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Antihypertensives Flashcards

1
Q

Agents along with drugs affecting the Sympathetic Nervous System

A

Alpha 1 - “-azosin”
B-blockers (NS) - Propranolol, Carvedilol, Pindolol, Timolol
B- blockers (S) - Metoprolol, Atenolol, Bisoprolol, Nebivolol

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2
Q

Agents along with drugs that interfere with the activity of renin- angiotensin

A

ACE inhibitors - “-pril”
AT1-R blockers - “-sartan”
Renin inhibitor - aliskerin

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3
Q

Calcium Channel Blockers

A

Phenylalkylamine - Verapamil
Benzothiazepine – Diltiazem
Dihydropyridine – “dipines”

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4
Q

Centrally acting A-2 agonist

A

Clonidine & Methyldopa

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5
Q

Direct vasodilators

A

Minoxidil, Nitroprusside, Hydralazine, Fenoldopam

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6
Q

Thiazide diuretics

A

Chlorothiazide

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7
Q

Renin Angiotensin route

A

Kidneys release renin.
The liver releases angiotensin pre-cursor.
These two make angiotensin I.
ACE converts angiotensin I -> angiotensin II. Angiotensin II acts on AT1 receptors to cause vasoconstriction & reacts w/ aldosterone to hold on to Na+ & let go of K+.

Vasoconstriction = increase in BP
Hypernatremia = increase in BP because in theory is makes our blood heavier which can cause edema and other stuff

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8
Q

Target of med: Heart

A

B1B & CCB – decrease cardio output (decrease volume out of the left ventricle = less contraction -> less pressure needed)
Which leads to a decrease in blood pressure because the heart does not have to work as hard

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9
Q

Target of med: kidney

A

ACEi, ARBs – decrease Na+ and decreases aldosterone
BB – decrease renin/angiotensin II
Diuretics – decrease blood volume/Total peripheral resistance (changes volume of blood with urine = decreased volume -> decreased pressure in vessels to get back to heart less pressure which lowers blood pressure)

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10
Q

Target of med: peripheral vasodilator

A

Vasodilators, ACEi, CCB – decrease TPR

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11
Q

Target of med: CNS/brain

A

CA sympathomimetics & BB – decrease TPR

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12
Q

Non med treatment

A

DASH Diet
Na+(<1500 mg/day) & ETOH (< 2 drinks/day; <1 drinks/day) limitation
Exercise programs
Weight loss for overweight patients
K+ supplementation if indicated (3500-5000 mg/day)

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13
Q

Treatment goals for hypertension

A

-ACC/AHA - <130/80 mmHg
-SBP of >140mmHg or DBP of >90 mmHg -should be tx w/ one or more medications
-Initial choices for primary HTN:
ACEi, ARBs, CCB, & Thiazide diuretics: (TAAC that Hypertension)

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14
Q

Thiazide diuertics and Thiazide like diuretics drugs

A

Hydrochlorothiazide (HCTZ), Chlorothiazide, Chlorthalidone, Indapamide.

don’t mind my thiazide (done mide thiazide )

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15
Q

Thiazide diuertics and Thiazide like diuretics drugs Use and MOA

A

Uses:
HTN – due to Na+ loss via urination & loss of edema (makes blood volume decrease in a sense makes blood light to not as much work to get it back to the heart)

MOA:
Secreted in the proximal tubule and acts in the early distal tubule. They inhibit the electro-neural Na+/Cl- cotransporter
This action increases K+ excretion = K+ sparing diuretics may also be used as well. (like spironolactone)
K+ cause patients to become hypokalemic

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16
Q

Thiazide diuertics and Thiazide like diuretics drugs side effects

A

Hypokalemia – CI in CHF, Cirrhosis, Diabetic, & Elderly (Hypokalemia S/S:
Cardiac arrhythmias
Muscle cramping/weakness
Lethargy)

Hypercalcemia – because youre holding onto calcium
Hyperglycemia – decrease insulin section
Hyperlipidemia – CI in pts w/ increased cholesterol & lipids
Uric acid reabsorption – CI in gout

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17
Q

ACE-Inhibitor Uses

A

Inhibits effects of Ang II
Dilates arteries & veins (CHF)
Decreases BP -> may have minor increase in HR (rare)
Baroreceptors are kept intact -> body can still detect changes and will accommodate
Decreases vascular hypertrophy
Increases life-expectancy for CHF pts

Not used in combo w/ Aliskiren or ARBs
Because work in the same system

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18
Q

ACE-Inhibitor Side effects

A

Hyperkalemia
Dry cough (MC) – Due to degradation of bradykinin which activates stretch receptors in the trachea.
Angioedema - esp. in A.A
Fetotoxicity

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19
Q

ARB’s MOA

A

Selectively block AT II type I receptors -> No AngII actions
Causes vasodilation & Na+/H20 excretion.
Decreasing TPR, plasma volume, CO, and BP
They don’t affect bradykinin -> no cough = use for when cough is intolerable

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20
Q

ARB’s USE

A

Just as effective in lowering BP
Renally & cardiac protective
Less effective in A.A unless combined w/ HCTZ
Not used in pregnancy!

21
Q

Aliserkin

What is inhibiting?
Not used in combo with? (2)

CI?

A

Directly inhibits renin secretion from kidney
Not used in combo w/ ARBs or ACEi because you will intensify all other actions -> will have increased side effects!
CI in pregnancy

22
Q

Verapamil are selective for what ?
what do they effect?
Used for?

May produce?

A

Selective for myocardium – effective for systemic vasodilator

Used to tx HTN, chronic angina, & arrhythmias

May produce cardiac depression & AV block

23
Q

Diltiazem is selective for what?

A

Intermediate b/w verapamil & dihydropyridines in its selectivity for vascular Ca2+ channels

24
Q

Verapamil
CI?
ADE?

A

CI in Beta blocker

Hyperprolactinemia – affect w/ dopamine
Constipation in 10% of pts

25
From the CCB which act directly on the heart and which does not? List strongest to weakest
Acts on the heart - verapamil and diltiazem Acts peripheral - nifedipine Nifedipine, verapamil, diltiazem
26
Dihydropyridines (Nifedipine) Does it decrease or increase BP? through what? Any changes on the heart rate? USES
Decreases BP through arteriolar smooth muscle relaxation & decreasing PVR No – mild HR changes due to working in the vasculature Uses: More effective in A.A or low-renin HTN Preferred medication for elderly pts ACEi + amlodipine(CCB) IS MORE EFFECTIVE than ACEi + HCTZ in reducing CV events Safe in pregnancy
27
Nifedipine ADE
Pretibial edema nausea flushing dizziness GINIGIVAL HYPERPLASIA Give a slow-release preparation to avoid reflex tachycardia
28
Nifedipine Act on? Decrease what? Increase what?
L-type Ca2+ channels = target in vascular smooth muscle Decrease BP peripherally Increases excretion of Na+ due to acting on renal afferent arterioles Decreases O2 consumption and increases supply through working on the coronary arteries
29
A1-Blockers drugs
“AZOSIN’S”
30
A1- Blockers Uses ADE:
blocks a-1 receptors in arteries & veins Use: A-1 blockers aren’t rec as monotherapy for HTN Doxazosin & Terazosin are used in urinary s/s of BPH by relaxing bladder/prostate muscles ADE: Prazosin causes 1st-dose hypotension so Give at bedtime. Only worried about patients w/ orthostatic hypotension. "A-1 but not recommend for monotherapy"
31
Beta blocker MOA?
Block myocardial B-1 receptors + in the juxtaglomerular apparatus = inhibiting renin release Very helpful in treating patients w/ high renin HTN Decrease HR, contractility, and Cardiac Output
32
1st gen Propanolol vs 2ND Generation: Atenolol, Esmolol, Betaxolol, & Metoprolol
Propanolol:Non-specific blockers of both B1 & B2 receptors Atenolol, Esmolol, Betaxolol, & Metoprolol: B1 selective at normal clinical doses Safe & beneficial in those w/ COPD
33
Acebutolol (B1 selective) Pindolol (Non-selective):
B1 receptor partial activators Slight sympathomimetic activity – bradycardia or negative inotropy in a resting heart
34
Labetalol - mixed a1-b blocker used when?
IV for hypertensive emergencies (Pheochromocytoma, pre-eclampsia)
35
Carvedilol – mixed a1-b blocker
3rd gen agents that decrease tachycardia through non-selective beta antagonism Decrease BP through a-1 antagonism
36
Nebivolol – B1 selective blocker w/ NO-mediated vasodilation (B3 agonist)
Promotes NO-mediated vasodilation Less ADEs than older BB
37
When do you use BB? Who is it less effective in? and what can it be less effective in compared to what?
Some arrhythmias Angina MI HF Hyperthyroidism BB are less effective in A.A patients BB are less effective in preventing CV events (esp. strokes) than ACEi, ARBs, CCBs, & diuretics.
38
BB ADE
Worsening of bronchospasm (Asthmatics/COPD) Hyperglycemia due to decreased insulin secretion Masks s/s of hypoglycemia (DM) Increases triglycerides, LDL, & cholesterol & decreases HDL CI in those on clonidine or cocaine due to unopposed a-AR vasoconstriction -> will increase ADEs of these meds ED w/ all BB Upregulation of B-receptors in the heart will cause tachycardia if withdrawal is too quick.
39
Centrally Acting Alpha-2 drugs
Clonidine Methyldopa Guanfacine
40
Centrally Acting Alpha-2 effects
Decrease sympathetic outflow from rostral ventrolateral medulla (RVLM) to heart & blood vessels Decrease in peripheral vascular resistance & HR
41
what kind of patient for each Centrally Acting Alpha-2 drug
Clonidine – hypertensive emergencies & a tertiary use in HTN (Patches is needed) Guanfacine (t1/2 =17hr) – add-on for refractory HTN Methyldopa – used for HTN in pregnancy - use this over nifedipine of aHTN
42
Centrally Acting Alpha-2 Side effects
Sedation, drowsiness, fatigue Clonidine withdrawal -> rebound HTN - TAPER OFF
43
Direct Vasodilators effect
Frequently produce reflex tachycardia & rarely cause orthostatic hypotension Dilate arteriolar smooth muscles & trigger reflex sympathetic stimulation -> increase catecholamine/renin secretion
44
Direct Vasodilator drugs
Hydralazine Minoxidil Diazoxide
45
Hydralazine
Direct vasodilator of arteriolar smooth muscles Given w/ BB to minimize the reflex increase in HR & CO Diuretics added to avoid sodium & fluid retention (through renin secretion) Isosorbide dinitrate (BiDil) for African Americans w/ CHF
46
Minoxidil use
Opens K+ ATP channels -> relaxes smooth muscles Potent dilator that rarely fails to lower BP. Reserved for severe HTN refractory to other drugs Dilates arterioles, but not veins Triggers reflex sympathetic stimulation -> Increases secretion of renin/catecholamines Other uses: hair growth due to hirsutism effects
47
Diazoxide use
Opens K+ channels on smooth muscles Decreases TPR by relaxing arterioles IV for hypertensive emergencies
48
ADEs of Direct Vasodilators
All cause rapid drop in TPR -> dizziness, palpitations, HA, & reflex tachycardia Hydralazine – autoimmune rxns – systemic lupus erythematosus, slow acetylators & high doses Minoxidil – Hypertrichosis (hair growth), tachycardia, fluid retention Diazoxide – pronounced tachycardia, hyperglycemia, hypertrichosis

Pharm (7 decks)

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