Exact hypotensive mechanism unknown Initial BP drop caused by diuresis Extracellular & plasma volume return to near pretreatment levels with chronic use but anti-hypertensive effects continue

Hypertension Drugs 2 Flashcards by Meghan May

In general, how do central alpha-2 agonists lower blood pressure?

by decreasing SNS outflow which reduces vascular tone & decreases HR

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What are some central alpha-2 agonists?

Clonidine
Guanabenz
α-Methyldopa

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What is the MOA of central alpha-2 agonists?

Stimulate α2-adrenergic receptors in the brain
– reduces sympathetic outflow from the brains vasomotor center
– increases vagal tone

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General adverse effects of central alpha-2 agonists?

– sodium/water retention
– abrupt discontinuation may cause rebound hypertension
– depression
– orthostatic hypotension
– dizziness

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Adverse effect specific to cloonidine?

anticholinergic side effects

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Adverse effects specific to methyldopa?

can cause hepatitis & hemolytic anemia (rare)

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In general, how do neuronal & ganglionic blocking agents lower BP?

decrease SNS outflow

decreases renin and inhibits alpha-1 both which reduce vascular tone
blocks beta-1 on heart decreasing HR

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What are some neuronal & ganglionic blocking agents?

Guanethidine
Guanadrel
Reserpine
Trimethaphan ganglionic

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Adverse effects of neuronal & ganglionic blocking agents?

– Sedation (reserpine)
– Depression (reserpine)
– decreased CO
– sodium/water retention
– increased gastric acid secretion (reserpine)
– diarrhea
– bradycardia

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In general, how do diuretics help lower BP?

decrease vascular volume causes decreased venous return therefore decreased CO
-however, causes reflex increased SNS

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What are some diuretic drugs?

Hydrochlorothiazide
Furosemide
Amiloride

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MOA of diuretics?

Exact hypotensive mechanism unknown
Initial BP drop caused by diuresis
Extracellular & plasma volume return to near pretreatment levels with chronic use but anti-hypertensive effects continue

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Potential adverse effects of diuretics?

– Electrolyte disturbances • potassium, magnesium, sodium, calcium
– Hyperglycemia
– Hypotension, orthostasis
– Lipid abnormalities
– Photosensitivity
– Ototoxicity
– Hyperuricemia, gout flare

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What are some aldosterone antagonists?

Spironolactone & Eplerenone

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What is the MOA of aldosterone antagonists?

Inhibit the renal (Na and H2O retention) and extra-renal (fibrosis, inflammation, etc.) actions of aldosterone

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What are the general classes of RAS inhibitors?

ACE inhibitors
AT1 blockers
renin inhibitor

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How do RAS inhibitors decreased BP?

block the effects of kidney mediated vasoconstriction which decreases vascular tone decreasing peripheral resistance

What are the ACE inhibitors?

Captopril
Enalapril
Lisinopril

What is the AT1 blocker?

Losartan

What is the renin inhibitor?

Aliskiren

MOA of ACE inhibitors?

Block angiotensin I to angiotensin II conversion by ACE (Angiotensin Converting
Enzyme) distributed in many
tissues

Secondary effects of ACE inhibitors?

Block bradykinin degradation; stimulate synthesis of other vasodilating substances such as prostaglandin E2 & prostacyclin
Prevent or regress left ventricular hypertrophy

What should we monitor in people with ACE inhibitors?

Monitor serum K+ & SCr within 4 weeks of initiation or dose increase

Adverse effects of ACE inhibitors?

– cough: up to 20% of patients due to increased bradykinin
– angioedema
– hyperkalemia: particularly in patients with CKD or DM
– neutropenia, agranulocytosis, proteinuria, glomerulonephritis, acute renal failure

MOA of ARB like losartan?

block AT1r which causes vasoconstriction and allows ATII to work on ATIIr causing vasodilation

Why do you get less cough with ARBs?

Do not block bradykinin breakdown

Adverse effects of ARB?

– orthostatic hypotension – renal insufficiency – hyperkalemia

Do ACE inhibitors and ARB work right away?

No, takes 4 to 6 weeks to see full effect

What is the MOA of renin inhibitor?

Inhibits angiotensinogen to angiotensin I conversion and Does not block bradykinin breakdown

What are the adverse effects of renin inhibitors?

orthostatic hypotension & hyperkalemia

What are ACE Inhibitor/ARB Precautions?

• Can cause acute kidney failure in certain patients – severe bilateral renal artery stenosis – severe stenosis in artery to solitary kidney • Pregnancy

ACE inhibitors and ARB’s Potential Drug Interactions?

– Medications which promote hyperkalemia – Medications that have activity which is sensitive to changes in serum K+ – Medications that may cause additive antihypertensive effects – NSAIDs

RAS inhibitors combo well with what?

diuretics

What are some lifestyle modifications that can help with hypertension?

- Reduce weight to normal BMI (<25kg/m2): 5-20 mmHg/10kg loss - DASH eating plan: 8-14 mmHg - Dietary sodium reduction: 2-8 mmHg - Increase physical activity: 4-9 mmHg - Reduce alcohol consumption: 2- 4 mmHg

What are JNC8 Recommendations for General Non-black Population?

* General population– Thiazide, CCB, ACEi, ARB (Grade B) * Black population – CCB or Thiazide (Grade B) Grade C for black patients with DM * DM– Thiazide, CCB, ACEi, ARB (Grade B) * CKD– ACEi or ARB (Grade B)

Guidelines for JNC8 combo therapy?

* Most patients require > 2 agents to control BP * A thiazide-type diuretic should be one of these agents unless contraindicated * Combination regimens should include a diuretic (preferably a thiazide) * Resistant hypertension: failure to achieve BP goal on full doses of 3 drug regimen including a diuretic

Special populations guideline: african americans?

response to diuretics & CCB greater than ACEI, ARB and beta-blockers angioedema is 2-4 fold higher

Special populations guideline: left ventricular hypertrophy?

Aggressive BP control regresses LVH…but hydralazine & minoxidil DO NOT!

Special populations guideline: elderly usually systolic HTN?

– Thiazide or CCB may be better tolerated

Special populations guideline: pregnancy?

– Methyldopa, beta-blockers, vasodilators (hydralazine) | – Avoid ACEI & ARBs

Special populations guideline: children/adolescents?

Avoid ACEI & ARBs in pregnant or sexually active girls