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MOD 2 > Pathophysiology of MI and Pharmacotherapy > Flashcards

Pathophysiology of MI and Pharmacotherapy Flashcards

1
Q

What are the gender trends with ischemic heart disease?

A
  • women have less anatomically obstructive CAD but have higher rates of MI mortality than men of same age
  • women are more likely to have **“atypical” symptoms **
  • greater hsCRP values compared to men (high sensitive C reative protein-very robust inflammatory response)
  • women have greater frequency of coronary plaque erosion (coronary endothelial and microvascular dysfunction)
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2
Q

What are the types of plaques in acute coronary syndrome (ACS)

A
  • ruptured (70%) —> non-stenotic (50%) and stenotic/reduction in lumen (20%)
  • nonruptured (30%) —-> erosion, calcified nodule
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3
Q

which are the three favorite arteries for an MI, and what areas of the heart do they supply?

A
  • Left Anterior Descending (50%): infarct of apical, anterior, and anteroseptal walls of left ventricle
  • Right coronary (30%): infarct of posterior basal region of left ventricle and posterior third of interventricular septum
  • Left circumflex (20%): infarct of lateral wall of left ventricle
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4
Q

Sudden occlusion of coronary artery often results in what type of infarction?

A

transmural (wall to wall)

-the area affected depends on the amount of collateral circulation

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5
Q

What do you see subendocardial necrosis?

A

-confined to the inner half of the left ventricle with a very thin layer of viable munscle present immediately beneath the endocardium

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6
Q

What is immediately expressed after the onset of MI?

A
  • HIF, activates genes involved in angiogenesis and energy metabolism
  • also see heat shock proteins, ubiquitin, fas, cytokines
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7
Q

Criteria for definition of MI (1 + 5)

A
  1. detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin) WITH atleast one of the following:
    a. ischemic symptoms
    b. new significant ST segment changes
    c. pathological Q waves
    d. imaging evidence of new loss of viable myocardium
    e. identification of intracoronary thrombus (by angiography or autopsy)
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8
Q

Major consequence of anoxia

A

anoxia –> less ATP –> impacts Ca pump –> Ca accumulates in myocardium cell –> free radicals from reperfusion –> cell death

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9
Q

What are serum biomarkers, why do we measure them, what are 3 important ones

A
  • when myocardial cells increase permeability due to alterations in plasma membrane, stuff gets out based on molecular weight (smaller MW get out first)
  • troponins, myoglobin, creatine kinase MB, and new markers (MB iosforms, CRP, MPO, sCD40, Annexin V)
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10
Q

For the following serum markers, list their relative molecular weight and detectability: Myoglobin, Cardiac Troponin T, Cardiac Troponin I, Creatine kinase MB (CK-MB)

Which troponin is not cardiac specific?

A
  • see figure
  • myoglobin is not cardiac specific, so not useful
  • troponin C is not cardiac specific
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11
Q

Which serum marker is highest at 8 hours after MI? 20 hours?

A

6 hours: Myoglobin

20: troponin

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12
Q

MI histopathology:

reversible damage:

irreversible damage:

A

reversible- cell swelling, hydropic and fatty change

irreversible - wavey appearance of myocardial fiber, cytoplasmic hypereosinophilia, contraction bands, nuclear pyknosis and karyolysis, chromatin half moon crescents

waviness of myocardial fiber = FIRST SIGN THAT SOMETHING IS WRONG!

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13
Q

given the timeline, what do you expect to see under light microscopy?

0-1/2 hours:

1/2-4 hours:

4-12 hours:

12-24 hours:

1-3 days:

A

see chart

recall: karyolysis = nuclear fading; pyknosis - nuclear shrinking; karyorrhexis- nuclear fragmentation

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14
Q

eline, what do you expect to see under light microscopy?

3-7 days:

7-10 days:

10-14 days:

2-8 weeks:

>2 months:

A

3-7 days: macrophages

7-10 days: granulation

10-14 days: granulation and collagen

2-8 weeks: collagen deposition

>2 months: scar

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15
Q

roughly what stage of MI is does this slide show

A

healing MI with granulation tissue: day 7-10

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16
Q

roughly what stage of MI is does this slide show

A

Healing MI with macropahges chewing up dead fibers, apoptotic PMNS: 3-7/10-14 days

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17
Q

What are the importance of contraction bands with respect to an MI

A
  • necrosis with contraction bands at time of reperfusion = irreversible injury to cardiomyocytes
  • the bands are eosinophilic transverse bands, made of hypercontracted sarcomeres
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18
Q

reperfusion injury

  • what type of death
  • cause of damage
A
  • after blood flow resumes, variable number of cells die mostly by apoptosis
  • damage by free radicals
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19
Q

how long does it take for an MI to become recognizable on a gross examination?

What is the most common pattern of acute ischemic necrosis

A
  • 12-24 hours
  • regional infarction, i.e. a large single area of coagulative necrosis
  • measures atleast 3 cm along one of axes and involves 50% of ventricular wall thickness
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20
Q

list the 7 most common complications of MI

A
  • pain
  • ventricular remodeling and dysfunction
  • cardiogenic shock
  • arrhythmias
  • pericarditis
  • thromboembolism
  • free wall rupture
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21
Q

which ventricle is most likely to rupture and why

A

Left ventricle is 7x more likely than right: even though it’s thicker, the idea is that hypertension may be a risk factor and high BP in LV increases local wall stress

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22
Q

What is mechanically occuring when you see symptoms with exertion (exertional angina) vs. symptoms at rest (unstable angina/MI)

A

exertional angina- clot that has not ruptured

unstable angina- ruptured clot with blood clot forming

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23
Q

definition of ischemia

  • symptoms
  • rarer symptoms
A

O2 demand >>>> O2 supply

  • chest pain, dyspnea, nausea, diaphoresis
  • *last two believed to result from vagal stimulation, more common with inferior wall ischemia**
  • more rare: urge to defecate, weakness, dizziness, palpitations, cold perspiration, send of impending doom
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24
Q

causes for sudden death from ischemia

A
  • usually caused by coronary artery disease
  • younger patients: hypertrophic cardiomyopathy (HCM)
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25
Q

What are the risk factors for ischemia? (7)

A
  1. prior coronary disease
  2. coronary risk equivalents (diabetes, peripheral artery disease, chronic kidney disease)
  3. hypertension
  4. hyperlipidemia
  5. family history
  6. smoking
  7. obesity, sedentary lifestyle
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26
Q

explain the concept of ST depressions

A
  • in figure: you see RV and LV in first drawing, blue portion is subendocardial ischemia
  • ischemia creates electrical currents going away from it
  • when lead looks at LV, it will see current heading towards it (since current is being driven away from the subendocardium)
  • raises baseline initially so then the EKG appears to have an ST depression
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27
Q

One important ischemic EKG change is T wave inversions. There are many causes for this, but list the 4 important ones. Why do you see the inversion?

A
  • raised intracerebral pressure (cerebral T waves)
  • resolving pericarditis
  • bundle branch blocks
  • ventricular hypertrophy
    mechanism: normally subendocardium repolarizes first, so you get a wave of repolarization from sub to epicardium = upwards T wave as it heads towards the lead facing from the outside.

In subendo ischemia, it gets damaged and gets repolarized last. This reverses the wave.

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28
Q

Explain the mechanisms behind ST elevations

A
  • ST elevation indicates transmural ischemia = entire wall is ischemic
  • see the wave going away from the EKG lead
  • now baseline is below the normal line
  • the heart depolarizes then repolarizes, making it look more elevated than the initial baseline
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29
Q

at what point duringdo you start to see inverted T waves in an ST elevation MI (STEMI)

A

1-2 days

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30
Q

in an anterior MI, which leads would you expect to see ST elevation?

A

V1, V2, V3, V4

31
Q

in a lateral MI, which leads would you expect to see ST elevation?

A

Leads I, aVL, V5, V6

32
Q

in an inferior MI, which leads would you expect to see ST elevation?

A

Leads aVF, II, III

33
Q

List the 5 ischemic syndromes

A
  1. ST-Elevation Myocardial Infarcion (STEMI)
  2. Non-ST-Elevation Myocardial Infarction (NSTEMI)
  3. unstable angina
  4. Variant/Prinzmetals angina
  5. stable angina
34
Q

Changes with infarction-gross and micro

0-4 hours:

4-12 hours:

12-24 hours:

5-10 days:

7 weeks:

A

0-4 hours: micro: hydropic and fatty change, t hen wavey myofibers

4-12 hours: gross: mottled; micro: necrosis, edema, hemorrhage

12-24 hours: gross: hyperemia; micro: surrounding tissue inflammation

5-10 days: gross: central yellowing; micro: granulation tissue

7 weeks: gross: gray-white scar; micro: scar

35
Q

Risks after infarction:

1-4 days:

5-10 days:

Weeks later:

A

1-4 days: arrhythmia

5-10 days: free wall rupture, tamponade, papillary muscle rupture, VSD (septal rupture)

Weeks later: dressler’s syndrome, aneurysm, LV thrombus/Cerebrovascular accident (CVA)

36
Q

3 causes for papillary muscle rupture

2 causes for septal rupture + type of murmur

A
  • papillary
    • acute mitral regurgitation (holosystolic)
    • heart failure, respiratory distress
    • inferior MIs
  • septal rupture
    • hypotension
    • right heart failure (increase JVP,edema)
    • loud, holosystolic murmur (thrill)
37
Q

weeks after an MI, the EKG shows ST elevation, PR segments are depressed. Name and describe the syndrome (5) + treatment

A

-a cause for ST elevations weeks after an MI can be due to pericarditis. This indicates Dressler’s syndrome

  • chest pain (sharp, pleuritic, worse when lying flat, improved when sitting up/lean forward)
  • pericardial friction rub (scratchy sound)
  • fever, leukocytosis
  • high ESR (erythrocyte sedimentation rate)
  • immune-mediated (details not known)
  • Tx: NSAIDs or steroids
38
Q

What are differenes/similarties between dressler’s and fibrinous pericarditis?

A
  • fibrinous can occur days after MI, not immune, extension of myocardial inflammation
  • dressler’s occurs WEEKS after, the pericarditis is considere a “post cardiac injury”
  • neither syndrome is life threatening, so DONT pinpoint it as a cause of death
39
Q

Secondary prevention for risk reduction of STEMI, NSTEMI, stable angina etc.

A
  • aspirin (low dose, 81 mg), less bleeding with lower dose
  • statins (atorvastatin, rosuvastatin) - pleiotrophic effects beyond LDL leveling, stabilize coronary plaques
40
Q

2 problems/complications with stents

A
  • restenosis
    • scar tissue over stent
    • re-occludes, usually not lifethreatening
    • slow return of angina
    • can use drug eluting stent to prevent this
  • thrombosis
    • acute closure of stent
    • same as STEMI- LIFE THREATENING
    • dual anti-platelet therapy for prevention
41
Q

Describe the antiplatelet therapy for preventing stent thrombosis

A
  • typically one year of:
    • aspirin (325 mg daily)
    • clopidogral (75 mg daily)
      • alternatives: prasugrel, ticagrelor
  • after one year, stent metal no longer exposed to blood
    • endothelialization
    • risk of thrombosis is lowered
    • cut back on antiplatelet therapy, most will still take lower dosed **aspirin **
42
Q

tombstoning

A

see this in a STEMI: tombstoning effect “goes up then down”

-ST elevation through V1-V5 = anterior myocardial infarction

43
Q

EKG suggest which artery is blocked by which leads show ST elevation

  • LAD
  • LCX
  • RCA
A
  • LAD: V1-V4 (anterior)
  • LCX: I, aVL, V5, V6 (lateral)
  • RCA: II, III, avF (inferior)
44
Q

“time is muscle” in STEMI

A
  • occluded coronary artery by blood clot
  • the longer it remains occluded:
    • more muscle dies
    • more likely pt dies
    • heart failure symptoms
    • hospitalization

aka MEDICAL EMERGENCY

45
Q

Treatment of STEMI

  • main objective
  • 2 options
A
  • objective is revascularization = open the artery
  • option 1: emergency angioplasty
    • mechanical opening of artery
    • should be done <90 min
    • more effective
  • option 2: thrombolysis
    • lysis of thrombus with drug
    • should be done <30 min
46
Q

supportive drug treatment for STEMI-given while you work to open the artery

A

Remember: STEMI is a thrombotic and an **ischemic **problem

thrombotic:

  • aspirin (inhibit platelet aggregation) 325 mg
  • heparin (inhibit clot formation)

ischemic:

  • beta blocker (to reduce O2 demand) i.e. metropolol
  • nitrates (reduce O2 demand) i.e. nitro drip
47
Q

alarms/cautions for when using beta blockers and nitrates

A
  • inferior MI stimulates vagal nerve + beta blocker –> bradycardia and AV block
  • nitrates lower preload, but if you have an RCA infarction, RV doesnt work to preload the LV, so LV becomes heavily dependent on volume in the body –> hypotension
48
Q

3 other STEMI treatments (aside from aspirin, heparin, beta blockers, and nitrates)

A
  • platelet inhibitor –> ADP receptor blocker –> clopidogrel
  • platelet inhibitor –> IIB/IIIA receptor blocker –> Eptifibatide
  • anticoagulant –> direct thrombin inhibitor –> bivalarudin
49
Q

What is a Non-ST-Elevation Myocardial Infarction (NSTEMI)? What do you see on EKG and lab work?

A
  • damage to tissue but EKG shows no ST elevation
  • lab work shows elevated cardiac biomarkers (signs of heart damage)
  • troponin
    • I and T are most common; increase 2-4 hours after MI
    • stay elevated for weeks
  • CK
  • CK-MB
    • increase 4-6 hours after MI
    • normalize wtihin 2-3 days
50
Q

creatinine kinase is found in multiple tissues, what ratio can be used in ischemia?

A

Several types of CK:

  • MM-skeletal muscle*
  • MB-cardiac*
  • BB-brain *

ratio of MB to total CK can be used in ischemia, (because high CK levels alone doesn’t necessarily mean MI, could be the MM type from a muscle disorder, i.e. rhabomyolysis)

51
Q

abdominal pain with isolated increase in AST levels

A

-need to rule out MI, some AST found in cardiac cells

52
Q

what is the most important difference between STEMI and NSTEMI?

A

there is no “ticking clock” with NSTEMI

  • artery not completely occluded
  • some blood flow distal to myocardium
  • no need for emergency angioplasty
  • no benefit to thrombolysis
53
Q

unstable angina:

  • symptoms
  • EKG
  • lab work
A
  • sudden onset substernal chest pain, nausea, diaphoresis
  • EKG: no ST elevation, but ST depression and T wave inversions
  • lab work: normal cardiac biomarkers

signs of chest pain at rest = on verge of having an NSTEMI

54
Q

stable angina:

symptoms

EKG

biomarkers

A
  • substernal chest pain with exercise
  • normal EKG and biomarkers
  • stress test: walks on treadmill–> chest pain –> EKG changes
55
Q

symptoms generally do not occur in stable angina until __% of artery is occluded

A

-70%

stress test produces symptoms

56
Q

why is there no role for heparin, tPA, and other antithrombotics in stable angina?

A

because blood clotting isn’t an issue, you have a stable plaque and that’s it.

57
Q

medical therapy for stable angina if you dont want/cant have vascularization procedures

A

-you have to rectify the oxygen supply/demand problem–like a SEESAW

  • increase O2 supply
    • vasodilate coronary arteries
    • increase diastole (recall coronary arteries are diffused during diastole)
  • decrease O2 demand–main determinants of work
    • decrease HR
    • decrease contractility
    • decrease afterload (BP)
    • decrease preload
58
Q
  • preload definition
  • what is the marker of preload
  • how to increase volume (3)
  • how to decrease preload (3)
A
  • def: how much blood the heart must pump, how much stretch is on fibers prior to contraction
  • marker = LV end diastolic volume (LVEDV)
  • increase preload:
    • add volume (blood, IVF)
    • slow heart rate –> more filling –> more volume
    • constrict veins (forces blood back to heart)
  • decrease preload:
    • remove volume (bleeding, dehydration)
    • raise heart rate
    • pool blood in veins (nitrates-dilators)
59
Q
  • afterload definition
  • how to decrease afterload
A
  • forces that resist forward flow of blood
    • blood pressure
    • aortic stenosis, HCM, etc.
  • decrease afterload:
    • lower BP
    • treat aortic valve disease, hypertrophic cardiomyopathy, etc.
60
Q

2 effects of HR with impact on O2:

-faster HR –> effect on diastole? —> effect on O2 delivery?

A

2 effects of HR with impact on O2:

  • more beats/min –> more O2 needed
  • length of diastole: faster HR –> shorter diastole –> less O2 delivery
61
Q

ejection time

  • definition
  • what its associated with
A
  • time to eject blood
  • tracks with LVEDV (another marker of preload)
  • more LVEDV = more ejection time = increase O2 demand
62
Q

nitrates

  • two mechanisms
  • effect on preload
  • reflex effect of nitrates, supplemental therapy
A
  • predominant mechanism: venous dilation
    • bigger veins = hold more blood = takes blood away from LV = lowers LVEDV
  • also dilates arteries (but way less than veins)
    • increases coronary perfusion
    • peripheral vasodilation –> BP will fall
  • preload DECREASES
  • preload falls –> reflex tries to maintain CO –> increase HR and contractility (increases O2 demand, exactly what we DONT want for angina
  • nitrates improve angina, but preload effects dominate
  • can administer BB or CCB to blunt reflex effect
63
Q

nitrates side effects (3)

A
  • headache (meningeal vasodilation)
  • flushing (skin vasodilation)
  • hypotension
64
Q

Monday disease

A

-workers in nitroglycerin manufacturing facilities

-regular NTG exposure –> tolerance

-lose tolerance over weekend

-monday morning headache due to reexposure: vasodilation, tachycardia, dizziness, headache

*tolerance with nitrates–drugs stop working after frequent use, avoid by not using drug continuously for more than 24 hours

*tolerance not demonstarted with once-daily isosorbide mononitrate

65
Q

CCB

  • action
  • drugs and their specific actions
A
  • negative inotropes
    • slow HR, decrease contractility
    • similar to beta blockers
    • verapamil, dilitiazem
  • vasodilators
    • decrease peripheral vascular resistance (afterload)
    • directly dilate coronary arteries
    • nifedipine (dihydropyridines)
66
Q

quiz self

A

see front

67
Q

quiz self

A

see front

68
Q

<4 hours:

gross changes

microscopic changes

complications

A

gross: none
microscopic: none
complications: cardiogenic shock (massive MI), CHF, arrythmias

69
Q

4-24 hours:

gross changes

microscopic changes

complications

A

gross: dark discoloration
microscopic: neutrophils
complications: arrhythmia

70
Q

1-3 days:

gross changes

microscopic changes

complications

A

gross changes: yellow discoloration

microscopic changes: neutrophils

complications: fibrinous pericarditis, presents as chest pain with friction rub

71
Q

4-7 days:

gross changes

microscopic changes

complications

A

gross changes: yellow discoloration

microscopic changes: macrophages

complications: rupture of ventricular free wall –> cardiac tamponade, rupture of IV septum –> shunt, rupture of papillary muscle –> mitral insufficiency/murmur

72
Q

1-3 weeks

gross changes

microscopic changes

complications

A

gross changes: red border emerges as granulation tissue enters from edge of infarct

microscopic changes: granulation tissue with plump fibroblasts, collagen, and blood vessels

complications: xx

73
Q

months:

gross changes

microscopic changes

complications

A

gross changes: white scar

microscopic changes: fibrosis

complications: aneurysm, mural thrombus, or dressler syndrome

MOD 2 (13 decks)

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