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Cardio pharmaco > Anti hypertensives > Flashcards

Anti hypertensives Flashcards

1
Q

First line antihypertensives

A
  • ACE-I
  • AT1 blockers
  • beta blockers
  • Ca channel blockers
  • Diuretics
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2
Q

ACE-I drugs

A

lisinopril, ‘-pril’

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3
Q

ACE-I MOA

A
  • 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
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4
Q

ACE-I clinical uses

A
  • hypertension
  • heart failure
  • following MI (reduce afterload & stress on heart)
  • renal insufficiency
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5
Q

ACE-I adverse effects

A
  • hypotension
  • acute renal failure
  • **angioedema & dry cough (bradykinin & substance P induced inflammation cause angioedema; bradykinin & PG reactions increase airway sensitivity
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6
Q

is ACE-I contraindicated in pregnancy

A

yes. potentially teratogenic

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7
Q

AT1 (angiotensin II type 1) blocker

A

valsartan, losartan ‘-sartan’

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8
Q

does AT1 blocker cause dry cough

A

no. bradykinin breakdown is not inhibited

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9
Q

AT1 blocker MOA

A

blocks receptor which angII binds to

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10
Q

is AT1 blocker contraindicated in pregnancy

A

yes

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11
Q

beta blockers drugs (selective, non selective)

A

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

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12
Q

MOA beta 1 blockers

A
  • 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)
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13
Q

MOA beta 2 blockers in airway constriction

A
  • 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
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14
Q

Behaviour of nebivolol (3rd gen beta blocker)

A
  • B1 selective in low dose/ fast metabolizers
  • non selective in high dose/ slow metabolizers
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15
Q

beta blocker clinical uses

A
  • hypertension (decrease pumping strength)
  • heart failure (decrease stress on heart)
  • angina
  • protect from post MI
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16
Q

beta blocker contraindicators

A
  • 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)
17
Q

beta blocker adverse effects

A
  • hypotension
  • bradycardia
  • AV nodal block
  • clinical depression, vivid dreams (beta blocker blues)
18
Q

Ca channel blockers

A
  • nifedipine, amlodipine (DHP channel blockers)
19
Q

Ca channel blockers MOA for hypertension

A
  • decrease contraction of smooth muscle -> decrease vascular tone -> vasodilation and decrease BP
20
Q

diuretics

21
Q

thiazide MOA

A
  • 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
22
Q

thiazide clinical uses

A
  • 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
23
Q

thiazide adverse effects

A
  • hypokalaemic metabolic acidosis
  • hyponatremia
  • hyperuricaemia
  • hyperglycaemia
  • hyperlipidaemia
  • hypercalcaemia
24
Q

thiazide used carefully with what drugs (DDI)

25
Q

Second line hypertensives

A
  • hydralazine (1st line HF)
  • mineralocorticoid receptor agonist (HF)
  • alpha adrenergic antagonists
26
Q

alpha adrenergic antagonists examples

A

prazosin, alfuzosin, terazosin, ‘-zosin’

27
Q

alpha adrenergic MOA

A

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

28
Q

time taken to reach peak plasma concentration & half life of alpha adrenergic antagonist drugs

A

2.5 hrs, t1/2 = 7hrs
extensively bound to plasma proteins

29
Q

metabolism of alpha adrenergic antagonists

A

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

30
Q

adverse effects of alpha adrenergic antagonists

A
  • reflex tachycardia, palpitations
  • orthostatic hypotension (low BP when sitting down)
  • urinary frequency
31
Q

alpha adrenergic antagonists clinical use

A
  • 2nd line anti hypertensive
  • urinary retention due to benign prostate hyperplasia
32
Q

1st line for HTN: ranking order

A

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

Cardio pharmaco (6 decks)

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