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CV2 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Increased blood pressure

A

associated with a progressive increase in the risk of stroke and cardiovascular disease

Risk however rises exponentially and not linear with pressure

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2
Q

Antihypertensive drugs

A

Vasodilators
Agents affecting adrenergic function
Diuretics
RAAS

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3
Q

Direct Arterial Vasodilators

A

Hydralazine-HTN, HF, oral long term
Minoxidil- K (atp) channel opener, HTN HF oral
Diazoxide- K channel openner, HTN emergencies, IV rapid

Counter regulatory Responses: potent reductions in perfusion activate baroreceptor reflex to increase sympathetic outflow, tachyphylaxis can cause loss of antihypertensive effect, relex release of renin

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4
Q

direct Arterial vasodilators Adverse effects

A

Sodium/water retention, tachycardia angina, minixidil can cause hair growth (hypertrichosis)

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5
Q

Calcium channel blockers

A

Nifedipine, Nicardipine, Amlodipine: dihydropyridines
Verapamil: Phenylalkylamine
Diltazem: benzothiazipine

MOA: arterial circulation (dominant), Vascular smooth muscle selectivity- dihydropyridines greater ratio vascular versus cardiac effects, Nimodipine cerebral vascular selective

USE: HTN/Angina/Vasopasm

Toxicity: bradycardia, aV block, flushing dizziness, nausea,constipation (verapamil), peripheral edema

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6
Q

Anithypertensive actions for calcium channel blockers

A

Dihydropyridines- Baroreceptor mediated reflex tachycardia due to potent vasodilating effects, do not alter conduction thru atrioventricular node

Non-dihydropyridines: decrease HR, slow atrioventricular nodal conduction

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7
Q

Nitroprusside

A

MOA: NO donors
Arterial and venous circulation

HTN emergencies- rapid reduction arterial pressure

Admin- IV, rapid offset after discontinuing, short duration

Toxicity: HTN, cyanide accumulation

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8
Q

Sympathetics nervous system

A
  • Heart (increased contractility, HR) Beta 1 receptor
  • Arterioles (vasoconstriction in the skin and viscera via alpha, vasodilatio in sk muscle/liver via Beta2)
  • Lungs (bronchodilation) beta 2
  • Kidney (increased renin) alpha 1 and beta 1
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9
Q

alpha 1 and alpha 2 blockers

A

Phenoxybenzamine and Phentolamine

Inhibit arterial vascular smooth muscle alpha1 receptors and venous smooth muscle a2 receptors –> vasodilation and blood pressure lowering
Inhibit sympathetic nerve ending a2 receptors leading to increased NE release
Increased NE release results in increased B 1 receptor mediated renin release

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10
Q

a 1 blockers

A

prazozin, terazosin, doxazosin

Small increase in heart rate- lack a2 venodilation
Does not block a2 , NE can inhibit its own release
Do not stimulate renin release

a1-blockers 1st dose Effect: orthostatic hypotension, transient dizziness, faintness, palpatation , reflex tachy, 1st dose at bedtime to minimize effect

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11
Q

Beta blockers receptors and adverse effects

A

Propranolol B1 and B2
Labetalol B1 B2 and a1
Metropolol, Atenolo B1

B1 receptors: heart kidney, stimulation increases HR, contractility, renin release

B2 receptors: Lungs, liver, pancreas, arteriolar smooth muscle
Stimulation causes bronchodilation and vasodilation, mediate insulin secretion and glycogenolysis

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12
Q

side effects of beta blockers

A

Glucose intolerance, masked hypoglycemia (B2)

bradycardia, dizziness (B1/B2)

Bronchospasm (B2)

Increased TGs and decreased HDL (B2)

CNS Depression, fatigue, sleep disturbances (B1/B2)
Reduced Cardiac output, exacerbation of heart failure (B1)
Impotence (B1/B2)
Exercise intolerance (B1/B2)

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13
Q

cardioselective B blockers: metropolol, atenolol

A

Greater affinity for B1 than B2 receptors. Inhibit B1 receptors at low to moderate dose, higher doses block B2 receptors
Safer in pts w/ bronchospastic disease, peripheral arterial disease, diabetes (exacerbate bronchospastic disease when selectivity lost at high doses, dose where selectivity lost varies from pt to pt )
Preferred B blockers for HTN

beter in younger kids, BP is more dependent on cardiac output in young adults

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14
Q

Central a 2 agonists

A

clonidine, guanabenz, amethyldopa
Stimulate a2 adrenergic receptors in brain (reduces sympathetic outflow from the brains vasomotor center) increases vagal tone

Adverse effects: Na and water retention, abrupt discontinuation can cause rebound HTN, depression, orthostatic hypotension and dizziness

Clonidine: anticholinergic side effects

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15
Q

Neural and ganglionic blockers

A

Gunnethidine, Reserpine

SE: brady cardia and decreased CO, Na and water retention, diarrhea, sedation (reserpine), depression (reserpine), gastric acid secretion

USed with diuretic to avoid fluid retention

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16
Q

diuretics

A

Fenoldopam, Furosemide, hydrochlorothiazide, spironolactone, eplerenone, amiloride

17
Q

Fenoldopam

A

MOA: selective renal vasodilation, decreases proximal tubule REAB–> diuresis

Use: HTN emergency, heart failure,

Toxicity: Increases intraocular pressure and should be avoided in pts with glaucoma

18
Q

Furosemide

A

Loop diuretic
MOA: inhibits Na K 2CL symporter in medullary and cortical thick ascending limb

USE: HTN HF EDEMA, less effective in chronic kidney disease

Toxicity: hypokalemic metabolic alkalosis, hypovolumia

19
Q

Hydrochlorothiazide

A

Thiazide diuretics

MOA: inhibits Na-Cl symporter in distal convoluted tubule

USE: HTN

Toxicity: hypokalemic metabolic alkalosis

20
Q

Amiloride

A

Sodium Channel inhibitors
MOA: Blocks sodium entry into principal cells of the collecting duct, Increases sodium excretion and decreases potassium excretion

USE: HTN (used in combo)

Toxicity: hyperkalemia

21
Q

Spironolactone and Eplerenone

A

MOA: blocks action of aldosterone on the late distal tubule and collecting duct
Increase sodium Excretion, Decrease potassium excretion

USE: HTN/ HF

Toxicity: hyperkalemia

effects wear off after long term use

22
Q

ACE inhibitors

A

Captopril, enalapril

Block Ang 1–>2 conversion

distributed in many tissue (primarily endothelial cells, blood vessels are the major angiotensin 2 production)

Block bradykinin degradation, stimulate synthesis of other sythesis of other vasodilating substances such as prostacyclin

23
Q

Losarton

A

Angiotensin 2 Receptor Blockers

Block Ang 2 type 1 receptorms, inhibit ANG2 actions in many tissue

Vascular smooth muscle, adrenal gland aldosterone release, SNS NE release, renal Na REAB, brain vasopressin secretion, heart contractility

24
Q

Aliskren

A

Renin inhibitor

25
Q

Ras inhibitors on renal hemodynamics

A

ANG 2 on renal hemodynamics, activates AT 1 receptors on renal vascular smooth muscle to reduce renal blood flow

ANG 2 influences glomerular filtration rate , slight increase

Hyperkalemia, can cause acute kidney failure in certain patients, contraindicated in pregnancy

Cough

26
Q

Hypertension epidemiology

A 
33% Adults with HTN
33 Million Essential HTN dignosis
1 million ED essential HTN 
33 thousand deaths from essential HTN and renal HTN
10 deaths per 100k deaths

82% aware, 75% under current treatment, 53 % controlled, 50% not controlled

Increased risk of stroke and IHD

Essential HTN- unknown cause 90%, secondary HTn 10%

Blood pressure increases with Age, faster increase in men, systolic more important than diastolic

27
Q

Preeclampsia

A

High blood pressure in pregnancy leads to heart disease, stroke, HBP
120-80 is actually elevated should be less

28
Q

Regulation of blood pressure

A

Hemodynamic factor (Bp= CO x tpr, CO= SV x hr)

Stroke volume: cardiac contractility, venous return (preload), resistance of LV to eject blood (afterload)

Blood pressure regulatoru systems: Heart, Blood vessel tone, kidney (volume), hormonal

29
Q

Blood pressure role of the kidney

A

increase in Na/H20 intake–> increase Blood volume–> decrease in sympathetic activity, ADH, RAAS, increase in ANP and prostaglandins–> Na/H20 excretion

Reflex and hormonal responses achieve only partial control

Pressure Natriuresis: Dominant physiological mechanism (increasng renal sodium excretion)

30
Q

blood pressure reflexes

A

Feedback mechanisms that continuously monitor arterial pressure

Baroreceptor reflex- mediated by receptors in the wall of the aortic arch and cartid sinuses
Negative feedback signals are sent to the circulation via the ANS, causing the BP to fall back to its baseline

31
Q

essential HTN

A

elevated BP for no reasin

Primary onset at 20-50, severity is mild to moderate, gradual progression, no signs, family history is genetic

32
Q

causes of HTN Obesity

A

Overactivation of SNS, impaired natriurises, RAAS increased, Insulin/leptin, corticosteroids, endothelial

CV2 (12 decks)

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