Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards




share
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

544 Pharm HTN, HF

Module 7

QuestionAnswer
Diuretics Decrease renal Na reabsorption which reduces water reabsorption
Thiazide Diuretics Prototype Hydrochlorothiazide
Thiazide Diuretic: HCTZ Site of Action Site of action: Distal Tubule
Thiazide Diuretic: HCTZ Mode of Action MOA- Competitive antagonism of Na/Cl cotransporter to decrease intravascular volume and direct vasodilatory effect
Thiazide Diuretic: HCTZ AE AE: LOW HYPOkalemia, hyperuricemia, hyperglycemia, dehydration. Less effective if CrCL
Potassium-Sparing Diuretics Prototypes Triamterene, Amiloride (Combo HCTZ/TMT- Maxide)
Potassium-Sparing Diuretics: Triamterene, Amiloride Site of Action Site of Action: Collecting Duct
Potassium-Sparing Diuretics: Triamterene, Amiloride MOA MOA: Na channel blockade; increase reabsorption of K
Potassium-Sparing Diuretics: Triamterene, Amiloride AE HYPERkalemia (HIGH K)
Beta Blockers do what? antagonism of catecholamines at Beta receptors Decrease CO by Decreasing HR and contractility (initial compensatory increase in PVR) decrease PVR longterm = decrease renin produces resting bradycardia and reduction in exercise-induced tachycardia
Beta Blockers AE Acute asthma, wheezing symptomatic bradycardia, fatigue, depression, HYPOglycemia, sexual dysfunction, detrimentally affects lipid profile Avoid sudden withdrawl
Non-selective Beta Blocker Prototype Prototype: Propranolol (Inderal)
Non-selective Beta Blocker Prototype: Propranolol (Inderal) MOA MOA: antagonizes catecholamines at B1 and B2 receptors, inhibition of sympathetically induced renin secretion
Non-selective Beta Blocker Prototype: Propranolol (Inderal) Contraindications CI in pt with asthma
Non-selective Beta Blocker Prototype: Propranolol (Inderal) Hepatically metabolized by: Hepatically metabolized by CYP2D6, 2C19
Beta 1 Selective Beta Blockers Prototypes Metoprolol (Lopressor, Toprol XL), atenolol, bisoprolol, esmolol Dose-dependent cardioselectivity Atenolol less lipid-soluble and Renally excreted unchanged Dose-dependent cardioselectivity Metoprolol Hepatically metabolized by CYP2D6
Partial B-Blockers (mixed agonist/antagonist) Acebutolol, carteolol, penbutolol, pindolol
Partial B-Blockers Acebutolol, carteolol, penbutolol, pindolol MOA: MOA: ISA (intrensic sympathemiminic Activity) -Less decrease in HR and CO -Agonist when Sympathetic tone is low (less resing bradycardia -antagonist when SNS is high; still blocks exercise-induced tachycardia
Mixed α1/β1/2 Blockers Prototypes Prototypes: Labetalol and Carvedilol
Mixed α1/β1/2 Blockers Carvedilol (Coreg) S(-) isomer - non-selective β-blockade R(+) isomer - α-blockade Primary use is in heart failure
Mixed α1/β1/2 Blockers Labetalol (Normodyne, Trandate) 3:1 β to α antagonism (orally) Used IV to treat hypertensive emergencies
α1- Blockers Protype Prototype Prazosin
α1- Blockers Protype Prototype Prazosin MOA MOA: Inhibitor Peripherial vasomotor tone, reducing VC and decreaseing SVR
α1- Blockers Protype Prototype Prazosin Precautions Precaution: “first dose effect” – postural hypotension
Can cause Na+/H2O retention when given without diuretic Prazosin- Alpha 1 Blocker
Prazosin- Alpha 1 Blocker Used to treat BPH
Prazosin- Alpha 1 Blocker hepatically metabolized by hepatically metabolized by non-cyp
Centrally Acting Agents MOA MOA Reduce sympathetic outflow from vasopressor centers in the brain stem
Centrally Acting Agents AE AE: Sedation Impaired concentration Nightmares Depression Vertigo EPS Lactation in men
Centrally Acting Agents Prototypes Protypes: Methyldopa (Aldomet)and Clonidine
Converted to alpha-methyldopamine and alpha-methylnorepinephrine in CNS Centrally Acting Agents Methyldopa (Aldomet)
Stimulates central α2 leading to a reduction in the activity of the vasomotor center Centrally Acting Agents Methyldopa (Aldomet)
Renal blood flow maintained – good in renal insufficiency Recommended for pregnant women Centrally Acting Agents Methyldopa (Aldomet)
Centrally Acting Agents Clonidine Site of Action Site of action: CNS non-adenergic binding sites and α2 receptor agonism
Centrally Acting Agents Clonidine BP reduction from decreased CO due to decreased HR and peripheral resistance Use with TCAs block effect Rebound hypertension with abrupt cessation PO or transdermal patch available 50/50 hepatic metabolism and renal excretion
Mixed α1/β1/2 Blockers Carvedilol (Coreg) is primarly used when the pt has what disease? Primarily used in heart failure
Mixed α1/β1/2 Blockers Labetalol is used IV to treat what? Used IV to treat hypertensive emergencies
beneficial for patients with renal insufficiency? Centrally Acting Agent Methyldopa (Aldomet)is beneficial for a pt with HTN and what disease
What HTN drug/class is recommended for pregnant women Centrally Acting Agent Methyldopa (Aldomet)
ACE Inhibitors Site of action: Site of action: ACE in endothelium
ACE Inhibitors Lisinopril, captopril, ramipril, enalapril, fosinopril, quinapril, benazepril
ACE Inhibitors MOA MOA: blocks ACE conversion of angiotensin I to angiotensin II; blocks inactivation of bradykinin
Ramipril, enalapril, benazepril, fosinopril are prodrugs. What class and what does prodrug mean? ACE Inhibitors; prodrugs mean that they have to be activated in their active form to produce an affect.
ACE Inhibitors Beneficial for Beneficial for diabetics with proteinuria (and or HTN)
ACE Inhibitors Adverse effects Adverse effects Hyperkalemia, angioedema, cough (bradykinin)
inhibiting Bradykinin and substance P will result in the side effect know as what? dry cough (caused why)
ACE Inhibitors Contraindications Contraindications Pregnancy, renal artery stenosis
ACE Inhibitors Comment: NSAIDs may impair effects by blocking bradykinin-mediated vasodilation
Angiotensin Receptor Blockers (ARBs) Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan
Angiotensin Receptor Blockers (ARBs) Site of action: Site of action: angiotensin II receptors
Angiotensin Receptor Blockers (ARBs) MOA MOA: Competitive binding results in decreased peripheral vasoconstriction
No effect on ACE or bradykinin Can cause hyperkalemia Contraindication: pregnancy Angiotensin Receptor Blockers (ARBs) Losartan, valsartan, candesartan, irbesartan, telmisartan, eprosartan
Direct Renin Inhibitors Site of action: Site of action: renin binding pocket
Direct Renin Inhibitors MOA Mechanism of action: prevents conversion of angiotensinogen to angiotensin I by renin
Direct Renin Inhibitors Okay in Pregnancy??? Contraindication: pregnancy
2 classes of CCB Dihydropyridines and Non-Dihydropyridines
CCB Calcium Channel Blockers prototypes Amlodipine, felodipine, nifedipine ER, nicardipine, nimodipine
Calcium Channel Blockers Dihydropyridines MOA: MOA: Block entry of extracellular calcium which is necessary for contraction Selectivity for smooth muscle over cardiac muscle Skeletal muscle unaffected since contraction not dependent on extracellular Ca
Calcium Channel Blockers Dihydropyridines AE: Adverse effects - peripheral edema, dizziness, headache, flushing, reflex tachycardia
Calcium Channel Blockers Dihydropyridines Metabolized by CYP3A4
Calcium Channel Blockers Non-Dihydropyridines Verapamil, diltiazem
Calcium Channel Blockers Non-Dihydropyridines MOA MOA: Blocks extracellular calcium entry SA and AV nodal tissue, other cardiac and arterial smooth muscle
Calcium Channel Blockers Non-Dihydropyridines Adverse effects: Adverse effects: conduction disturbances Diltiazem: ha, bradycardia, edema, heart failure Verapamil: constipation, dizziness, heart failure
Calcium Channel Blockers Non-Dihydropyridines Substrates and inhibitors of CYP3A4
NO formation K+ channel openers D1 stimulation Vasodilators
Hydralazine Vasodilators MOA MOA Stimulates NO synthesis from endogenous sources in endothelial cells Dilates arterioles only
Well-absorbed but rapidly metabolism by first-pass Variable effect due to variable acetylation Hydralazine Vasodilators
Hydralazine Vasodilators AE Adverse effects SLE-like syndrome with higher doses
Nitroprusside Vasodilators MOA MOA Gives off NO itself which then enters smooth muscle Arterial AND venous dilation
Nitroprusside Vasodilators Duration of action IV only Hypertensive emergency Short duration of action
Nitroprusside Vasodilators AE Adverse effects - cyanide toxicity
Nitroprusside Vasodilators AE CAN BE ENHANCED IF PT HAS WHAT INSUFFICIENCY? WHAT AE? AE: Cyanide toxicity Insufficiency: liver and kidney
Fenoldopam Vasodilators MOA MOA: D1-dopamine receptor agonism Decreased PVR and increased renal blood flow, diuresis, natriuresis Minimal adrenergic effects
Fenoldopam Vasodilators is used at what times Use: hypertensive emergency
Minoxidil Vasodilators MOA K+ channel opener Produce hyperpolarization of smooth muscle membrane reducing excitation and contraction = vasodilation
Minoxidil Vasodilators Half-life Half-life of 4 hours but active metabolite can cause persistence of hypotensive effect for 24 hours
Minoxidil Vasodilators AE Adverse effects: hypertrichosis
What is the first-line therapy in tx HTN? First-line therapy is thiazide diuretic unless there is a “compelling indication.”
T/F: In many cases, it is more effective to add a second agent from a different drug class than to increase the dose of the first agent. True
First-line therapy is thiazide diuretic unless there is a “compelling indication.” What are the Complling Indications Heart failure MI High CVD risk DM Chronic Kidney Disease Recurrent stroke prevention Isolated Systolic HTN
Rx's Heart Failure Thiazide diuretic, β-blocker, ACEI, ARB, aldosterone antagonist
Rx's MI β-blocker, ACEI, aldosterone antagonist
Rx's High CVD Risk Thiazide, β-blocker, ACEI, CCB
Rx's DM Thiazide diuretic, β-blocker, ACEI, ARB, CCB
Rx's Chronic kidney disease ACEI or ARB
Rx's Recurrent stroke prevention: Thiazide diuretic, ACEI
Rx's Isolated systolic hypertension: Thiazide diuretic, CCB
HTN Urgency Diastolic pressure >120 with evidence of progressive end organ damage Goal: decrease DBP to 100-105 within 24 hrs Clonidine
Hypertensive Crisis Diastolic pressure >120 with evidence of end organ failure Goal: decrease DBP 100-105 asap Nitroprusside, NTG, Labetalol, Fenoldopam
Diuretics Indications Heart Failure Systolic HTN
Diuretics CI Gout
BB Indications Migraines tachyarrhythmias
BB CI asthma heart block
A-blockers Indications BPH
A-Blockers CI Heart Failure
CCBs Indications Systollic HTN
CCBs CI Heart Block
ACEIs Indications Heart Failure Previous MI Diabetic Nephropathy
ACEIs CI RAS Pregnancy HYPERkalemia
ARBs Indications ACEI-associated cough Diabetic nephropathy Heart Failure
ARBs CI RAS Pregnancy HYPERkalemia
Down-regulation of sympathetic tone β1-blockers α1-blockers α2-agonists
Modulation of vascular smooth tone Calcium-channel blocker Potassium-channel openers
Reduction of intravascular volume Diuretics
Modulation of renin-angiotensin-aldosterone system ACE Inhibitors ARBs
Created by: tguymon1