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CV 3 > HTN Pharmacology > Flashcards

HTN Pharmacology Flashcards

1
Q

Hydralazine MOA and use/administration, class

A

ARTERIAL VASODILATOR

MOA: unknown

use: HTN and Heart Failure
administration: oral, long term use

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2
Q

Minoxidil Class, MOA and use/administration

A

ARTERIAL VASODILATOR

MOA: K/ATP channel opener (K efflux)

use: HTN, HF, oral long term

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3
Q

Diazoxide Class, MOA and use/administration

A

ARTERIAL DILATOR

MOA: Non-selective K channel opener

use: HTN emergencies
administration: IV rapid response

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4
Q

What are the 3 counter regulatory responses to vasodilation from an arterial vasodilator?

A
  1. low perfusion pressure activates baroreceptors to increase sympthetic outflow
  2. leads to taachyphylaxis (quick removal of drug) and therefore elss anti-hypertensive effects
  3. release of renin (which increases peripheral resistance and cardiac output)
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5
Q

what are the adverse effects of direct arterial vasodilators?

A
  • sodium and water retention: due to increases in renin and angiotensin II
  • tachycardia/angina: due to baroreflex activation leading to increased contractility and increased HR
  • Minoxidil can cause hair growth (hypertrichosis)
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6
Q

WHat are the 3 classes of Ca channel blockers and what drugs are in each class?

A

Dihydropyridines: Nifedipine, Nicardipine, Amlodipine

Phenylalkylamine: Verapamil

Benxothiazapine: Diltiazem

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7
Q

What is the MOA for Ca channel blockers? How about the uses? Toxicity?

A
  • MOA:
    • Arterial Circulation (dominant)
    • Vascular smooth muscle selectivity- diydropyridines have more vascular than caridac effects
    • Nimodipine has selective cerebral vascular effects
  • use: HTN, Angina, Vasospasm
  • Toxicity:
    • Cardiac: bradycardia, AV block
    • flushing dizziness, nausea, constipation (verapamil), peripheral edema
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8
Q

How do Dihydropyridines and Non-dihydropyridines influence HR and AV conduction

A

Dihydropyridines: barorreceptor mediated reflex tachycardia due to potent vasodilatory effects, do not alter conduciton through AV node (main goal is vasodilation)

Non-Dihydropyridines: decrease HR, slow AV nodal conduction

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9
Q

What are the effects of Nitroprusside? What is the MOA of Nitroprusside? use? adminitration? toxicity?

A
  • Effects:
    • arterial : decrease tone, decrease resistance, decrease BP
    • Venous: decrease venous return (therefore SV), increase HS (due to decrease in pre-load)
      • so effects on CO are unkown bc decrease SV and increase HR
  • Mixed (arterial and venous) vasodilator
  • MOA: NO donor, activates GC to increase cGMP leading to vasodilation
  • Use: HTN emergencies, rapid reduction in arterial pressure
  • Administration: IV duration is 15-30 min and offset is 1-10 min (why it is good for emergencies)
  • toxicity? hypotension and cyanide accumulation
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10
Q

What are the effects of sympathtic influence on the heart, vessels, lungs, kidneys? What receptors cause these effects?

What is the effect of a2?

A

Heart: Increase in contractility and HR (beta1)

Vessels: Vasoconstriction of skin/ viscera ( alpha 1), Vasodilation of skeletal muscle/ liver (beta 2)

Lungs: bronchodilation (beta 2)

Kidneys: Increased renin (alpha 1, beta 1)

a2 is the breaks. It stops sympathtic activity.

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11
Q

Fun physio question: Why does sympathitic stimulation cause vasoconstriciton, but increase blood flow to skeltal muscles. How is this possible????

A

Bc NE is working on different receptors at different locations! in skin and viscera NE binds to a1 and cause vasocontriction,

In skeletal muscle it binds to b2 receptors causing vasdilation.

This is how you can run away form a bear! You don’t need any bloo dgoing to your skin and viscera, you want it all going to your muscles!

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12
Q

What are the effects of non-selective a1/a2 blockers? What are 2 examples?

A
  • Effects:
    • a1: decrease arterial tone, decrease peripheral resitance, decrease BP
    • a2: decrease venous tone, decrease venous return, decrease CO, decrease BP
    • inhibit a2 leading to increased NE release
    • increased NE release leads to increased B1 driven renin release

Phenoxybenzamine, Phentolamine

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13
Q

What are 3 alpha 1 receptor blockers? What do they cause?

A

Prazosin, Terazosin, Doxazosin

  • smaller increase in HR than a1/a2 bc they lack the a2 venodilation (decreasing preload would cause relexive tachycardia. You don’t see this here)
  • doesn’t block a2 so NE can inhibit its own release
  • do not stimulate renin relase
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14
Q

Why would you want to give the first dose of prazosin, terazosin or doxazosin at bedtime?

A

there is significant “first dose effect” for selective a1 inhibitors

this means that within the first 3 hours of the first does the patient will experience relex tachycardia and orthostatic hypotension

If they are already laying down for bed then they won’t really be symptomatic

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15
Q

What is the general effect of a beta blocker?

A
  • decrease HR and contractility to decrease CO and therefore BP
  • decrease renin release to block vasoconstriction, decrease peripheral resistance and therefore CO and BP
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16
Q

Where are B1 receptors located and what does stimulation cause?

Where are B2 receptors located and what does stimulation cause?

A
  • B1:
    • Heart and kidney
    • stimulation increases HR , contractility, renin release
  • B2:
    • lungs, liver, pancreas, arteriolar smooth muscle
    • stimulation causes bronchodilation and vasodilation
    • Also mediates insulin secretion and glycogenolysis (pancreas)
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17
Q

What are the potential adverse effects for B Blockers and what B receptors are each side effect related to?

A
  • glucose intolerance, masked ypoglycemia (B2)
  • bradycardia/dizziness (B1/B2)
  • Bronchospasm (B2)
  • Increased TG 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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18
Q

What are the cardioselective B Blockers? What patient population would it be better to use a selective blocker?

A

Metoprolol, Atenolol

Greater affinity for B1 than B2

At high doses loses selectivity and can cause B2 blockade. This dose is different in different people.

Safer in pts. with bronchospastic disease, peripheral arterial disease, diabetes

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19
Q

In what age group are B Blockers MOST effective? Why?

A

Young adults!

Because when you are young (20-29) BP is more dependent on CO (decreasing contractility and HR decrease CO bc contractility imacts SV and CO= SV*HR)

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20
Q

How does renin level relate to the efficacy of B blockers? Why?

A

At high renin levels B blocks are more effective than at low renin levels

Why: Renin release is mediated by B1 receptor.

SO if a person has HTN due to high renin levels, blocking rening release will be very effective!

But if somone’s HTN is unrelated to renin (aka they have low renin levels and still have HTN) then blocking renin relase won’t be effetive.

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21
Q

What are the general effects of an a2 agonist?

A

Decrease SNS by upregulating negative feedback on NE release (decrease NE release) which will:

  • decrease HR (less NE at B1)
    • decreases CO
  • decrease venous tone (???)
    • decreases CO
  • decrease renin release (less NE causing B1 mediated renin release.)
    • this decreases vascular tone, peripheral resistance and therefore BP
22
Q

List 3 central a2 adrenergic agonists

what are their effects and where do they occur?

What are some adverse effects?

A

Clonidine, Guanabenz, a-Methyldopa

  • They stimulate a2 adrenergic receptors in the brain which
    • reduces sympathetic outflow form the brains vasomotor center
    • increases vagal tone
  • Adverse effects:
    • Na/H20 retention (due to no NE block, so more NE, so more B1 mediated renin release)
    • Abrupt iscontinuation can cause rebound hypertension
    • depression
    • orthostatic hypotention and dizziness
    • Clonidine: anticholinergic side effects
      *
23
Q

What are the general effects of Neuronal and ganglionic blockade?

A

Decreases SNS

  • decrease arterial vascular tone
    • decrease peripheral resistance,CO and therefore BP
  • decrease renin release (NE at B1 stimulates renin release)
    • decreae peripheral reisstance….
  • decrease venous tone
  • decrease HR (less NE at B1 on heart)
    • decrease Co and therefore BP
24
Q

What are 2 Ganglionic and neuronal blcokers? What are their adverse effects? What other drug is suggested to be given with them?

A

Guanethidine and reserpine

use with a diuretic (preferably a thiazide) to avoid fluid retention

adverse effects:

  • bradycardia and decrease CO
  • sodium and water retention
  • diarrhea
  • sedation (reserpine)
  • depression (reserpine)
  • gastric acid secretion (reserpine)

***note reserpine has extra effects beacuse it can cross the BBB***

25
Q

Summary:

  • alpha receptor antagonists lower BP primarily through ________
  • alpha1 receptor antagonists also demonstrate first dose effect that requires ________
  • B receptor blockers lower BP by decreasing ______ and are more efective in _________patients and patients with ______ renin levels
  • central a2 receptor agonist and neuronal ganglionic blockers decrease __________ to lower BP
  • Na/H20 retention is a side effect of central a2 agonists and neuronal/ganglionic blockers that require______
A
  • a receptor antagonist lower BP primarily through arterial dilation
  • a1 receptor antagonists also demonstrate first dose effect that requires 1st dose at bedtime (prazosin, terazosin, doxazosin)
  • B clockers lower BP by decreasing CO an are more effective in young adults and pts with high renin levels
  • central a2 agonists and neuronal ganglionic blockers decrease sympathetic nervous system activity to lower BP
  • Na/H20 retention is an adverse effect of central a2 receptor agonists and neuronal and ganglionic blockers that typically require use with a diuretic
26
Q

How do diuretics impact blood pressure?

A

decrease vascular volume which decreases venous return, which decreases CO, which decreases BP

they also activate the RAA system

27
Q

What kind of drug is Fenoldopam/where does it work?

What is the MOA?

use?

toxicity?

A

Renal Vasodilator-works at the glomerulus

MOA: selective renal vasodilaiton, decreases proximal tubule reabsoprtion resulting in diuresis

use: HTN emergency and heart failure (works fast, but after a few hours BP returns)
toxicity: increases intraocular pressure and should be avoided in patients wiht glaucoma

28
Q

What class of drug is Furosemide/ where does it work?

What is the MOA?

use?

toxicity?

A

Loop diuretic-thick ascending limb

MOA: inhibits Na/K/2Cl symporter in medullary and cortical thick ascending limb

use: HTN emergency, HF, edema. less effective in chronic kidney disease
toxicity: hypokalemic metabolic alkalosis, hypovolemia

29
Q

What kind of drug is Hydrochlorothiazide/ where does it work?

MOA

use

toxicity

A

Thiazide diuretic- distal tubule

MOA: inhibit Na/Cl symporter in distal convoluted tubule

use: HTN
toxicity: hypokalmeia metabolic alkalosis

30
Q

What kind of drug is amiloride/where does it work? MOA? use? toxicity?

A

Amiloride- Sodium channel blocker-late and distal collecting duct

MOA: block Na entry into principal cells of the collecting duct, increase Na excretion, decrease K excretion

use: HTN, usually in combination
toxicity: hyperkalemia (esp if given alone)

31
Q

Generally how do aldosterone antagonists impact BP? MOA? What are 2 antagonists?

A

they decrease vascular volume which will decrease venous return which will decrease CO which will decrease BP

Spironolactone, Eplerenone

MOA: Block aldosterone on late distal tubule and collecting duct, this increases Na excretion (blocks na channel effects), decreases K excretion (blocks luminal Na/K/ATPase)

use: HTN, heart failure
toxicity: hyperkalemia

32
Q

What happens if you use a diuretic for long-term BP treatment?

A

The exact long-term antihypertensive mechanism is unknown

  • there is an initial BP drop from diuresis which causes:
    • reduced plasma and stroke volume ecreases CO
    • causes compensatory increase in peripheral vascular resistance
  • BUT extracellular and plasma volume return to almost pretreatment levels w chronic use
    • peripheral vascular resistance becomes lower than pretreatment levels
    • results in chronic antihypertensive effects

***SO volume levels go back to baseline but for some unknown reason the peripheral resitance stays decreased, so diuretics continue to decrease BP even after volume has returned to baseline

33
Q

What are 3 ACE inhibitors? what is their MOA? where do they work? what else is ACE responsible?

A

Captorpil, Enalapril, Lisinopril

MOA: Block Angiotensin Converting Enzyme (ACE) to block the conversion from Angiotensin I to Angiotnsin II

ACE is distributed all over tissues but primarily in in endothelial cells. Blood vessels are a major site for angiotensin II production

ACE degrades peptides like bradykinin so ACE inhibitors block bradykinin degradation, which stimulates the activation of other vasodilating substances such as prostacyclin

34
Q

What is the main AT1 blocker? MOA? where do they work/what are the effects?

A
  • Losartan- Angiotensin II receptor blocker
  • MOA: Block Angiotensin II type I receptor (AT1) also called ARBs (angiotensin receptor blockers)
  • ARBs inhibit AngII in many tissues
    • vascular smooth muscle-blocks vasoconstriction
    • adrenal gland aldosterone release
    • blocks SNS NE release
    • inhibits renal Na reabsorption
    • blocks brain vasopressin secretion
    • decreases heart contractility
35
Q

What is Aliskiren?

A

renin inhibitor!

inhibits conversion of angiotensinogen to angiotensin I

FDA approved for monotherapy and combo therpay with other anti-hypertensives

36
Q

How does AngII influence renal hemodynamics? WHat does this mean for the effect of RAS inhibitors?

A
  • AngII activates AT1 receptors on renal vascular smooth muscle to reduce renal blood flow
  • angiotensin Ii influence glomerular filtration rate (GFR) by several mechanisms
  • afferent arteriolar constriction reduces infraglomerular pressure and tends to reduce GFR
  • mesangial cell contraction decreases the glomerular capillary surface area available for filtration and decreases GFR
  • efferent arteriolar constriction increases intraglomerular pressure and tends to increase GFR
  • overall GFR is slightly reduced by AngII

SO RAS inhibitor slightly increase GFR

37
Q

How long does it take for a RAS to maximally lower blood pressure?

A

4-6 weeks

38
Q

what are the potential adverse effect of RAS inhibitors?

A
  • hyperkalemia- monitor plasma K on office visit 4-6 wks after initiation
  • acute kidney failure in pts. with:
    • severe bilateral renal artery stenosis
    • severe stenosis in artery to solitary kidney
  • contraindicated in pregnancy
  • cough caused by ACE inhibitors (due to increase in bradykinin)
  • Angioedema- more prevalent in ACE inhibitors *require immediate stop of ACE inhibitor
39
Q

RAS inhibitors may have interactions with drugs that _____

A

medications hich promote hyperkalemia

medications that have activity which is sensitive to chanegs in serum K

medications that may cause addditive antihypertensive effects

NSAIDs- bc NSAIDs already cause damamge to kidney function

40
Q

summary:

  • RAS inhibitors lower BP primarily through ________ and secondarily through ____________
  • ACE inhibitors lowe BP by decreasing ___________ levels and increasing ________ levels
  • Angiotensin type 1 receptor blockers (ARBs) have a number of effects based on ___________
  • ____________ are the newest class of RAS inhibitors
  • RAS inhibitors slightly _________ renal blood flow and glomerular filtration rate
  • RAS inhibitor adverse effects include _______
A
  • RAS inhibitors lower BP primarily through vasodilation and secondarily through decreasing renal Na reabsorption
  • ACE inhibitors lower BP by decreasing AngII levels and increasing bradykinin levels
  • Angiotensin type 1 receptor blockers (ARBs) have a number of effects based on AngII sites of action
  • Renin inhibitors are the newest class of RAS inhibitors
  • RAS inhibitors slightly increase renal blood flow and glomerular filtration rate
  • RAS inhibitor adverse effects include hyperkalemia, acute kidney failure, cough and angioedema
41
Q

What are the JNC 7 lifestyle modifications?

A
  • reduce weight to normal BMI
  • Dash diet/ sodium intake reduction
  • dietary sodium reduction
  • increased physical activity
  • reduce alcohol consumption
42
Q

WHat is the JNC7 BP goal? what about JNC8?

A

JNC7 BP<140/90. (no age recccomendations)

JNC8 BP<150/90, 60 and older, or if you have CKD or diabetes you want to keep 140/90

43
Q

According to the JNC7 reccomendations what are first line anti-hypertensive agents? How about JNC8?

A
  • JNC7: thiazide diuretics for all people
  • JNC8:
    • General population: Thiazide, CCB, ACEi, ARB
    • black: CCB or thiazide
    • DM: THiazide, CCB, ACEi, ARB
    • CKD: ACEi or ARB
44
Q

WHat are the reccomendations for:

  • elderly with isolated systolc HTN:
  • pregnancy:
  • children/adolescents:
  • African American
  • LVH
A
  • elderly with isolated systolc HTN: Thiazide or CCB may be better tolerated
  • pregnancy: methyldopa, beta blockers, vasodilators (hydralazine)
    • avoid ACEi or ARBs
  • children/adolescents: avoid ACEi or ARBs in pregnant or sexually active girls
  • African Americans: Response to diuretics and CCB> ACEi ARB, beta blocker. also angioedema 2-4X higher
  • Left ventricular hypertrophy: aggressive LV control regresses LVH
45
Q

What parameters do you need to monitor if you are taking a

diuretic

B blocker

RAS

CCB

A

diuretic: blood pressure, BUN/creatinine, serum electrolytes (K, Mg, Na), uric acids for thiazides

B Blocker: BP, HR

RAS: BP, BUN/creatinine, serum K

CCB: BP, HR

46
Q

what do you do if goal BP is not met with treatment…

after 1 month:

with 2 medications:

other classes of drugs may be added if….

A

1 month: increase dose of initial drug, or add a second drug (thiazide CCB, ACEi, ARB)

with 2 medications: add and titrate a third (thiazide, CCB, ACEi, ARB)

other classes of drugs may be added if goal BP is not met w 3 meds, OR contraindicated to thiazide (don’t use ACE and ARB together), ACE/ARB or CCB

47
Q

What are 4 anti-hypertensive combnation therapies?

A
  • diuretics and RAS inhibitors
  • directic vasodilators- add diuretic to reduce flid retention and reflex tachycardia
  • B-Blockers: add diuretic to reduce fluid retention and reflex tachycardia
  • Neuroanl and ganglionic blockers (Guanethidine or reserpine): add diuretic to reduce fluid retention
48
Q

How many agents do most people require to control blood pressure? what drug should be included unless contraindicated?

A

over 2!

A thiazide diuretic should be included unless contraindicated

49
Q

What is resistant hypertension? How do we often treat these patients?

A

failure to achieve blood pressure goal on full doses of 3 drug regimen including a diuretic. these people often require 4 drugs to get BP control.

Renal denervation!

50
Q

What is a hypertensive crisis? WHat is the difference between a hypertensive urgency and a hypertensive emergency? WHat drug is often used for HTN crisis and why must you be careful using this drug?

A

Blood pressure> 180/120

you must reduce it gradually

hypertensive urgency: elevated BP, no progressive organ damage

hypertensive emergency: acute or progressing target organ damage

Nitroprusside: caution with high intracranial pressure, azotemia, or chronic kidney disease

51
Q

what drugs are often used for HTN crisis? what are their special indications?

A

Sodium nitroprusside- Most HTN emergency, caution with increased intracranial pressure or chronic kidney disease (may lead to cyanide toxicity)

Fenoldopam- most HTN emergencies, caution with glaucoma (may cause tachycardia, headache, flushing)

Hydralazine- Eclampsia (may cause tahcycardia)

Hypertensive crisis can be treated with diazoxide, sodium nitroprusside, or fenoldopam

52
Q

What is the take-away from the sprint trial?

A

intensive blood pressure intervention is reccomended. decreasing systolic from 140 to 120 decreased risk of CV event by 27%

CV 3 (7 decks)

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