HTN-1 Flashcards by Brooklyn Underwood

Normal BP

<120/80 mmHg

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Elevated BP

120-129 mmHg / ≤ 80 mmHG

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Stage 1 Hypertension BP

≥ 130 mmHg systolic
OR
≥ 80 mmHf diastolic

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Stage 2 Hypertension BP

≥ 140 mmHg systolic
OR
≥ 90 mmHg diastolic

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Hypertensive Urgency / Emergency BP

≥ 180 mmHg systolic
OR
≥ 120 mmHg diastolic

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What are the hypertension risk factors

Age
FH
Smoking
Obesity
Metabolic Syndrome
High alcohol intake
Diabetes
High sodium intake
Dyslipidemia

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What are the two major processes that regulate BP

-baroreceptors and the sympathetic nervous system
-renin-angiotensin aldosterone system

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Pathophysiology of decreased BP on alpha and beta receptors

decrease BP
decrease signal to brain
increase sympathetic nervous system
increase catecholamines

alpha increase peripheral resistance
beta effects heart

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Pathophysiology of decreased BP in blood volume

decrease BP
decrease signal to kidneys
renin -> angio -> angio II vasoconstrictor
aldosterone increases sodium and water

results in higher blood volume

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What are the secondary causes of hypertension

renal disease
Cushing’s disease
pheochromocytoma
pregnancy
sleep apnea
contraceptives
sympathomimetics
NSAIDs
steroids
SSRIs/SNRIs
cocaine
nicotine
amphetamines
licorice

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What is the primary goal of treating hypertension

reduce morbidity and mortality by decreasing the risk of target organ damage

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What are the best practices for checking BP

sit for 5 minutes
no caffeine
arm placement
correct cuff size
check both arms
feet flat on floor
not talking
clothing removed from where cuff placed

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Higher CVD risk = more important to have a ______ goal and assure we get there ________

tighter
quickly

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What is the CV risk for stage 1 hypertension and ASCVD or 10 year CVD risk ≥ 10%

high CV risk

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What is the CV risk for stage 1 hypertension and no ASCVD and 10-year CVD risk < 10%

Low CV risk

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What are the ASCVD risks

ACS (acute coronary syndrome) CAD (coronary artery syndrome)
PAD (peripheral artery disease)
TIA (transient ischemic attack)
Stroke
MI (myocardial infarction)
Angina (stable or unstable)
CABG or PCI/stent (coronary/arterial revascularization)

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What calculation can you use for a patient between the ages of 40-79 to estimate risk of CV event in the next 10 years

American College of Cardiology Risk Calculator

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If a patient is less than 40 and has 2 or more risk factors included in calculation (smoking, african american, HLD, DM) they are considered what kind of CV risk

High CV risk

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If a patient has an elevated BP (120-129/<80) what is their recommendations

Start with nonpharmacologic therapy, reassess BP in 3-6 months

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If a patient has stage 1 hypertension and a high CV risk what is their recommendation

-Start with nonpharmacologic and pharmacologic therapy
-Reassess BP in 1 month
-If at goal reassess 3-6 months
-Not at goal reassess for adherence and intensification of therapy

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If a patient has stage 1 hypertension and a low CV risk what is their recommendation

-Start with nonpharmacologic therapy
-Reassess BP in 3-6 months
-Not at goal consider pharmacologic therapy

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If a patient has stage 2 hypertension what is their recommendation

-Start with nonpharmacologic and pharmacologic therapy
-Reassess BP in 1 month
-At goal reassess 3-6 months
-Not at goal asses for adherence and consider intensification of therapy

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Food considerations for improving BP

Na+ restriction
High-fiber and natural foods
Limit high saturated fats
Low-fat dairy products

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Lifestyle consideration for improving BP

Exercise
Aerobic activity
Dynamic resistance
Isometric resistance
Moderate alcohol
Smoking cessation

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cardiac output times peripheral resistance equals

blood pressure

What two things effect cardiac output

cardiac (heart rate, heart contraction) volume control (renal renin-angiotension, aldosterone)

What two things effect peripheral resistance

sympathetic control (vasoconstrictor, vasodilator) humoral (catecholamines, prostagandins)

What part of the renal system is not permeable to water

distal convoluted tubule

What part of the renal system is not permeable to salt

thin descending tubule

Where are thiazide agents located

distal convoluted tubule

Where are loop diuretics located

thick ascending tubule

Where are potassium sparing agents located

collecting tubule

What are diuretics mechanism of action

decreases extracellular volume, enhancing sodium excretion in the urine, leading to a decrease in cardiac output

What is the most frequent used class of antihypertensive agents in the US

thiazide diuretics

Results of thiazide diuretics

high K+ secretion causing hypokalemic because K+ is not reabsorbed

What drug class do these belong to: hydrochlorothiazide (hydrodiuril) chlorthalidone (hygroton) Indapamide Metolazone

thiazide diuretics

What is the GFR goal of kidneys

<30 ml/min

ACE and ARBs will ________ diuretic induced loss of K+

counteract

Hydrochlorothiazide primary and secondary site

primary: kidney secondary: vascular smooth muscle cells

What drug class do these belong to: furosemide (lasix) bumetanide (bumex) ethacrynic acid (edecrin) torsemide (demadex)

Loop diuretic (block Na/K/Cl

What diuretics is the highest capacity especially if renal function is not normal and has the highest capacity Na/Cl/K pump

loop diuretics (twice a day medications for hypertension, heart failure, and ascites)

Loop diuretics increase the urinary secretion of what ions

na cl ca mg K+

What drug class do these belong to: amiloride (midamor) triamterene (dyrenium)

potassium sparing channel blockers

What drug class do these belong to: spironolactone (aldactone) eplerenone (inspra)

potassium sparing receptor blockers

What class of diuretic can you not use with ACE and ARBs

potassium sparing

What is the function of potassium sparing channel blockers

block pore of the epithelial sodium channel (decrease volume, hyperkalemic)

What is the function of potassium sparing receptor blockers

steroid hormone produced by adrenal gland regulate Na+, K+, and acid/base balance in blood

Potassium sparing diuretics ________ transepithelial _____ transport

enhances NaCl

ACE inhibition

-BP is decreased due to decrease in blood volume, peripheral resistance and cardiac load -inhibit vasoconstriction and release of aldosterone which inhibits the retention of sodium and water

What does ACE inhibition do to bradykinin

increases it

What do all ACE inhibitors end in

"-pril"

What do ACE-I treat

chronic renal disease aldosterone (they tend to enhance the efficacy of diuretic drugs) young middle-aged Caucasians

Adverse effects of ACE-I

-rise in serum K+ -caution with K+-sparing diuretics, K+ supplements, NSAIDs, beta-blockers -bradykinin: dry cough, angioedema -dysgeusia -contradicted with pregnancy

ARBs do not inhibit ACE-mediated degradation of ___________

bradykinin

What do all AT1 receptor blockers end in

"-sartan"

What do AT1 and AT2 do

AT1: vascular, myocardial tissue, kidney, brain, and adrenal glomerulosa cells AT2: adrenal medulla, kidney, CNS

What are the three steps of AT1 receptor activation

Altered Peripheral Resistance (direct vasoconstriction, enhance sympathetic discharge) Altered Renal Function (increase Na+ reabsorption in the proximal tubule and distal tubule) Altered Cardiac Function (relax smooth muscle to promote vasodilation, increase salt and water secretion, reduce plasma volume decreasing cellular hypertrophy)

AT1 receptor blockers treatment

high angiotenstion II: volume depketion, renovascular hypertension, cardiac function, cirrhosis no bradykinin not effective in old, blacks, low-renin patients

Adverse effects of AT1 receptors

insignificant rise in serum K+ (hyperkalemia) contraindicated in pregnancy

Aliskiren hemifuramate (tekturna)

-inhibits the catalytic activity of renin producing Ang1, Ang2, aldosterone which decreases BP -systolic and diastolyic -monotherapy and combo therapy -contraindicated in pregnancy

When do you start two medicines for hypertension

>30 mmHg above systolic or >20 mmHg diastolic African American: >20mmHg above systolic or >10mmHG diastolic

What numbers of BP is a hypertension emergency

>180 systolic or >120 diastolic

What medicine to use for systolic heart failure (SHF/CHF)

ACE and beta blocker

What medicine to use for post-MI

ACE-I and beta blocker

What medicine to use for diabetes with albuminuria

ACE-I or ARB

What medicine to use for CKD with albuminuria

ACE-I or ARB

What medicine to use for stroke

ACE-I or ARB

If there are no compelling indications for hypertension what are the trifecta of choices to use

thiazide diuretics (-pine) ACE-I and ARBs Calcium Channel Blockers

If patients are over 60 or black what is the recommended medication class to use

thiazide or calcium channel blocker (beta blocker NOT recommended)

What do alpha blockers cause

orthostatic hypotension (important to titrate slow and start low)

Central alpha 2 agonists

Only for resistant hypertension or hypertensive emergency ADRs don't go away (adverse drug reaction) Avoid in HF Alcohol dependence ADHD ER formulation Methyldopa used in pregnancy

Vasodilators

Resistant HTN (systolic) Use with diuretic to decrease fluid retention

Moderate dose of 2 or more medications are _____ effective than high doses of one medication

Thiazides and CCBs cause ____ excretion and vasodilation

Na+

ACE-I and ARBs improve ____-induced edema by causing venule dilations

CCB (calcium channel blocker)

ACE and ARBs may improve ___________ from thiazides

hypokalemia

When should a follow-up be after starting/changing therapy

2-4 weeks

When should a follow-up be if BP is stable and controlled

3-6 months

Diuretics increase the excretion of electrolytes and water from the body ______ affecting protein, vitamin, glucose, or amino acid reabsorption

without

Diuretics are used to treat _____ and hypertension

edema

What is the primary target organ of diuretics where they interfere with reabsorption of ions

kindey

What are osmotics site of action and mechanism of action

Site: proximal tubule mechanism: osmotic effects decrease sodium and water reabsorption

What are carbonic anhydrase inhibitors site of action and mechanism of action

site: proximal convoluted tubule mechanism: inhibition of renal carbonic anhydrase decreases sodium bicarbonate reabsorption

What are thiazides site of action and mechanism of action

site: thick ascending loop and distal tubule mechanism: inhibit na/cl symporter

What are loop or high ceiling site of action and mechanism of action

site: thick ascending limb mechanism: inhibit na/k/cl transport system

What are potassium-sparing site of action and mechanism of action

site: distal tubule and collecting duct mechanism: inhibit sodium and water reabsorption by competitive inhibition of aldosterone or blockage of sodium channels

What are osmotics MOA

decrease na and h2o reabsorption

Osmotics are ______ polar and have a ______ molecular weight

highly low

Are osmotics secreted as charged or uncharged parent drugs

uncharged

Carbonic anhydrase inhibitors MOA

inhibit carbonic anhydrase which decreases H+ exchange for Na+ ion in the kidney. Lose Na, HCO3, and H2O

Carbonic anhydrase inhibitors treat what

glaucoma and acidify urine (result in metabolic acidiosis)

Sulfonamides are ______ and are common with all CAIs

acidic

Methyls improve ________

lipophilicity

Secondary aliphatic amines _______ water solubility

increase

An ionizable amino group cause ______ water solubility

higher

MOA of thiazides

compete for Cl- binding of Na/Cl symport which inhibits reabsorption of Na and Cl ions -> hyponatremia, hypokalemia, hypomagnesia

In thiazides what group is important at position 6

EWG

In thiazides what is present at position 3 and 4

double bond to make them more active

In thiazides what is at position 3 to increase a longer duration of action

alkyls to increase lipid solubility

What is the duration of action of loops or high ceiling diuretics

short duration of action to cause excretions of ions

What is the only loop without sulfur

ethacrynic

MOA of loops

Inhibit Na/K/Cl symporter, may alter warfarin, ototoxicity with ethacrynic acid

Potassium Sparing side effects

do not use with ACE-I or ARBs sexual side effects due to nonselective binding receptors

What is present at position 9 or 11 in potassium sparing

epoxide

What is replaced at position 7 in potassium sparing diuretics

thioester with ester

What is present at position 17 in potassium-sparing diuretics

gamma lactone ring

What is MOA of potassium-sparing diuretics

bind to negatively charged regions of Na channel (weak bases)

What do ACE-I's cut

dipeptides

ACE needs zinc in order to do what

bind by ionic bond with amines then zinc helps dipeptide cleavage, hydrogen bond between substrate and ACE

ACE-I have _____ bioavailability and undergo phase 1 metabolism by ________

low esterases

What ring minics the C-terminal in ACE-I

N-ring

Large hydrophobic rings ______ potency

increase

___________ group is best for zinc binding in ACE-I because they shorten duration of action

sulfhydryl

Esterification produces orally bioavailable prodrugs in ACE-I because zinc binding to which two groups is optimal

carboxylate phosphinate

ACE-I are usually acidic excepts for which two drugs because they contain amines

captopril fosinopril

In ARBs esters need to be _______ in order to produce a free acid

hydrolyzed

ARBs need an _______ group

acidic and it has to be ortho

The tetrazole ring in ARBs need to be ______

ionized

Incomplete absorption in ARBs results in _____ lipid solubility and _____ bioavailability because the drug is unchanged

low low

Renin Inhibitors MOA

enzyme secreted by kidneys to decrease glomerular filtration rate resulting in low BP

What functional group do you want in renin inhibitors to mimic their sites

isopropyl