AntiHypertensives Flashcards

1
Q

Alpha 1 blockers

Examples
use
MOA
S/E
C/I
A

Examples: Doxazosin
Prazosin

USE: Hypertension
benign prostatic hypertrophy

MOA; peripheral vascular smooth muscle relaxation leads to vasodilation which leads to a decrease in systemic vascular resistance which leads to a decrease in blood pressure
Decrease in prostatic and bladder neck contraction leads to improvement of urinary flow through the prostate and out of the urethra

Side Effects: Orthostatic hypotension, dizziness, nasal congestion

Contraindication: Cataract eye surgery

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2
Q

Beta 1 selective blockers

Examples
Use
MOA
S/E
C/I
A

Examples: ATENOLOL METOPROLOL

Use: HTN Arrhythmias HF Glaucoma Migraine prophylaxis

MOA: Blocks β1→ ↓CO → ↓BP
Blocks beta 1 leading to a decrease in cardiac output and hence a decrease in blood pressure.

S/Es: Erectile dysfunction, bradycardia, HF, seizures, dyslipidemia, COPD/asthma exacerbation

Contraindications: Depression
Asthma
Raynaud’s phenomenon
Worsening of COPD

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3
Q

NON SELECTIVE BETA 1, BETA 2 AND ALPHA 1

Examples
Use
MOA
S/E
C/I
A

Examples: CARVEDILOL LABETALOL

Use: Chronic congestive HF in addition to ACE and diuretics.
HTN

MOA: Blocks β1→ ↓HR & ↓contractility
Blocks β2→ bronchoconstriction
α1 → Vascular smooth muscle relaxation (vasodilation) → ↓BP

S/Es: Dizziness Hypotension Bradycardia

C/I : Cardiac failure
Severe bradycardia Asthma
Greater than first degree heart block

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4
Q

CENTRALLY ACTING ADRENERGIC DRUGS

Examples
use
MOA
S/E

A

Examples: CLONIDINE METHYLDOPA→ METHYL- NOREPINEPHRINE

Use: Hypertension, useful in patient with renal disease

MOA: Stimulates α-receptors in the presynaptic vasomotor→ reduced NE→ ↓vasoconstrictio n/ ↓SVR and ↓CO &↓HR→↓BP

S/Es: Rebound HTN (if withdrawn quickly) Bradycardia Sedation

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5
Q

CALCIUM CHANNEL BLOCKERS / DIHYDROPYRIDINES

Examples
Use
MOA
S/Es
C/Is
A

Examples: AMLODIPINE FELODIPINE NICARDIPINE NIFEDIPINE

Use: Hypertension
Angina pectoris

MOA: Inhibits L-type Ca2+-channels in vascular smooth muscle → Blocks entry of Ca2+ → inhibits contraction → vasodilation ↓SVR → ↓BP

S/Es: Dizziness
Headache
Peripheral edema
Gingival hypertrophy

C/Is: Hypotension
HF
Unstable angina

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6
Q

NON - DIHYDROPYRIDINES

Examples
Use
MOA
S/Es
C/Is
A

Examples: Verapamil
Dilitiazem

Use: Hypertension
Angina

MOA: Blocks L-type Ca2+-channels in vascular smooth muscle & cardiac cells → ↓contractility, ↓HR, ↓conduction → ↓ BP

S/Es: Excessieve bradycardia
Cardiac conduction abnormalities

C/Is: Severe hypotension or cardiogenic shock

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7
Q

Mechanism of action Diuretics

A

They increase urine output by affecting different areas of the kidney

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8
Q

MOA of Thiazides

A
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9
Q

MOA of Loop diuretics

A

Affect LOH and decrease sodium reabsorption but cause an increase of calcium in urine.

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10
Q

MOA of Potassium sparing diuretics.

A

Block sodium-potassium pump or block aldosterone to reduce production of pumps—> Leading to an increase of potassium absorption and decrease sodium absorption

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11
Q

MOA of calcium channel blockers

A

Block L type calcium channel—> Leading to no calcium entry–> Leading to no smooth muscle cell contraction —–>Reduces blood pressure

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12
Q

MOA of Beta blockers

A

Block b1 leading to a reduction in heart rate and heart contractility (inotropic and chronotropic) leading to a reduction in blood pressure.

Decrease renin release in juxtaglomeluar cells, leading to a decrease in bp and a decrease in aldosterone means decrease in NA2+ Leading a decrease in blood volume and a decrease in cardiac output

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13
Q

ACE Inhibitors

A

Block ACE by preventing angiotensin 1 conversion to angiotensin 2
Preventing vasoconstriction.
Reducing Blood pressure

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14
Q

ARBs/ Sortans

A

Block AT1 receptor on vessels preventing vasoconstriction

Leading to a decrease in Blood pressure.

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15
Q

Renin Inhibitors

A

Inhibits renin, leading to a decrease in bp and aldosterone

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16
Q

1st line treatment of hypertension

A

ACEi

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17
Q

2ND 1st line treatment of hypertension

A

ARBs

18
Q

what patient has an increased level of ANG-1

A

Patient taking ACE because there is no ANG1–>ANG2 conversion

19
Q

Divisions of calcium channel blockers

A

Dihydropyridines eg nifedipine, amlodipine. Have an affinity to vessels

Non-Dihydropyridines eg verapamil. Have an affinity to the heart and AV conduction (side effect- arrhythmia’s)

20
Q

Side Effect of beta blockers

A

hyperkalemia d/t decrease of aldosterone.
Fatigue
Bradycardia

21
Q

ACE Inhibitors S/E and drug names

A

Dry cough due to increase in bradykinin. ACE is responsible for bradykinin degradation but when ACE is inhibited it does not degrade bradykinin leading to a dry cough.

Examples: Captopril, Ramipril, Benzaopril

22
Q

In what patient is beta blocker indicated

A

patients with a history of MI

23
Q

Beta blocker contraindications

A

Asthma, COPD, AV BLOCKS, PSORIASIS

24
Q

Can we use diuretics in pregnancy

A

it is not advised because

  1. An increase in sodium excretion leads to frequent urination which can cause discomfort
  2. Diuretics are teratogenic (they disturb the development of the embryo or fetus)
  3. They are lipophilic so they cross the placenta and may decrease fatal heart rate
25
Q

What is the only condition in which a beta blocker can be prescribed without cardiac history.

A

Pregnancy

26
Q

Discuss the masking effect of hypoglycaemia

A

Beta blockers should not be given to patients with diabetes mellitus.

Masking effect of glycemic;
It will cause fatigue (The patient won’t know where from because the decrease in cardiac output leads to a decrease in oxygen delivery to cells causes fatigue)

Bradycardia will mask the tachycardia normally caused by hypoglycaemia

Dizziness (Masked by beta blocker because circulation will also be decreased here)

27
Q

What antihypertensives should never mix

A

ACEi and Sartans

Beta blockers and calcium channel blockers

28
Q

Which diuretics have the side effect of hyperkalemia

A

Potassium sparing diuretics such as spironolactone

29
Q

Which diuretics have the side effect of and increase in uric acid (hyperuricemia)

A

Thiazides

eg hydrocholorothiazide, chlorothiazide

30
Q

which diuretics cause hypokalaemia

A

Thiazides

31
Q

Adverse effects of thiazides

A
hypercalcemia
hyperuricema
hypokalaemia 
hypotension
hyponatriema
hypercalcemia
32
Q

Adverse effects of loop diuretics

A
Ototoxicity
Hyperuricemia
Hypotension
Hypokalaemia 
Hypomagnesemia
33
Q

Adverse effect of potassium sparing diuretics

A

Hyperkalemia
Spironolactone may cause gynacamastia in men and irregular menstrual period in women because it may stimulate progesterone and hormone receptors.

34
Q

Which diuretics have the side effects of

  1. Hypokalaemia
  2. Hyperuricemia
  3. Hypotension
A

Lood diuretics and thiazides

35
Q

Where do thiazides work

A

Thiazides work in the distal tubule by inhibiting NaCL Co-Transporter
eg chlorothiazide, hydrochlorothiazide

36
Q

Where do loop diuretics work

A

Loop diuretics work in the ascending LOH, by inhibiting the sodium-potassium-chloride co transporter eg furosemide, bumetadine

37
Q

where does potassium sparing diuretics work

A

Potassium sparing directs work in the collecting ducts by inhibiting sodium transporter (spironolactone) and antagonises aldosterone (amiloride)

38
Q

Which diuretics may cause hyperuricemia in the treatment of hypertension.

*Who is at risk for hyperuricemia

A

Loop directics eg furosemide
Thiazides eg chlorothiazide and hydrochlorothiazide

Which interferes with uric acid secretion leading to hyperuricemia

*Hyperuricemia usually precede gout, sodium urate crystals get deposited in joints

39
Q

How do ARBs/Sartans work in hypertension

A

They bind to angiotensin receptor 1 on vessels, where angiotensin 2 usually binds leading to a decrease in blood pressure
because vasoconstriction won’t occur

40
Q

Who are ARBs/Sartans contraindicated in ?

Is angiotensin 1 level high or low on ARBs/Sartans?

A

Example: Losartan, Condesartan
Pregnant women

ANG 2 is higher in patients using ACEi because ANG1 won’t get converted to ANG2 because is blocked