Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSII Pharmacology > Unit 4 - Coronary Artery Disease > Flashcards

Unit 4 - Coronary Artery Disease Flashcards

1
Q

what kind of exams are coronary angiograms?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is angina VS acute MI?

A

angina: larger artery that is slowly occluding

acute MI: smaller and fast artery occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

in who does angina usually occur?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe the metabolic effects of ischemia

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

elevated extracellular K+

  • due to increased cell membrane permeability to K+ during plateau phase of AP (leak outwards)
  • lactate and phosphate follow K+ out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what causes the increased circulating FFA in ischemia?

A

sympathetic activation from MI

  • liposomal phospholipase is activated to break down membrane phospholipids
  • LCFA accumulate in intracellular space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the gradient between ischemic cells and normal cells?

A

“injury current”

  • partial depolarization
  • shortened AP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the diastolic injury current?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the systolic injury current?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which injury current should one focus on?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

stress test on treadmill for 6-12 minutes (Bruce protocol)

-valid if patient reaches 85% of max predicted HR (220 - age)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is coronary steal? what causes this?

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do electron beam CT sans do?

A

identify Ca++ in coronaries

  • use Ca++ score to correlate probability of significant coronary disease
  • variable results
  • most useful in predicting absence of CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the 2 objectives of medical management of CAD?

A
  1. prevent MI and death (increase quantity of life)

2. reduce symptoms of angina and occurence of ischemia (increase quality of life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what should the first intervention of CAD treatment be?

A

identify and treat risk factors for CVD:

  • lipid abnormalities
  • smoking
  • diabetes
  • HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

when someone is allergic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ticlopidine

  • what is it?
  • mechanism?
  • use in angina?
  • ASE?
A

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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

clopidogrel

  • what is it?
  • mechanism?
  • ASE?
A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Prasugrel

  • what is it?
  • mechanism?
  • ASE?
A

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
Q

Ticagrelor

  • what is it?
  • mechanism?
  • ASE?
A

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
Q

dipyridamole

  • what is it?
  • mechanism?
  • ASE?
A

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
Q

cilostazol

  • what is it?
  • mechanism?
  • ASE?
A

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
Q

what does angiotensin II do?

A

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
Q

what is kininase II? what does it do?

A

another name for ACE

-degrades bradykinin to inactive fragments

27
Q

what does bradykinin do?

A

vasodilator that increases vascular permeability

  • plays role in cough and angioedema
  • increased if using ACEi
28
Q

what is angioedema?

A

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
Q

what are important ASE of ACEi?

A
  • 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
Q

what does stimulation of B1 receptors do to the heart?

A
  • increase contractility, HR, and condunction through AV node
  • -increases O2 demand
31
Q

why are B2 blockers avoided in CAD?

A

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
Q

what is the goal of B1 blockers?

A

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
Q

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

A

increase survival immediately post-MI

34
Q

what are contraindications to using BB?

A
  • 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
Q

what is sick sinus syndrome?

A

sino-atrial node may not work all the time

36
Q

what are side effects for beta-blockers?

A
  • fatigue
  • decreased exercise tolerance (CO doesn’t go up)
  • lethargy
  • insomnia
  • worsening claudication
  • impotence (more common if nonselective)
37
Q

what do BB do to lower risk of CV events?

A

they don’t

-can only be used to treat symptoms, but not long-term impact

38
Q

mechanism of nitrates?

A

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
Q

what do nitrates cause overall?

A
  • 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
Q

what does endothelial-derived NO do?

A
  • inhibits platelet aggregation

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

41
Q

dosing of nitrates?

A

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

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

42
Q

what are nitrate contraindications?

A
  • 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
Q

what are side effects of nitrates?

A
  • 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
Q

what do calcium channel blockers do?

A

reduce transmembrane flux of Ca via Ca channels

  • tension decreased –> vasodilation
  • negative inotrope –> cardiac muscle relaxes
45
Q

what are the types of CCB? names?

A
  1. vasoselective dihydropyridines
    - end in “dipine”
  2. non-dihydropyridines
    - verapamil and diltiazem
46
Q

mechanism of dihydropyridines?

A

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
Q

mechanism of non-dihydropyridines?

A
  • 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
Q

what is verapamil?

A

non-dihydropyridine CCB

  • phenylalkylamine class
  • relatively selective for myocardium
  • less effective as systemic vasodilator
49
Q

what is diltiazem?

A

non-dihydropyridine CCB

  • benzothiazepine class
  • intermediate between verapamil and dihydropyridines
50
Q

what are contraindications for CCB?

A
  • overt decompensated HF (would give even lower EF)

- bradycardia, sinus node dysfunction, or high-degree AV block (non-dihydropyridines)

51
Q

what are ASE of CCB?

A
  • hypotension
  • worsening HF
  • peripehral edema
  • constpiation
  • headache
  • flushing
  • bradycardia
  • AV block

MSII Pharmacology (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions