Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVS drugs > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

What are the first line antihypertensive drugs?

A
  1. Angiotensin inhibitors (ACE-is) and (ARBs)
  2. Beta blockers
  3. Calcium Channel Blockers
  4. Diuretics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some common ACE-Is?

A
  1. Lisinopril (Long half-life)
  2. Enalapril (Long half-life)
  3. Captopril (Short half-life)

All drugs -pril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mechanism of ACE-Is

A
  • Blocks conversion of Ang1 to Ang2
  • Lesser vasoconstriction and aldosterone levels
  • Lower aldosterone levels will lead to lower Na+/H2O retention thereby lowering BP
  • Decrease peripheral resistance and reduce BP
  • Blocks inactivation of Bradykinin
    -Bradykinin levels increase
  • Forms NO and PG which causes vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are ACE-Is excreted

A

Renal excretion, decreased dose in renal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Side effects of ACE-Is

A
  1. Severe Hypotension (All hypertensive drugs can cause Hypotension)
  2. No reflex sympathetic activation, ACE-Is reset pressure sensor sensitivity, blocking baroreceptor reflex
  3. Acute renal failure
  4. Hyperkalemia, increase K+ retention in bloodstream
  5. Angioedema/Dry cough induced by bradykinin and Substance P
  6. Angioedema (Allergic run, lip tongue swelling)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which group is ACE-Is contraindicated in?

A

Pregnant woman

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Clinical indications for ACE-Is

A
  • Hypertension
  • Cardiac failure (Following MI, together with aspirin, beta-blocker and statins)
  • Renal insufficiency (Decrease efferent arteriole vasoconstriction, decrease glomerular pressure, decrease proteinuria and increases function)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name some common Ang2 Type 1 (AT1) receptor blockers

A
  1. Losartan
  2. Valsartan
  3. Candesartan

all dugs -sartan
(Medications of choice if ACE-Is cannot be tolerated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why doesn’t AT1 cause dry cough

A

Angiotensin II type I inhibitors don’t increase the bradykinin levels, thus no bradykinin effect systemically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some common beta blockers?

A

Non selective:
1. Propanolol
2. Pindolol
3. Carvedilol

Cardioselective:
1. Atenolol
2. Bisoprolol
3. Metoprolol XL

Mixed (3rd Generation):
1. Nebivolol (Beta 1 selective in lower dose, non-selective in higher dose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define cardioselective

A

Selective inhibits Beta 1 adrenoceptors (works on the heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Nebivolol mechanism

A

Decreases vascular resistance by stimualting β-3 receptors and activating NO synthase in the vasculature
Release of NO for vasodilatory effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mechanism of beta blockers in hypertension

A
  • Diminish phase 4 depolarisation
  • Depress automaticity
  • Prolong AV conduction
  • Decrease Heart rate and contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does beta-1 adrenoceptor antagonist reduce BP

A
  1. Decreases contractility of calcium channels, leading to decreased Calcium influx and Ca-calmodulin complex formation
  2. Inactivation of MLCK and hence unable to convert Myosin-LC to Myosin-LC# which deactivates it and reduce contraction
  3. Relaxation of cardiac muscles and reduce contractility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why are non-selective beta blockers (Propranolol) contraindicated in asthmatic patients

A
  • Blocking beta 2 receptors on smooth muscles prevents the relaxation of the muscles (phosphorylation of MLCK and deactivate it)
  • Asthma very easily provokes this problem
  • Adrenaline originally provides a base level of broncho relaxation
  • Without which due to beta blockers, there will no longer be a baseline level of dilation for smooth muscles, increasing chances of an asthma attack
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Adverse effects of Beta Blockers

A
  1. Bradycardia
  2. CNS: Mild sedation, vivid dreams
  3. Asthma
  4. Withdrawal symptoms: Upregulation or super sensitivity of adrenoceptors
  5. Contraindicated in diabetic patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why are beta blockers dangerous for diabetic patients?

A

Masking of Hypoglycemia Symptoms:

Symptoms of hypoglycemia, such as tachycardia and palpitations, are partly mediated by the release of adrenaline (epinephrine), which activates beta receptors.

Beta blockers block the effects of adrenaline, which can prevent the typical symptoms of hypoglycemia, leading to delayed recognition and treatment of low blood sugar levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are some typical calcium channel blockers?

A

DHP CCB
1. Nifedipine
2. Felodipine

Non DHP CCB
1. Verapamil
2. Diltiazem

19
Q

What’s the difference between DHP and non DHP CCB?

A

DHP predominantly work on smooth muscle cells whereas non-DHP acts on cardiac cells

Therefore as a cardiac depressant: Verapamil&raquo_space; Diltiazem&raquo_space; Nifedipine
However, as a Vasodilator: Nifedipine&raquo_space; Diltiazem&raquo_space; Verapamil

20
Q

Mechanism of Nifedipine (DHP)

A
  • Preferentially targets L type calcium channels in smooth muscle cells
  • Binds to and blocks L type Calcium channels
  • Decreased frequency of Ca2+ channel opening in response to cell membrane depolarisation → decreased transmembrane Ca2+ current
  • Vascular smooth muscles relax leading to vasodilation → decrease PVR → decreased afterload → decreased BP
  • Ca2+ binds to Calmodulin forming Calcium-calmodulin complex, activates Cam-kinase
  • Cam-kinase converts myosin light chain kinase to phosphorylated myosin light chain kinase
21
Q

Mechanism of non-DHP (Verapamil)

A
  1. Blocks Ca2+ channes
  2. Decrease intracellular Ca2+
  3. Decrease SA/AV node conduction
  4. Decrease supraventricular, re-entry tachycardia
22
Q

Adverse effects of DHP CCB

A
  • Headache
  • Peripheral edema
  • Flushing
  • Reflex tachycardia
  • Gingival hyperplasia
23
Q

Adverse effects of non-DHP CCB

A
  • Cardiac depression: Bradycardia, AV block, Heart failure
    Due to decrease HR and contractility, inhibition of signal transaction from atrium to ventricle thus cannot be used to treat heart failure
24
Q

Route of administration of CCB

A
  1. Oral high first pass effect
  2. Verapamil and Nifedipine also IV
  3. More selective for cardiac muscle (Verapamil > Diltiazem)
25
Q

What are the 3 main classes of diuretics?

A
  1. Loop diuretics
  2. Thiazides
  3. K+ Sparing diuretics
26
Q

Which part of the renal system does loop diuretics work on?

A

Thick ascending loop of hence

27
Q

Examples of loop diuretics?

A

Furosemide and other sulfonamides (Strongest diuretics)

28
Q

Mechanism of loop diuretics

A

Inhibits the function of the Na+K+2Cl- co-transporter (NKCC co transporter)

Reduce Na+, Cl-, Mg2+ and Ca2+ from getting reabsorbed back into the bloodstream

Counters the countercurrent multiplier mechanism

Reduces the osmolarity difference between the intercellular space and the descending loop of henle thus less water diffuses out of the descending loop of henle

More water excreted as urine -> BP decreases

29
Q

Pk of loop diuretics

A

Rapidly absorbed
Rapid response upon IV injection
Lasts for 2-3h
Eliminated by tubular secretion as well as by glomerular filtration

30
Q

Clinical uses of loop diuretics

A
  • Acute pulmonary edema and other edema
  • Acute hyperkalemia
  • Acute renal failure
  • Anion overdose, toxic ingestion of bromide fluoride iodide
    -Severe Hypertension
31
Q

Adverse effects of loop diuretics

A
  • Hypokalaemia, metabolic alkalosis
    • Loss of ions like Cl- lead to compensatory mechanism of body by increasing HCO3- ions, thus it is in relative excess and hence leading to metabolic alkalosis
    • Cellular uptake of H+ ions caused by hypokalaemia in exchange for K+ ions will further increase the concentration of bicarbonate ions in the bloodstream

-Ototoxicity (Avoid with aminoglycoside)

32
Q

Name common thiazides

A

Hydrochlorothiazide, Chlorthiazide

33
Q

Where does thiazides work on

A

Early Distal Convoluted Tubule

34
Q

Mechanism of thiazides

A
  • Blocking the Na+/Cl- transporter
  • Less Na+ & Cl- absorbed into cell
  • Thus less water reabsorbed into cell and more lost in urine
  • Less Na+ pumped into blood by Na+/K+ ATPase and less K+ pumped in
  • Lower Na+ in cell and thus more Na+ will get pumped in by Na+/Ca2+ co transporter
  • Enhances Ca2+ reabsorption from tubular lumen
35
Q

Clinical uses of thiazides

A
  • Hypertension (preferred)
  • Congestive heart failure
  • Nephrolithiasis (kidney stones) due to idiopathic hypercalciuria (excessive amounts of calcium in blood)
    • Less calcium in the urine
    • More calcium reabsorbed into the bloodstream thus prevention of hypercalciuria
    • Reduce the effect of nephrolithiasis
  • Nephrogenic diabetes insipidus.
36
Q

Adverse effects of thiazides

A
  1. Hypokaemic metabolic acidosis
  2. Hyponatremia
  3. Hyperuricemia and gout (High uric acid reabsorption)
  4. Hyperglycemia
  5. Hypercalcemia
37
Q

Types of K+ Sparing diuretics

A

Aldosterone receptor antagonists
1. Spironolactone
2. Epleronone

ENAC (Epithelial NA channel) blockers
1. Triamterine
2. Amiloride

38
Q

Mechanism of Spironolactone

A
  1. Inhibits the binding of aldosterone to certain transcription factors (aldosterone receptors) in the nucleus of the principal cells and hence down regulates transcription and translation of certain proteins like ENAC, K+ transporter, Na+/K+ ATPase transporters
  2. Less ENAC, less Na+ reabsorption into the cell, and hence less water gets reabsorbed as well
  3. Less intracellular Na+, less K+ will be transported into the cell through Na+/K+ ATPase which is also down regulated
  4. Less K+ channels thus less K+ lost into tubular lumen
  5. More Na+ and water lost through lumen but less K+ lost thus termed potassium sparing
39
Q

Clinical indications for K+ sparing diuretics

A
  • Hypertension
  • Hypokalaemia (due to K+ retaining functions)
  • Hyperaldosteronism
40
Q

PK of K+ sparing diuretics

A
  • Spironolactone has rather slow onset, need several days before full therapeutic effect is reached
  • Triamterene is metabolised by the liver, shorter half life and must be given more frequently than amiloride
41
Q

Adverse effects of K+ sparing diuretics

A
  1. Hyperkalaemia
  2. Metabolic acidosis (Less H+ ATPase synthesised in alpha intercalated cells thus less H+ last into tubular lumen, more H+ retained in blood)
  3. Gynecomastia (for spiranolactone)
  4. Acute renal failure (Triamterene + indomethacin)
  5. Kidney stones (with triamterene)
42
Q

Name some 2nd line anti hypertensives

A
  1. Hydralazine
  2. Mineralocorticoid receptor antagonist
  3. Alpha-adrenergic receptors
43
Q

Mechanism of hydralazine

A
  • Direct arteriole vasodilator
  • Inhibit inositol trisphosphate (IP3)-induced release of calcium from the smooth muscle cells sarcoplasmic reticulum
  • Reduces peripheral resistance → compensatory release of epinephrine / norepinephrine → increase venous return and cardiac output
44
Q

Indications

A
  1. First line drug for heart failure
  2. Second line drug for hypertension

CVS drugs (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions