Cardiovascular pharmacology Flashcards

(58 cards)

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
What is renin, and where is it stored?
Proteolytic enzyme * Stored in juxtaglomerular cells in kidneys
26
What causes the release of renin?
Released; response to : 1. sympathetic activation of B1 receptors, 2. systemic hypotension, 3. decreased tubular Na+
27
What is the mechanism for the release of renin?
↓ arterial pressure = ↓ renal perfusion + baroreflex mediated sympathetic activation of renal β1 induce release of renin
28
What is the function of aldosterone?
Mineralocorticoid * Increase sodium reabsorption (promote sodium retention)
29
Function of ADH
ADH (also known as vasopressin) is a posterior pituitary peptide hormone. * Antidiuretic action on the kidney and powerful vasoconstrictor.
30
What is an example of class 2 Angiotensin-Converting Enzyme inhibitor? (ACEI)
Enalapril
31
What is an example of Angiotensin II receptor blockers (ARBs)
Losartan
32
MOA of ACE-Inhibitors
Inhibit ACE1 which converts angiotensin I to angiotensin II
33
Where do ACE-Is act?
Act preferentially on angiotensin-sensitive vascular beds including kidney, heart and brain
34
Antihypertensive effectiveness is increased by what?
Antihypertensive effectiveness increased by * Low salt diet * Enhanced renin secretion (patients on diuretics
35
What are the indications of ACEIs? (6)
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
Why are ACEIs preferred in diabetic pts?
Lack negative effects on glucose tolerance and blood lipids * Reduce microalbuminuria
37
Why are ACEs preferred in patients in congestive heart failure?
Counteract overall metabolic-hormonal abnormalities * Indirect diuretic effect via inhibition of aldosterone production
38
5 contraindications of ACEIs
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
What are the general cautions for the use of ACEIs?
* 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
5 adverse effects of ACEIs
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
ROA of ACEIs
Administer orally (bioavailability ranges from 25%-75%)
42
Metabolism of ACEIs
Varying degrees of first pass hepatic metabolism, several has active metabolites
43
How is enalapril excreted?
Excreted predominantly in the urine as enalaprilat (active metabolite) and unchanged drug
44
What are the adverse effects of enalapril? (3)
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
3 Contraindications of enalapril
Bilateral renal artery stenosis, hyperkalaemia, pregnancy
46
Drug interactions with enalapril
Other antihypertensives (hypotension) * Potassium-sparing diuretics / potassium supplements * ARBs * High-dose aspirin & all NSAIDs * Digoxin & lithium * Trimethoprim
47
MOA of angiotensin receptor blockers (ARBs)
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
What is an advantage of using ARBs instead of ACEIs?
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
Adverse effects of ARBs (3)
Adverse effects: hyperkalemia, neutropenia, increase hepatic aminotransferase enzymes
50
I contraindication and 1 caution of ARBs
Contraindication: pregnancy – cause foetal injury and death * Caution in patient with renal artery stenosis
51
Lorsatan metabolism
First pass metabolism to an active metabolite
52
Half life of Losartan vs half-life of its active metabolite
Half-life (losartan): 1.5-2.5 hours * Half-life (active metabolite): 6-9 hours
53
PPB of Losartan
99% PPB
54
Maximal effect of Losartan
Maximal antihypertensive effect: 3-6 weeks of tx
55
T/F: Losartan is not uricosuric
F
56
Contraindications of Losartan (3)
Bilateral renal artery stenosis, hyperkalaemia, pregnancy
57
Cautions of losartan
* Unilateral renal artery stenosis, pre-existing renal insufficiency, hypersensitivity (angioedema) to ACEIs
58
Adverse effects of Losartan
* Dizziness, dose-related orthostatic hypotension * Hyperkalaemia, raised liver enzymes