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PDA II > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

85-90% of patients with HTN have this form, no specific cause can be established

A

essential hypertension

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2
Q

only 10-15% of patients with HTN have this form, specific cause of HTN identified (HTN due to another disease, can correct disease to fix the HTN but can’t do this with other form of HTN), could be caused by renovascular disease (increased fluid retention and pressure), pheochromocytoma (adrenal gland tumor), primary hyperaldosteronism (too much aldosterone from adrenal glands, water retention from kidneys), Cushing’s disease (too much cortisol so retention of water)

A

secondary hypertension

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3
Q

genetics and family history, race (blacks>whites), gender (men>premenopausal women), diabetes (Type 1)

A

non-modifiable risk factors for essential HTN

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4
Q

obesity, sedentary lifestyle, sodium intake, hyperlipidemia, smoking, alcohol intake

A

modifiable risk factors for essential HTN

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5
Q

which type of blood vessels contribute the most to resistance?

A

arterioles

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6
Q

what does BP equal (hydraulic equation)?

A

(HR x SV) x PVR

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7
Q

if blood pressure decreases, what happens to carotid baroreceptor activity?

A

decreases (less pressure means less stretch, less action potentials)

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8
Q

if blood pressure decreases, what happens to CNS activity, adrenal medulla activity, epi release, PVR and therefore afterload on the heart, venous return and therefore preload on the heart, NE release, and HR/contractility?

A

increases

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9
Q

if blood pressure decreases, what happens to vagal nucleus (parasympathetic) activity, and ACh release?

A

decreases

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10
Q

if blood pressure decreases, what happens to renal blood flow, K+ reabsorption?

A

decreases

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11
Q

if blood pressure decreases, what happens to renin, angiotensin I/II, vasoconstriction and therefore PVR, aldosterone, Na+ and H2O reabsorption and therefore plasma volume?

A

increases

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12
Q
  • all of these drugs act by stimulating alpha 2 receptors in the brain stem (because alpha 2 downregulates NE for negative feedback loop –> these drugs decrease NE release), also act at sympathetic varicosities, decrease sympathetic nervous system outflow,
  • PHYSIOLOGICAL EFFECTS: less NE from SNS so decreased HR, decreased contractility and SV, decreased PVR, decrease venous tone for decreased preload
  • have substantial toxicity/side effects: sedation, dry mouth, dizziness, nausea, sleep disturbances, nightmares/vivid dreams
  • severe overdose consequences: hypotension, respiratory depression, bradycardia, coma, death
  • rebound HTN: increased alpha and beta receptor number (upregulation) and increased NE
  • NOT FIRST LINE THERAPY, usually used in combination with diuretics
  • CONTRAINDICATIONS: tricyclic antidepressants, depression
A

centrally acting sympatholytics (alpha 2 adrenergic agonists) –> clonidine, methyldopa, guanabenz

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13
Q

this drug is an analog of L-dopa that enters the CNS where it is converted to alpha-methylnorepinephrine (NE with a methyl group) that replaces NE in the nerve terminal (selectively enhance binding to alpha 2 on presynaptic terminal), binds with greater affinity for alpha 2 compared to NE

A

methyldopa (alpha 2 agonist)

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14
Q

these drugs have high lipid solubility so they rapidly enter the CNS, binds to alpha 2 receptors preferentially, inhibits synaptic NE release, similar efficacy in treating HTN

A

clonidine, guanabenz (direct alpha 2 agonists)

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15
Q
  • both of these drugs in this class decrease adrenergic synaptic transmission but through different MOAs
  • PHYSIOLOGICAL EFFECTS: decreased PVR, HR, and SV
  • rare use now (not available in US), short-term antihypertensive therapy (aneurysms and surgical hypertension)
  • Toxicity/side effects: postural hypotension, diarrhea (PNS is dominant), CNS sedation, depression, receptor upregulation (HTN crisis/rebound), drug interactions (efficacy is decreased when combined with drugs that decrease neuronal NE reuptake like tricyclic antidepressants and cocaine)
A

adrenergic neuron blocking agents (reserpine, guanethidine)

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16
Q

this drug irreversibly binds to VMAT antiporter of vesicles in central and peripheral adrenergic neurons leading to neurons losing the ability to concentrate and release NE into synapse

A

reserpine

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17
Q

this drug is actively transported into neurons via the presynaptic NE transporter (uptake-1), replaces NE with an inactive neurotransmitter, depletes stored NE in neurons, too polar to enter CNS so not centrally acting (act on peripheral)

A

guanethidine

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18
Q

affinity for a specific receptor subtype (beta 1 vs beta 2 vs nonselective)

A

selectivity of beta blockers

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19
Q

receptor ligand with partial agonist activity for a particular receptor

A

intrinsic sympathomimetic activity (ISA), pindolol, acebutolol

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20
Q

ability of a beta blocker to cross lipid membranes

A

lipophilicity

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21
Q

what beta blocker has high lipophilicity?

A

propranolol

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22
Q

what beta blockers have moderate lipophilicity?

A

timolol, metoprolol, pindolol

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23
Q

what beta blockers have low lipophilicity?

A

nadolol, atenolol, acebutolol

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24
Q

what beta blockers are beta 1 selective antagonists?

A

metoprolol, atenolol, acebutolol, esmolol, nebivolol

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25
Q

what beta blockers are beta and alpha 1 antagonists?

A

labetalol, carvedilol

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26
Q

what beta blockers are non-selective antagonists (block beta 1 and 2)?

A

propranolol, nadolol, timolol, pindolol

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27
Q

which beta blocker also vasodilates blood vessels through NO (nitric oxide) at higher doses?

A

nebivolol

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28
Q
  • PHYSIOLOGICAL EFFECTS: decreased HR, decreased contractility (SV), decreased renin release (decreased plasma volume so decreased SV)
  • used for all degrees of hypertension, ischemic heart disease, antiarrhythmic drugs, heart failure
  • TOXICITY/SIDE EFFECTS: cardiovascular effects (beta 1, bradycardia, heart failure, low exercise tolerance), rebound HTN effect (due to higher receptor number), bronchospasm (beta 2 in patients prone to spasms like in asthma patients), CNS effects with lipid soluble beta 2 antagonists (fatigue, depression, nightmares), metabolic effects (no ISA increased triglycerides, blunted recovery from hypoglycemia in beta 2 antagonists)
  • CONTRAINDICATIONS: asthma, chronic obstructive lung disease (blocks beta 2 mediated bronchorelaxation), diabetes (blocks beta 2 mediated mobilization of glucose), plasma lipid disorders (increased triglycerides/LDLs, decreased HDLs)
A

beta adrenergic receptor antagonists (beta blockers)

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29
Q

beta blockers that are preferred in patients prone to bronchospasm, diabetes, peripheral artery disease (PAD)

A

beta 1 selective like metoprolol

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30
Q

beta blockers that are useful in patients with bradycardia and hyperlipidemia

A

beta blockers with ISA like acebutolol

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31
Q

beta blockers that are useful in heart failure patients

A

beta blockers with alpha 1 blocking like carvedilol

32
Q
  • all of these are chemical analogs of each other, alpha 1 blockade is much greater than alpha 2 blockade (“alpha 1 selective”)
  • PHYSIOLOGICAL EFFECTS: arterial (inhibition of tonic vasoconstriction, decreased PVR), venous (decreased venous return for decreased preload, decreased SV)
  • INDICATIONS: mild to moderate hypertension, severe HTN but usually as combined therapy (effects enhanced by beta blockers and diuretics)
  • TOXICITY/SIDE EFFECTS: 1st dose effect (postural hypotension and syncope so advise to take first dose at bedtime to minimize these problems), headache, dizziness, drowsiness, CNS effects (vivid dreams, depression), favorable lipid effects (reduce triglycerides, LDLs, total cholesterol while increasing HDLs)
  • CONTRAINDICATIONS: decreased liver function (these are extensively metabolized by the liver)
A

alpha 1 adrenergic receptor antagonists

33
Q

which drug is a 1st generation alpha 1 adrenergic receptor antagonist that has specifically vascular alpha 1B receptor blocking?

A

prazosin

34
Q

which drugs are 2nd generation alpha 1 adrenergic receptor antagonists that have both prostatic alpha 1A and vascular alpha 1B adrenergic blocking?

A

terazosin, doxazosin

35
Q
  • these drugs have high efficacy due to 25% of filtered solutes are reabsorbed in ATL (ascending thin limb in loop of Henle), distal segments of the nephron do not possess reabsorptive capacity to buffer effects of the drug
  • MOA: blocks Na+/K+/2Cl- symport in ATL leading to large increase in Na+ and Cl- excretion into the urine, increases excretion of K+ into the urine(the natriuretic effect creates a diuretic effect) leading to rapid and large naturesis for concomitant diuresis
  • TOXICITY/ADVERSE EFFECTS: fluid and electrolytes imbalances –> plasma Na+ depletion and hyponatremia, hypokalemia, hypocalcemia, drug induced ototoxicity, most are sulfonamides (allergic reactions), GI distress (nausea, vomiting, diarrhea), increased urinary frequency
  • CV INDICATIONS: often reserved for refractory HTN or edema following vasodilator therapy, moderate-severe heart failure
  • CONTRAINDICATIONS: severe Na+ and volume depletion (dehydration), hypersensitivity to sulfonamides
A

loop diuretics - furosemide, torsemide, bumetanide

36
Q

does water follow sodium in cells? (if Na+ is leaving the cell, does water also leave the cell?)

A

Yes

37
Q

organic acids, extensively bound to plasma proteins but they are secreted by organic acid transport system into lumen of PCT and available to symports in ATL (have to be in urine to go to symports), action is dependent on renal function (not going to work in a kidney that isn’t producing urine), simultaneous use of NSAIDs or probenecid which can compete for weak acid secretion in the PCT can reduce efficacy

A

unique features of loop diuretics

38
Q
  • generally the most prescribed first line therapy for HTN
  • MOA: inhibits Na+/Cl- symport in DCT, reduces Na+/Cl-/K+ reabsorption
  • EFFECTS: 5% increase in Na+ excretion, only moderate because 90% of filtered solutes are reabsorbed BEFORE reaching DCT
  • RESULTS: mild-moderate, sustained diuretic effects, synergistic effect with loop diuretics
  • potassium wasting (more Na+ in the urine, more sodium goes into cell which kicks out a K+ ion), wide range of half lives due to variable plasma protein binding, since they are sulfonamides they are secreted into lumen of PCT by organic acid secretory pathway (effectiveness dependent on renal function, competes with other organic acids for secretion, drug interactions)
  • TOXICITY/ADVERSE EFFECTS: most common is fluid/electrolyte imbalances (hypotension, hypokalemia, hyponatremia, hypochloremia), relatively rare would be CNS (vertigo, headache, paresthesia), GI (nausea, vomiting, anorexia, cramping), sexual (impotence, reduced libido), dermatological (rashes, photosensitivity)
  • INDICATIONS: often single initial therapy for HTN, mild-moderate heart failure
  • CONTRAINDICATIONS: decreased liver function (highly metabolized by liver), hypersensitivity to sulfonamides, concomitant cardiac glycoside therapy (increases risk of arrhythmias)
A

thiazide and thiazide-like diuretics - chlorothiazide, hydrochlorothiazide, indapamide

39
Q
  • all drugs within this general category decrease Na+ reabsorption in CT via Na+ channels but have differing MOAs
A

K+ sparing diuretics - pteridines (triamterene, amiloride), aldosterone antagonists (spironolactone, eplerenone)

40
Q
  • MOA: blocks Na+ channels in renal DCT and CT, specific for renal epithelial Na+ channels, does not affect K+ secretion directly, must be secreted into lumen of PCT by organic base secretory pathway
  • these drug do not allow Na+ to enter cell or K+ to leave cells, more Na+/Cl- in urine, less K+ in urine
  • URINARY EFFECTS: mild natriuresis, only 2% increase of Na+/Cl- excretion because most of the Na+ has already been absorbed
  • RESULTS/USES: mild diuretic effects as single therapy, limited use as single agents but useful in combination with thiazide/loop diuretics to reduce K+ wasting
  • TOXICITY: hyperkalemia (increased risk with other factors promoting K+ retention like renal failure, ACE inhibitors, K+ supplements), renal stones, interstitial nephritis, nausea, vomiting, dizziness, cramps, headache
A

K+ sparing diuretics - pteridines (triamterene, amiloride)

41
Q
  • MOA: block aldosterone receptors late in distal tubules and collecting tubules
  • GENERAL EFFECTS: slow onset consistent with MOA, efficacy is a function of endogenous aldosterone (aldosterone in blood), only class of diuretic that DOES NOT depend on renal filtration or secretion to be effective, aldosterone means water reabsorption so with this class of drugs blocking aldosterone then there will be less water reabsorption (diuretic effect)
  • EFFECTS IN THE KIDNEY: increase the number of active Na+ channels and increase Na+ gradient across cell, urinary Na+/Cl- increase whereas urinary K+ decreases
  • USES: limited use as a single agent in HTN, useful in combo with thiazide or loop diuretics to reduce K+ wasting, primary hyperaldosteronism (adrenal adenomas), secondary hyperaldosteronism (heart failure, hepatic cirrhosis, nephrotic syndrome)
  • TOXICITY/INTERACTIONS: hyperkalemia (can be life threatening, increased risk with other factors promoting K+ retention like renal failure, ACE inhibitors, K+ supplements, CONTRAINDICATED in patients with increased risk of hyperkalemia), steroid effects (gynecomastia, impotence, hirsutism, deepening voice, menstrual irregularities, etc), CNS effects (lethargy, confusion), CONTRAINDICATED in patients with gastric bleeding/peptic ulcers because these drugs make that bleeding worse
A

K+ sparing diuretics - aldosterone antagonists (spironolactone, eplerenone)

42
Q

how do arterial dilators decrease BP?

A

reduce PVR by vasodilating

43
Q

how do venous dilators decrease BP?

A

decrease CO by reducing venous return (preload)

44
Q

potent vasoconstriction (AT1 receptors), enhances noradrenergic activity (increase NE release and decrease NE reuptake), increase sympathetic tone from CNS, increase catecholamines from adrenal gland (minor), net effect is increase in PVR leading to increased BP

A

angiotensin II rapid pressor effects on BP

45
Q

increase Na+ reabsorption in PCT directly, increase aldosterone release from adrenal gland (increased Na+ reabsorption in CT), decreased renal blood flow (decreased filtration), net effect is increased Na+ retention that leads to increased plasma volume and increased BP

A

angiotensin II slow pressor effects on BP

46
Q

the _______ of ACE inhibitors have 100-1000 fold less potency as direct ACE inhibitors but much better bioavailability, metabolized to active form (-prilat) in the body, once metabolized to active form all have good (dose-dependent) efficacy

A

prodrugs

47
Q

which ACE inhibitors are active forms?

A

captopril and lisinopril

48
Q

which ACE inhibitors are prodrug forms?

A

enalapril, quinapril, benazepril, fosinopril, ramipril

49
Q
  • PHYSIOLOGICAL EFFECTS: arterial dilation (less angiotensin II to bind to its AT1R, decreased plasma volume (renal effects, decreased angiotensin II mediated release of aldosterone, decreased Na+ reabsorption, increased renal blood flow)
  • RESULTS: no change in HR, decreased SV, decreased PVR
  • INDICATIONS: mild-moderate HTN, very effective (50% effective as single therapy, about 90% as combination therapy), heart failure
  • UNIQUE FEATURES: elimination heavily dependent on renal excretion, elderly African Americans do not respond as well
  • SIDE EFFECTS: generally well tolerated, hypotension, dry cough (5-20% of patients because of increased bradykinins), angioneurotic edema (less than 1% of patients, mucosal swelling over the period of minutes to several hours, bradykinins involved)
  • CONTRAINDICATIONS: pregnancy (fetal pathologies, death), renal impairment
A

ACE inhibitors - lisinopril, captopril, enalapril, quinapril, benazepril, fosinopril, ramipril

50
Q
  • MOA: AT1 receptor antagonists, no partial agonist activity
  • Effectively inhibits both rapid and slow pressor effects of angiotensin II
  • ADVANTAGES: reduced incidence of cough because no inhibition of breakdown of bradykinins
  • SIDE EFFECTS: hypotension, hyperkalemia, fetal pathologies and death (contraindicated in pregnancy)
  • USES: mild-moderate HTN, useful in HTN patients who cannot tolerate other drugs
  • Similar efficacy between all antagonists, 50% responder rates for single therapy, 70% with HCTZ diuretic
A

angiotensin II receptor antagonists (ARBs) - losartan, valsartan, candesartan, olmesartan medoxomil

51
Q
  • low molecular weight, competitive inhibitor of renin (binds active site of renin preventing it from cleaving angiotensinogen to angiotensin I, results in decreased ang-I, ang-II, and plasma renin activity
  • approved for treatment of HTN, equal efficacy as ACE-I and HCTZ in mild-moderate HTN, equal efficacy as lisinopril in severe HTN
  • recommend for patients intolerant to other anti-HTN meds or in combo with others to treat resistant HTN
A

direct renin inhibitor (DRIs) - aliskiren

52
Q

which calcium channel blockers are dihydropyridines?

A

nifedipine, amlodipine, felodipine, isradipine, nicardipine, nimodipine, nisoldipine

53
Q

which calcium channel blockers are cardioprotective?

A

verapamil, diltiazem

54
Q
  • MOA: bind to L-type Ca2+ channels, inhibits influx of Ca2+, lowers free, intracellular Ca2+
  • RESULTS: inhibits muscle contraction, arterioles dilate because can’t contract without intracellular Ca2+, decreased PVR, decreased HR and SV in cardiac muscle
  • antihypertensive effects due to cardiac activity (decreased cardiac output, decreased contractility and HR), and vascular activity (decreased PVR because of relaxation of VSM)
  • INDICATIONS: mild-moderate HTN (cautious/avoid use of dihydros in patients with ischemic heart disease or conduction abnormalities), anti-anginal/antiarrhythmics (not dihydros generally)
  • TOXICITY/SIDE EFFECTS: bradycardia, decreased cardiac contractility, dizziness, edema, flushing, constipation (these drugs slow peristalsis in the GIT)
A

calcium channel blockers - -dipines and cardioprotective (verapamil, diltiazem)

55
Q

do the cardioprotective calcium channel blockers have more selectivity for cardiac or vascular effects?

A

cardiac

56
Q

do the dihydropyridines calcium channel blockers have more selectivity for cardiac of vascular effects?

A

vascular

57
Q
  • all decrease PVR but mechanisms of action differ
  • PHYSIOLOGICAL EFFECTS: decreased PVR is main effect, no change of venous capacitance (preload/venous return, ONLY ACT ON ARTERIES NOT VEINS), decreased renal artery resistance (increased renal blood flow)
  • MAJOR LIMITATIONS: large and rapid decrease in BP produces decreased baroreceptor activity which leads to increased SNS tone, increased SNS tone results in increased HR, increased cardiac inotropy (force of contraction and SV), increased renin release for increased ang-II and fluid retention, DIFFICULT TO MAINTAIN THE REDUCTION IN BP
  • can be used in combination with diuretics or beta blockers to maintain lower BP
  • INDICATIONS: moderate-severe HTN (usually not as sole therapy), avoid in HTN with ischemic heart disease, decreased liver function (primary site of metabolism)
  • COMMON SIDE EFFECTS: hypotension, tachycardia, sodium/fluid retention, edema, headache, nausea, skin flushing
A

arterial vasodilators - hydralazine, minoxidil

58
Q
  • MOA: uncertain, partially through endothelial derived relaxing factor/nitric oxide, partially by direct vasodilation, partially by Ca2+ inhibition
  • UNIQUE FEATURES: active metabolites mediate response, acetylation dependent metabolism so slow acetylators have increased plasma levels (accumulation of the drug in plasma)
A

hydralazine - arterial vasodilator

59
Q
  • MOA: opens K+ channels (K+ leaves cells) in smooth muscle cells, hyperpolarizes plasma membrane (more negative so further away from depolarization threshold, makes it harder to contract so less likely to contract), relaxes arterial smooth muscle cells
  • UNIQUE FEATURES: more potent than other arterial vasodilator, often used after failure of other treatments
A

minoxidil - arterial vasodilator

60
Q
  • intrinsic defect in heart function resulting in decreased cardiac output and decreased peripheral blood flow, no cure for this except for heart transplant
  • causes include ischemia (coronary artery disease, 50-60%), cardiomyopathies (idiopathic dilated, idiopathic hypertrophic, viral, familial, postpartum 30-40%), cardiac overload syndromes (chronic HTN, chronic anemia, valvular/congenital, chronic alcoholism), chemotherapy
  • common signs/symptoms: dyspnea, fatigue, SOB, peripheral edema (venous pooling), pulmonary edema, impairment of renal/liver function, increased SNS activation (increased HR at rest, increased circulating catecholamines, this is baroreceptor activity)
A

heart failure

61
Q

heart failure that has systolic dysfunction, idiopathic dilated cardiomyopathy, ischemia, MI, etc, characterized by large dilated ventricular chambers, squeezing problem

A

HFrEF (heart failure with reduced ejection fraction)

62
Q

heart failure that has diastolic dysfunction, long standing HTN, hypertrophic cardiomyopathy, aortic valve stenosis, etc, thickened poorly compliant ventricular walls with small lumen volumes, filling problem

A

HFpEF (heart failure with preserved ejection fraction)

63
Q

when there is an intrinsic defect in the heart, what happens to CO, SV, BP, baroreceptors?

A

decreased

64
Q

when there is an intrinsic defect in the heart, what happens to CNS, renin, angiotensin II, aldosterone, fluid retention, blood volume, preload, PVR, venous return, HR, force of contraction, afterload, wall stress, and MVO2?

A

increased

65
Q

enhance contractility (mostly HFrEF) through increased force of contraction (inotropes), reduce preload through reducing blood volume (diuretics), reduce afterload through reducing PVR (vasodilators)

A

common pharmacological interventions in HF

66
Q
  • this drug directly increases cardiac contractility through increased force of contraction and increased velocity of contraction with a net result of increased SV and CO
  • MOA: inhibits Na+/K+ ATPase enzyme (inhibits active transport of Na+ out of cell leading to an accumulation of Na+ in cell so accumulation of Ca2+ in cell, high potency and specificity), accumulation of Na+ inside cell slows down the pump that pumps Na+ in and Ca2+ out so there is an increase in Ca2+ inside cell leading to greater contraction of heart muscle
  • PHYSIOLOGICAL EFFECTS: increase contractility (increased CO, SV), decrease SNS activity (decrease HR and afterload leading to increased contraction because less going against contraction), decreases conduction of atrial arrhythmias (improves efficiency, reduces sudden death, useful in HF patients with atrial arrhythmias)
  • RELATIVELY NARROW THERAPEUTIC INDEX: difficult to monitor symptoms of toxicity because many of them mimic symptoms of HF (fatigue, edema)
  • TOXICITY: arrhythmias, heart block, anorexia, nausea, vomiting, diarrhea, headache/neurological pain, fatigue, stupor/confusion, visual problems, gynecomastia, skin rashes
A

cardiac glycoside - digoxin

67
Q

how does taking potassium treat cardiac glycoside toxicity?

A

the potassium competes with drug binding in heart tissue

68
Q
  • main use: short-term IV inotropic support usually in a hospital setting
  • advantages: potent, rapid onset of action, quickly metabolized, allows titratable IV dosing
  • disadvantages: tolerance with long term use that necessitates drug holiday, tachyarrhythmias, can provoke ischemia
A

sympathomimetics - dobutamine, dopamine

69
Q
  • this drug is most helpful at a slow infusion rate, stimulation of dopamine receptors on VSM and presynaptic terminals of postganglionic sympathetic nerves relaxes VSM for vasodilation of renal blood vessels leading to increased GFR and diuresis and inhibition of NE release leading to vasodilation
  • increases contractility, can increase HR/afterload/PVR at higher infusion rates, can increase renal blood flow at renal dose
A

sympathomimetic - dopamine

70
Q
  • this drug is a racemic mixture that increases inotropy (force of contraction) but not chronotropy (heart rate), some decrease in PVR because - enantiomer is counteracted by + enantiomer and beta 2 activity
  • increases contractility, no change in heart rate, decrease in PVR/afterload, no change in renal blood flow
A

sympathomimetic - dobutamine

71
Q
  • MOA: relatively selective phosphodiesterase III enzyme (PDE-III) inhibitor that allows an accumulation of cAMP inside of cells, increased vasodilation/decrease PVR, increased cAMP for increased in Ca2+ influx into heart leading to increased contractility and SV because these drugs inhibit the breakdown/inactivation of cAMP
  • PHYSIOLOGICAL EFFECTS: increased inotropy/contractility for increased SV, decreased PVR/afterload, net effect is increased CO
  • USES: short term inotropic support usually in hospital setting usually for only acute HF, shorter half life so can titrate dose (this is the drug used for dobutamine holiday), long term chronic use associated with increased mortality/hospitalizations in severe HF
  • NOT first line therapy and limited use in HFpEF
A

phosphodiesterase inhibitor - milrinone

72
Q

if we need increased cardiac output in a HF patient, what drug do we use?

A

digoxin

73
Q

if we want to decrease fluid retention and venoconstriction, what drugs do we use?

A

diuretics

74
Q

if we want to decrease vasoconstriction, what drugs do we use?

A

vasodilators for better ventricular performance

75
Q
  • MOA: first drug in the combo inhibits neprilysin (which normally degrades brain-type natriuretic peptide/BNP into inactive metabolites, BNP typically increases vasodilation so we want more of this in HF so this drug inhibits the breakdown of BNP for an increase in BNP), second drug in the combo inhibits angiotensin II from binding to AT1 receptor which normally causes vasoconstriction so this drug’s inhibition of that causes vasodilation which is beneficial in HF
  • side effects similar to enalapril but greater risk of hypotension with similar risk of cough
A

sacubitril/valsartan (ENTRESTO)

76
Q
  • this drug increases SV and decreases circulating NE in HF patients
  • prevents catecholamine toxicity on myocytes, hemodynamic effects (decreased afterload), anti-ischemic effects (decreased MVO2), antiarrhythmic effects
A

carvedilol - alpha 1 selective and nonselective beta blocker

77
Q
  • MOA: SGLT2 in PCT is main site of filtered glucose reabsorption so reduced glucose reabsorption (since these are SGLT2 inhibitors) means increased urinary excretion and reduced glucose in plasma
  • adverse effects: dehydration and hypotension, diabetic ketoacidosis in type 2 diabetes patients, hypoglycemia if used with insulin or sulfonylureas, increased genital mycotic infections/UTIs/urination because of glycosuria
  • drug interactions: diuretics (increased risk of severe dehydration), insulin/sulfonylureas (hypoglycemia)
A

SGLT2 inhibitors - empagliflozin, dapagliflozin, canagliflozin

PDA II (4 decks)

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