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CVS M2 > Hypertension Drugs > Flashcards

Hypertension Drugs Flashcards

1
Q

What are the types of first line hypertension drugs?

A
  1. ACE-inhibitors (-pril)
  2. Angiotensin Receptor Blockers (-sartan)
  3. Beta-Blockers (-olol)
  4. Calcium Channel Blockers (-dipine + verapamil)
  5. Diuretics (Thiazides) (indapamide, hydrochlorothiazide)
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2
Q

Write out the two flowcharts of control of blood pressure

A

Compare to slides

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2
Q

What is the mechanism of action of ACE inhibitors?

A
  1. Inhibits ACE enzymes so less Ang II
  2. Blocks the inactivation of bradykinin = bradykinin increases, leads to production of NO, PG, ultimately causing vasodilation
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3
Q

What are the clinical uses of ACE inhibitors?

A
  1. Hypertension
  2. Cardiac Failure
  3. Following MI
  4. Renal Insufficiency
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4
Q

What are the adverse effects of ACE inhibitors?

A
  1. Severe Hypotension
  2. Acute Renal Failure
  3. Hyperkalemia
  4. Angioedema (bradykinin and substance P induced “inflammatory-like” responses) & Dry Cough (bradykinin & PG increased sensitivity of bradykinin-dependent airway sensory nerve fibres)
  5. NO in pregnancy
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5
Q

What is the mechanism of action of AT1 blockers?

A

Block action of angiotensin 2 by preventing it from binding to AT1 receptor

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6
Q

What are the adverse effects of AT1 blockers?

A
  1. Dry Cough (less than ACE Inhibitors)
  2. NO to pregnancy
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7
Q

What is the mechanism of action of beta blockers?

A
  1. Blocking beta adrenergic receptor prevents signalling to activate adenylate cyclase
  2. ATP not converted to cAMP
  3. PKA not activated
  4. Calcium channel not opened
  5. No calcium, no CICR, no Ca-calmodulin complex
  6. MLCK not activated
  7. Myosin LC not phosphorylated to active form
  8. Reduced contraction of heart
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8
Q

What are the main types of beta blockers?

A

Non-Selective:
1. Propanolol
2. Pindolol
3. Carvedilol

Cardioselective:
1. Atenolol
2. Bisprolol
3. Metoprolol

Mixed:
1. Nebivolol
- beta 1 selective in low dose
- non-selective in high dose
- vasodilatory effects via NO release

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9
Q

Which beta blockers can also be used to treat heart failure?

A
  1. Carvedilol
  2. Bisoprolol
  3. Metoprolol
  4. Nebivolol
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10
Q

What are the clinical uses of beta blockers?

A
  1. Hypertension
  2. Cardiac Failure
  3. Following MI
  4. Abnormal Heart Rhythm
  5. Anxiety Disorders
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11
Q

What are the adverse effects of beta blockers?

A

Hypotension
Bradycardia
AV nodal block
Reduced Exercise Capacity
Bronchoconstriction
CNS: Vivid Dreams, Clinical Depression

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12
Q

What is the mechanism of action of thiazides?

A
  1. Inhibit NaCl reabsorption at DCT by blocking the transporter
  2. Enhance Ca reabsorption in DCT
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13
Q

What are the clinical uses of thiazides?

A
  1. HTN
  2. Heart Failure
  3. Nephroloithiasis due to idiopathic hypercalcemia
  4. Nephrogenic Diabetes Insipidus
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14
Q

What are the adverse effects of thiazides?

A
  1. Hypokalemic Metabolic Acidosis
  2. Hyponatremia
  3. Hyperurecemia
  4. Hyperglycemia
  5. Hyperlipidemia
  6. Hypercalcemia
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15
Q

What is the mechanism of action of calcium channel blockers?

A
  1. Calcium channel not opened
  2. No calcium, no CICR, no Ca-calmodulin complex
  3. MLCK not activated
  4. Myosin LC not phosphorylated to active form
  5. Reduced contraction of heart
16
Q

What are the clinical uses of calcium channel blockers?

A
  1. HTN
  2. Stable Angina (Amlodipine)
  3. MI and Stroke Prevention (Amlopidine)
17
Q

What are adverse effects of calcium channel blockers?

A
  1. Hypotension
  2. Heart Failure
  3. Myocardial Infarction
18
Q

Some of the calcium channel blockers have multiple uses? What are the drugs and their respective uses?

A
  1. Verapamil, Diltiazem = Antiarrythmics and Anti HTN
  2. Nifedipine, Amlodipine = Anti HTN, Anti Angina
19
Q

What are second line anti-hypertensives?

A
  1. Hydralazine
  2. Mineralocorticoid receptor antagonists (-lactones)
  3. Alpha-adrenergic antagonists (-zosins)
20
Q

What is the mechanism of action of alpha1 antagonists?

A

oppose alpha1 mediated vasoconstriction, keeping vasodilation, reducing peripheral resistances, reducing BP

21
Q

What is the peak plasma concentration time and half life of alpha1 antagonists?

A
  1. 2.5h
  2. t half 7h
22
Q

How is alpha1-antagonists transported in the body?

A

extensively bound to plasma proteins

23
Q

How is alpha1-antagonists metabolised and excreted?

A

metabolised in liver, excreted in feces and bile

24
Q

What are the advantages of using alpha1 antagonists?

A
  1. Does not affect renal blood flow & GFR (safe to use in renal impaired patients)
  2. No teratogenicity
25
Q

What other condition can alpha1 antagonists be used for?

A

BPH

26
Q

What are adverse effects of alpha1 antagonists?

A

Reflex tachycardia, orthostatic hypotension, palpitations, depression, urinary frequency, flushing

CVS M2 (10 decks)

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