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

Pathology of Heart Disease II and III Flashcards

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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
When did this MI probably occur? why?
Months ago - lots of Scar Tissue
26
• In what part of Coronary Arteries is Atherosclerosis most commonly seen? why?
* Most commonly seen at the proximal end of the coronary vessels * This is the area where flow is the **MOST TURBULENT**
27
\*\*\*\*What is the youngest this infarct can be?
\*\*3 months at the youngest because of how extensive the collagen deposition is.
28
What two early interventions are very effective at minimizing damage caused by clogged coronary arteries? • Risks associated?
* Thrombolysis (alteplas) - may shoot microemboli to brain * Angioplasty - may cause reperfusion injury
29
What are two causes of sudden cardiac death?
* **HUGE MI or * ARRYTHMIA (even w/o myocyte necrosis)**
30
\*\*Ischemia
Lack of Blood Flow to Tissue
31
What gross changes in the heart would you see in a hypertensive patient?
• **Ventricular Hypertrophy** from **Pressure Overload** because myocytes must adapt to push against increased afterload
32
How long does it take myocardium to lose function in ischemic injury? • What are some cellular changes that have occured?
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)
33
\*\*Angina Pectoris Stable vs. Unstable • Differentiate in Terms of Symptoms and Occlusion.
**Stable Angina** • **70%** of More occlusion • **chest pain on exertion** **Unstable Angina** • **90%** of More occlusion • Occurs with **less exertion** or even **while resting**
34
\*\*\*\*\*What is seen here?
\*\*Boxcar nuclei in the myocardium of a Hypertensive Patient (note: this can be due to pulmonary hypertension too)
35
What chemical markers are used for Myocardial Infarction? • Times when they are the most useful?
**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
36
\*\*\*\*\*What is seen here?
• Myocardium of a Normal Adult
37
**Contraction Bands** • what are they associated with? • where are they typically seen? **• CAUSE?**
**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
\*\*Mural Thrombus, que es?
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
T or F: **ischemia even if not peristent may causes improper heart contraction and cause electrical instability.**
TRUE - you may get rid of the thrombus but the heart still won't work right
40
\*\*\*what has occured here?
Recent Infarct with stretching and thinning of myocardial wall
41
What are the steps in athlerosclerotic plaque formation?
* 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
\*\*\*Would you suspect that this patient has chest pain? • At Rest or on Exertion?
YES, this is ~90% occlusion so they probably have unstable angina and have pain even while at rest
43
How can someone survive with a COMPLETE occlusion of their Left Antierior Descending (LAD) coranary artery?
• If this occlusion happened slow enough it is possible that **collaterals** developed between it and another coronary artery
44
\*\*\*\*What has occured here?
• Fibrinous Pericarditis
45
\*\*\*\*When did this person's MI occur? • what is likely the gross appearance?
**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
What cuases Chronic Ischemic Heart Disease with Congestive Heart Failure?
* Progressive **Cardiac Decompensation** after an **acute Myocardial Infarction** * **Small ischemic insults** eventually causing failure
47
When are you at the greatest risk of developing an aneurysm as a result of MI?
• **mural infarcts** may leave behind thinned/weakened scar tissue that may become an **aneurysm**
48
\*\*\*\*What has happened here?
• Myocardial Infarction - graying out of endocardium indicates that no blood is getting there = coagulative necrosis
49
50
\*\*\*\*When did this injury likely occur? why?
1-3 weeks ago because you can see **new blood vessel formation and debris from dead myocytes**
51
\*\*Critical Stenosis
* 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
What are some complications of infarction?
* Ventricular Muscle Rupture * Papillary Muscle Rupture * Aneurysm Formation * Mural Thrombus * Arrhythmia * Pericarditis * CHR
53
At what point does irreversible myocardial damage occur?
• Severe ischemia lasting **longer than ~20**-40 **minutes** causes myocyte death and coagulative necrosis
54
\*\*Contraction Band
Caused by Reperfusion injury - result of EXCESS CALCIUM release in the cells
55
What marker is most useful in measuring a re-infarct?
CK-MB, because Troponin will stay elevated but another spike in CK may indicate a patient has had a second infarction
56
\*\*\*\*When did this MI likely occur? why?
1-3 weeks ago because we see **MACROPHAGES, Vessel formation, and debris from dead myocytes**
57
\*\*\*\*What has occurred here?
Anterior wall Myocardial Rupture
58
Someone occlusions of coronary vessels spontaneously resolve. How does this happen?
• Occlusions may clear by **lysis** or **relaxation of spasm**
59
When is myocardial **rupture** most likely to occur? where?
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
\*\*Cardiac Tamponade
\*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
\*\*Arrhythmia
Can result from MI
62
What is Cor Pulmonale?
• **Right Ventricular Hypertrophy** and **Dilation** due to **Primary Disorders** of the **lung** parenchyma or pulmonary vasculature
63
T or F: myocytes actually die in myocardial infarction.
True
64
Who are you most likely to see a myocardial infarction in? • MOST COMMON CAUSE?
* 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
\*\*\*\*What is this called? • when is likely to occur in association with an MI?
Hemopericardium - 3-7 days after an MI if the wall ruptures
66
What are the other causes of Ischemic Heart Disease (aside from 90% of cases caused by athlerosclerosis)? • Give Examples of Each of these Processes
* **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
\*\*Aneurysm
68
\*\*\*\*What has occurred here?
Papillary Muscle Rupture
69
\*\*\*\*When did this MI likely occur? why?
Months ago - **EXTENSIVE collagen deposition** has occurred, myocytes have NO nuclei
70
\*\*Congestive Heart Failure
71
\*\*\*\*What is seen here?
* **SEVERE athlerosclerosis of Aorta** * Atheromatous Plaques have undergone **ULCERATION** * Ulceration has resulted in Overyling **mural** **thrombus**
72
What is your most probable site of injury in occlusion of: ## Footnote **• Left Anterior Descending Coronary Artery** **• Right Coronary Artery** **• Left Circumflex Coronary Artery**
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
When risks are associated with a ruptured myocardium?
• **Hemopericardium** which can lead to **Tamponade**
74
What do arrhythmias put patients at a high risk of?
Arrhythmia puts you at a risk of MURAL THROMBOSIS
75
What are some causes of **chronic cor pulmonale**?
Emphysema, COPD, Alpha-1-antitrypsin
76
\*\*Myocardial Infarct
Death of tissue in myocardium typically 20-40 minutes after arterial occlusion in the coronaries
77
\*\*Atherosclerotic Vascular Disease • what Heart problems (beside heart attack) does this often lead to?
• Often leads to **ischemic heart disease**
78
\*\*\*\*What process has occurred here?
Athlerosclerotic Plaque Rupture - causes by exposure of the atherlosclerotic lipid core/collagen to clotting factors
79
What happens in to the following during Angina? • Blood Supply • Sensation • Myocytes
**Ischemia** is occuring, which is **painful** BUT **does NOT cause MYOCYTES to die.**
80
What often causes **acute cor pulmonale**? What changes will the heart shwo?
**Caused by EMBOLISM** typically leads to **right ventricular DILATION** (not hypertrophy)
81
What is a transmural infarct? • What piece of tissue in that area remains perfused?
* Transmural infarct = full thickness of the myocardium * Typically the Subendothelial area remains perfused because of exposure to blood within the heart
82
What is the underlying process that causes most of ischemic heart disease?
* Athlerosclerosis causes MOST IHD * Underlying cause of Athlerosclerosis = **INFLAMMATION**
83
What **microscopic appearance** would you expect to see in the heart tissue of a **hypertensive patient**?
* Increased Transverse Diameter * Nuclear enlargment with hyperchromasia = **BOXCAR NUCLEI - this appearance comes from increased DNA production needed for cellular hypertrophy** **•** intracellular fibrosis
84
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
**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
\*\*Reperfusion Injury
Caused by blood rushing back into tissue leading to PMN infiltration and ROS from O2, characterized by contraction lines
86
\*\*Hypertension
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
\*\*\*\*What has occurred here?
Ventricular Septal Rupture
88
\*\*\*What is shown here?
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
\*\*Thromboembolism
• Thombus that gets displaced and most likely will infarct another organ or area
90
What sequence of events leads to thrombus formation after plaque rupture?
* 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
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
* 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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