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CVS drugs > Anti Hypertensives > Flashcards

Anti Hypertensives Flashcards

1
Q

Classes of drugs used as anti hypertensives

A

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

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

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2
Q

Which class of drugs end with -pril?

A

ACE inhibitors
Lisinopril, Captopril, Enalapril

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3
Q

MOA of Lisinopril

A
  • 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
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4
Q

Clinical uses of ACE Inhibitors

A
  1. Hypertension
  2. Cardiac failure
  3. Following myocardial infarction (protective effect)
  4. Renal insufficiency
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5
Q

Adverse effects of ACE INHIBITORS

A
  • Severe hypotension
  • Acute renal failure
  • Hyperkalaemia
  • Angioedema and dry cough (due to
  • bradykinin accumulation)
  • Contraindicated in pregnancy
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6
Q

Which patients are ACE inhibitors and ARBs contraindicated in?

A

PREGNANT

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7
Q

What does AT1/ARBs blockers end in?

A
  • sartan
    Valsartan, Losartan, Candesartan, Telmisartan
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8
Q

MOA of Valsartan

A
  • 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
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9
Q

Does sartans cause dry cough?

A

No, as they no longer affect the bradykinin pathways

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10
Q

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

A

DRY COUGH

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11
Q

Beta blocker MOA

A

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

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12
Q

Examples of beta blockers

A

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)

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13
Q

Example of non selective beta blockers

A

propranolol, pindolol, carvedilol

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14
Q

Example of selective beta blockers

A

Beta 1 selective: atenolol, bisoprolol, metoprolol XL

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15
Q

Dose dependent selectivity beta blocker example

A

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

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16
Q

Beta blockers contraindicated in which patients?

A
  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.)

17
Q

Clinical uses of beta blockers

A
  1. Hypertension
  2. Cardiac failure (HR decreases, increasing ventricular filling, more CO)
  3. Following myocardial infarction
  4. Abnormal heart rhythm
  5. Anxiety disorders
18
Q

Adverse effects of beta blockers

A
  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
19
Q

What kind of CCB is used in HTN?

A

DHP CCB
Nifedipine, amlodipine

20
Q

MOA of Nifedipine, Amlodipine

A

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

21
Q

Clinical uses of DHP CCB

A
  1. Hypertension
  2. Stable angina (amlodipine)
  3. Reduce risk of MI and stroke (amlodipine)
22
Q

Adverse effects of DHP CCB

A
  1. Hypotension
  2. Heart failure
23
Q

Which channels do Thiazides act on

A

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

24
Q

Side effect of Thiazide on Ca2+ reabsorption

A

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

25
Q

Uses of Thiazide

A
  1. Hypertension
  2. Congestive heart failure
  3. Nephrolithiasis due to idiopathic hypercalciuria (kidney stones)
  4. Nephrogenic diabetes insipidus
26
Q

Adverse effects of thiazide

A
  1. Hypokalemic metabolic alkalosis
  2. Hyponatraemia
  3. Hyperuricemia
  4. Hyperglycaemia (contraindicated in diabetics)
  5. Hyperlipidaemia
  6. Hypercalcaemia
27
Q

What are 2nd line drugs for HTN

A
  1. Alpha adrenergic antagonists
  2. Hydralazine
28
Q

Which class of drugs end with -zosins

A

Alpha adrenergic antagonists
Prazosin, Alfuzosin, Terazosin

29
Q

MOA of Prazosin

A

A-adrenergic antagonists oppose a1-mediated vasoconstriction

Keeps the vessel tone lower, reducing peripheral vascular resistance → reduces BP

30
Q

Can alpha adrenergic antagonists be used in pregnancy

A

yes

31
Q

Adverse effects of a adrenergic antagonists

A

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

32
Q

Clinical uses of a adrenergic antagonists

A
  1. Symptomatic relief of urine retention due to benign prostate hyperplasia
  2. Hypertension
33
Q

MOA of Hydralazine

A
  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)
34
Q

Clinical uses of Hydralazine

A
  1. HFrEF (in combination with isosorbide dinitrate, orally, 1st line)
  2. Essential hypertension (2nd line)
  3. Acute-onset, severe peripartum or postpartum hypertension (IV)
35
Q

Adverse effects of Hydralazine

A
  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)

CVS drugs (6 decks)

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