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PHARMACOLOGY > Cardiovascular pharmacology > Flashcards

Cardiovascular pharmacology Flashcards

1
Q

List 4 types of drugs that fall under cardiac therapy

A

Cardiac glycosides
Antiarrhythmics
Cardiac stimulants
Vasodilators (cardiac disease)

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2
Q

List 3 non-selective beta blocking agents

A

Propranolol
Sotalol
Timolol

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3
Q

List 5 B1 selective drugs

A

Atenolol
Bisoprolol
ESMOLOL
Metoprolol
Nevibilol

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4
Q

Name 2 drugs that are vasodilatory non-B1 selective

A

Carvedilol
Labetalol

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5
Q

Which Beta-blocking agents are cardioselective and are preferred in angina?

A

B1-selective

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6
Q

Which beta blockers are contra-indicated in asthma and COPD?

A

Non-selective beta blockers

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7
Q

Which beta blockers are preferred in CCF

A

Vasodilatory non-B1 selective

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8
Q

Which specific drug is cautioned in asthma?

A

Carvedilol

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9
Q

Which class is preferred in acute coronary syndrome/acute MI, and arrhythmias

A

B1 selective

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10
Q

Which B blocking agent is used as 5th line treatment of Hypertension?

A

B1 selective agent

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11
Q

4 indications for the use of non-selective agents

A

Essential tremor
Symptomatic anxiety
Adjunct in thyrotoxicosis
Migraine prophylaxis

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12
Q

Which beta blockers are lipid soluble (3)

A

propranolol, metoprolol, labetalol

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13
Q

Which beta blockers have the least lipid-solubility? What is the advantage of low lipid-solubility?

A

Atenolol and sotalol
Advantage: fewer CNS adverse effects

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14
Q

6 side effects of beta blockers

A

Bradycardia
Bronchospasm
Masking hypoglycaemia
Fatigue
Cold extremities
Cholesterol dysregulation

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15
Q

Name 2 CNS effects associated with beta blockers

A

insomnia, depression
Lipid soluble: propranolol,
metoprolol, labetalol (MPL - mnemonic)

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16
Q

Contra-indications/cautions of beta blockers

A

Asthma & COPD
Heart block
Diabetes mellitus
Depression (non-selectives)

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17
Q

Name 3 alpha-1 blocking agents

A

Doxazosin
* Prazosin
* Terazosin

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18
Q

3 Indications of alpha-1 blockers

A

Hypertension 4th line (not monotherapy)
Pheochromocytoma-associated hypertension
Benign prostatic hypertrophy (BPH)

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19
Q

What type of formulation is used in alpha1 blockers?

A

Controlled release formulation (daily dose)

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20
Q

Explain metabolism and elimination of alpha1 blockers

A

Extensively metabolised in the liver and excreted mainly as
metabolites in the faeces

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21
Q

COntraindications of alpha-1 blockers

A

Contraindications: Hypersensitivity,
* For controlled-release tablets: history of GI obstruction, oesophageal
obstruction, decreased lumen diameter of GIT

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22
Q

when should alpha 1 blockers be cautioned?

A

In hepatic impairment

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23
Q

Adverse effects of alpha1 blockers (10)

A

First dose hypotension, hypotension, dizziness, vertigo, headache, fatigue
* Orthostatic hypotension, palpitations, nausea

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24
Q

What are the 3 functions of the RAAS system?

A

Coordinate renal and
cardiovascular functions
* Homeostatic control of blood
volume
* Electrolyte balance
* Vascular resistance

25
Q

What is renin, and where is it stored?

A

Proteolytic enzyme
* Stored in juxtaglomerular cells in
kidneys

26
Q

What causes the release of renin?

A

Released; response to :
1. sympathetic activation of B1 receptors,
2. systemic hypotension,
3. decreased tubular Na+

27
Q

What is the mechanism for the release of renin?

A

↓ arterial pressure = ↓ renal
perfusion + baroreflex mediated
sympathetic activation of renal β1
induce release of renin

28
Q

What is the function of aldosterone?

A

Mineralocorticoid
* Increase sodium reabsorption
(promote sodium retention)

29
Q

Function of ADH

A

ADH (also known as vasopressin)
is a posterior pituitary peptide hormone.
* Antidiuretic action on the kidney and powerful vasoconstrictor.

30
Q

What is an example of class 2 Angiotensin-Converting Enzyme inhibitor? (ACEI)

A

Enalapril

31
Q

What is an example of Angiotensin II receptor blockers (ARBs)

A

Losartan

32
Q

MOA of ACE-Inhibitors

A

Inhibit ACE1 which converts angiotensin I to angiotensin II

33
Q

Where do ACE-Is act?

A

Act preferentially on angiotensin-sensitive vascular beds including
kidney, heart and brain

34
Q

Antihypertensive effectiveness is increased by what?

A

Antihypertensive effectiveness increased by
* Low salt diet
* Enhanced renin secretion (patients
on diuretics

35
Q

What are the indications of ACEIs? (6)

A

Indications:
* Hypertension (enhanced by low salt diet) – in Black patients they are less effective in the absence of diuretics
* Reduce mortality in patients with heart failure
* Prevent post-infarct heart failure
* Reduce cardiovascular outcomes in patient at high risk of IHD
* Renoprotective in patients with diabetes mellitus (diabetic
nephropathy) and renal disease with proteinuria
* Prevent progression of chronic kidney disease

36
Q

Why are ACEIs preferred in diabetic pts?

A

Lack negative effects on glucose tolerance and blood lipids
* Reduce microalbuminuria

37
Q

Why are ACEs preferred in patients in congestive heart failure?

A

Counteract overall metabolic-hormonal abnormalities
* Indirect diuretic effect via inhibition of aldosterone production

38
Q

5 contraindications of ACEIs

A

Pregnancy - teratogenic
* History of angioedema and hyperkalaemia
* Bilateral renal artery stenosis or stenosis of an artery to a dominant/single kidney
* Aortic valve stenosis
* Severe renal impairment (eGFR <30ml/min) – unless specialist dose-adjusted

39
Q

What are the general cautions for the use of ACEIs?

A
  • Angioedema rare, but important adverse effect (caused by inhibition of
    bradykinin degradation) – more common in Black patients and those with history
    of allergy
  • Combination with ARBs should be avoided
40
Q

5 adverse effects of ACEIs

A

Adverse effects:
* Dry cough
* Angioedema
* Hyperkalaemia (due to reduced
aldosterone secretion)
* Hypotension
* In patients with bilateral renal artery
stenosis: precipitate renal failure,
because AT2 usually constrict
efferent arterioles and maintains
pressure in the glomerulus for
filtration

41
Q

ROA of ACEIs

A

Administer orally (bioavailability ranges from 25%-75%)

42
Q

Metabolism of ACEIs

A

Varying degrees of first pass hepatic metabolism, several has active
metabolites

43
Q

How is enalapril excreted?

A

Excreted predominantly in the urine as enalaprilat (active metabolite)
and unchanged drug

44
Q

What are the adverse effects of enalapril? (3)

A

Dry cough most common usually happen in early phase of tx (can
happen after many years on tx)
* Angioedema (can happen after many years on tx)
* Hyperkalaemia

45
Q

3 Contraindications of enalapril

A

Bilateral renal artery stenosis, hyperkalaemia, pregnancy

46
Q

Drug interactions with enalapril

A

Other antihypertensives (hypotension)
* Potassium-sparing diuretics / potassium supplements
* ARBs
* High-dose aspirin & all NSAIDs
* Digoxin & lithium
* Trimethoprim

47
Q

MOA of angiotensin receptor blockers (ARBs)

A

Selectively block AT1 receptors (antagonising effects of ATII)
* Reduce vasoconstriction, aldosterone secretion, sodium reabsorption by the proximal tubule and norepinephrine release from sympathetic nerve terminals

48
Q

What is an advantage of using ARBs instead of ACEIs?

A

Equally effective (as ACEIs) in treating hypertension and rarely cause dry cough.
Safe to use in diabetes mellitus (do not affect serum glucose), gout (do not increase serum uric acid levels), dyslipidaemias (do not increase cholesterol levels), ACEI-mediated angioedema (only 8% cross-reactivity)

49
Q

Adverse effects of ARBs (3)

A

Adverse effects: hyperkalemia, neutropenia, increase hepatic
aminotransferase enzymes

50
Q

I contraindication and 1 caution of ARBs

A

Contraindication: pregnancy – cause foetal injury and death
* Caution in patient with renal artery stenosis

51
Q

Lorsatan metabolism

A

First pass metabolism to an active metabolite

52
Q

Half life of Losartan vs half-life of its active metabolite

A

Half-life (losartan): 1.5-2.5 hours
* Half-life (active metabolite): 6-9 hours

53
Q

PPB of Losartan

A

99% PPB

54
Q

Maximal effect of Losartan

A

Maximal antihypertensive effect: 3-6 weeks of tx

55
Q

T/F: Losartan is not uricosuric

A

F

56
Q

Contraindications of Losartan (3)

A

Bilateral renal artery stenosis, hyperkalaemia, pregnancy

57
Q

Cautions of losartan

A
  • Unilateral renal artery stenosis, pre-existing renal insufficiency,
    hypersensitivity (angioedema) to ACEIs
58
Q

Adverse effects of Losartan

A
  • Dizziness, dose-related orthostatic hypotension
  • Hyperkalaemia, raised liver enzymes

PHARMACOLOGY (30 decks)

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