Unit 4 - Coronary Artery Disease Flashcards Preview

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Flashcards in Unit 4 - Coronary Artery Disease Deck (51):
1

what kind of exams are coronary angiograms?

anatomical tests, not physiological; can visualize lesion but not discover if pathological or not

2

what is angina VS acute MI?

angina: larger artery that is slowly occluding
acute MI: smaller and fast artery occlusion

3

in who does angina usually occur?

-most commonly in patients with CAD involving at least one epicardial artery
-patients with valvular heart disease, hypertrophic cardiomyopathy, and uncontrolled HTN
-may have normal coronary arteries secondary to spasm or endothelial dysfunction

4

describe the metabolic effects of ischemia

-anaerobic glycolysis takes over, but cannot maintain
-ATP and creatine phosphate levels call
-intracellular and extracellular acidosis develops
-extracellular levels of K+, lactate, PO4, and FA levels rise

5

what is the most important contributor to electrophysiologic changes of ischemia? what else follows this?

elevated extracellular K+
-due to increased cell membrane permeability to K+ during plateau phase of AP (leak outwards)
-lactate and phosphate follow K+ out

6

what causes the increased circulating FFA in ischemia?

sympathetic activation from MI
-liposomal phospholipase is activated to break down membrane phospholipids
-LCFA accumulate in intracellular space

7

what is the gradient between ischemic cells and normal cells?

"injury current"
-partial depolarization
-shortened AP

8

what is the diastolic injury current?

phase 4 intracellular positive current flows from less negative ischemic cells to more negative normal cells

9

what is the systolic injury current?

during phase 2/3, shortening of AP causes intracellular potential of ischemic cells to be more negative than normal cells
-this causes intracellular positive current to flow from normal to ischemic cells --> ST-depression

10

which injury current should one focus on?

the systolic current (more negative ischemic flows to less negative healthy)
-in subendocardial injury --> ST depression

11

what is a noninvasive diagnosis of ischemia if one can exercise?

stress test on treadmill for 6-12 minutes (Bruce protocol)
-valid if patient reaches 85% of max predicted HR (220 - age)

12

what does an EKG diagnosis of ischemia look like? what if it is abnormal?

if normal baseline ECG to compare
-positive will have at least 1 mm of horizontal/downsloping ST depression
-use imaging if abnormal --> echocardiograph to look at induced wall motion abnormalities

13

what is a noninvasive diagnosis of ischemia if one cannot exercise?

pharmacologic stress test
-dobutamine (stimulate B1 receptors to increase contractility and HR)
-adenosine/dipyridamole (coronary vasodilators to inhibit cellular uptake and degradation of adenosine)
--stenotic arteries don't respond to these

14

what is coronary steal? what causes this?

pharmacological perfusion mismatch when healthy coronary arteries are dilated but unhealthy ones are constricted
-drugs cause more O2 to healthy, less to unhealthy
-occurs if use antiplatelet or pharmacologic stress test adeosine and dipyridamole

15

what do electron beam CT sans do?

identify Ca++ in coronaries
-use Ca++ score to correlate probability of significant coronary disease
-variable results
-most useful in predicting absence of CAD

16

what are the 2 objectives of medical management of CAD?

1. prevent MI and death (increase quantity of life)
2. reduce symptoms of angina and occurence of ischemia (increase quality of life)

17

what should the first intervention of CAD treatment be?

identify and treat risk factors for CVD:
-lipid abnormalities
-smoking
-diabetes
-HTN

18

what is the only time you don't use aspirin?

when someone is allergic

19

ticlopidine
-what is it?
-mechanism?
-use in angina?
-ASE?

thienopyridine derivative that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
-reduces blood viscosity by decreasing plasma fibrinogen
-increases RBC deformity
-has NOT shown a decrease in adverse events in patients with stable angina
-induces neutropenia and rarely TTP (require WBC monitoring)

20

clopidogrel
-what is it?
-mechanism?
-ASE?

thienopyridine derivative that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
-more potent than ticlopidine or aspirin; moreso used after stent placement
-selectively and irreversibly inhibits binding of adenosine diphosphate to platelet receptors --> blocks adenosine diphosphate-dependent activation of glycoprotein IIb/IIIa complex
-increased bleeding risk, so must monitor

21

Prasugrel
-what is it?
-mechanism?
-ASE?

thienopyridine class that inhibits platelet aggregation by adenosine phsophate (blocks ADP receptors)
-irreversibly binds to P2Y12 receptor (GPCR chemoreceptor for ADP)
-used to decrease thrombotic events in people w/ stents placed
-while less MI, more bleeding risk, thus limited to patients less than 75 yo and greater than 60 kg, w/o history of stroke or TIA

22

Ticagrelor
-what is it?
-mechanism?
-ASE?

adenosine derivative
-blocks ADP receptors like thienopyridines, but at different site from ADP; thus reversible blocckade
-doesn't need hepatic activation, so can be used in liver dysfunction
-has faster onset of action, and faster elimination, thus needs more doses (less compliance)
-greater rates of non-lethal bleeding
-doses of aspirin above 100 mg decrease effectiveness of ticagrelor

23

dipyridamole
-what is it?
-mechanism?
-ASE?

pyrimido-pyrimidine derivative
-increases intracellular platelet cAMP
--inhibits phosphodiesterase
--activates adenylate cyclase
--inhibits uptake of adenosine from vascular endothelium and RBCs
-limited use b/c vasodilates coronary arteries to enhance exercise-induced ischemia

24

cilostazol
-what is it?
-mechanism?
-ASE?

quinolinone derivative that inhibits cellular phosphodiesterase
-causes increase in CAMP to inhibit platelet aggregation
-causes vasodilation --> increased morbidity and mortality in HF patients
-used primarily as treatment for calduication with peripheral vascular disease

25

what does angiotensin II do?

cause vasoconstriction of arterioles throughout body
-more constriction in efferent than afferent arterioles --> blood building up in glomerulus to increase glomerular pressure
-acts on adrenal cortex to release aldosterone to increase Na and water retention from kidneys
-stimulates ADH release from posterior pituitary to increase water reabsorption from kidney

26

what is kininase II? what does it do?

another name for ACE
-degrades bradykinin to inactive fragments

27

what does bradykinin do?

vasodilator that increases vascular permeability
-plays role in cough and angioedema
-increased if using ACEi

28

what is angioedema?

swelling of skin around the mouth, mucosa of mouth and throat, and tongue
-can be fatal if occludes airways (thus must always beware when using ACEi)

29

what are important ASE of ACEi?

-dry cough (10-30%, most common)
-hypotension
-hyperkalemia (decreased aldosterone)
-angioedema (0.1%, very rare, but can be fatal)
--can occur at any time during treatment

30

what does stimulation of B1 receptors do to the heart?

-increase contractility, HR, and condunction through AV node
--increases O2 demand

31

why are B2 blockers avoided in CAD?

B2 receptors in vascular smooth muscle cause vasodilation; thus inhibiting would cause vasoconstriction b/c removes counteraction to vasoconstriction caused by alpha-adrenergic stimulation

32

what is the goal of B1 blockers?

class II antiarrhythmics
-decrease contractility and HR to decrease myocardial O2 demand
-inhibits sympathetic influences on cardiac electrical activity, increase AP duration, and EFP

33

what do both anti-ischemia and anti-arrythmic effects of B-blockers make them good for?

increase survival immediately post-MI

34

what are contraindications to using BB?

-severe bradycardia
-high degree of AV block (BB could make it complete)
-sick sinus syndrome
-unstable LV failure
-asthma and bronchospastic disease
-severe depression
-peripheral vascular disease

35

what is sick sinus syndrome?

sino-atrial node may not work all the time

36

what are side effects for beta-blockers?

-fatigue
-decreased exercise tolerance (CO doesn't go up)
-lethargy
-insomnia
-worsening claudication
-impotence (more common if nonselective)

37

what do BB do to lower risk of CV events?

they don't
-can only be used to treat symptoms, but not long-term impact

38

mechanism of nitrates?

endothelium-independent vasodilators
-interact w/ enzymes and intracellular sulfhydryl groups that reduce nitrate groups to NO
--NO activates smooth muscle soluble guanylyl cyclase to make cGMP
---cGMP inhibits Ca++ entry into cell, thus decreasing intracellular Ca++ concentration, and increasing relaxation/vasodilation

39

what do nitrates cause overall?

-dilation of large epiccardial coronary arteries and collateral vessels
-increase myocardial O2 delivery to relieve coronary vasospasm in patients w/o CAD (true vasospastic, Prinzmetal's angina)
-venous dilation predominates in doses given (redues venous pressure to reduce preload)
--decreased wall stress reduces O2 demand, and improves subendocardial blood flow

40

what does endothelial-derived NO do?

-inhibits platelet aggregation
-inhibits leukocyte-endothelial interactions (anti-inflammatory effects)

41

dosing of nitrates?

immediate effect: sublingual tablets or spray (standard dose 0.4 mg)

long-acting: oral (Isorbide di/mononitrate) or transdermal (ointment, patch)

42

what are nitrate contraindications?

-hypertrophic cardiomyopathy
-severe aortic stenosis
-significant hypotension
-use of PDE inhibitors for erectile dysfunction (PDEi inhibit cGMP degradation; thus together would cause buildup and over-vasodilation)

43

what are side effects of nitrates?

-nitrate tolerance with chronic use
--depletion of tissue sulfhydryl groups or scavenging of NO by superoxide anion
--O2. produces peroxynitrite to inhibit guanylyl cyclase
--counteract w/ infrequent dosing or nitrate-free periods (8 to 12 hours)
-headaches (vasodilation increases pressure in skull)
-hypotension
-Bezold-Jarisch reflex --> bradycardia
--marked increase inv agal efferent discharge to heart caused by stimulation of cardiac sensory receptors

44

what do calcium channel blockers do?

reduce transmembrane flux of Ca via Ca channels
-tension decreased --> vasodilation
-negative inotrope --> cardiac muscle relaxes

45

what are the types of CCB? names?

1. vasoselective dihydropyridines
-end in "dipine"
2. non-dihydropyridines
-verapamil and diltiazem

46

mechanism of dihydropyridines?

tend to be vasoselective
-dilate epicardial coronary arteries --> relieve coronary vasospasm
-dilate arteriolar resistance vessels --> reduce systemic vascular resistance and decrease arterial pressure
-first generation agents have negative inotropic effect --> negative inotropic effect (decrease myocardial contractility)

47

mechanism of non-dihydropyridines?

-vasodilation
-true negative inotropes, decreasing myocardial contractility
-decrease firing rate of aberrant pacemaker sites within heart
-decrease conduction velocity and prolong repolarization in SA node and AV node (decrease HR)

48

what is verapamil?

non-dihydropyridine CCB
-phenylalkylamine class
-relatively selective for myocardium
-less effective as systemic vasodilator

49

what is diltiazem?

non-dihydropyridine CCB
-benzothiazepine class
-intermediate between verapamil and dihydropyridines

50

what are contraindications for CCB?

-overt decompensated HF (would give even lower EF)
-bradycardia, sinus node dysfunction, or high-degree AV block (non-dihydropyridines)

51

what are ASE of CCB?

-hypotension
-worsening HF
-peripehral edema
-constpiation
-headache
-flushing
-bradycardia
-AV block