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Pathology Pre-Midterm > module 6 CVS continued:Angina and MI > Flashcards

module 6 CVS continued:Angina and MI Flashcards

1
Q

What is angina

A

Intermittent chest pain or discomfort due to transient, reversible myocardial ischemia – not infarction and NO myocyte death

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2
Q

There are three types of angina, each card will go through one. 1. Typical (Stable)

A
  1. Typical (Stable): associated with increased demand
    predictable chest pain with certain levels of exertion
    Most common form
    due to critical stenosis and reduction of coronary perfusion due to fixed stenosis
    Pain is crushing or squeezing, substernal and may radiate down the right arm
    Relieved by rest and vasodilators
    If plaque ruptures see on EKG = ST segment depression but normal cardiac enzymes
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3
Q
  1. Unstable (crescendo angina)
A

Pain that occurs with progressively increasing frequency and is precipitated with progressively less effort, often occurs at rest and tends to be more prolonged duration
Induced by disruption of plaque with superimposed thrombosis and possibly vasospasm
Harbinger of subsequent MI (per infarction angina)
Responds to nitro (aka vasodilators)
ST depression on EKG
No elevated cardiac enzymes

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4
Q
  1. Prinzmetal (variant) Angina
A

Occurs at rest and awakens patient from sleep
Associated with ST segment elevation, indicative of transmural ischemia
Cause and mechanism not clear
May be due to coronary artery spasm
Responds to vasodilators
Middle aged females
Cardiac enzymes are normal

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5
Q

What is a myocardial infarction (MI)

A

Superimposed thrombus on an atherosclerotic plaque thats unstable/ruptures
Indicates the development of an area of myocardial necrosis caused by local ischemia

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6
Q

There are two types of MI, transmural and subendocardial. What is a transmural MI?

A

Full thickness of ventricular wall, associated with plaque disruption and superimposed thrombosis
Much more serious
ST segment elevation

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7
Q

What is a subendocardial MI?

A

Inner 1/3rd of ventricular wall affected
Associated with stenosing coronary atherosclerosis
Less serious
Gunshot wounds and bleeding out the myocardial wall is the last place to bleed out and therefore you get an infarct
Could be due to a plaque disruption or superimposed thrombus as well
ST depression

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8
Q

Most MI’s (90%) are due to coronary artery occlusion. The three coronary arteries affected are, LAD, left circumflex and right coronary artery. Explain the areas of the heart each of these arteries supply

A

Left Anterior Descending (LAD): percent of infarcts 50% supplies anterior 2/3rd of septum and anterior free wall
Left circumflex: percent of infarcts 20% supplies lateral free wall
Right Coronary Artery: percent of infarcts 30% supplies posterior 1/3 septum and posterior (inferior) free wall

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9
Q

Coronary artery obstruction leads to the loss of critical blood supply to the myocardium which indicates functional, biochemical, and morphological consequences. What are some features in the first hour of an MI?

A

Onset = ATP depletion
In 2 minutes = loss of contractility
ATP reduced to half in 10 minutes and 10% in 40 minutes
Irreversible cell injury = 20-40 minutes

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10
Q

What is the presentation for an MI?

A 
Sharp substernal chest pain radiating to arm 
diaphoresis 
palpitations 
nausea 
dyspnea
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11
Q

Does nitro help for an MI?

A

Nope because with an MI you are actively infarcting

note pain is due to acute inflammation from bradykinin

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12
Q

What investigations would you do for an MI?

A

EKG – ST elevation
Troponin I – rise in 2-4 hours ; peak at 48 hours and disappears 7-10 days
CK-MB — rise in 2-4 hours ; peak at 24 hours ; disappears in 3 days (72 hours); use to check for re-infarction

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13
Q

On gross image of an MI how do you tell the difference between an old and new MI?

A 
New= yellow 
Old = white (this is due to fibrosis)
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14
Q

What is the sequence of events for an MI?

A

Coagulative necrosis —- inflammation and resorption of necrotic myocardium —- formation of granulation tissue —-organization of granulation tissue to form a collagen rich scar tissue

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15
Q

There is a distant time line for an MI, each card will go through the events that happen. 1. 0-30 minutes

A

0-30 minutes – nothing on histology and possibly injury can be reversed

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16
Q
  1. 30 minutes - 4 hours
A

Wavy fibers: Stretching and buckling of non contractile dead fibers

  • –myocardium is passively stretching
  • –this is the time period you would need to do TPA
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17
Q
  1. 4 hours - 12 hours
A

Gross: Few dark mottling
Micro: Early coagulation necrosis, edema, hemorrhage –all protein denatured with loss of nuclei

18
Q
  1. 12 hours - 24 hours
A

Gross: dark mottling (uneven spots)
Micro: early neutrophils infiltrate
coagulative necrosis and pyknosis
contraction bands (vertical lines) (associated with reperfusion—bringing Ca back in and hypercontraction — no oxygen, no ATP to relax myocardial fibers)

19
Q
  1. 1-3 days
A

Gross: mottling and yellow/tan center
Micro: Heavy neutrophilic infiltrate in the myocardium
upper right corner

20
Q
  1. 3-7 days
A

Gross: central softening; yellow/tan center and hyperemic border: due to hemorrhage
Micro: macrophages appear and the myofibers are breaking down
myocardium becomes extremely soft because macrophages are eating necrotic debrie so this is when you see rupture complications

21
Q
  1. 7-10 days
A

Gross: max softening again risk of rupture; no myocytes or collagen
Micro: well developed phagocytosis and extensive macrophages

22
Q
  1. 10-14 days
A

Gross: red/gray depressed border
Micro: active granulation tissue
lower left corner

23
Q
  1. 2-8 weeks
A

Gross: firm, gray/white, scarring complete
Micro: increased collagen and decreased cellularity
type III collagen and making angiogenesis

24
Q
  1. 2+ months
A 
Gross: scar complete 
Micro: dense collagenous scar 
no more angiogenesis so this is type I collagen
lower left corner 
aneurysm
25
Q

What is the most common cause of death in the first 24 hours of an MI?

A

Arrhythmias or VFIB
(also most common complication)
(need tight junctions for conduction; dead cells/scars impede transmission)

26
Q

Complications mostly occur between 3-10 days because macrophages have engulfed debrie and the myocardium is soft and vulnerable to rupture. Each card will go through the various complications of an MI. 1 –>

A
  1. Rupture of the free wall of the myocardium (most common)(circumflex) — pericardial temponde (Diastolic dysfunction) —- becks triad (muffled heart sounds, increased jugular veins and hypotension)
27
Q

The second complication of an MI —>

A
  1. IV septum rupture —- leads to a left to right shunt, gives you higher pressure on the right —-so acquired VSD —leads to pulmonary edema —- leads to an LAD occlusion —– leads to this because LAD supplies the anterior 2/3 of the IV septum
28
Q

If a patient has an IV septum rupture what will the patient present with?

A

Pansystolic murmur — loudest in left lower sternal border
and breathlessness due to pulmonary edema
(one time you will see oxygenated blood in the right ventricle coming from the left ventricle)

29
Q

The third complication of an MI is —>

A
  1. Papillary muscle rupture: supplied by the right coronary artery so if you have a right coronary artery occlusion then papillary muscle ruptures
    Affects mitral valve and if this rupture then you get regur ( when the mitral valve closes its regur, closed during systole —> however because the valve is now leaky the blood goes back to the left atrium (normally would go to the aorta) –> pulmonary system and lungs)
30
Q

If a patient has a papillary muscle rupture what will the patient present with?

A

Pansystolic murmur loudest at the apex because this is where the mitral valve is
patient is breathlessnesss due to the pulmonary edema

31
Q

The 4th complication of an MI is —>

A
  1. Months later – left ventricular aneurysm after fully formed scar
    Fibrosis scar is much weaker then proper myocardium
    Stasis (blood not moving) —- leading to mural thrombus —embolize — goes to artery of LE —- gangrene —- or could go to brain aka MCA called embolic stoke and this is a red infarct
32
Q

What is heart failure or congestive heart failure?

A

Inability of the heart, working at normal or elevated filling pressure, to pump enough blood to meet the metabolic demands of the body

33
Q

The etiology of heart failure is either systolic dysfunction (Contraction) or diastolic dysfunction (filling). Explain systolic dysfunction

A

Systolic dysfunction (Contraction): inability to contract properly (decreased ejection fraction)

  • MI
  • HTN
  • Volume overload (valvular regur)
  • Cardiomyopathy (dilated enlarged flabby or restrictive fibrosis of endocardium)
34
Q

Explain diastolic dysfunction (filling)

A

Diastolic Dysfunction (filling): inability of heart chamber to relax/expand and fill sufficiently during diastole

  • massive ventricular hypertrophy
  • senile cardiac amyloidosis: transthyretin
  • -systemic amyloidosis: AL
  • -constrictive pericarditis: inflammation of pericardium
  • -cardiac tamponade
35
Q

On autopsy of the heart how would you distinguish diastolic failure compared to systolic failure?

A

Diastolic Failure: thick heart walls

Systolic Failure: thin heart walls

36
Q

What are the 5 categories of heart disease?

A
  1. Ischemic heart disease/Coronary Artery disease (IHD/CAD)
  2. Hypertensive heart disease (LVH)
  3. Valvular heart disease
  4. Cardiomyopathy (primary myocardial disease)
  5. Congenital Heart Disease
37
Q

What is ischemic heart disease/coronary artery disease?

A

Generic term for imbalance between myocardial need for and supply of oxygenated blood
–fixed atherosclerotic plaque occluding coronary artery + new superimposed thrombus and/or vasospasm

38
Q

What are the four clinical syndromes of ischemic heart disease?

A
  1. Various forms of angina
  2. Acute MI
  3. Sudden cardiac death
  4. Chronic ischemic heart disease with CHF
    (note: acute coronary syndrome applies to MI, unstable angina and sudden cardiac death)
39
Q

90% of cases of IHD/CAD is?

A

Atherosclerosis

40
Q

What are the different pathogenesis for ischemic heart disease?

A
  1. Coronary obstruction: atherosclerotic lesions causing at least 75% reduction = critical stenosis
  2. Acute plaque changes: disruption of plaque: inability to withstand imposed mechanical stresses. (plaque= hemorrhage, rupture or erosion)
  3. Coronary artery thrombosis: plaque rupture, erosion or ulceration
  4. Vasoconstriction: increased mechanical shear forces that can contribute to plaque rupture
41
Q

What is the difference between stenosis and incompetence/regurgitation or insufficiency?

A

Stenosis: failure of a valve to open completely – impeding forward flow
Incompetence:Failure of a valve to close completely (allowing reversed flow)

Pathology Pre-Midterm (35 decks)

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