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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
Adverse effects of dihydropyridine (amlodipine)?
1. Reflex tachycardia 2. Peripheral oedema (more vasodilation and thus peripheral pooling) 3. Headache 4. Flushing 5. Hypotension 6. Dizziness
26
Describe MoA of verapamil (non-dihydropyridine - phenylalkylamine)
-cardiac-selective (SA node and cardiomyocyte) 1. Decrease HR and contractility —> decrease CO —> decrease BP
27
Adverse effects of verapamil (phenylalkylamine)?
1. Bradycardia (decreased HR) 2. AV block (blocks SA mode) 3. Constipation
28
Clinical uses of verapamil?
HTN, angina, a-fib
29
Describe MoA for diltiazem (benzothiazepine)
- 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
Describe adverse effects of diltiazem
1. Reflex tachycardia 2. Peripheral oedema 3. Headache 4. Flushing 5. Bradycardia 6. AV block 7. A-fib 8. Constipation
31
Clinical uses of diltiazem?
HTN, angina, a-fib
32
What are some common examples of beta receptor antagonists?
1. Metoprolol 2. Atenolol 3. Nebivolol
33
Describe MoA of beta blockers
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
Effects of beta blockers?
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
Adverse effects of beta blockers?
1. Bradycardia 2. Fatigue 3. Cold extremities 4. Bronchoconstriction 5. Nightmares 6. Hypoglycaemia
36
Contraindications of beta blockers?
1. Asthma 2. COPD 3. Bradycardia 4. Peripheral vascular disease 5. DM
37
Contraindication of vascular selective CCB?
Tachyarrhythmias, heart failure
38
Contraindication of cardio-selective CCB?
Heart failure, bradycardia, AV block
39
What drugs are first line hypertensives?
1. ACEI and ARBs 2. Vascular selective CCB 3. Thiazide diuretics (if >65yo)
40
What drugs are second-line antihypertensives?
1. Cardio-selective CCB 2. Beta blockers
41
What is an example of alpha-1 receptor antagonist?
Prazosin
42
Describe MoA of alpha-1 receptor antagonists
- block alpha-1 receptor in vascular smooth muscle —> blockage of SM excitatory effects —> vasodilation
43
Adverse effects of alpha-1 receptor antagonist?
1. Postural hypotension 2. Dizziness 3. Headache 4. Oedema 5. Nasal congestion
44
Common examples of alpha 2 agonists?
Clonidine, methyldopa, moxonidine
45
Describe MoA of alpha 2 receptor agonists
-autoinhibitory - inhibit further NA release, and thus decrease SNS outflow -constant reduction of SNS outflow can cause up-regulation of SNS receptors
46
Drug interaction of alpha 2 receptor agonist?
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
what will sudden cessation of alpha-2 agonists cause?
1. Sudden and dangerous increase in BP (rebound HTN) 2. Withdrawal syndrome: rapid increase in BP, headache, flushing, sweating, insomnia, agitation, tremor
48
Common adverse effects of alpha-2 agonists?
1. Drowsiness 2. Fatigue 3. Bradycardia 4. Dizziness —> due to reduced SNS activity
49
Third line antihypertensives?
Alpha-1 receptor antagonists
50
Last line antihypertensives?
Alpha-2 agonists
51
Contraindication of alpha-1 antagonists?
Avoid use in elderly
52
Contraindication of alpha-2 agonists?
1. Bradycardia 2. AV block 3. Peripheral vascular disease 4. Depression 5. DM
53
When would antihypertensive drug therapy be considered? (3 scenarios relative to CVD risk)
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
What can you pair ACEI/ARB with for combination therapy?
1. Thiazide 2. CCB 3. Dihydropyridine CCB + thiazide
55
What can you pair beta-blocker with in combination therapy?
1. Thiazide 2. Dihydropyridine CCB (amlodipine)
56
What do you want to avoid pairing with beta blocker?
Diltiazem or verapamil (non-dihydropyridine CCBs) —> risk of severe bradycardia and heart block (double effects of blocking heart SNS effects)
57
What do you want to avoid pairing with ACEI?
ARBs —> risk of increasing renal complications

Pharmacology 201 (4 decks)

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