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Pharm > Antihypertensives > Flashcards

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
Q

From the CCB
which act directly on the heart and which does not?
List strongest to weakest

A

Acts on the heart - verapamil and diltiazem
Acts peripheral - nifedipine

Nifedipine, verapamil, diltiazem

26
Q

Dihydropyridines (Nifedipine)

Does it decrease or increase BP? through what?
Any changes on the heart rate?

USES

A

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
Q

Nifedipine ADE

A

Pretibial edema
nausea
flushing
dizziness
GINIGIVAL HYPERPLASIA
Give a slow-release preparation to avoid reflex tachycardia

28
Q

Nifedipine
Act on?
Decrease what? Increase what?

A

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
Q

A1-Blockers drugs

A

“AZOSIN’S”

30
Q

A1- Blockers
Uses
ADE:

A

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
Q

Beta blocker
MOA?

A

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
Q

1st gen Propanolol vs
2ND Generation: Atenolol, Esmolol, Betaxolol, & Metoprolol

A

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
Q

Acebutolol (B1 selective)
Pindolol (Non-selective):

A

B1 receptor partial activators
Slight sympathomimetic activity – bradycardia or negative inotropy in a resting heart

34
Q

Labetalol - mixed a1-b blocker
used when?

A

IV for hypertensive emergencies (Pheochromocytoma, pre-eclampsia)

35
Q

Carvedilol – mixed a1-b blocker

A

3rd gen agents that decrease tachycardia through non-selective beta antagonism

Decrease BP through a-1 antagonism

36
Q

Nebivolol – B1 selective blocker w/ NO-mediated vasodilation (B3 agonist)

A

Promotes NO-mediated vasodilation
Less ADEs than older BB

37
Q

When do you use BB?
Who is it less effective in? and what can it be less effective in compared to what?

A

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
Q

BB ADE

A

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
Q

Centrally Acting Alpha-2 drugs

A

Clonidine
Methyldopa
Guanfacine

40
Q

Centrally Acting Alpha-2 effects

A

Decrease sympathetic outflow from rostral ventrolateral medulla (RVLM) to heart & blood vessels
Decrease in peripheral vascular resistance & HR

41
Q

what kind of patient for each Centrally Acting Alpha-2 drug

A

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
Q

Centrally Acting Alpha-2 Side effects

A

Sedation, drowsiness, fatigue
Clonidine withdrawal -> rebound HTN
- TAPER OFF

43
Q

Direct Vasodilators effect

A

Frequently produce reflex tachycardia & rarely cause orthostatic hypotension

Dilate arteriolar smooth muscles & trigger reflex sympathetic stimulation -> increase catecholamine/renin secretion

44
Q

Direct Vasodilator drugs

A

Hydralazine
Minoxidil
Diazoxide

45
Q

Hydralazine

A

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
Q

Minoxidil use

A

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
Q

Diazoxide use

A

Opens K+ channels on smooth muscles
Decreases TPR by relaxing arterioles
IV for hypertensive emergencies

48
Q

ADEs of Direct Vasodilators

A

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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