Anti Hypertensives

Question 1

Classes of drugs used as anti hypertensives

Answer 1

1.ACE-i, ARBs
2.Beta blockers
3.Calcium channel blockers
4.Diuretics (Thiazides)

(2nd line)
5.A-adrenoceptor blocking agents
6.Hydralazine

Question 2

Which class of drugs end with -pril?

Answer 2

ACE inhibitors
Lisinopril, Captopril, Enalapril

Question 3

MOA of Lisinopril

Answer 3

• Inhibits ACE which converts Angiotensin I to Angiotensin II
• Decrease in angiotensin II = decrease in aldosterone secretion and decrease in vasoconstriction
• Decrease in aldosterone decreases Na+ and H2O retention
• Since arterial blood pressure = CO x peripheral resistance
• Decrease blood volume (decrease CO) and decrease vasoconstriction (decrease peripheral resistance) → decrease blood pressure
• Prevents the breakdown of bradykinin to its inactive states
• Bradykinin accumulation results in the activation of prostaglandins and nitric oxide (NO) → further vasodilation

Question 4

Clinical uses of ACE Inhibitors

Answer 4

1. Hypertension
2. Cardiac failure
3. Following myocardial infarction (protective effect)
4. Renal insufficiency

Question 5

Adverse effects of ACE INHIBITORS

Answer 5

• Severe hypotension
• Acute renal failure
• Hyperkalaemia
• Angioedema and dry cough (due to
• bradykinin accumulation)
• Contraindicated in pregnancy

Question 6

Which patients are ACE inhibitors and ARBs contraindicated in?

Answer 6

PREGNANT

Question 7

What does AT1/ARBs blockers end in?

Answer 7

• sartan
  Valsartan, Losartan, Candesartan, Telmisartan

Question 8

MOA of Valsartan

Answer 8

• Blocks angiotensin II type 1 receptor (AT1)
  Prevents the binding of angiotensin II to AT1 to exhibit its effects (vasoconstriction, ADH secretion, aldosterone production, stimulate thirst) → decrease BP

Question 9

Does sartans cause dry cough?

Answer 9

No, as they no longer affect the bradykinin pathways

Question 10

What is one side effect observed in use with ACE inhibitors but not AT1 blockers

Answer 10

DRY COUGH

Question 11

Beta blocker MOA

Answer 11

B1-blockers bind to the beta receptors and decrease myocyte contractility
Decrease contractility and heart rate thus reducing bp

Question 12

Examples of beta blockers

Answer 12

Non-selective: propranolol, pindolol, carvedilol

Beta 1 selective: atenolol, bisoprolol, metoprolol XL

Dose-dependent: Nebivolol (beta 1 selective in low doses, non selective in high doses, also has vasodilatory effects through NO release)

Question 13

Example of non selective beta blockers

Answer 13

propranolol, pindolol, carvedilol

Question 14

Example of selective beta blockers

Answer 14

Beta 1 selective: atenolol, bisoprolol, metoprolol XL

Question 15

Dose dependent selectivity beta blocker example

Answer 15

Dose-dependent: Nebivolol (beta 1 selective in low doses, non selective in high doses, also has vasodilatory effects through NO release)

Question 16

Beta blockers contraindicated in which patients?

Answer 16

1. Avoid giving ASTHMATICS patients non-selective beta blockers as they can bind to b2 receptors and cause beta-blocker associated bronchoconstriction
2. Contraindicated in DIABETICS as it can mask the symptoms of hypoglycaemia

(Beta blockers can mask some of the typical symptoms of low blood sugar (hypoglycemia), such as rapid heartbeat and tremors. This can make it challenging for individuals with diabetes to recognize when their blood sugar is too low and may delay appropriate intervention.)

Question 17

Clinical uses of beta blockers

Answer 17

1. Hypertension
2. Cardiac failure (HR decreases, increasing ventricular filling, more CO)
3. Following myocardial infarction
4. Abnormal heart rhythm
5. Anxiety disorders

Question 18

Adverse effects of beta blockers

Answer 18

1. Bradycardia
2. Reflex tachycardia
3. AV nodal block
4. Reduced exercise capacity (heart does not pump as much)
5. Bronchoconstriction (CONTRAINDICATED IN ASTHMATICS)
6. Beta-blocker blues: clinical depression

Question 19

What kind of CCB is used in HTN?

Answer 19

DHP CCB
Nifedipine, amlodipine

Question 20

MOA of Nifedipine, Amlodipine

Answer 20

Blocks the calcium channel → prevent entry of Ca2+ into cell
Prevent formation of Ca2+-calmodulin complex → MLCK inactivation → no myosin LC activation
No contraction of cell
Relax blood vessels (vasodilation) + Decrease cardiac contractility and CO
Decrease BP

Question 21

Clinical uses of DHP CCB

Answer 21

1. Hypertension
2. Stable angina (amlodipine)
3. Reduce risk of MI and stroke (amlodipine)

Question 22

Adverse effects of DHP CCB

Answer 22

1. Hypotension
2. Heart failure

Question 23

Which channels do Thiazides act on

Answer 23

Blocks the Na/Cl channel at the distal convoluted tubule

Inhibits Na+ reabsorption and therefore decreased fluid reabsorption
Decrease blood volume → decrease CO → decrease blood pressure

Question 24

Side effect of Thiazide on Ca2+ reabsorption

Answer 24

Since the Na+/Ca2+ channel at the basolateral aspect, is working better, more Ca2+ is drawn out from the lumen in exchange for Na+ –> hypercalcaemia

Question 25

Uses of Thiazide

Answer 25

1. Hypertension 2. Congestive heart failure 3. Nephrolithiasis due to idiopathic hypercalciuria (kidney stones) 4. Nephrogenic diabetes insipidus

Question 26

Adverse effects of thiazide

Answer 26

1. Hypokalemic metabolic alkalosis 2. Hyponatraemia 3. Hyperuricemia 4. Hyperglycaemia (contraindicated in diabetics) 5. Hyperlipidaemia 6. Hypercalcaemia

Question 27

What are 2nd line drugs for HTN

Answer 27

1. Alpha adrenergic antagonists 2. Hydralazine

Question 28

Which class of drugs end with -zosins

Answer 28

Alpha adrenergic antagonists Prazosin, Alfuzosin, Terazosin

Question 29

MOA of Prazosin

Answer 29

A-adrenergic antagonists oppose a1-mediated vasoconstriction Keeps the vessel tone lower, reducing peripheral vascular resistance → reduces BP

Question 30

Can alpha adrenergic antagonists be used in pregnancy

Answer 30

yes

Question 31

Adverse effects of a adrenergic antagonists

Answer 31

Reflex tachycardia (due to reduced BP) Depression Urinary frequency Flushing Palpitations

Question 32

Clinical uses of a adrenergic antagonists

Answer 32

1. Symptomatic relief of urine retention due to benign prostate hyperplasia 2. Hypertension

Question 33

MOA of Hydralazine

Answer 33

1. Direct arterial vasodilator → decreases peripheral vascular resistance Inhibits IP3-induced release of Ca2+ from smooth muscle cell sarcoplasmic reticulum 2. Can trigger compensatory NE/adrenaline release by the sympathetic NS (thus increasing CO and useful in HFrEF)

Question 34

Clinical uses of Hydralazine

Answer 34

1. HFrEF (in combination with isosorbide dinitrate, orally, 1st line) 2. Essential hypertension (2nd line) 3. Acute-onset, severe peripartum or postpartum hypertension (IV)

Question 35

Adverse effects of Hydralazine

Answer 35

1. Symptoms associated with baroreflex-associated sympathetic activation: Flushing, tachycardia Hypotension 2. Hydralazine-induced lupus syndrome (HILS): - autoimmune- like symptoms - can be resolved by stopping hydralazine 3. Contraindicated in coronary HD (because hydralazine stimulates the SNS → increase CO → increase oxygen demand → triggering angina)