hypertension Flashcards by Jasmin Maisuria

how is diagnosis of HTN made

blood-pressure dependent
Do not wait for symptoms as they are typically asymptomatic
Silent Killer

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normal BP

<120 and <80

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stage 1

130-139 or 80-89

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elevated BP

120-129 and <80

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what does adrenaline do

constricts

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stage 2

> 140 or >90

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what does nitric oxide do

dilates

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what do baroreflexes do

help regulate rapid adjustments in BP by communicating with the brain

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Binds to its receptors and causes
o Direct vasoconstriction
o Increased sympathetic tone
o Causes release of aldosterone

angiotensin 2

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Steroid produced by adrenal cortex
o Most potent mineralocorticoid
o Alters renal function = increased Na+ loop absorption, fluid
retention, increased in vascular volume
o Alters cardiac structure = cardiac growth factors, cardiac
remodeling

aldosterone

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do drugs cause a new function in the body?

no, only modify existing functions

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drug that interacts with a receptor to stimulate a response

agonist

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drug that interacts with a receptor, but does not stimulate a response

antagonist

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○ PVR and reduce CO

Sympatholytics (sympathoplegics

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○ Removes sodium and reduces blood volume

Diuretics

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○ PVR and possibly blood volume

Angiotensin inhibitor

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Relax vascular smooth muscle → dilating resistance vessels → capacitance

vasodilators

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Inhibit the sympathetic nervous system
They work best in combination therapy with diuretic
Central acting: Clonidine and Alpha-methyldopa
Spinal cord releases Norepinephrine → increases HR, contractility, preload, resistance
BP = CO x R → All lead to increased BP!
These medications inhibit these response

sympatholytics

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alpha 2 agonist
● When receptor stimulated, it inhibits NE from fusing with cell membrane
● Response = reduced sympathetic outflow = inhibited SNS = reduced BP + HR
● Lipid-soluble, easily enters brain, short half life (8-12 hours) and thus given BID
dosing
Indication:
Not readily used, seen as 3rd agent in clinical use (refractory HTN to 2 or more agents)
Works well with withdrawal
● Withdrawal from depressants such as alcohol or opioids, the SNS is no longer
inhibited and large SNS outflow occurs

Sympatholytics: Clonidine (Catapres)

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Sympatholytics: Clonidine (Catapres) adverse effects

● Dry mouth
● Sedation
● Inhibition of ejaculatio

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Sympatholytics: Clonidine (Catapres) contraindications

● Depression (stop medication if occurs)
● Do not use with TCAs (block alpha receptor)
Do not stop abruptly at higher doses (>1mg/day), can cause hypertensive crisis***
Wean slowly over 2-3 weeks while starting another agent

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MOA
● Follows the pathway that is used to make NE
● Alpha-2 agonist
● Inhibits synthesis of NE
● Thus less sympathetic outflow, reduces BP and HR (does not affect CO or blood flow
to vital organs)
Indications
● Pregnancy
● HTN complicated by kidney disease (no decrease in renal blood flow

Sympatholytics: Methyldopa (Aldomet)

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May cause a false positive Coombs test (autoimmune hemolytic anemia)
Adverse Effects
● Effect of medication may last even when no longer in circulation
● Sedation
● Dry mouth
● Mental concentration or feels like mind is foggy
● Postural hypotension
● Lactation in both genders (increased prolactin secretion)
Contraindications
● Caution with known depression

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Sympatholytics: Methyldopa (Aldomet)

MOA
● NE attaches to cell through Beta 1 receptor
● Beta 1 blockers affect NE effect on the cell = Beta antagonist → reducing SNS
effect
● Beta 1 receptors found in heart on nodal cells (SA node, AV node) and
contractile cells
○ Decreased signal to nodal cell → decreased HR → decreased CO = decreased BP
○ Decreased signal to contractile cell → decreased contractility → dec SV/CO = dec BP
● Atenolol, Bisoprolol, Esmolol, Metoprolol (all cardioselective)

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Sympatholytics: Beta Blockers

was first one discovered and found to work concomitantly with ischemic heart disease ● This is still in use but for other indications, such as headache prevention ● May see used in pregnancy for tachyarrhythmias ● Not cardioselective, working on both beta 1 and beta 2 receptors, and thus not readily used for HTN any longer Reduced mortality post-MI and heart failure Can help reduce reflex tachycardi

propranolol

Liver excretion, short half life (4-6 hours), but comes in XR for daily use or SR works well with heart failure patients (succinate only

Metoprolol (Toprol)

Excreted in urine (renal dosing) and given in daily dosing

Atenolol (Tenormin)

Indications ● HTN + ischemic heart disease ● HTN + heart failure ● Situational anxiety (presentation), essential tremor Adverse effects ● Bradycardia and reduced HR during exercise ● Hypotension ● CNS: Fatigue, lethargy, insomnia, hallucinations ● Erectile dysfunction ● Watch out for hypoglycemia unawareness ● Normal tachycardia, diaphoresis, sense of doom, all may be blunted due to BB

Sympatholytics: BB

MOA ● Blocks alpha 1 receptors on venous and arterial smooth muscle cells ○ NE can not bind the receptor = alpha 1 antagonist ○ Causes arteries to relax → vasodilation → decreased R → decreased BP ○ Venodilation → decreased preload → decreased CO → decreased BP ● Selective = Prazosin (Minipress), Terazosin (Hytrin), Doxazosin (Cardura) ● Non-selective = Phentolamine, Phenoxybenzamine

Sympatholytics: Alpha blockers

Sympatholytics: BB Contraindications

● Cardiogenic shock ● Non-selective avoid in asthma ● Decompensated heart failure ● Avoid abrupt cessation or initiation: ○ Start low and titrate slowly every 1-2 weeks ○ Wean slowly at least over 2-3 weeks ● Do not use with Non-dihydropyridine CCBs (Verapamil, Diltiazem), cause severe bradycardia and AV block

Indications ● Selective = BPH ● Non-selective = hypertensive crisis, pheochromocytoma, MAO-I + tyramine (cheese/wine) Adverse Effects ● Watch out for reflex tachycardia = compensatory mechanism/baroreflex ● First dose phenomenon = some experience postural hypotension with first dose, start low and at bedtime ● HA, dizziness, hypotension Contraindication ● Patient who is preload dependent → orthostasis Possible false positive ANA test

Sympatholytics: Alpha blockers

● Reduces resistance via alpha blocking, but does not significantly affect HR or CO ● Pheo or hypetensive emergencie

Labetalol

● Start 6.25mg BID, half life 7-10 hours ● Reduced mortality in heart failure patient

Carvedilol = Coreg

● Vasodilation not from alpha blocking, may be due to endothelial release of NO ● Men note less ED effects, less sedating

Nebivolol = Bystolic

● Used in intraoperative and postoperative hypertension ● Short half life (9-10 minutes) = great drug to use if worried about toxicity of drug due to such short half life

Esmolol = Brevibloc

Hydrochlorothiazide = HCTZ Chlorthalidone = old drug, studies show reduced cardiac events, and more effective than HCTZ (longer duration of action) Red-headed step child MOA Inhibits reabsorption of water and sodium in distal convoluted tubule (DCT) Consequently excrete sodium, water, and chloride Can lead to hyponatremia

thiazides

MOA Excretion of sodium through urine Subsequent blood volume reduction and CO drops, R increases temporarily About 2 months later CO returns to normal, R declines Monotherapy for mild HTN, combination with alpha or beta blockers for moderate to severe See 10-15mmHg reduction

diuretics

Indications: Volume overload (CHF, cirrhosis) Moderate to severe HTN When patient has medications with sodium-retaining attributes Acute hypercalcemia Helps more with symptomatic volume overload (peripheral edema, breathing/ pulmonary edema) Adverse Events: Hyponatremia, hypokalemia, metabolic alkalosis, hypocalcemia CAN be used if CrCl <30 (but is nephrotoxic when combined with others) Contraindications: Increases uric acid, try to avoid with gout history May be ototoxic (rapid IV administration

loop diuretics

Indications: Mild HTN with normal renal and cardiac function Iatrogenic volume overload (given a lot of fluids during hospitalization) Mild edema Calcium nephrolithiasis—reduces calcium in urine and may prevent recurrence Adverse Effects: Can elicit gout flare and worsen dyslipidemia Hyponatremia, hypokalemia, metabolic alkalosis Can be nephrotoxic Caution: avoid with sulfa allergy as it contains a sulfonamide group

thiazides

Furosemide = Lasix “Lasts six hours” Bumetanide = Bumex Torsemide = Demadex MOA Inhibits sodium and water reabsorption at ascending limb of loop of Henle Increases water excretion Increases excretion of sodium, potassium, and calcium

loop diuretics

Spironolactone = Aldactone MOA = Potassium-sparing diuretic, blocks aldosterone receptor competitively at DCT/collecting tubule Prevents Na+ and water reabsorption Prevents K+ and H+ excretion Indication = Very mild diuretic, heart failure, ascites in cirrhosis, acne (weakly blocking androgen receptors), hypokalemia due to other diuretics Adverse effects = dry skin, hyperkalemia, gynecomastia (blocking sex hormones) Contraindication = pregnancy

Aldosterone receptor blockers

● Beta 1 cells on kidney are activated by SNS through NE, trigger kidney to excrete renin ● If poor perfusion to kidneys (low CO), stimulates cells in kidney to produce renin ● Renin interacts with Angiotensinogen that is made by the liver, converts to Angiotensin I ● Angiotensin I goes to the lungs where ACE converts it to Angiotensin II ● Angiotensin II acts on the heart, adrenal cortex, CNS, kidney tubules

Renin-Angiotensin-Aldosterone Inhibitors

Lisinopril = Zesteril Enalapril = Vasotec MOA Reduce vasoconstriction, reduce aldosterone, reduce ADH production, reduce glomerular BP 1. Inhibits ACE in the lungs: blocks conversion of angiotensin I to angiotensin II Angiotensin II is a potent vasoconstrictor, by lowering it also lowers aldosterone and thus decreases sodium and water retention 2. ACE normally converts bradykinin to other metabolites, but by inhibiting ACE bradykinin increases in the system → agitation of cough receptors or inflammation leading to capillary leakage (angioedema) 3. Lowers BP by lowering R = no reflex increase in CO, HR, or contractility

Renin-Angiotensin-Aldosterone Inhibitors: ACE Inhibitors

Indications ● HTN + ischemic heart disease (do not cause reflex SNS) ○ Start 24 hrs after AMI, improves function, decreases mortality, used with BBs ● HTN + CKD (reduce proteinuria and maintained renal function) ○ Utilized in diabetic patient for renal protection ● HTN + diastolic dysfunction ● HF = In combination with BBs, both decrease mortality Great option as first line agent in general, but always use in DM and/or CKD if no contraindications = slows progression of diabetic neuropathy and decreases albuminuria (ARBs have same benefits)

Renin-Angiotensin-Aldosterone Inhibitors: ACE Inhibitors

Adverse Effects ● Persistent, dry cough (can occur any time, resolves with discontinuation, 10%) ● Angioedema = <1%, can be fatal ● Hyperkalemia = diet changes to avoid K+-rich foods (bananas, beans, potatoes, salmon, salt substitutes), caution with K+-sparing diuretics (Spironolactone) ● Increased creatinine (reduces GFR → decreases creatinine clearance) o ARF in patients with bilateral renal artery stenosis (reversible when stopped) Contraindications ● Patients with prior angioedema, avoid in pregnancy, monitor for renal impairment (renal excretion) ● Avoid potassium supplements or potassium-sparing diuretics

Renin-Angiotensin-Aldosterone Inhibitors: ACE Inhibitors

Cozaar = Losartan Diovan = Valsartan MOA Binds to Angiotensin II receptors to block action of Angiotensin II Reduce vasoconstriction, reduce ADH, reduce Aldosterone secretion, reduce glomerular

Renin-Angiotensin-Aldosterone Inhibitors: Angiotensin II Receptor Blockers (ARBs

Venodilators: Dilate vein and thus reduce preload (mild effect) Arterial dilators: Dilate arteries and thus reduce resistance ● ("-dipines") = block calcium channel on smooth muscle cell and inhibits contraction → reduce resistance → reduce BP ○ Amlodipine (Norvasc), Nifedipine (Procardia) ○ Used for angina or cardiac vasospasms ○ Can use with beta blockers ■ Can lead to bradycardia and AV block (dangerous if pre-existing conduction issues) ○ Only find dihydropyridine calcium channels on the smooth muscle cells

vasodilators Dihydropyridine calcium channel blockers

Indications Same for ACE-I, but generally used when patient has cough reaction to ACE-I HF: Combo with BBs if ACEI not tolerated Adverse Effects Hyperkalemia (by reducing aldosterone) Increased creatinine (reduces GFR → decreases creatinine clearance) Contraindications Teratogenic (avoid in pregnancy

Renin-Angiotensin-Aldosterone Inhibitors: Angiotensin II Receptor Blockers (ARBs)

These calcium receptors are on cardiac myocytes AND vascular smooth muscle Verapamil = Calan Diltiazem = Cardizem Used for chronic stable angina and Printzmetal's angina, rate control in SVT/Afib/Aflutter, rare for HTN unless compelling reason MOA Reduce cell contractility → reduce CO → reduce BP (vasodilation) Block action at nodal cell → reduce HR →→ reduce BP Have anti-anginal and anti-arrhythmic effects

vasodilators Non-dihydropyridine calcium channel blockers:

Indications Refer to other lecture for further uses Amlodipine as common first agent >50yo or AA Adverse Effects ● CCB = Reflex tachycardia (baroreceptor → CNS → increased HR), peripheral swelling at higher doses, dizziness/fatigue, gingival hyperplasia ● NonD CCB = Bradycardia, major DDI with 3A4 inhibitors ● All CCB = orthostatic HOTN, constipation (esp Verapamil) Contraindication Decompensated HF = non-dihydropyridines, negative inotropic effect, poor CO, reduce contractility further, leads to shock Short-acting Nifedipine may increase MI and thus not used for HT

vasodilators

MOA Direct-acting vasodilator → stimulates cell through cGMP → inhibit arterial smooth muscle → arterial vasodilation (decreases resistance) Reflex tachycardia and renin secretion = tachycardia can be blocked by BBs, fluid retention can be blocked with diuretic Indications = severe HTN, usually given with BB and diuretic, with nitrates for HF esp AA Adverse Effects = Reflex tachycardia, HA, angina, can cause drug-induced SLE-like symptoms at high doses (muscle/joint pain, flu-like symptoms), mild orthostasis, peripheral neuritis (prevented with administration of B6 (pyridoxine)) Contraindications May avoid with FH of lupus (SLE-symptoms resolve with discontinuation) It IS safe in pregnancy

Vasodilators: Hydralazine

Same as Hydralazine, but even more potent than Hydralazine and used when maxed doses of Hydralazine reached Active metabolite is a potent arteriolar vasodilator, decreases R Greater SNS response, must be used with BB (reflex tachycardia) or loop diuretic (renin secretion) Generally only used for hair growth topically (Rogaine) ADRs: Severe sodium and water retention (can lead to volume overload, edema, HF)

Vasodilators: Minoxidil

Work by increasing/releasing nitric oxide that leads to action on the cell MOA: Intense dilation by relaxing smooth muscle in arterioles and venules, decreases preload and afterload, causes reflex tachycardia Indication: hypertensive emergency (given IV, PO poisonous as it converts to cyanide), severe HF, aortic dissection (along with BB, opioid, and surgery) Adverse Effects: can give off cyanide molecule that leads to toxicity (rare with IV), leads to lactic acidosis Contraindication Known CAD (drug will overdilate unblocked coronary arteries and reduce flow to moderately restricted artery → coronary steal syndrome

Vasodilators: Nitro dilators Nitroprusside

Consider if you have patient on 3 medications and all 3 are near or at maximum dosing without appropriate control. Look for RAS/renal causes Make sure at least one of the 3 medications is a diuretic

resistant hypertension

Very high BP with signs of organ damage ● >180mmHg SBP, >120mmHg DBP ● Brain, renal, cardiovascular compromise ● Slowly decrease BP to 160/100, risk of stroke if corrects too quickly Hypertensive encephalopathy (malignant HTN): severe HA, confused, seizures Intracranial hemorrhage: Thunderclap headache Acute MI Eclampsia

hypertensive emergency

Stage 2 Hypertension without signs of organ damage Generally agreed to be >120mmHg DBP Goal is to reduce BP within a few hours

hypertensive urgency

hypertension Flashcards

(56 cards)