AntiHypertensives Flashcards
Alpha 1 blockers
Examples use MOA S/E C/I
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
Beta 1 selective blockers
Examples Use MOA S/E C/I
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
NON SELECTIVE BETA 1, BETA 2 AND ALPHA 1
Examples Use MOA S/E C/I
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
CENTRALLY ACTING ADRENERGIC DRUGS
Examples
use
MOA
S/E
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S/Es: Rebound HTN (if withdrawn quickly) Bradycardia Sedation
CALCIUM CHANNEL BLOCKERS / DIHYDROPYRIDINES
Examples Use MOA S/Es C/Is
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
NON - DIHYDROPYRIDINES
Examples Use MOA S/Es C/Is
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
Mechanism of action Diuretics
They increase urine output by affecting different areas of the kidney
MOA of Thiazides
MOA of Loop diuretics
Affect LOH and decrease sodium reabsorption but cause an increase of calcium in urine.
MOA of Potassium sparing diuretics.
Block sodium-potassium pump or block aldosterone to reduce production of pumps—> Leading to an increase of potassium absorption and decrease sodium absorption
MOA of calcium channel blockers
Block L type calcium channel—> Leading to no calcium entry–> Leading to no smooth muscle cell contraction —–>Reduces blood pressure
MOA of Beta blockers
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
ACE Inhibitors
Block ACE by preventing angiotensin 1 conversion to angiotensin 2
Preventing vasoconstriction.
Reducing Blood pressure
ARBs/ Sortans
Block AT1 receptor on vessels preventing vasoconstriction
Leading to a decrease in Blood pressure.
Renin Inhibitors
Inhibits renin, leading to a decrease in bp and aldosterone
1st line treatment of hypertension
ACEi
2ND 1st line treatment of hypertension
ARBs
what patient has an increased level of ANG-1
Patient taking ACE because there is no ANG1–>ANG2 conversion
Divisions of calcium channel blockers
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)
Side Effect of beta blockers
hyperkalemia d/t decrease of aldosterone.
Fatigue
Bradycardia
ACE Inhibitors S/E and drug names
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
In what patient is beta blocker indicated
patients with a history of MI
Beta blocker contraindications
Asthma, COPD, AV BLOCKS, PSORIASIS
Can we use diuretics in pregnancy
it is not advised because
- An increase in sodium excretion leads to frequent urination which can cause discomfort
- Diuretics are teratogenic (they disturb the development of the embryo or fetus)
- They are lipophilic so they cross the placenta and may decrease fatal heart rate
What is the only condition in which a beta blocker can be prescribed without cardiac history.
Pregnancy
Discuss the masking effect of hypoglycaemia
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)
What antihypertensives should never mix
ACEi and Sartans
Beta blockers and calcium channel blockers
Which diuretics have the side effect of hyperkalemia
Potassium sparing diuretics such as spironolactone
Which diuretics have the side effect of and increase in uric acid (hyperuricemia)
Thiazides
eg hydrocholorothiazide, chlorothiazide
which diuretics cause hypokalaemia
Thiazides
Adverse effects of thiazides
hypercalcemia hyperuricema hypokalaemia hypotension hyponatriema hypercalcemia
Adverse effects of loop diuretics
Ototoxicity Hyperuricemia Hypotension Hypokalaemia Hypomagnesemia
Adverse effect of potassium sparing diuretics
Hyperkalemia
Spironolactone may cause gynacamastia in men and irregular menstrual period in women because it may stimulate progesterone and hormone receptors.
Which diuretics have the side effects of
- Hypokalaemia
- Hyperuricemia
- Hypotension
Lood diuretics and thiazides
Where do thiazides work
Thiazides work in the distal tubule by inhibiting NaCL Co-Transporter
eg chlorothiazide, hydrochlorothiazide
Where do loop diuretics work
Loop diuretics work in the ascending LOH, by inhibiting the sodium-potassium-chloride co transporter eg furosemide, bumetadine
where does potassium sparing diuretics work
Potassium sparing directs work in the collecting ducts by inhibiting sodium transporter (spironolactone) and antagonises aldosterone (amiloride)
Which diuretics may cause hyperuricemia in the treatment of hypertension.
*Who is at risk for hyperuricemia
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
How do ARBs/Sartans work in hypertension
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
Who are ARBs/Sartans contraindicated in ?
Is angiotensin 1 level high or low on ARBs/Sartans?
Example: Losartan, Condesartan
Pregnant women
ANG 2 is higher in patients using ACEi because ANG1 won’t get converted to ANG2 because is blocked
