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Year 4 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is the mechanism of action for angiotensin converting enzyme (ACE) inhinbitors?

A
  • ACE inhibitors block conversion of angiotensin I to angiotensin II and also inhibit the breakdown of bradykinin
  • Reduce the effects of angiotensin II-induced vasoconstriction, sodium retention and aldosterone release.
  • Reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
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2
Q

What are some examples of ACE inhibitors?

A
  • Enalapril
  • Perindopril
  • Ramapril
  • Lisinopril
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3
Q

What are the indications for an ACE inhibitor?

A
  • Hypertension
  • Chronic systolic heart failure as part of standard treatment (eg with beta-blocker, diuretics)
  • Diabetic nephropathy
  • Prevention of progressive renal failure in patients with persistent proteinuria (>1 g daily)
  • Post MI
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4
Q

What are the side effects of ACE inhibitors?

A
  • Dry cough
  • 10% hypotension
  • fatigue
  • hyperkalemia
  • renal insufficiency
  • angioedema
  • Rash - some are photosensitive
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5
Q

What are the contraindications of an ACE inhibitor?

A
  • Bilateral renal artery stenosis
  • pregnancy
  • caution in decreased GFR
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6
Q

What is the mechanism of action of angiotensin II antagonists and angiotensin receptor antagonists (ARA) or blockers (ARB), AKA sartans?

A
  • Competitively block binding of angiotensin II to type 1 angiotensin (AT1) receptors.
  • They reduce angiotensin II-induced vasoconstriction, sodium reabsorption and aldosterone release.
  • They also reduce the effect of angiotensin II on sympathetic nervous activity and growth factors.
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7
Q

What are some examples of angiotensin II antagonists and angiotensin receptor antagonists (ARA) or blockers (ARB)?

A
  • Candesartan
  • Irbesartan
  • Valsartan
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8
Q

What are the indications for an ARB?

A
  • Hypertension
  • Chronic systolic heart failure as part of standard treatment (eg with beta-blocker, diuretics) in patients unable to tolerate ACE inhibitors.
  • Same as ACEI, although evidence is generally less for ARBs; often used when ACEI are not tolerated
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9
Q

What are the side effects of an ARB?

A
  • dizziness, headache
  • 10% hypotension
  • fatigue
  • hyperkalemia
  • renal insufficiency
  • angioedema
  • Rash - some are photosensitive
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10
Q

What are the contraindications of ARBs?

A
  • Bilateral renal artery stenosis
  • pregnancy
  • caution in decreased GFR
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11
Q

What is the mechanism of action of ß-blockers?

A
  • Competitively block beta receptors in heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver.
  • Beta-blockers reduce heart rate, BP and cardiac contractility; also depress sinus node rate and slow conduction through the atrioventricular (AV) node, and prolong atrial refractory periods.
  • The affinity of individual beta-blockers for beta receptors varies
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12
Q

What are some examples of ß-blockers?

A
  • ß1 antagonists - atenolol, metoprolol, bisoprolol
  • ß1/ß2 antagonists - propranolol
  • α1/ß1/ß2 antagonists - labetalol, carvedilol
  • ß1 antagonists with intrinsic sympathomimetic activity - acebutalol
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13
Q

What are the indications of use for a ß-blocker?

A
  • Hypertension
  • Angina
  • Tachyarrhythmias
  • MI
  • Chronic systolic heart failure as part of standard treatment (eg with ACE inhibitor, diuretics)
  • Prevention of migraine
  • Propranolol - prevents variceal bleeding in cirrhosis.
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14
Q

What are the side effects of a ß-blocker?

A
  • bradycardia, hypotension, orthostatic hypotension (especially carvedilol, labetalol)
  • transient worsening of heart failure (when treatment starts)
  • nausea, diarrhoea, bronchospasm, dyspnoea
  • cold extremities, exacerbation of Raynaud’s phenomenon
  • fatigue, dizziness, abnormal vision
  • alteration of glucose and lipid metabolism
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15
Q

What are the contraindications to ß-blockers?

A
  • Sinus bradycardia
  • 2nd or 3rd degree heart block
  • hypotension
  • Wolff-Parkinson-White syndrome
  • Caution in asthma,
  • claudication
  • Raynaud’s phenomenon
  • decompensated CHF
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16
Q

What are the practical points to know about ACE inhibitors?

A
  • when starting an ACE inhibitor:
    • stop potassium supplements and potassium-sparing diuretics
    • in heart failure, consider reducing dose or withholding other diuretics for 24 hours before starting an ACE inhibitor
    • review use of NSAIDs (including selective COX‑2 inhibitors)
    • start with a low dose
  • check renal function and electrolytes before starting an ACE inhibitor and review after 1–2 weeks
17
Q

What are the practical points of an ARB?

A
  • when starting a sartan:
    • stop potassium supplements and potassium-sparing diuretics
    • in heart failure, consider reducing dose or withholding other diuretics for 24 hours before starting a sartan
    • review use of NSAIDs (including selective COX‑2 inhibitors)
    • start with a low dose
  • check renal function and electrolytes before starting a sartan and review after 1–2 weeks
  • unlike ACE inhibitors, sartans do not inhibit the breakdown of bradykinin and may be useful if an ACE inhibitor is not tolerated because they:
    • cause less cough than ACE inhibitors
    • may be used if there is a history of angioedema caused by an ACE inhibitor (with close monitoring as there is a small risk of recurrence)
  • maximum antihypertensive effect occurs about 4–6 weeks after starting treatment
18
Q

What are the practical points of a ß-blocker?

A
  • beta-blockers are not usually recommended first line for uncomplicated essential hypertension; they are associated with reduced protection against stroke in the elderly (most comparative studies used atenolol, which is associated with higher cardiovascular mortality and stroke compared to other antihypertensives)
  • when stopping treatment, reduce dosage gradually, eg over at least 2 weeks; avoid abrupt withdrawal as it may exacerbate angina, or precipitate rebound hypertension, MI or arrhythmias
19
Q

What is the mechanism of action of calcium channel blockers?

Benzothiazepines and phenylalkylamines (non-dihydropyridines).

A
  • Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
  • Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
  • Non-dihydropyridines: diltiazem and verapamil act on cardiac and arteriolar smooth muscle. They reduce cardiac contractility, heart rate and conduction, with verapamil having the greater effect. Diltiazem has a greater effect on arteriolar smooth muscle than verapamil.
20
Q

What is the mechanism of action of calcium channel blockers?

Dihydropyridines

A
  • Block inward current of calcium into cells in vascular smooth muscle, myocardium and cardiac conducting system via L‑type calcium channels.
  • Act on coronary arteriolar smooth muscle to reduce vascular resistance and myocardial oxygen requirements, relieving angina symptoms.
  • Dihydropyridines act mainly on arteriolar smooth muscle to reduce peripheral vascular resistance and BP. They have minimal effect on myocardial cells.
21
Q

What are some examples of non-dihydropyridines calcium channel blockers?

A
  • diltiazem
  • verapamil
22
Q

What are some examples of dihydropyridines calcium channel blockers?

A
  • Amlodipine
  • Nifedipine
  • Felodipine
23
Q

What are the indications of use for a calcium channel blocker?

A
  • Hypertension
  • Angina
24
Q

What are the side effects of calcium channel blockers?

A
  • nausea
  • vasodilatory effects: including headache, flushing, dizziness, hypotension, peripheral oedema
25
Q

What are the contraindications of use for calcium channel blockers?

A
  • Non-dihydropyridines:
    • Sinus bradycardia
    • 2nd or 3rd degree heart block
    • hypotension
    • Wolffe-Parkinson-White syndrome
    • CHF
  • Dihydropyridines
    • Severe aortic stenosis and liver failure
26
Q

What is the effect of an acetylcholinesterase inhibitor or anticholinesterase?

A

An acetylcholinesterase inhibitor or anticholinesterase is a chemical that inhibits the cholinesterase enzyme from breaking down acetylcholine (ACh), so increasing both the level and duration of action of the neurotransmitter acetylcholine.

ACh can stimulate postganglionic receptors to produce effects such as:

  • Salivation
  • Lacrimation
  • Defecation
  • Micturition
  • Sweating
  • Miosis
  • Bradycardia, and
  • Bronchospasm.

Year 4 (25 decks)

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