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Pharmacology 201 > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

What are the three mechanisms that antihypertensives work along?

A
  1. Reduced TPR
  2. Reduced CO
  3. Reduced autonomic sympathetic outflow
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2
Q

What drugs work to reduce TPR?

A
  1. ACEI
  2. ARBs
  3. Alpha-1 receptor antagonists
  4. Vascular-selective CCB
  5. Thiazide diuretics
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3
Q

What drug works to reduce CO?

A
  1. Beta-receptor antagonists
  2. Cardio-selective CCB
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4
Q

What drug reduces autonomic sympathetic outflow?

A

Alpha-2 receptor agonists

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5
Q

Describe MoA of ACEI

A

Inhibit ACE, which then inhibit conversion of AI into AII, thus production of AII

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6
Q

What are some common ACEIs?

A

Captopril, enalapril, ramipril, fosinopril, lisinopril, perindopril

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7
Q

Describe MoA of ARBs

A

Inhibit the action of angiotensin II on AT1 receptors

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8
Q

What are some common ARBs?

A

Candesartan, irbesartan, losartan, valsartan, eprosartan

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9
Q

What is the therapeutic effects of ACEI and ARBs?

A
  1. Decreased vasoconstriction —> decreased BP
  2. Decreased Aldo secretion —> decreased Na and water retention —> decreased K excretion —> decreased BV —> decreased BP
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10
Q

What are the common adverse effects of ACEI and ARBs?

A
  1. Hypotension
  2. Dizziness
  3. Hyperkalaemia
  4. Dry cough (in ACEI due to accumulation of bradykinin)
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11
Q

List common examples of thiazide diuretics?

A
  1. Hydrochlorothiazide
  2. Indapamide
  3. Chlorthalidone
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12
Q

Describe MoA of thiazide diuretics

A
  1. Inactivate NA/Co cotransporter in distal tubule of kidneys —> loss of Na, Cl and water
  2. Vasodilation through unknown mechanism
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13
Q

what are the adverse effects of thiazide diuretics?

A
  1. Postural hypotension
  2. Dizziness
  3. Hypokalaemia
  4. Hyperuricaemia
  5. Hyperglycaemia
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14
Q

What are the contraindications in ACEI and ARBs?

A
  1. Hyperkalaemia
  2. Pregnancy
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15
Q

What are the contraindications in thiazide diuretics?

A
  1. Glucose intolerance
  2. DM
  3. Gout
  4. Pregnancy
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16
Q

Describe MoA of CCB

A

Blocks L-type voltage gated calcium channels in cardiac and smooth muscle

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17
Q

What is the effect of CCB in cardiac muscle cells?

A
  1. Decreased HR
  2. Decreased AV conduction
  3. Decreased myocardial contractility
    —> net reduction in CO and thus BP
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18
Q

What is the effect of CCB in smooth muscle cells?

A
  • no intracellular calcium = no contraction
    1. Decrease vascular smooth muscle contraction
    2. Decrease vascular tone —> vasodilation
    —> net reduction in vascular resistance and thus BP
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19
Q

What are the 3 classes of CCB?

A
  1. Dihydropyridine
  2. Non-dihydropyridine (phenylalkylamine)
  3. Non-dihydropyridine (benzothiazepine)
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20
Q

Example of dihydropyridine?

A

Amlodipine, celvidipine, felodipine, lecarnidipine, nimodipine

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21
Q

Example of phenylalkylamine?

A

Verapamil

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22
Q

Example of bezothiazepine?

A

Diltiazem

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23
Q

Describe MoA of dihydropyridine CCB (amlodipine)

A
  • vascular selective
    1. Arterial vasodilation —> decreased arterial pressure (BP)
24
Q

Clinical uses of dihydropyridine (amlodipine)?

A

HTN, angina

25
Q

Adverse effects of dihydropyridine (amlodipine)?

A
  1. Reflex tachycardia
  2. Peripheral oedema (more vasodilation and thus peripheral pooling)
  3. Headache
  4. Flushing
  5. Hypotension
  6. Dizziness
26
Q

Describe MoA of verapamil (non-dihydropyridine - phenylalkylamine)

A

-cardiac-selective (SA node and cardiomyocyte)
1. Decrease HR and contractility —> decrease CO —> decrease BP

27
Q

Adverse effects of verapamil (phenylalkylamine)?

A
  1. Bradycardia (decreased HR)
  2. AV block (blocks SA mode)
  3. Constipation
28
Q

Clinical uses of verapamil?

A

HTN, angina, a-fib

29
Q

Describe MoA for diltiazem (benzothiazepine)

A
  • both cardiac and vascular selective, but less effects on cardiac cells than verapamil
    —> works on both SA node, cardiac and vascular SM
    1. Arterial vasodilation —> decrease BP
    2. Decreased HR and contractility —> decreased CO and BP
30
Q

Describe adverse effects of diltiazem

A
  1. Reflex tachycardia
  2. Peripheral oedema
  3. Headache
  4. Flushing
  5. Bradycardia
  6. AV block
  7. A-fib
  8. Constipation
31
Q

Clinical uses of diltiazem?

A

HTN, angina, a-fib

32
Q

What are some common examples of beta receptor antagonists?

A
  1. Metoprolol
  2. Atenolol
  3. Nebivolol
33
Q

Describe MoA of beta blockers

A

Blocks beta 1 receptor in cardiac muscle
1. Activation of beta 1 receptor normally increases intracellular calcium via increase cAMP and PKA (blocking this receptor would mean intracellular calcium decreases)
2. Opposes SNS action - less HR, AV conduction, contractility
3. Less CO and thus BP

34
Q

Effects of beta blockers?

A
  1. Decreased HR and contractility
  2. Decreased AV conduction
  3. Decreased automacity
  4. Decreased oxygen consumption by myocardium
  5. Negative inotropic (contractility) and chronotropic (rate)
  6. Decreased CO and BP
    —> overall reduction in SNS effects on cardiac muscle
35
Q

Adverse effects of beta blockers?

A
  1. Bradycardia
  2. Fatigue
  3. Cold extremities
  4. Bronchoconstriction
  5. Nightmares
  6. Hypoglycaemia
36
Q

Contraindications of beta blockers?

A
  1. Asthma
  2. COPD
  3. Bradycardia
  4. Peripheral vascular disease
  5. DM
37
Q

Contraindication of vascular selective CCB?

A

Tachyarrhythmias, heart failure

38
Q

Contraindication of cardio-selective CCB?

A

Heart failure, bradycardia, AV block

39
Q

What drugs are first line hypertensives?

A
  1. ACEI and ARBs
  2. Vascular selective CCB
  3. Thiazide diuretics (if >65yo)
40
Q

What drugs are second-line antihypertensives?

A
  1. Cardio-selective CCB
  2. Beta blockers
41
Q

What is an example of alpha-1 receptor antagonist?

A

Prazosin

42
Q

Describe MoA of alpha-1 receptor antagonists

A
  • block alpha-1 receptor in vascular smooth muscle —> blockage of SM excitatory effects —> vasodilation
43
Q

Adverse effects of alpha-1 receptor antagonist?

A
  1. Postural hypotension
  2. Dizziness
  3. Headache
  4. Oedema
  5. Nasal congestion
44
Q

Common examples of alpha 2 agonists?

A

Clonidine, methyldopa, moxonidine

45
Q

Describe MoA of alpha 2 receptor agonists

A

-autoinhibitory - inhibit further NA release, and thus decrease SNS outflow
-constant reduction of SNS outflow can cause up-regulation of SNS receptors

46
Q

Drug interaction of alpha 2 receptor agonist?

A

Increased sensitivity to sympathomimetics - due to up-regulation of SNS receptors secondary to constant reduction of SNS outflow
E.g. alpha-1 agonists —> can cause sudden and dangerous increase in BP

47
Q

what will sudden cessation of alpha-2 agonists cause?

A
  1. Sudden and dangerous increase in BP (rebound HTN)
  2. Withdrawal syndrome: rapid increase in BP, headache, flushing, sweating, insomnia, agitation, tremor
48
Q

Common adverse effects of alpha-2 agonists?

A
  1. Drowsiness
  2. Fatigue
  3. Bradycardia
  4. Dizziness
    —> due to reduced SNS activity
49
Q

Third line antihypertensives?

A

Alpha-1 receptor antagonists

50
Q

Last line antihypertensives?

A

Alpha-2 agonists

51
Q

Contraindication of alpha-1 antagonists?

A

Avoid use in elderly

52
Q

Contraindication of alpha-2 agonists?

A
  1. Bradycardia
  2. AV block
  3. Peripheral vascular disease
  4. Depression
  5. DM
53
Q

When would antihypertensive drug therapy be considered? (3 scenarios relative to CVD risk)

A
  1. High risk (>15% CVD risk)
  2. Moderate risk (10-15%): if BP is consistently > 140/90mmHg or if other CVD risk factors are present
  3. Low risk (less than 10%): if BP consistently > 160/100mmHg
54
Q

What can you pair ACEI/ARB with for combination therapy?

A
  1. Thiazide
  2. CCB
  3. Dihydropyridine CCB + thiazide
55
Q

What can you pair beta-blocker with in combination therapy?

A
  1. Thiazide
  2. Dihydropyridine CCB (amlodipine)
56
Q

What do you want to avoid pairing with beta blocker?

A

Diltiazem or verapamil (non-dihydropyridine CCBs)
—> risk of severe bradycardia and heart block (double effects of blocking heart SNS effects)

57
Q

What do you want to avoid pairing with ACEI?

A

ARBs
—> risk of increasing renal complications

Pharmacology 201 (4 decks)

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