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Cardio - Gupta > Pathology of Heart Disease II and III > Flashcards

Pathology of Heart Disease II and III Flashcards

1
Q

****How long ago did this MI occur? why?

A

3-4 weeks ago - because there is extensive collagen with few remaining fibers

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2
Q

*****What has occurred here?

A

Apical Left Ventricular Aneurysm

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3
Q

What findings are you likely to see at at the GROSS and LIGHT MICROSCOPY level at the following time points following a heart attack?

  • 10-14 days
  • 2 months
A

10-14 days
Gross: Red-Grey
LM: New vessels and collagen deposition

2 months
Gross: Scar
LM: DENSE COLLAGENOUS SCAR

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4
Q

**cor pulmonale

A

Right Side Ventricular enlargement due to primary lung dysfunction

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5
Q

What is the Appearance of a Heart in someone that has Chronic Ischemic Heart Disease?

A

**LEFT Ventricular HYPERTROPHY and DILATION -often you can see scarred areas of pervious healed infarcts

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6
Q

*****WHAT IS THIS????

A

MURAL THROMBOSIS

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7
Q

**Collateral Circulation

• why could this be important in ischemic heart disease?

A

• ischemic heart disease is caused by poor fluid flow through vessels. If this occurs slow enough collateral circulation may form allowing for tissue perfusion despite complete occlusion of Coronary Arteries.

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8
Q

***When did this Myocardial Infarction probably occur?

A

3-7 days ago - gross appearance of necrosis with hyperemic area surrounding it

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9
Q

**Thrombus

•what often causes this in IHD?

A

IHD - most often caused by Atherosclerosis, therefore most thrombi likely form due to EXPOSED NECROTIC TISSUE or SUBENDOTHELIAL collagen from a plaque

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10
Q

****What changes can you see in the heart as a result of the thrombus?

A

• Ischemic changes are seen (before coag. necrosis). You can see DARKENING of the myocytes as they become a deeper red color

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11
Q

*****What is seen in this histology (move from left to right) ?
• Reversibility of Injury?

A
  • endocardium - may not be dead, still fairly pink
  • Myocardium (left) - Definitely dead - Vacuolar changes and Absence of nucleus conferms this
  • Myocardium (right) - still fairly well perfused but we can see Spead out and Swollen Cells
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12
Q

Prinzmetal Angina
• cause
• angina type

A

STABLE angina caused by vessel spasm

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13
Q

What is this?

A

Chronic Cor Pulmonale - Right Ventricle is Dilated and Hypertrophied with HUGE trabeculae

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14
Q

****When did this MI occur? why?

A

1-3 weeks ago because you can see macrophages and fibroblasts

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15
Q

****Was the appearance of the heart here most likely caused by an acute event or chronic?

• how do you know?

A

• Collateral Circulation development implies that this happened over an extended period of time

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16
Q

****What is seen here?

A

• Boxcar nucleus in top left corner of picture - indicative of hypertension (specifically pulmonary HTN in this pt)

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17
Q

What does ACUTE CORONARY SYNDROME refer to?

A

any of the three catastrophic manifestions of IHD

  • UNSTABLE ANGINA
  • ACUTE MI
  • SCD (sudden cardiac death)
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18
Q

****What is wrong with the appearance of this left ventricle? why has this happened?

A

• Left Atrium - Dilated due to HUGE HYPERTROPHIED ventricle (probably the result of HTN)

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19
Q

****When did this MI most likely occur?

A

• 1-2 days before death

• You can see contraction bands and neutrophils
• most nuclei are gone
• acute inflammation is kicking in

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20
Q

*****When did this MI occur?
• what intervention likely took place to stop it?
• histological features?

A
  • Day 1 after MI
  • Contraction Bands and Lack of Nuclei indicates Necrosis

• Contraction bands may have been caused by placement of a stent when the patient was hospitalized (or pt. may have naturally cleared clot)

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21
Q

****When did this myocardial infarction occur? why?

A

2-3 days ago

  • Extensive acute inflammatory infiltrate
  • Myocardial fibers are necrotic with no nuclei
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22
Q

What findings are you likely to see at at the GROSS and LIGHT MICROSCOPY level at the following time points following a heart attack?

  • 12 - 24 hours
  • 3 - 7 days
  • 7 - 10 days
A

12 - 24 hours
Gross: Dark Mottling
LM: Neurtophilic Infiltrate; Marginal contraction with BAND necrosis

3 - 7 days
Gross: Yellow tan Soft
LM: Macrophages

7 - 10 days
Gross: Yellow tan Soft
LM: Granulation Tissue

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23
Q

What is Ischemic Heart Disease?

• Most common cause?

A
  • consequence of reduced coronary blood flow
  • 90% of cases of Ischemic Heart Disease are due to ATHEROSCLEROTIC VASCULAR DISEASE
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24
Q

***What is the darker colored material in this artery?

A

Calcium

• Note: this plaque looks pretty stable with lipid core being completely surrounded by fibrous tissue

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25
Q

When did this MI probably occur? why?

A

Months ago - lots of Scar Tissue

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26
Q

• In what part of Coronary Arteries is Atherosclerosis most commonly seen? why?

A
  • Most commonly seen at the proximal end of the coronary vessels
  • This is the area where flow is the MOST TURBULENT
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27
Q

****What is the youngest this infarct can be?

A

**3 months at the youngest because of how extensive the collagen deposition is.

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28
Q

What two early interventions are very effective at minimizing damage caused by clogged coronary arteries?

• Risks associated?

A
  • Thrombolysis (alteplas) - may shoot microemboli to brain
  • Angioplasty - may cause reperfusion injury
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29
Q

What are two causes of sudden cardiac death?

A
  • **HUGE MI or
  • ARRYTHMIA (even w/o myocyte necrosis)**
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30
Q

**Ischemia

A

Lack of Blood Flow to Tissue

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31
Q

What gross changes in the heart would you see in a hypertensive patient?

A

• Ventricular Hypertrophy from Pressure Overload because myocytes must adapt to push against increased afterload

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32
Q

How long does it take myocardium to lose function in ischemic injury?

• What are some cellular changes that have occured?

A

Time:
• No perfusion for 1 minute leads to LOSS OF FUNCTION

Damage:
• Tissue damage at this point is likely reversible

• involves: myofibrillar relaxation, glycogen depletion, mitochondrial swelling

(note: glycogen depleted b/c of ineffecient glycolysis used for energy instead of ox-phos)

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33
Q

**Angina Pectoris Stable vs. Unstable

• Differentiate in Terms of Symptoms and Occlusion.

A

Stable Angina
• 70% of More occlusion
• chest pain on exertion

Unstable Angina
• 90% of More occlusion
• Occurs with less exertion or even while resting

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34
Q

*****What is seen here?

A

**Boxcar nuclei in the myocardium of a Hypertensive Patient (note: this can be due to pulmonary hypertension too)

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35
Q

What chemical markers are used for Myocardial Infarction?
• Times when they are the most useful?

A

Myoglobin - Peaks 1st ~4hrs and rapidly declines
• NOT SPECIFIC could be raised after excercise

CK-MB - Peaks ~10hrs and declines much more slowly
• More Specific

Troponin I - Peaks at around 1 day
• Very Specific - slow to rise but stays up for a long time

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36
Q

*****What is seen here?

A

• Myocardium of a Normal Adult

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37
Q

Contraction Bands
• what are they associated with?
• where are they typically seen?
• CAUSE?

A

Association:
• REPERFUSION, perioperative ischemia (during surgery), Sudden Cardiac Death

Where:
• Typically at margin of infarct in MI

CAUSE: ****
• HYPERCONTRACTION due to massive calcium influx

38
Q

**Mural Thrombus, que es?

A

Thrombus that forms on the wall of an organ (typically wall of atria or ventricles if they are not contracting properly and blood is becoming stagnant) - e.g. fibriallation

39
Q

T or F: ischemia even if not peristent may causes improper heart contraction and cause electrical instability.

A

TRUE - you may get rid of the thrombus but the heart still won’t work right

40
Q

***what has occured here?

A

Recent Infarct with stretching and thinning of myocardial wall

41
Q

What are the steps in athlerosclerotic plaque formation?

A
  • Endothelial Cell injury attracts Luekocytes
  • Macrophages come in with T-cell (secrete IFN-gammma)
  • MATRIX is produced over the athlerosclerotic LIPID CORE
  • METALLOPROTEINASES (secreted by macrophages) Destabilize Plaques
  • Plaque Rupture and THROMBOSIS
42
Q

***Would you suspect that this patient has chest pain?

• At Rest or on Exertion?

A

YES, this is ~90% occlusion so they probably have unstable angina and have pain even while at rest

43
Q

How can someone survive with a COMPLETE occlusion of their Left Antierior Descending (LAD) coranary artery?

A

• If this occlusion happened slow enough it is possible that collaterals developed between it and another coronary artery

44
Q

****What has occured here?

A

• Fibrinous Pericarditis

45
Q

****When did this person’s MI occur?
• what is likely the gross appearance?

A

Wavy Fibers = 1.5-4 hours

BUT we see some neurtophils (12-24 hr marker) and dissappearance of nuclei so it may actually be a bit older

***NO Changes in the gross appearance have occurred yet (these start at >12 hours)

46
Q

What cuases Chronic Ischemic Heart Disease with Congestive Heart Failure?

A
  • Progressive Cardiac Decompensation after an acute Myocardial Infarction
  • Small ischemic insults eventually causing failure
47
Q

When are you at the greatest risk of developing an aneurysm as a result of MI?

A

• mural infarcts may leave behind thinned/weakened scar tissue that may become an aneurysm

48
Q

****What has happened here?

A

• Myocardial Infarction - graying out of endocardium indicates that no blood is getting there = coagulative necrosis

49
Q
A
50
Q

****When did this injury likely occur? why?

A

1-3 weeks ago because you can see new blood vessel formation and debris from dead myocytes

51
Q

**Critical Stenosis

A
  • Classified as having 70% occlusion of the vessel lumen if - these people typically have stable angina
  • Greater than 90% occlusion people probably have unstable angina
52
Q

What are some complications of infarction?

A
  • Ventricular Muscle Rupture
  • Papillary Muscle Rupture
  • Aneurysm Formation
  • Mural Thrombus
  • Arrhythmia
  • Pericarditis
  • CHR
53
Q

At what point does irreversible myocardial damage occur?

A

• Severe ischemia lasting longer than ~20-40 minutes causes myocyte death and coagulative necrosis

54
Q

**Contraction Band

A

Caused by Reperfusion injury - result of EXCESS CALCIUM release in the cells

55
Q

What marker is most useful in measuring a re-infarct?

A

CK-MB, because Troponin will stay elevated but another spike in CK may indicate a patient has had a second infarction

56
Q

****When did this MI likely occur? why?

A

1-3 weeks ago because we see MACROPHAGES, Vessel formation, and debris from dead myocytes

57
Q

****What has occurred here?

A

Anterior wall Myocardial Rupture

58
Q

Someone occlusions of coronary vessels spontaneously resolve. How does this happen?

A

• Occlusions may clear by lysis or relaxation of spasm

59
Q

When is myocardial rupture most likely to occur? where?

A

Most likely 3-7 days post-infarction - being FEMALE and OVER 60 are some risk factors for this happening

*Most often occurs in anterior ventricular wall

*Results in Hemopericardium

****NOTE: this is not associated with aneurysm which occurs months after MI

60
Q

**Cardiac Tamponade

A

*During the first 3-7 days when the heart is most suscepitble, it may rupture and leak a TON of blood into the pericardium leading to compression of the heart and inability to beat (the latter process = TAMPONADE)

61
Q

**Arrhythmia

A

Can result from MI

62
Q

What is Cor Pulmonale?

A

• Right Ventricular Hypertrophy and Dilation due to Primary Disorders of the lung parenchyma or pulmonary vasculature

63
Q

T or F: myocytes actually die in myocardial infarction.

A

True

64
Q

Who are you most likely to see a myocardial infarction in?

• MOST COMMON CAUSE?

A
  • Males WHITE OR BLACK between 40 and 60
  • After Menopause they are common in women too
  • MOST myocardial infarctions are from ACUTE CORONARY THROMBOSIS
65
Q

****What is this called?

• when is likely to occur in association with an MI?

A

Hemopericardium - 3-7 days after an MI if the wall ruptures

66
Q

What are the other causes of Ischemic Heart Disease (aside from 90% of cases caused by athlerosclerosis)?

• Give Examples of Each of these Processes

A
  • Increased Demand - with increased HR or Hypertension
  • Diminished Blood Volume - seen in HYPOTENSION and shock (e.g. gunshot wound)
  • Diminished Oxygenation - due to pneumonia or CHF
  • Diminished O2 carrying capicity - Anemia or Lead Poisoning
67
Q

**Aneurysm

A
68
Q

****What has occurred here?

A

Papillary Muscle Rupture

69
Q

****When did this MI likely occur? why?

A

Months ago - EXTENSIVE collagen deposition has occurred, myocytes have NO nuclei

70
Q

**Congestive Heart Failure

A
71
Q

****What is seen here?

A
  • SEVERE athlerosclerosis of Aorta
  • Atheromatous Plaques have undergone ULCERATION
  • Ulceration has resulted in Overyling mural thrombus
72
Q

What is your most probable site of injury in occlusion of:

• Left Anterior Descending Coronary Artery

• Right Coronary Artery

• Left Circumflex Coronary Artery

A

LAD:

  • Antertior APEX of Left Ventricle
  • ANTERIOR 2/3 of intraventicular Septum

RCA:

  • Posterior Left Ventricle
  • Posterior 1/3 of Intraventricular Septum

LC:

• Lateral Left Ventricle

73
Q

When risks are associated with a ruptured myocardium?

A

• Hemopericardium which can lead to Tamponade

74
Q

What do arrhythmias put patients at a high risk of?

A

Arrhythmia puts you at a risk of MURAL THROMBOSIS

75
Q

What are some causes of chronic cor pulmonale?

A

Emphysema, COPD, Alpha-1-antitrypsin

76
Q

**Myocardial Infarct

A

Death of tissue in myocardium typically 20-40 minutes after arterial occlusion in the coronaries

77
Q

**Atherosclerotic Vascular Disease

• what Heart problems (beside heart attack) does this often lead to?

A

• Often leads to ischemic heart disease

78
Q

****What process has occurred here?

A

Athlerosclerotic Plaque Rupture - causes by exposure of the atherlosclerotic lipid core/collagen to clotting factors

79
Q

What happens in to the following during Angina?
• Blood Supply
• Sensation
• Myocytes

A

Ischemia is occuring, which is painful BUT does NOT cause MYOCYTES to die.

80
Q

What often causes acute cor pulmonale? What changes will the heart shwo?

A

Caused by EMBOLISM typically leads to right ventricular DILATION (not hypertrophy)

81
Q

What is a transmural infarct?

• What piece of tissue in that area remains perfused?

A
  • Transmural infarct = full thickness of the myocardium
  • Typically the Subendothelial area remains perfused because of exposure to blood within the heart
82
Q

What is the underlying process that causes most of ischemic heart disease?

A
  • Athlerosclerosis causes MOST IHD
  • Underlying cause of Athlerosclerosis = INFLAMMATION
83
Q

What microscopic appearance would you expect to see in the heart tissue of a hypertensive patient?

A
  • Increased Transverse Diameter
  • Nuclear enlargment with hyperchromasia = BOXCAR NUCLEI - this appearance comes from increased DNA production needed for cellular hypertrophy

• intracellular fibrosis

84
Q

What findings are you likely to see at at the GROSS, LIGHT MICROSCOPY, and EM level at the following time points following a heart attack?

  • 0 - 1.5 hours
  • 1.4 - 4 hours
  • 4 - 12 hours
A

0 - 1.5 hours
Gross - nothing
LM - nada
EM - Relaxation of Myofibrils; Glycogen Loss; Mitochondrial swelling

1.5 - 4 hours
Gross - none
LM - maybe Wavy Fibers
EM - Sarcolemmal Disruption; mitochondrial amorphous densities

4 - 12 hours
Gross - none
LM - Edemia and Hemorrhage, coagulative necrosis
EM - not important at this point

85
Q

**Reperfusion Injury

A

Caused by blood rushing back into tissue leading to PMN infiltration and ROS from O2, characterized by contraction lines

86
Q

**Hypertension

A

Causes increased afterload and boxcar nuclei that are hyperchomic due to increased DNA production to allow for ventricular hypertrophy (a compensatory mechanism to try to maintain SV)

87
Q

****What has occurred here?

A

Ventricular Septal Rupture

88
Q

***What is shown here?

A

Coronary Atherosclerosis complicated by Hemorrhage into the atheromatous Plaque

• This is more like an ulceration where an exposed area has been carved out by the metalloproteinases and you get bleeding of the plaque?

89
Q

**Thromboembolism

A

• Thombus that gets displaced and most likely will infarct another organ or area

90
Q

What sequence of events leads to thrombus formation after plaque rupture?

A
  • Atheromatous plaque is suddenly disrupted by intraplaque hemorrhage or mechanical forces => necrotic plaque tissue and collagen is exposed
  • Platelets adhere (via vWF Gp1b and Gp1a/11a) and release TXA2, ADP, and Serotonin => more aggregation and vasospasm
  • Tissue Factor initiates Coag. cascade
  • within MINUTES complete occlusion can occur
91
Q

When are you most likely to get the following after a Myocardial Infarction?

  • Pericardial Friction Rub
  • Aneurysm
  • Mural Thrombus
  • Autoimmune Pericarditis (Dressler syndrome)
  • Rupture of ventricular Wall/IV septum/Papillary m.
  • Arrythmia
A
  • Mural Thrombus - 1.5 - 4 hrs.
  • Arrythmia - within 12 hours
  • Pericardial Friction Rub - 2-3 days
  • Rupture of ventricular Wall/IV septum/Papillary - 3-6 days
  • Autoimmune Pericarditis (Dressler syndrome) - 1-8wks

• Aneurysm - months

Cardio - Gupta (12 decks)

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