Antihypertensives Flashcards

1
Q

Name 4 first line treatments for hypertension

A
  1. ACE-Inhibitors, AT I Blockers
  2. Beta blockers
  3. Calcium channel blockers
  4. Diuretics (Thiazides)
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2
Q

Name 3 second line treatments for hypertension

A
  1. Alpha blockers
  2. Mineralocorticoid receptor antagonists
  3. Hydralazine
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3
Q

Name 2 ACE-I and give their suffix

A

Lisinopril, enalopril, captopril
Suffix is pril

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4
Q

Give 2 MOA of ACE-I

A

Overall decrease in BP by:
1. Inhibiting conversion of Ang I to Ang II (causing decreased vasoconstriction and aldosterone)
2. Inhibiting breakdown of bradykinin (causing increase in NO and PG thus increasing vasodilation)

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5
Q

Give 4 clinical uses of ACE-I

A
  1. Hypertension
  2. Cardiac failure
  3. Renal insufficiency
  4. Following myocardial infarction
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6
Q

Give 5 ADRs of ACE-I

A
  1. Severe hypotension
  2. Hyperkalemia
  3. Acute renal failure
  4. Dry cough
  5. Angioedema
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7
Q

How does ACE-I cause dry cough?

A

Increased accumulation of bradykinin and PG which is postulated to increase sensitivity of bradykinin-dependent airway sensory nerve fibres

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8
Q

How does ACE-I cause angioedema?

A

Increased PG and NO production causes inflammatory like responses like vasodilation, thus causing extravasation of plasma fluid into interstitial space

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9
Q

ACE-I is contraindicated in

A

Pregnancy (due to increase risk of fatal renal failure)

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10
Q

Name 2 AT1 blockers and give their suffix

A
  1. Losartan, Valsartan, Candesartan, Irbesartan, Telmisartan
  2. suffix is -sartan
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11
Q

MOA of Angiotensin II Type 1 blockers

A

Directly binds to Ang II Type 1 receptors, which prevents the binding of Ang II, thus decreasing Ang II effects, eventually lowers BP (similar to ACE-Is)

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12
Q

Which side effect of ACE-I is reduced with AT 1 blocker and why?

A

Reduced dry cough / productive cough.
AT 1 blocker does not interfere with breakdown of bradykinin

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13
Q

Name 3 non-selective beta blockers

A
  1. Propanolol
  2. Pindolol
  3. Carvedilol
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14
Q

A non-selective beta blocker that can be used to treat both hypertension and heart failure

A

Carvedilol

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15
Q

Name 3 cardioselective beta 1 blockers

A
  1. Atenolol
  2. Bisoprolol
  3. Metoprolol XL / metoprolol succinate
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16
Q

Name 2 cardioselective beta 1 blockers that can be used to treat both hypertension and heart failure

A

Bisoprolol and metoprolol XL

17
Q

Name a 3rd generation / mixed beta blocker

A

Nebivolol

18
Q

Give 2 MOA / features of nebivolol

A
  1. Dose dependent selectivity: cardioselective at low doses, but non-selective at high doses
  2. Vasodilation effect due to NO release
19
Q

Give 5 clinical uses of beta blockers

A
  1. Hypertension
  2. Cardiac failure
  3. Arrythmias
  4. Following myocardial infarction
  5. Anxiety disorders
20
Q

Give 6 ADRs of beta blockers

A
  1. Hypotension
  2. Bradycardia
  3. Bronchoconstriction especially in asthmatics
  4. AV nodal block
  5. Decreased exercise capacity
  6. CNS Effects: vivid dreams, CNS depressant (beta-blocker blues)
21
Q

Name the 2 types of beta blocker blockades

A
  1. beta 1 blockade
  2. beta 2 blockade
22
Q

How does beta 1 blockade result in decreased cardiac contraction?

A

Inhibits activation of adenylyl cyclase, thus inhibiting cAMP production, causing inhibition of PKA, thus inhibiting CICR, decreasing formation of Ca-calmodulin complex, decrease activation of MLCK, inhibit actvation of myosin LC, thus decrease contraction

23
Q

How does beta 2 blockade cause bronchoconstriction / smooth muscle contraction

A

Inhibit cAMP production, thus inhibiting phosphorylation of MLCK, decrease bronchodilation, thus increase bronchoconstriction

24
Q

Which part of the nephron do thiazides work at?

A

Distal convoluted tubule

25
Q

MOA of thiazides

A

Inhibits Na+Cl- reabsorption by blocking the apical Na+ Cl- cotransporter of the DCT cells, leading to increased activity of the basolateral Na+ Ca2+ exchanger, thus enhancing calcium reabsorption

26
Q

Name 2 thiazides

A
  1. Hydrochlorothiazide
  2. Indapamide
27
Q

Name a class of drugs that interferes with thiazide action and explain why

A

NSAIDs
Action of thiazides depend on renal PG synthesis. NSAIDs reduce PG synthesis, thus interfere with thiazide action

28
Q

Name 4 clinical uses for thiazides

A
  1. Hypertension
  2. Congestive heart failure
  3. Nephrolithiasis due to idiopathic hypercalciuria
  4. Nephrogenic diabetes insipidus
29
Q

Name 6 ADRs of thiazides

A
  1. Hypokalemia metabolic alkalosis
  2. Hyponatremia
  3. Hyperglycemia
  4. Hyperlipidemia
  5. Hyperuricemia
  6. Hypercalcemia
30
Q

Name 3 alpha-1 adrenergic antagonists and state their suffix

A
  1. Prazosin
  2. Alfuzosin
  3. Terazosin
    Suffix: -zosin
31
Q

MOA of alpha 1 adrenergic antagonists

A

Antagonises / reduces alpha 1 mediated vasoconstriction effect, which keeps vessels dilated, thus increasing TPR which lowers BP

32
Q

Alpha-1 antagonists are safe to use in 2 kinds of patients

A
  1. Renal impairment: No effect on renal blood flow and GFR
  2. Pregnant patients: No known teratogenicity
33
Q

Name 3 common early ADRs of alpha-1 antagonists

A
  1. Reflex tachycardia
  2. Palpitations
  3. Orthostatic hypotension
34
Q

Name 3 other ADRs of alpha-1 antagonists

A
  1. Depression
  2. Urinary frequency
  3. Flushing