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544 Pharm HTN, HF
Module 7
| Question | Answer |
|---|---|
| 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
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