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PDA II > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

type of angina characterized by lumen that is narrowed by plaque, inappropriate vasoconstriction, less than normal blood flow that could be fine at rest but noticeable with exercise

A

stable angina

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2
Q

type of angina characterized by a ruptured plaque, platelet aggregation, thrombus formation, unopposed vasoconstriction, pain even at rest

A

unstable angina

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3
Q

type of angina characterized by no overt plaques, intense vasospasm with pain that comes and goes

A

variant angina

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4
Q

age, gender, family history of premature this, hypercholesterolemia, hypertension, smoking, type II diabetes, sedentary lifestyle, obesity, and more

A

risk factors for coronary artery disease (CAD)

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5
Q

what are the main determinants of myocardial oxygen demand?

A

heart rate, contractility, afterload, preload

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6
Q

what is the main determinant of myocardial oxygen supply?

A

coronary blood flow (greater demand necessitates greater flow)

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7
Q

this class of drugs delivers nitric oxide to vessels: nitrate compound is denitrated by mitochondrial aldehyde dehydrogenase (mtALDH, higher concentration of mtALDH in veins so more NO in veins) which forms nitric oxide (NO), this increases cGMP which decreases calcium levels inside cells so less contraction of vessels leading to relaxation of vascular smooth muscle cells (veins more than arteries)

A

organic nitrates mechanism of action

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8
Q

class of drugs whose primary action is venodilation which decreases preload (greatest effect in veins because mtALDH mostly found in veins), coronary artery dilation, some arteriolar dilation (decreased afterload), net result is decreased myocardial oxygen demand with increased oxygen supply in some situations

A

physiological effects of organic nitrates

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9
Q

hepatic glutathione-organic nitrate reductase converts these drugs into inactive metabolites, high first pass metabolism, high capacity, limited oral bioavailability (sublingual forms have rapid onset but shorter duration, oral/transdermal forms have slower onset but longer duration)

A

metabolism of organic nitrates

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10
Q

what is the use of sublingual organic nitrates like sublingual nitroglycerine or isosorbide dintrate?

A

to relieve acute angina

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11
Q

what is the use of oral/dermal organic nitrates like nitroglycerin ointment, nitroglycerin dermal patches, oral isosorbide dinitrate?

A

for prophylaxis of angina

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12
Q

continuous exposure of these drugs leads to tachyphylaxis (rapid development of tolerance) because following repeated/prolonged use these drugs oxidize mtALDH and decrease its activity (longer the enzyme is exposed to drug less able to remove NO from drug)

A

limitations of organic nitrates

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13
Q
  • side effects of these drugs include orthostatic hypotension, tachycardia, throbbing headache, dizziness, flushing of skin
  • contraindications include PDE5 inhibitors for erectile dysfunction (combo use leads to hypotension, SNS activation and increased MVO2)
A

side effects/contraindications of organic nitrates

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14
Q

what are organic nitrates mainly used for (what types of angina)?

A

stable and variant angina, somewhat helpful in unstable

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15
Q

what is the main effect of calcium channel blockers?

A

decrease intracellular calcium

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16
Q

primary physiological effects: decreased heart rate, contractility, conduction velocity all for decreased oxygen demand

A

physiological effects of cardioprotective calcium channel blockers (diltiazem, verapamil)

17
Q

primary physiological effects: decreased afterload for decreased oxygen demand, but if decrease BP too fast there will be an increase in SNS activity leading to an increase in oxygen demand

A

physiological effects of dihydropyridine calcium channel blockers (nifedipine, amlodipine, felodipine)

18
Q

nifedipine XL, amlodipine, felodipine are more (slowly/quickly) absorbed for (less/more) tachycardia

A

slowly, less

19
Q
  • decrease myocardial oxygen consumption due to decreased contractility and heart rate, relaxation of coronary smooth muscle cells
  • net effects: decreased oxygen demand and vasospasms
  • main uses: variant and stable angina
  • toxicity/side effects: bradycardia, heart block, dizziness, edema, flushing, constipation
A

diltiazem and verapamil calcium channel blockers

20
Q
  • physiological effects: reduces myocardial oxygen consumption through decreased force of contraction and heart rate (decreased oxygen demand), slightly increases coronary flow to ischemia areas (due to increased perfusion time of ventricles leading to slight increase in oxygen supply, not consistent)
  • net effects: decreased myocardial oxygen consumption and slight increase in coronary blood flow
A

beta blockers (selective and nonselective)

21
Q

why are nonselective beta blockers contraindicated/cautious use in variant angina?

A

if block beta 2 receptors the alpha 1 receptor activity will be unchecked because usually there is a balance between beta 2 and alpha 1 leading to more vasoconstriction

21
Q

toxicity/side effects: bradycardia, heart failure, low exercise tolerance, rebound effect due to more beta 1 receptors (increase angina if abruptly stop), bronchospasm with nonselective, CNS effects with lipophilic nonselective (fatigue, depression, nightmares)

A

toxicity and side effects of beta blockers

21
Q

what are the main uses of beta blockers in angina?

A

stable and unstable angina

22
Q

this drug blocks the late Na+ current during the cardiac action potential (this current is increased during ischemia), increased late Na+ current results in increased intracellular Na+ which causes increased intracellular Ca2+, increased Ca2+ results in increased contractility and increased oxygen demand — this drug BLOCKS all that, reduces calcium overload which decreases ventricular stiffness, diastolic wall tension, cardiac contractility (these changes reduce myocardial oxygen consumption)

A

ranolazine

23
Q

unstable angina (acute coronary syndromes), atrial fibrillation, pulmonary embolism, deep vein thrombosis, heart failure, stroke, different procedures

A

uses of anticoagulants

24
Q

which takes longer, the intrinsic pathway (activated partial thromboplastin time aPTT) or extrinsic pathway (prothrombin time PT)?

A

intrinsic

25
Q

what is the enzyme that converts prothrombin (II) to thrombin (IIa)?

A

Xa (prothrombin activator)

26
Q

what is the enzyme that converts fibrinogen to fibrin?

A

IIa (thrombin)

27
Q

heterogeneous mixture of sulfated glycosaminoglycans, naturally occuring in mast cells, have both unfractionated and low molecular weight, not orally active (must be given IV or SC), active site is the pentasaccharide (five sugar) sequence

A

heparins

28
Q

MOA: circulating antithrombin (produced by liver) has a low affinity to bind and inactivate Xa and IIa, this drug binds to circulating antithrombin and increases its affinity for IIa and Xa (1000x), the complex of this drug-antithrombin-FIIa/FXa are rapidly removed by liver (suicide inhibition)

A

heparins

29
Q

are low molecular weight heparins better at inhibiting Xa or IIa?

A

Xa

30
Q

this heparin is just the pentasaccharide fragment, SC injection, eliminated unchanged in the urine so contraindicated in patients with low creatinine clearance, effect lasts days after discontinuing drug (no antidote at this time), less likely to induce thrombocytopenia

A

fondaparinux

31
Q
  • side effects: bleeding (dose related), heparin induced thrombocytopenia, osteoporosis (long term use, relatively rare)
  • contraindications: active bleeding, coagulopathies (hemophilia, significant thrombocytopenia), hypersensitivity to pork or beef products, severe hypertension, intracranial hemorrhage
A

unfractionated heparin

32
Q

what is needed as a cofactor for inhibition by heparins?

A

antithrombin

33
Q

these drugs do not need antithrombin as a cofactor for inhibition, work as direct FXa inhibitors (DOACs)

A

direct FXa inhibitors - rivaroxaban (Xarelto), apixaban (Eliquis), edoxaban (Sazaysa)

34
Q
  • reversal agent for FXa inhibitors
  • MOA: recombinant modified human factor Xa decoy, higher affinity to the FXa inhibitor than natural FXa
A

andexanet alfa (AndexXa)

35
Q
  • direct oral competitive thrombin (FIIa) inhibitor, approved for prevention of emboli with Afib, VTE, hip/knee replacements
  • doesn’t req
A

PDA II (4 decks)

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