anti hypertensives

Question 1

First line antihypertensives

Answer 1

• ACE-I- AT1 blockers
• beta blockers
• Ca channel blockers
• Diuretics

Question 2

ACE-I drugs

Answer 2

lisinopril, ‘-pril’

Question 3

ACE-I MOA

Answer 3

• binds to angiotensin converter enzyme, prevent angI->angII, reduce angII, reduce water retention via RAAS
• prevent breakdown of bradykinin, which induces NO release & PG activation for vasodilation

Question 4

ACE-I clinical uses

Answer 4

• hypertension
• heart failure
• following MI (reduce afterload & stress on heart)- renal insufficiency

Question 5

ACE-I adverse effects

Answer 5

• hypotension
• acute renal failure
• **angioedema & dry cough (bradykinin & substance P induced inflammation cause angioedema; bradykinin & PG reactions increase airway sensitivity

Question 6

is ACE-I contraindicated in pregnancy

Answer 6

yes. potentially teratogenic

Question 7

AT1 (angiotensin II type 1) blocker

Answer 7

valsartan, losartan ‘-sartan’

Question 8

does AT1 blocker cause dry cough

Answer 8

no. bradykinin breakdown is not inhibited

Question 9

AT1 blocker MOA

Answer 9

blocks receptor which angII binds to

Question 10

is AT1 blocker contraindicated in pregnancy

Answer 10

yes

Question 11

beta blockers drugs (selective, non selective)

Answer 11

non selective
- carvedilol
beta1
- bisoprolol, metoprolol XL
3rd gen
- nebivolol

Question 12

MOA beta 1 blockers

Answer 12

• block B1 receptors, prevent activation of adenylyl cyclase -> ATP not converted to cAMP (cannot activate PKA) -> influx of Ca2+ through Ca channel does not occur -> no CICR
• no formation of actin
  -myosin complex, less contraction (heart beats slower)

Question 13

MOA beta 2 blockers in airway constriction

Answer 13

• block beta receptors, prevent activation of adenylyl cyclase -> ATP not converted to cAMP -> cAMP cannot phosphorylate & inactivate MLCK in smooth muscles via B2 receptor binding -> MLCK in active form, induces contraction in airway

Question 14

Behaviour of nebivolol (3rd gen beta blocker)

Answer 14

• B1 selective in low dose/ fast metabolizers
• non selective in high dose/ slow metabolizers

Question 15

beta blocker clinical uses

Answer 15

• hypertension (decrease pumping strength)
• heart failure (decrease stress on heart)
• angina
• protect from post MI

Question 16

beta blocker contraindicators

Answer 16

• non selective/ 3rd gen -> relatively contraindicated in asthma due to side effect of bronchoconstriction (salbutamol unable to relieve in event of asthma attack due to B2 blockage)

Question 17

beta blocker adverse effects

Answer 17

• hypotension
• bradycardia
• AV nodal block
• clinical depression, vivid dreams (beta blocker blues)

Question 18

Ca channel blockers

Answer 18

• nifedipine, amlodipine (DHP channel blockers)

Question 19

Ca channel blockers MOA for hypertension

Answer 19

• decrease contraction of smooth muscle -> decrease vascular tone -> vasodilation and decrease BP

Question 20

diuretics

Answer 20

thiazide

Question 21

thiazide MOA

Answer 21

• block Na+/Cl- transporter at distal convoluted tubule -> reduce ion uptake -> reduce water uptake and retention-> more urine
• cause increase Ca2+ retention (in replacement of Na+) at distal convoluted tubule

Question 22

thiazide clinical uses

Answer 22

• hypertension
• congestive HF (blood builds up in body due to HF; too much volume)
• nephrolithiasis (kidney stones) by removing Ca2+ from urine
• nephrogenic diabetes insipidus (inability to concentrate urine) by preventing reabsorption of ions

Question 23

thiazide adverse effects

Answer 23

• hypokalaemic metabolic alkalosis
• hyponatremia
• hyperuricaemia
• hyperglycaemia
• hyperlipidaemia
• hypercalcaemia

Question 24

thiazide used carefully with what drugs (DDI)

Answer 24

NSAIDs

Question 25

Second line hypertensives

Answer 25

- hydralazine (1st line HF) - mineralocorticoid receptor antagonist (HF) - alpha adrenergic antagonists

Question 26

alpha adrenergic antagonists examples

Answer 26

prazosin, alfuzosin, terazosin, '-zosin'

Question 27

alpha adrenergic MOA

Answer 27

prevent a1-receptor mediated vascular smooth muscle constriction -> lower vessel tone -> decrease peripheral resistance

Question 28

metabolism of alpha adrenergic antagonists

Answer 28

metabolised by liver, excreted in faeces; can use in patients with renal failure

Question 29

adverse effects of alpha adrenergic antagonists

Answer 29

- reflex tachycardia, palpitations - orthostatic hypotension (low BP when sitting down) - urinary frequency

Question 30

alpha adrenergic antagonists clinical use

Answer 30

- 2nd line anti hypertensive - urinary retention due to benign prostate hyperplasia

Question 31

1st line for HTN: ranking order

Answer 31

A: ACE-I B: beta blocker C: Ca channel blocker D: Diuretics - thiazide