabsorption
283
Q

effects of vasopressin

A
  • Helps raise BP and thus establish a more adequate circulation
284
Q

metabolism of vasopressin

A

hepatic and renal

285
Q

excretion of vasopressin

A

renal

286
Q

administration of vasopressin

A

IV

287
Q

indication of vasopressin

A

hypovolaemic shock

288
Q

contraindication of vasopressin

A

hypersensitivity

289
Q

adverse effects of vasopressin

A
  • Sweating
  • Nausea
  • Diarrhoea
  • Angina
290
Q

monitoring of vasopressin

A

adverse effects
pt fluid status and electrolytes level

291
Q

MOA of dopamine

A
  • At low dose:
    Activate D1 receptors in renal and mesenteric arteries, which increases adenylate cyclase > increased cAMP and PKA > inhibition of MLCK > vascular SM relaxation and vasodilation
  • At medium dose:
    Activates D1 and beta 1 receptors – increases CO and maintain renal blood flow
  • At high dose:
    Activated alpha-1 and beta-1 receptors
292
Q

effects of dopamine

A
  • Helps raise BP and thus establish a more adequate circulation
293
Q

metabolism of dopamine

A

hepatic, renal, and plasma (monoamine oxidase)

294
Q

excretion of dopamine

A

renal

295
Q

administration of dopamine

A

IV

296
Q

indication of dopamine

A

hypovoalemic shock

297
Q

contraindications of dopamine

A
  • Hypersensitivity
  • Uncorrected tachyarrhythmias
  • Ventricular fibrillation
298
Q

adverse effects of dopamine

A
  • Arrhythmia
  • Tachycardia
  • Angina
  • Palpitation
  • Bradycardia
  • Hypotension
  • Hypertension
  • Vasoconstriction
  • Headache
  • Nausea
  • Ectopic beats
299
Q

monitoring of dopamine

A

for adverse effects - ECG, BP
pt fluid and electrolyte levels

300
Q

common examples of inotropics

A

dobutamine
isoprenaline

301
Q

MOA of dobutamine

A
  • beta agonist (positive inotropes)
  • increases CO via positive chronotropic (HR) and inotropic (contractility) actions
  • minor effect at alpha-1 receptors, hence little effect on peripheral vascular resistance
302
Q

effects of dobutamine

A
  • increase CO via positive chronotropic and inotropic actions
303
Q

metabolism of dobutamine

A

hepatic and tissue

304
Q

excretion of dobutamine

A

renal

305
Q

administration of inotropics

A

IV

306
Q

indication of inotropics

A

hypovolaemic shock

307
Q

contraindication for dobutamine

A

hypersensitivity

308
Q

adverse effects of dobutamine

A
  • Tachyarrhythmia
  • Hypertension
  • Angina
  • Headache
  • Nausea
  • Ectopic beats
  • Palpitations
309
Q

monitoring of dobutamine

A

ECG, BP
fluid levels

310
Q

MOA of isoprenaline

A
  • beta agonist (positive inotropes)
  • increases CO via positive chronotropic (HR) and inotropic (contractility) actions
  • no effect on alpha-1 receptors, so either maintain or increase systolic BP, and decrease diastolic BP by lowering peripheral resistance (beta 1 and 2 effects)
311
Q

effects of isoprenaline

A
  • increase CO via positive chronotropic and inotropic actions
312
Q

metabolism of isoprenaline

A

hepatic

313
Q

exception fo isoprenaline

A

renal

314
Q

contraindications of isoprenaline

A
  • Hypersensitivity
  • Concomitant use with adrenaline
  • Pre-existing ventricular arrhythmias
  • Tachyarrhythmia
  • MI
  • Angina
315
Q

adverse effects of isoprenaline

A
  • Tachycardia
  • Ectopic beats
  • Arrhythmias
  • Platelet aggregation inhibition
  • Hypotension
  • Tachyarrhythmia
  • Ischemia
  • V-fib
316
Q

monitoring of isoprenaline

A

ECG, BP

317
Q

common example of antimuscarinics

A

atropine

318
Q

MOA of atropine

A
  • Nonselective muscarinic receptor antagonist
  • Blocks M2 receptors via Gi on myocardial cells causes an increased rate of firing at SA node and increased conduction velocity through AV node
319
Q

effects of atropine

A
  • Increased conduction at AV node
  • Increased rate at SA node
320
Q

metabolism of atropine

A

hepatic

321
Q

excretion of atropine

A

mainly renal

322
Q

administration of atropine

A

IV

323
Q

indication of atropine

A

bradycardia
AV block

324
Q

contraindication of atropine

A

hypersensitivity

325
Q

adverse effects of atropine

A
  • M3 receptor antagonist effects (relaxation of smooth muscle and decreased glandular secretions):
  • Constipation
  • Urinary retention
  • Blurred vision
  • Dry mouth
  • Dry eyes
326
Q

MOA of digoxin

A
  1. Increases PNS activity (vagal tone) > slow SA node (decreased HR) and AV conduction (negative chronotrope and dromotrope)
  2. Blocks Na/K ATPase on cardiac muscle cell membrane > blocks sodium efflux > Na+ accumulates intracellularly > affects Na+ gradient for Na/Ca exchanger > exchanger is indirectly inhibited by the accumulation of sodium > Ca2+ cannot leave via exchanger as there’s no gradient for sodium influx > calcium accumulates intracellularly as well
327
Q

effects of digoxin

A
  • Decreased HR via SA node and decreased AV conduction (negative chronotropic and dromotropic effects)
  • More intracellular sodium and calcium > positive inotropic effects
  • Proarrhythmic effects
328
Q

metabolism of digoxin

A

hepatic

329
Q

excretion of digoxin

A

mainly renal

330
Q

administration of digoxin

A

oral / IV

331
Q

indication of digoxin

A
  • A-fib (rate control)
    > slows HR and increase contractility)
332
Q

contraindication of digoxin

A
  • Hypersensitivity
  • V-fib

**increased risk of toxicity:
* Renal impairment
* Hypokalaemia (decreased competition for K binding site on Na/K ATPase – toxic effects but no increase in digoxin plasma levels)

333
Q

adverse effects of digoxin

A

**narrow therapeutic index – ineffective below the range, and toxic above the range:
- anorexia – below
- nausea – mid-range
- vomiting – above
* Other signs of toxicity:
- Diarrhoea
- Vision disturbances (halo around objects)
- Confusion
- Agitation
- Life-threatening arrhythmias (atrial or ventricular)
- AV block

334
Q

monitoring for digoxin

A
  • Digoxin plasma levels
  • Renal function
  • K levels
  • ECG recording?
335
Q

MOA of adenosine

A
  • Activates A1 receptors on AV node > inhibits adenylate cyclase > decreased cAMP and PKA > increased outward K current, decreased funny current and Ca influx
336
Q

effects of adenosine

A

decreases AV conduction

337
Q

metabolism of adenosine

A

Phosphorylation to adenosine monophosphate by adenosine kinase, or via deamination to inosine by adenosine deaminase in cytosol

338
Q

excretion of adenosine

A

Via specific nucleoside transporter into RBCs

339
Q

administration of adenosine

A

IV?

340
Q

indication of adenosine

A
  • Supraventricular tachycardia (SVT)
341
Q

contraindication of adenosine

A
  • Hypersensitivity
  • Pre-existing second/ third degree AV block
  • Pt w asthma and COPD
342
Q

adverse effects of adenosine

A
  • Flushing
  • Chest pain
  • Dyspnoea
  • Anxiety
  • Bronchospasm
    ** short-lived effects – 15seconds
343
Q

monitoring of adenosine

A
  • ECG recordings
  • Adverse effects
344
Q

common examples of K channel blockers

A

amiodarone
sotalol

345
Q

MOA of K channel blockers (sotalol and amiodarone)

A
  • Bind and block potassium channels (prevent K efflux) that are responsible for phase 3 repolarisation
346
Q

effects of sotalol and amiodarone

A
  • Slows repolarisation and increases effective (absolute) refractory period
347
Q

metabolism of amiodarone

A

hepatic

348
Q

excretion of amiodarone

A

biliary

349
Q

administration of sotalol and amiodarone

A

oral/ IV

350
Q

indication of sotalol and amiodarone

A
  • Ventricular/atrial arrhythmia
351
Q

contraindication of amiodarone

A
  • Hypersensitivity
  • Preexisting second/ third degree AV block
  • Cardiogenic shock
352
Q

contraindication of sotalol

A
  • Hypersensitivity
  • Preexisting second/ third degree AV block
  • Cardiogenic shock
  • Sinus bradycardia
353
Q

adverse effects of amiodarone

A
  • Hyper/hypothyroidism – dependent on pt pre-existing thyroid hormone levels
  • Pulmonary fibrosis
  • Skin abnormalities
  • GI disturbances
  • Corneal deposits
  • Peripheral neuropathy
  • Liver damage
  • Ventricular arrhythmia (torsades de pointes)
354
Q

adverse effects of sotalol

A
  • Proarrhythmic effects – inc. torsades de pointes (due to increased AP duration)
  • Bradycardia
  • Fatigue
  • Cold extremities
  • Bronchoconstriction
  • Nightmares
  • Hypoglycaemia
355
Q

monitoring for amiodarone

A
  • Hyper/hypothyroidism (thyroid function test)
  • Pulmonary fibrosis (chest XRAY)
356
Q

monitoring for sotalol

A
  • For adverse effects
  • ECG recordings
  • Plasma levels
357
Q

3 classes of sodium channel blockers

A
  1. class Ia: disopyramide (intermediate disso rate)
  2. class Ib: lidocaine (fastest disso rate)
  3. class Ic: flecainide (slowest disso rate)
358
Q

MOA of sodium channel blockers

A
  • Bind and block fast sodium channels that are responsible for rapid depolarisation (phase 0) of non-nodal cardiac AP
359
Q

effects of sodium channel blockers

A
  • Blocking sodium channels reduced velocity of AP transmission within the heart (reduced conduction veloity) – this can suppress tachyarrhythmias that are caused by abnormal conduction
    ** the slower a cell depolarises, the more slowly adjacent cells will become depolarised, which leads to a slower transmission of AP b/n cells
360
Q

metabolism of sodium channel blockers

A

hepatic

361
Q

excretion of sodium channel blockers

A

renal

362
Q

administration of disopyramide

A
  • Orally, either q6h, q12h – doasge dependent on weight
363
Q

administration of lidocaine

A

Slow IV bolus over 2-3 minutes

364
Q

administration of flecainide

A

Orally, twice daily / IV

365
Q

indication of dispyramide

A
  • Serious ventricular arrhythmia (second line)
366
Q

indication of lidocaine

A

serious ventricular arrhythmia

367
Q

indication of flecainide

A
  • Atrial or ventricular arrhythmia (second line)
368
Q

contraindication of disopyramide and lidocaine

A
  • Hypersensitivity
  • Preexisting second/ third degree AV block
369
Q

contraindication of flecainide

A
  • Hypersensitivity
  • Preexisting second/ third degree AV block
  • RBBB
370
Q

adverse effects of sodium channel blockers

A
  • Cardiovascular effects:
  • Arrhythmias (effect greatest for flecainide, least for lidocaine) – proarrhythmic effects
  • AV block and worsening heart failure (flecainide)
  • CNS effects:
  • Drowsiness
  • Dizziness
  • Confusion
  • Anticholinergic effects: (only disopyramide)
  • Tachycardia
  • Dry mouth
  • Constipation
371
Q

monitoring of sodium channel blockers

A

plasma levels
pt response - adverse effects
ECG recordings - arrhythmias

Pharmacology 201 (4 decks)

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