Myocardial Infarction Flashcards

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1
Q

Cause of MI ?

A
  1. Rupture of the atherosclerosis with thrombosis
  2. Complete occlusion of coronary artery
  3. CA vasosapsm
  4. Prinzmetal angina
  5. Emboli
  6. Vasculitis-Kawasaki Disease
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2
Q

Cell injury in MI ?

A

Necrosis of cardiacx] myocytes

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3
Q

Dyspnea manifesto in MI ?

A

Total function oif heart is impaired = Pulmonary congestionnand edema = Dyspnea

73

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4
Q

Presenations of MI ?

A
  1. Chest pain = >20minutes
  2. Diaphoresis
  3. Pain radiates left arm — jaw
  4. Dyspnea

Not releived by nitroglycerine

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5
Q

Involvement in MI ?

A
  1. LV
  2. RV
  3. Both atria are spared
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6
Q

EKG changes in MI ?

A
  1. Initially = Subendocardial ischemia = ST depression
  2. Severe ischemia = Traansmural ischemia = ST elevation
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6
Q

Occlusion in MI ?

A
  1. Left ant descending artery = ant wall & ant septum of LV = 45%
  2. Right coronary artery = post wall & post septum & papillae muscle LV
  3. left circumflex artery = lateral wall of LV
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7
Q

Mmembrane damage fate in MI ?

A

Leakage of cardiac enzyme s= Marker of MI

74

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7
Q

Hallmark of MI ?

A

Membrane damage

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8
Q

Cardiac marker in mI ?

A
  1. Troponin I
  2. CK-MB
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9
Q

Troponin I details time—

A

Rise 2-4 hr after infraction
peak = 24 hr
normal = 7-10 day

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10
Q

CK-MB????

A

Level rise =4-6 hr
peak = 24 hr
normal = 72 hr

creatinine kinase MB

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11
Q

Tx of MI ?

A
  1. Aspirine/Heparin = Limit thrombosis
  2. O2 = minimize ischemia
  3. Nitrates = vasodialtion
  4. Beta blocker = dec O2
  5. ACEi = dec LV dilation
  6. Fibrinolytic /angioplasty = open blocked vessels

74

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12
Q

Reperfusion of irreversibly = C ainflux = Hypercontraction of myofibrills == Contraction band necrosis

A

in MI

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13
Q

Further damaging myocytes
after return of O2 + inflammatory cells create = Free radicles

A

Reperfusion injury

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13
Q

Which kind of necrosis in MI ?

A

Coagulative necrosis

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14
Q

Day 1 necrosis time ?

A

<4 hour = changes = No changes

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14
Q

Complications of MI ___+++

A

74 Whole CHART IN PATHOMA-

15
Q

Coagulative necrosis features ?

A
  1. Pyknosis
  2. Kariokinesis’
  3. Kryptosis

3 feature of CN

15
Q

Day1 —– Week 1 ?

A

Inflammation by Neutrophil + Macrophage

16
Q

1-3 days heart condition ?

A

Fibrinous pericarditis
(Chest pain + Friction rub )

17
Q

4-7 days infarction ?

A

Rupture of ventricular wall
-cardiac temponade
-papillary muscle rupture
-mitral insufficiency
-IV septum defect = Shunt

18
Q

Granulation tissue with plump fibrosis blood vessels seen in ?

A

1-3 weeks
red border emerge

19
Q

After months complications ?

A
  1. White scar
  2. Fibrosis
  3. Mural thrombus
  4. Dressler syndrome
20
Q

Dressler syndrome?

A

AB against own pericardium

74

21
Q

Cause of sudden cardiac death ?

A
  1. Fatal ventricular arrhythmia
  2. Mitral valve prolapse
  3. Cardiomyopathy
  4. Cocaine abuse
22
Q

Chronic ischemic heart disease progression ?

A

CHF

23
Q

CHRONIC ischemic damage +/- ischemia = ????

A

CIHD

24
Q

Irreversible cell injury typical sign ?

UWorld

A

Mitochondrial Vacuolization

UW

25
Q

Leads of ST elevation and Q waves indication ??

Left circulflex artery = Lateral wall of LV = Infraction =

UW

A

I aVL

UW

26
Q

Free wall rupture results in –

UW

A
  1. Cardiac temponade
  2. Hypotension
  3. Shock
  4. Cardiac arrest
26
Q

Autpsy of MI ????

UW

A

Slitlike tear at the site of infarction in the LV wall

uW

27
Q

Inferior wall lead in ECG ?

UW

A

II III aVF

27
Q

Which chamber is relatively protected from MI ?

UW

A

RV

27
Q

Devastating but uncommon complications of transmural MI ?

UWorld

A

LV free wall rupture

UW

28
Q

Which factors protect RV from MI ?

UW

A
  1. Small muscle mass with high capacity to increase O2 extraction
  2. Perfusion throughout the cardiac cycle
  3. Heightened ischemic preconditioning
29
Q

same shit revise&raquo_space;»

UW

A

ST-elevation myocardial infarction involves transmural (full-thickness) infarction of the myocardial wall, and usually
results from acute atherosclerotic plaque rupture with the development of overlying thrombus that fully occludes the
coronary artery lumen. It classically presents with sudden-onset substernal chest pain that is not relieved by rest or
short-acting nitrates. ECG demonstrates ST elevation in the affected leads with subsequent development of Q waves.
[37]

30
Q

After the onset of severe ischemia leading to myocardial infarction (MI), early signs of coagulative necrosis do not
become apparent when ??

UWorld

A

Light microscopy untill 4 hours after the onset of MI

UWorld

31
Q

cellular and
mitochondrial swelling that is observed histologically why ?

UW

A

=Ion pump failure
=ATP deficiency during ischemia
=Intracellular accumulation of Na & Ca
=Draw free water into the cell
=Cellular swelling

UWorld

32
Q

Why papillary muscle rupture in MI ?

UW

A

Papillary muscle = Supplied solely by Pst Decending Artery
Its susceptible to ischemic rupture

32
Q

How fibrosis after MI occur ??

UW

A

Transforming growth factor-Beta = Reduce inflmmation = Promote tissue remodelling = Fibroblast proliferation = collagen deposition

UWorld

33
Q

Life threatening complication of MI that occurs 3-5 days after ??

UW

A

Papillary muscle rupture

34
Q
A