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Renal Pharm > Anti-Hypertensives > Flashcards

Anti-Hypertensives Flashcards

1
Q

Dry mouth; sedation; rebound hypertension (on withdrawal)

A

Clonidine

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2
Q

Reflex tachycardia; Postural hypotension

A

Prazosin; Doxazosin

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3
Q

Sedation; postural hypotension (in volume depleted patients)

A

Methyldopa (Aldomet)

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4
Q

Therapy for hypertension during pregnancy

A

Methyldopa (Aldomet);

Clonidine

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5
Q

Used mainly in men with hypertension plus BPH

A

Prazosin; Doxazosin

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6
Q

βAdrenoceptor antagonists

Non-selective (competitively blocks β1 + β2 adrenoceptors)

(i) βBlockers (via β1) → ↓HR & ↓CO → ↓BP
(ii) β1Blockade → ↓Renin release
(iii) Blockade of β autoreceptors → ↓Sympathetic tone

A

Propranolol

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7
Q

– Dry cough
– Angioedema
– Teratogenic
Hyperkalemia

A

Captopril, Lisinopril, Enalapril, Ramipril

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8
Q

Do not enhance dilator effects of bradykinin

A

AT1- Receptor antagonists

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9
Q

β-Antagonists with Vasodilator Activities

β1 blocker + Vasodilation due to ↑Endothelial Nitric oxide (NO) release

Racemic mixture

D‐isomer → highly selective β1‐blocker;
L‐isomer → Vasodilation via ↑NO release

A

Nebivolol

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10
Q

– Hyperkalemia
– Renal impairment
– Potential teratogen

A

Aliskiren

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11
Q

(i) Reflex tachycardia;
(ii) Fluid retention;
(iii) Excessive hair growth;
(iv) Headaches/Flushing
excess cerebral/cutaneous dilation

A

Minoxidil; Pinacidil

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12
Q

↓Renin release (Kidney):
– ↓Angiotensin II/↓Arteriolar resistance
– ↓Aldosterone → ↓Na+ retention & ↓Blood volume

A

β blockers

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13
Q

a peripheral arteriolar dilator via agonist action at D1 receptors

A

Fenoldopam

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14
Q

Absorbed incompletely from the GIT;

Hardly cross the blood‐brain‐barrier

A

Hydrophilic β blockers

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15
Q

↓Ang. II & Aldosterone secretion; Dilates via ↓in Bradykinin breakdown or Increase in bradykinin secretions

A

Captopril, Lisinopril, Enalapril, Ramipril

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16
Q

Angioedema; teratogenic

A

Losartan, Candesartan, Valsartan, Eprosartan

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17
Q

AT1- Receptor antagonists

Blocks Angiotensin II actions at AT1 Receptors → ↓Vasoconstriction and ↓Aldosterone effects

A

Losartan, Candesartan, Valsartan, Eprosartan

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18
Q

Blood pressure (B.P.) =

A

C.O. x P.R.

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19
Q

bradycardia & cardiac conduction problems; impotence, peripheral vascular insufficiency, hyperglycemia, diabetes, asthma

Withdrawal s/s
nervousness, tachycardia, increase BP

A

Propranolol

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20
Q

Cardiac output (C.O) depends on

A

Stroke Volume (SV) & Heart Rate (HR)

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21
Q

Centrally‐acting sympatholytics

preferential α2 agonist stimulates
central presynaptic α2 adrenergic receptors →
↓Peripheral sympathetic drive via ↓NE release

A

Clonidine

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22
Q

Centrally‐acting sympatholytics
prodrug for methylnorepinephrine

Forms αmethylNE (an α2-agonist)
Central α2-agonism → ↓ Sympathetic tone

A

Methyldopa (Aldomet)

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23
Q

chemically‐related to thiazides but has no diuretic activity

Opens K+ channels → Hyperpolarization & prolonged dilation

  • Long‐lasting arteriolar dilation → rapid fall in systemic vascular resistance and fall in BP
  • Extensively bound to serum albumin & to vascular tissue; Dilates via the opening of K+ channels
A

Diazoxide

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24
Q

Contraindicated in asthma patients

Not effective in African American patients
Avoid nonselective blockers in COPD patients

A

Propranolol

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25
Q

dilates arterioles but not veins

A

Hydralazine

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26
Q

Drug accumulate in patients with
↓hepatic blood flow, e.g., elderly, liver
cirrhosis, & congestive heart failure

A

Lipophilic β blockers

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27
Q

Effectively treats hypertension, particularly in the elderly

A

Nifedipine; Amlodipine; Verapamil; Diltiazem

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28
Q

Elimination T1/2 = 1‐5 h

A

Lipophilic β blockers

29
Q

Elimination T1/2: ↑ when GFR is ↓, e.g.,

elderly, renal insufficiency

A

Hydrophilic β blockers

30
Q

excessive lowering of BP; accumulation of cyanide byproduct of its metabolism

A

Sodium nitroprusside

31
Q

Excreted unchanged or as active

metabolites by the kidney

A

Hydrophilic β blockers

32
Q

Extensive metabolism in gut wall & the
liver (1st pass effect) → Low oral
bioavailability (10‐30%)

A

Lipophilic β blockers

33
Q

extensively metabolized;
excreted in urine [Tó = 6 h; Dosed
once/day; ↓Renal function → ↓Dose]

A

Atenolol

34
Q

Heart Rate (HR) depends on

A

sympathetic & parasympathetic

activities

35
Q

Hydrophilic β blockers

A

Atenolol, Esmolol, Labetolol,

Carteolol, Nadolol

36
Q

hypertension in pregnancy, & hypertension due to phaechromocytoma

A

Labetolol

37
Q

Hypotension
Peripheral edema
Headache/dizziness

A

Nifedipine; Amlodipine

38
Q

Hypotension
Peripheral edema
Headache/dizziness
Cardiodepression

A

Verapamil; Diltiazem

39
Q

KATP channel activators

Selectively dilate arterioles via increases
in K+ efflux through KATP channels

Opens K+ channels → VSM hyperpolarization & relaxation

A

Minoxidil; Pinacidil

40
Q

L-Type Ca2+ channel Blockers

Dihydropyridines (DHPs): Greater block of vascular versus cardiac Ca2+ channels

Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol

A

Nifedipine; Amlodipine

41
Q

L-Type Ca2+ channel Blockers

equi-active on heart & blood vessels

Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol

A

Verapamil; Diltiazem

42
Q

Lipophilic β blockers

A

Propranolol, Metoprolol , Pindolol,

Timolol

43
Q

management of hypertensive emergency; administered with diuretic

A

Sodium nitroprusside
Hydralazine
Fenoldopam
Diazoxide

44
Q

metabolized by

hepatic CYP2D6; T1/2 = 4‐6 h

A

Metoprolol (β1‐selective)

45
Q

Metabolized rapidly
by RBC esterases; T1/2 = 9‐10 min, given by
constant IV infusion

A

Esmolol (β1 blocker)

46
Q

Modulation of central sympathetic drive to the

periphery

A

Lipophilic β‐blockers, e.g., propranolol

47
Q

More effective blocker of RAS than ACE inhibitors

A

AT1- Receptor antagonists

48
Q

nitric oxide donor → Dilation of both arteries & veins

Activates soluble guanylate cyclase (sGC) → ↑Cellular cGMP & VSM cell relaxation & ↓BP

A

Sodium nitroprusside

49
Q

No changes to Cardiac output, serum glucose or lipids

A

ACE Inhibitors

50
Q

Peripheral Resistance (PR) determined by?

A

arteriolar tone

51
Q

Peripheral α‐Adrenoceptor Blockers

Selective αblockade → Arterial dilation

A

Prazosin; Doxazosin

52
Q

Preferred in hypertensive diabetic patients (delay the onset/progression of diabetic renal damage)

A

Captopril, Lisinopril, Enalapril, Ramipril

53
Q

Contraindication: PREGNANCY

A

Captopril, Lisinopril, Enalapril, Ramipril; Losartan, Candesartan, Valsartan, Eprosartan; Aliskiren

54
Q

Primarily to treat severe or intractable

hypertension

A

Minoxidil; Pinacidil

55
Q

Purpose(s) of Poly‐therapy

A 
1. Synergy of efficacy
Vasodilators → Na+ retention &
↑Sympathetic activity (SA)
Diuretics & β‐blockers → ↑Na+
excretion & ↓HR via SA node
2. Enhance long‐term beneficial effect
ACE inhibitors (ACEIs) prevent renal damage in Stage 2 HPT patients;
ACEI → ≈10 mmHg ↓BP
3. Toxicity prevents use of max. dose in mono‐therapy
56
Q

Rapidly, completely absorbed in GIT; easy

entry to CNS → Central side effects

A

Lipophilic β blockers

57
Q

Reflex sympathetic activation → Tachycardia; ↓Insulin release (due to Kchannel opening); Edema (salt and water retention)

A

Diazoxide

58
Q

Reflex tachycardia; headache, flushing & ↑Intraocular pressure

A

Fenoldopam

59
Q

Renin inhibitors
Inhibits the enzyme activity of Renin
– ↓Angiotensin I and Angiotensin II formation
– ↓Aldosterone production and activity

A

Aliskiren

60
Q

Stroke Volume (SV) depends on:

A

Plasma volume & Venous return

61
Q

Sympathetic nerve terminal blockers

adrenergic amine release blocker

A

Guanadrel

62
Q

T1/2 = 6‐24 h; No interaction with liver metabolized

drugs

A

Hydrophilic β blockers

63
Q

Useful in hypertensive patients with predisposition to, or with asthma, diabetes, or peripheral vascular disease

A

Metoprolol

64
Q

VMAT; Vesicular monoamine
transporter blocker

Sympathetic nerve terminal blockers

A

Reserpine

65
Q

β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists;
stimulates as well as blocks β-receptors)

↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP

A

Pindolol

66
Q

β-Antagonists with Vasodilator Activities

α1- + β-adrenergic blockade

has 3:1 ratio of β:α antagonism after oral dosing

A

Labetolol

67
Q

β-Antagonists with Vasodilator Activities

β2-agonism + β-adrenergic blockade

A

Celiprolol

68
Q

β1-Selective (Cardio-selective; β1 receptors predominate in the heart)

A

Metoprolol

69
Q

β2 Agonist activity > β2 Antagonist activity, thus beneficial in treatment of Peripheral Vascular Disease

A

Pindolol

Renal Pharm (14 decks)

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