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3.2a CVS Pathology 1 Flashcards

0
Q

This can help predict if there is cardiomegaly or atrophy

A

Weight of the heart

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1
Q

Normal weight of the heart for males and females

A

Female: 250-300 gm
Male: 300-350 gm

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2
Q

Normal thickness of the free wall do the heart for RV and LV

A

RV: 0.3-0.5 cm
LV: 1.3-1.5 cm

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3
Q

This is important in recognizing hypertrophy and dilatation

A

Thickness of the free wall

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4
Q

This can mean the ff:

  1. Increase in organ size
  2. Greater heart weight
  3. Greater ventricular thickness
A

Hypertrophy

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5
Q

This mean refers to an enlarged chamber size accompanied by thinning of the left ventricle

A

Dilatation

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6
Q

This refers to an increase in cardiac weight or size (owing to hypertrophy or dilatation)

A

Cardiomegaly

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7
Q

Enumerate the layers of the heart (4)

A
  1. Endocardium
  2. Myocardium
  3. Pericardium
  4. Epicardium
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8
Q

Which layer of the heart is being described?

  1. Lines the chambers and valves
  2. Cardiac conduction system can be found here
A

Epicardium

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9
Q

It is a collection of specialized striate muscle cells

A

Cardiac myocytes

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10
Q

It is the functional intracellular contractile unit of cardiac muscle

A

Sarcomere

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11
Q

What are the regulatory proteins of the sarcomere? (2)

A
  1. Troponin

2. Tropomyosin

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12
Q

What is the importance of regulatory proteins (Troponin, tropomyosin)?

A

Important diagnostically: they are released to indicate myocardial injury

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13
Q
  1. It is the sac that encloses the heart

2. The outermost layer of the heart

A

Pericardium

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14
Q

It is the visceral pericardium

A

Epicardium

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15
Q

What area the specialized excitatory and conducting myocytes? (4)

A
  1. SA node
  2. AV node
  3. Bundle of His
  4. Right and left bundle branches
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16
Q

Cardiac myocytes relies almost entirely on this process for its energy needs

A

Ox phos

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17
Q

Differentiat epicardial coronary arteries from intramural arteries

A

Epicardial: run along external surface of the heart
Intramural: penetrate myocardium

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18
Q

What are the major epicardial coronary arteries? (3)

A
  1. Left anterior descending a. (LAD)
  2. Left circumflex a. (LCX)
  3. Right coronary artery
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19
Q

What does the LAD supply? (3)

A
  1. Anterior wall
  2. Anterior 2/3 of septum
  3. Entire apex

Circumferentially

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20
Q

What does LCX supply? (1)

A

Left posterolateral aspect of the heart

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21
Q

What does the right coronary artery supply? (2)

A
  1. Posterior 1/3 of septum

2. Inferior and posterior wall of the heart

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22
Q

These maintain unidirectional flow of blood through the heart

A

Cardiac valves

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23
Q

The function of _____ depends on the mobility, pliability, structural integrity of the leaflets (tricuspid, mitral) or cusps (aortic, pulmonic)

A

Heart valves

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24
Q

What are semilunar valves? (2)

A
  1. Aortic

2. Pulmonary

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25
Q

What are the atrioventricular valves? (2)

A
  1. Mitral

2. Tricuspid

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26
Q

These valves depend on the integrity and coordination of movement of the cuspal attachment

A

Semilunar valves (aortic, pulmonic)

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27
Q

These valves depend on:

  1. Leaflets and their attachments
  2. Tendinous connections to papillary muscle of ventricular wall
A

Atrioventricular valves (mitral, tricuspid)

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28
Q

What can cause regurgitation in the semilunar valves? (1)

A

Dilatation of aortic root

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29
Q

What can causes regurgitation in atrioventricular valves? (3)

A
  1. Left ventricular dilatation
  2. Ruptured tendon
  3. Papillary muscle dysfunction
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30
Q

What are the (3) pathological changes of valves?

A
  1. Damage to collagen (weakens leaflets; ie. mitral valve prolapse)
  2. Nodular calcification (ie. calcific aortic stenosis)
  3. Fibrotic thickening (ie. RHD)
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31
Q

Which cardiac pathology is being described:
1. Results from impaired cardiac function that renders heart muscle unable to maintain an output sufficient for the metabolic requirements of tissues and organs

  1. It is the final common pathway of many heart diseases
  2. Most often develop due to cumulative effects of chronic work overload or ischemic heart disease
A

CHF

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32
Q

Simply, it is defined as a state that develops when the heart fails to maintain adequate cardiac output to meet the demand of the body

A

CHF

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33
Q

Normal CO = ?

A

4200 mL/min

4-8 L/min

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34
Q

It is the volume of blood ejected

A

Cardiac output

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35
Q

Heart failure is characterized by? (3)

A
  1. Forward failure: diminished CO
  2. Backward failure: damming of blood in venous system
  3. Both
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36
Q

Compensatory mechanisms in CHF (3)

A
  1. Frank-Starling mechanism
  2. Myocardial hypertrophy
  3. Activation of neuronumoral systems
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37
Q

In this compensatory mechanism:
Greater volume of blood entering the heart during diastole (end diastolic volume) = greater volume of blood ejected during systole (stroke volume)

A

Frank-Starling mechanism

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38
Q

Compensatory mechanism:

  1. With or without cardiac chamber dilatation
  2. LVH –> increased contractility
  3. Left ventricular “remodeling” –> increased stroke volume
A

Myocardial hypertrophy

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39
Q

What happens in left ventricular remodeling? (3)

A
  1. Deposition of new sarcomeres
  2. Increased length and width of muscle fibers
  3. Increased weight of heart
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40
Q

It is an important indication of heart failure

A

Left ventricular remodeling

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41
Q

It is a compensatory response of the myocardium to increased mechanical work.

A

Myocardial hypertrophy
-the pattern of hypertrophy reflects the nature of the stimulus:

  1. In aortic or mitral valve regurgitation = volume overload
  2. In systemic HPN or aortic stenosis = pressure overload
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42
Q

Characterized by:

  1. Dilation with increased ventricular diameter
  2. Muscle mass and wall thickness (not necessarily be increased; may be normal or less than normal) are increased in proportion to diameter of chamber
  3. Deposition of sarcomeres (cell length and width area increased)
A

Volume overload

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43
Q

Characterized by:

  1. Concentric hypertrophy of LV
  2. Reduced cavity diameter
  3. Predominant deposition of sarcomeres is parallel to long axes of cells (cross-sectional area of myocytes is expanded but cell length is not)
A

Pressure overload

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44
Q

Increased mass + normal wall thickness

A

Volume overload

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45
Q

Increased mass + thickened left ventricular wall

A

Pressure overload

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46
Q

What are the neuro hormonal systems activated in CHF (3)

A
  1. NE/Epi
  2. RAAS activation
  3. Atrial natriuretic peptide release
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47
Q

Effects of NE/Epi (compensatory mechanism of CHF) (3)

A

Increased:

  1. HR
  2. Contraction
  3. Vascular resistance
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48
Q

Effects of RAAS activation (compensatory mechanism of CHF)

A

In chronological order: increased

  1. Tubular reabsorption of sodium and water
  2. Blood volume
  3. Venous return
  4. Preload
  5. Force of contraction

–> augments CO

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49
Q

Effects of atrial natriuretic peptide release (compensatory mechanism of CHF)

A

Increased tubular reabsorption of sodium and water

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50
Q

Basis for myocardial contractile failure (4)

A
  1. Death of myocytes, loss of vital elements
  2. Overworked and fatigued cardiac muscles
  3. Altered gene expression (due to prolonged hemodynamics overload)
  4. Re-expression of protein synthesis analogous to that in fetal cardiac development
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51
Q

What are huge early mediators of hypertrophy? (4)

A
  1. c-fos
  2. c-myc
  3. c-jun
  4. EGR1
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52
Q

Describe pathologic hypertrophy (4)

A
  1. Increased protein synthesis
  2. Induction of fetal gene program
  3. Synthesis of abnormal contractile protein isoforms that reduce excitation-coupling
  4. Fibrosis, reduced vasculature
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53
Q

Cardiac dysfunction is characterized by (3)

A
  1. Heart failure
  2. Arrhythmias
  3. Neurohumoral stimulation
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54
Q

What are the FUNCTIONAL modifications that follow neurohumoral stimulation in heart failure (4)

A
  1. Increased inotropy
  2. Increased HR
  3. Vasoconstriction
  4. Salt and water retention
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55
Q

What are the STRUCTURAL modifications that follow neurohumoral stimulation in heart failure (3)

A
  1. Hypertrophy
  2. Increased nonmuscular tissue
  3. Increased expression of adult cardiac genes
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56
Q

Mechanisms of Cardiac Dysfunction (5)

A
  1. Pump failure
  2. Obstruction to flow
  3. Regurgitant flow
  4. Disorders of cardiac conduction
  5. Shunt anomalies (Disruption of normal circulatory continuity)
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57
Q

Pump failure is exemplified by?

A

Acute MI

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58
Q

Obstruction to flow is exemplified by?

A

Aortic valve stenosis

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59
Q

Regurgitant flow is exemplified by?

A

Aortic regurgitation

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60
Q

Disorders of cardiac conduction is exemplified by?

A

Arrhythmias

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61
Q

Shunt anomalies are exemplified by? (2)

A

Infarct

Ischemia

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62
Q

In this mechanism of a cardiac dysfunction:

(+) necrosis/death of heart muscle –> cannot pump blood/failure to contract –> affect stroke volume

A

Pump blood

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63
Q

In this mechanism of a cardiac dysfunction:

  1. Aortic valve is calcified and stenosic, (+) LV Outflow
  2. Size and aperture of aortic valve is significantly reduced –> reduced blood flow
A

Obstruction to flow

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64
Q

In this mechanism of a cardiac dysfunction:

  1. There is increased back flow of blood into LV chamber –> greater volume of blood retaine in LV chamber
  2. Problem is volume overload
  3. It is seen in valvular dilatation or insufficiency
A

Regurgitant flow

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65
Q

In this mechanism of a cardiac dysfunction:
1. (+) opening between ventricular chambers –> free communication between chambers –> disruption of normal circulatory function –> CHF

A

Disruption of normal circulatory continuity/Shunt Anomalies

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66
Q

Etiology of CHF (8)

A
  1. Myocardial dysfunction
  2. Ventricular overload
  3. Restrictive disease
  4. Electrical disorders
  5. Iatrogenic
  6. Conduction system failure
  7. Valvular failure
  8. Cardiac malformations
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67
Q

What is the most common final pathway of many cardiac diseases?

A

CHF

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68
Q

What is the mechanism behind myocardial dysfunction?

A

Direct impairment of myocardial contractility

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69
Q

What is the mechanism behind ventricular overload?

A

Excessive pressure or volume, or high output states

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70
Q

What is the mechanism behind restrictive disease?

A

Reduced myocardial expansion

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71
Q

What is the mechanism behind electrical disorders?

A

Disrupted electrical function

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72
Q

What is the mechanism behind conduction system failure?

A

Electrical conduction dysfunction

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73
Q

What is the mechanism behind valvular failure? (3)

A

Inflammation
Degenerative
Congenital

74
Q

What is the mechanism behind cardiac malformations?

A

Congenital

75
Q

The ff are examples of which etiology of CHF?

  1. Ischemic heart disease
  2. Dilated cardiomyopathy
A

Myocardial dysfunction

76
Q 
The ff are examples of which etiology of CHF?
(Pressure)
1. HPN
2. Aortic stenosis
3. Pulmonary embolism
4. Cor pulmonale

(Volume)

  1. Aortic regurgitation
  2. Mitral regurgitation

(High output states)

  1. Pregnancy
  2. Anemia
  3. Thyrotoxicosis
A

Ventricular overload

77
Q 
The ff are examples of which etiology of CHF?
(Myocardial)
1. Restrictive/Ischemic cardiomyopathy 
2. Amyloidosis
3. Myocarditis

(Pericardial)

  1. Pericarditis
  2. Tamponade
A

Restrictive disease

78
Q

The ff are examples of which etiology of CHF?

  1. Pathological tachycardia
  2. Heart block
A

Electrical disorders

79
Q

The ff are examples of which etiology of CHF?
1. Radiation

(Drugs)

  1. Doxyrubucin
  2. Cocaine
A

Iatrogenic

80
Q

The ff are examples of which etiology of CHF?

  1. Acute MI
  2. Arrhythmia
A

Conduction system failure

81
Q

The ff are examples of which etiology of CHF?

  1. Endocarditis
  2. RHD
  3. Calcific aortic stenosis
  4. Pulmonary stenosis
  5. Tricuspid atresia
A

Valvular failure

82
Q

The ff are examples of which etiology of CHF?

  1. VSD
  2. ASD
  3. PDA
  4. TOF
  5. Coarctation of aorta
A

Cardiac malformations

83
Q

What are the most frequent clinical conditions associated with CHF? (2)

A
  1. MI

2. Valvular disease

84
Q

Types of CHF is categorized as to what? (3)

A
  1. Systolic or diastolic dysfunction
  2. Anatomic location
  3. High output failure or low output failure
85
Q

What is the main pathology in systolic dysfunction?

A

Problem during contraction

86
Q

The ff are examples of which type of CHF?

  1. IHD
  2. Hypertensive Heart Disease (HHD)
  3. Dilated Cardiomyopathy (D-CMP)
A

Systolic dysfunction

87
Q

Most systolic dysfunction affects which chamber of the heart?

A

Left ventricle

88
Q

It is the most common cause of heart failure

A

Systolic dysfunction

89
Q

This type of CHF produces a forward type of failure

A

Systolic dysfunction

90
Q

This type has the s/sx of pulmonary congestion and edema

Explanation:

  1. Blood dammed into lungs d/t love force of contraction –> pulmonary edema and congestion
  2. Blood tends to be dammed into left ventricle –> volume overload reflected in left atrium and pulmonary vasculature
A

Systolic dysfunction

91
Q

What is the Pathophysiology of systolic dysfunction?

A

Progressive degeneration of myocardial contractile function

92
Q

Main pathology in diastolic dysfunction

A

Inability of heart muscle to relax/reduced ventricular compliance

Explanation:
Blood volume contributes to preload, which enhances myocardial contractility. Since heart ms cannot relax, heart becomes stiff thereby decreasing preload –> affects:
1. Ejection fraction
2. CO (relatively preserved at rest but LV is stiff so heart is unable to increase its output in response to metabolic demands of peripheral tissues)
3. SV

93
Q

This type of CHF is seen in:

  1. Massive LVH
  2. Amyloidosis
  3. Constrictive pericarditis
  4. Myocardial fibrosis
A

Diastolic dysfunction

Explanation:
Heart is stiff + reduced diameter –> reduced. Look volume in ventricular cavity

94
Q

Which organ is immediately affected in left sided heart failure due to its proximity?

A

Lungs

Explanation:
Because LV a cannot expand, any increase in filling pressure is immediately referred back to pulmonary circulation –> rapid onset of pulmonary edema (“flash pulmonary edema”)

95
Q

Aside from the lungs, left sided heart failure affects (2) other organs

A
  1. Kidneys (reduced renal blood flow)
    Explanation: decreased CO –> reduced renal perfusion –> activation of RAAS –> induces salt and water retention! expansion of interstitial and intra vascular fluid volumes (increased blood volume, edema)
  2. Brain (hypoxic encephalopathy)
    This can progress to stupor and coma
96
Q

Clinical features of left sided heart failure (5)

A
  1. Pulmonary symptoms (dyspnea, blood tinged sputum, elevated pulmonary wedge pressure, rales, cough)
  2. Increased HR, cardiomegaly
  3. Cyanosis
  4. Hypoxic encephalopathy
  5. Edema
97
Q

This type of CHF is characterized by RV hypertrophy/dilatation with associated RA dilatation

A

Right sided heart failure

98
Q

What are the causes right sided heart failure? (5)

A
  1. Pulmonary embolism
  2. Intrinsic lung disease (COPD, cystic fibrosis)
  3. Kyphoscoliosis
  4. Pneumoconiosis
  5. Schistosomiasis
99
Q

Mechanism behind right sided heart failure

A

Increased pulmonary vascular resistance (d/t increased pulmonary vascular resistance and/or hypoxic vascular response)

100
Q

What is the classical feature of right sided heart failure?

A

Nutmeg liver (due to chronic passive congestion)

101
Q

The ff morphological characteristics can be seen in which type of CHF?

  1. Congestive hepatomegaly, centrilobular necrosis, sclerosis, NUTMEG LIVER
  2. Congestive splenomegaly
  3. Right ventricular dilatation/hypertrophy
  4. Congestion (kidneys)
  5. Hypoxic encephalopathy
A

Right sided heart failure

102
Q

The ff are clinical features of which type of CHF?

  1. Splanchnic congestion (hepatosplenomegaly)
  2. Increased hepatojugular reflex or jugular venous distention (d/t increased pressure in RV and RA)
  3. Dependent edema (d/t increased venous hydrostatic pressure)
  4. Transudative effusions (ascitis, pleural effusion)
  5. Cyanosis
A

Right sided heart failure

103
Q

Type of CHF:

  1. Heart failure secondary to pumping excessive volume of blood
  2. Causes anemia, hyperthyroidism, high fever, shunts between an artery and a vein
A

High output failure

104
Q

Type of CHF:

  1. Secondary to ischemic heart disease, HPN, dilated cardiomyopathy, vulvar/pericardial disease
  2. The more common type of heart failure
A

Low output heart failure

105
Q

A group of related heart disorders resulting from an imbalance between the blood supply to the heart (perfusion) and it’s demand for oxygen –> myocardial ischemia

106
Q
  1. This brings about an insufficiency of oxygen

2. Reduces the availability of nutrients and removal of metabolites

107
Q

(4) syndromes of IHD

A
  1. Acute myocardial infarction
  2. Angina pectoris
  3. Chronic IHD with heart failure
  4. Sudden cardiac death
108
Q

IHD is also known as (2)

A
  1. CAD

2. CHD

109
Q

This condition is the most important form of IHD wherein ischemia causes the death of heart muscle

A

Acute myocardial infarction

110
Q

In this condition, ischemia is of insufficient severity to cause infarction but may be a precursor of MI

A

Angina pectoris

111
Q

The central unifying problem of the 4 syndromes of IHD

A

Reduction/insufficient coronary blood flow

112
Q

Non-modifiable risk factors in IHD (3)

A
  1. Age
  2. Gender (males > females)
  3. Familial disposition
113
Q

Modifiable risk factors in IHD (4)

A
  1. Diet/Hyperlipidemia
    Lipids deposited in coronary arteries
  2. HPN
    Associated with LVH
  3. DM
    Alteration in lipids, carbs, Peripheral vascular disease, Hyperlipidemia
  4. Cigarette smoking
    Carcinogenic; byproducts toxic to endothelium which could lead to development of atheroma or thrombus
114
Q

Folic acid and other B vitamins break down what?

A

Homocysteine:

Increased levels may promote atherosclerosis by damaging inner lining of arteries and promoting blood clots

115
Q

Inflammatory mediators in IHD (3) that cause endothelial injury

A

Increased

  1. C-reactive protein
  2. Ferritin
  3. Leukocyte count
116
Q

Thrombotic mediators in IHD (2) that increase risk for thrombus formation

A
  1. Increased fibrinogen

2. Inherited polymorphism

117
Q

Other lipids that are risk factors in IHD (2) (abnormal lipid metabolism)

A
  1. Genetic variation in Lipoprotein (LPA) gene region

2. ApoE polymorphism

118
Q

A risk factor in IHD that inhibits LDL oxidation

A

Antioxidants

119
Q

A risk factor in IHD that is a drug with antioxidant properties

A

Resveratrol

120
Q

Pathogenesis of IHD

A

Decreased/Insufficient coronary perfusion relative to myocardial demand

121
Q

In the Pathogenesis of IHD, there is decreased/Insufficient coronary perfusion relative to myocardial demand due to (4)

A
  1. Fixed stenosing atherosclerosis
  2. Fissure, break, rupture, ulceration, hemorrhage
  3. Coronary artery thrombosis
  4. Coronary artery vasoconstriction/vasospasm
122
Q

What is the critical level of stenosis in fixed stenosing atherosclerosis?

A

70% - at this fixed level of obstruction, compensatory coronary artery vasodilation is insufficient to my moderate increases in myocardial oxygen demand leading to ischemia

123
Q

What is Fixed Coronary Atherosclerosis?

A

Coronary artery with stable atheroma, no acute plaque change

124
Q

It is the underlying cause of angina pectoris

A

Fixed Coronary Atherosclerosis

125
Q

Most involved vessels in Fixed Coronary Atherosclerosis (3)

A
  1. LAD
  2. LCX
  3. RCS
126
Q

Acute plaque change is associated with acute coronary syndromes (3)

A
  1. Unstable angina
  2. Acute MI
  3. Sudden cardiac death
127
Q

What follows acute plaque change in IHD?

A

Thrombosis leading to complete obstruction

128
Q

Occlusive thrombus is associated with?

A

Acute transmural myocardial infarction

129
Q

Partial occlusive thrombus is subendocardial infarction is associated with? (2)

A
  1. Unstable angina

2. Sudden cardiac death

130
Q

Non-atheromatous coronary arterial occlusive happen in <10% of cases (6)

A
  1. Embolism
  2. Dissecting aneurysm
  3. Vasospasm
  4. Congenital anomaly
  5. Trauma
131
Q

Inflammation causes coronary obstruction (minority of cases wherein preexisting coronary artery vasculitis causes IHD), what is the initial lesion?

A

Interaction between endothelial cells and circulating leukocytes

132
Q

What is the role of vasoconstriciton in IHD?

A

Reduction in lumen size –> increase in local mechanical forces —> increase risk of plaque rupture

133
Q
  1. Paroxysmal, recurrent substernal/precordial chest pains

2. Caused by transient (15s-15min) myocardial ischemia that falls short in inducing an infarction

A

Angina pectoris

134
Q

It is increased myocardial demand and decreased myocardial perfusion secondary to:

  1. Chronic stenosing coronary atherosclerosis
  2. Disrupted atherosclerotic plaque
  3. Vasospasm
  4. Thrombosis
  5. Coronary artery embolism
A

Angina pectoris

135
Q

What are the (3) types of angina pectoris?

A
  1. Stable/Typical AP
  2. Prinzmetal/Variant AP
  3. Unstable/Crescendo AP
136
Q
  1. Most common form of AP
  2. Caused by reduction of perfusion (in chronic stenosing coronary artery atherosclerosis)
  3. Transient, precipitated by exertion or emotion
  4. Relieved by rest and vasodilators
A

Stable/Typical AP

137
Q

Type of AP with:

  1. Uncommon pattern of episodic angina occurring at rest (unrelated to activity, HR, BP)
  2. Caused by coronary VASOSPASM
  3. ECG changes suggestive of transmural ischemia (ST segment elevation)
  4. Responded promptly to vasodilators (nitroglycerin) and CCB
A

Prinzmetal/Variant AP

138
Q

Type of AP:

  1. Occurs in 90% vessel block
  2. Caused by disruption of atherosclerotic plaque with superimposed partial/mural thrombosis, embolization, vasospasm
  3. Often occurs at rest
  4. Precursor to subsequent acute MI (hence called pre-infarction/Q-wave angina)
A

Unstable/Crescendo AP

139
Q

This type of AP has a localized area of cardiac muscle necrosis due to ischemia

140
Q 
The ff are risk factors of which syndrome of IHD?
(Major)
1. HPN
2. Cigarette smoking
3. DM
4. Hyperlipidemia

(Minor)

  1. Obesity
  2. Sex
  3. Age
  4. Stress
  5. Physical activity
141
Q

Pathogenesis of acute MI (6)

A
  1. Coronary artery occlusion
  2. Increased myocardial demand (hypertrophy, tachycardia)
  3. Hemodynamic compromise (Hypotension)
  4. Vasospasm
  5. Emboli
  6. Unexplained (vasculitis, hematologist abnormalities, cardiac surgery)
142
Q

Sequence of coronary artery thrombosis (4)

A
  1. Disruption of atheromatous plaque
  2. Subendothelial collagen exposed
  3. Extrinsic coagulation pathway activation
  4. Occlusive thrombus forms
143
Q

Biochemical changes in AMI (3)

A
  1. Anaerobic glycolysis
    (aerobic mechanisms cease in ischemia)
  2. Decreased in high energy phosphates
    (ATP, creatinine phosphates)
  3. Lactic acidosis
    (accumulation of break down products)
144
Q

Reversible ultrastructural changes in AMI (4)

A
  1. Mitochondrial swelling
  2. Myofibrillar relaxation
  3. Glycogen depletion
  4. Sarcolemmal membrane damage
145
Q

The predominant mechanism in myocardial function damage (1)

A

Coagulation necrosis

146
Q

Region first affected by myocardial function damage

A

Subendocardial region with wavefront progression –> transmural (wall) thickness of ischemic zone

147
Q

Pathologic forms of AMI (2)

A
  1. Transmural infarction

2. Subendocardial infarction

148
Q

Type of AMI:

  1. Its necrosis involves full/nearly full thickness of the myocardium
  2. Aka ST elevation infarcts
  3. It’s associated with: chronic atherosclerotic obstruction, acute opaque change, superimposed complete thrombosis
  4. Heart appears dark and mottled in its early stages
A

Transmural infarction

149
Q

Type of AMI:

  1. Necrosis is limited to inner 1/3 or 1/2 of ventricle
  2. Aka Non-ST elevation infarct
  3. Associated with: diffuse stenosing coronary artery atherosclerosis WITHOUT thrombosis and acute plaque change, partially obstructing coronary artery
A

Subendocardial infarction

150
Q

What stain is suede for early recognition of AMI?

A

Triphenyl tetra-zolium chloride

  1. Normal: stains magenta red
  2. Infarcted: unstained/pale area
151
Q

What is the hallmark of AMI (gross)?

A

Coagulation necrosis of myocardium

152
Q

Gross features of AMI that happen in the indicated time:

  1. 30mins aft infarct
  2. 4-12hours after
  3. 18-24hours after
  4. 6weeks after
A
  1. No manifestation at gross level
  2. Gross changes are evident
  3. Pale to cyanotic
  4. Pale, fibrous scar
153
Q

Microscopic features of AMI in the indicated times:

  1. Within 1 hour
  2. At 12-17 hours
  3. 3-7 days
  4. 7-10 days
A
  1. Intracellular edema, wavy fibers at periphery
  2. Neutrophilic infiltration, myocyte coagulation necrosis, dead myocytes are hypereosinophilic with loss of nuclei
  3. Disintegration of dead myofibers
  4. Fibrous scar
154
Q

Factors affecting severity of AMI (6)

A
  1. Location
  2. Severity of obstruction
  3. Rate of development of occlusion
  4. Duration of occlusion
  5. Extent of collateral vessels
  6. Metabolic demands of myocardium
155
Q

Sequence of changes in AMI (gross, prominent findings) (5)

A
  1. No gross change
  2. Vague pallor, softening
  3. Yellow pallor
  4. Central pallor with red border
  5. White firm scar
156
Q

Sequence of changes in AMI (microscopic, prominent findings) (5)

A
  1. Waxy myocyte fibers
  2. Coagulation necrosis
  3. Neutrophilic infiltrate, then macrophages
  4. Granulation tissue
  5. Fibrotic scar
157
Q

Gross features of AMI 1-10 days post infarct:

  1. Day 1-3
  2. Day 3-7
  3. Day 7-10
A
  1. Day 1-3: mottling with yellow-tan infarct center
  2. Day 3-7: hyperemic border, central yellow-tan softening
  3. Day 7-10: maximally yellow-tan and soft, depressed
    red-tan margins
158
Q

Light microscopic features of AMI 1-10 days post infarct:

  1. Day 1-3
  2. Day 3-7
  3. Day 7-10
A
  1. Day 1-3: coagulation necrosis, loss of nuclei and striations, interstitial neutrophilic infiltrates
  2. Day 3-7: start of disintegration of dead myofibers, dying neutrophils, early phagocytosis of dead cells by macrophages at infarct border
  3. Day 7-10: well developed phagocytosis of dead cells, early formation of fibrovascular granulation tissue at margin
159
Q

Gross features of AMI day 10 onwards post infarct:

  1. 10-14 days
  2. 2-8 weeks
  3. > 2 months
A
  1. 10-14 days: red-gray depressed infarct borders
  2. 2-8 weeks: gray-whit scar
  3. > 2 months: complete scarring
160
Q

Microscopic features of AMI day 10 onwards post infarct:

  1. 10-14 days
  2. 2-8 weeks
  3. > 2 months
A
  1. 10-14 days: well established granulation tissue with new blood vessels and collagen deposition
  2. 2-8 weeks: increased collagen deposition, decreased cellularity
  3. > 2 months: dense collagenous scar
161
Q
  1. The best way to rescue myocardial ischemic myocardium

2. It may completely prevent necrosis

A

Reperfusion

162
Q

How is AMI diagnosed (using what)? (3)

A
  1. Clinical symptoms
  2. Presence of myocardial proteins (tropomyosin, Troponin) in plasma
  3. ECG changes
163
Q

S/Sx of AMI (3)

A
  1. Rapid, weak pulse
  2. Diaphoresis
  3. Dyspnea –> pulmonary congestion and edema
164
Q

ECG feature in AMI

A

New Q waves

165
Q

Serum markers of AMI (3)

A
  1. CK-MB (creatinine kinase enzymes)
  2. Troponin I and T
  3. LDH
166
Q

Complications of MI (9)

A
  1. Contractile dysfunction
  2. Arrhythmias
  3. Right ventricular infarction
  4. Mural thrombus, embolism
  5. Ventricular aneurysms
  6. Pericarditis
  7. Rupture
  8. Infarct extension
  9. Infarct expansion
167
Q

The complications and prognosis of MI is dependent on (3) things:

A
  1. Infarct size
  2. Location
  3. Factional thickness of damaged myocardial wall
168
Q

This type of infarct has a higher probability of cardiogenic shock, arrhythmias, late CHF

A

Large transmural infarcts

169
Q

This type of infarct has greater risk of free wall rupture, expansion, mural thrombi, aneurysm

A

Anterior transmural infarct

170
Q

This type of infarct is more likely to be complicated by conduction blocks, right ventricular involvement, or both

A

Posterior transmural infarct

171
Q

Which has a worse clinical course, anterior or posterior/inferior infarcts?

172
Q

Treatment of AMI (5)

A
  1. Thrombolysis
  2. Angioplasty
  3. Stent
  4. Coronary bypass surgery
  5. Altered morphology
173
Q
  1. It is also known as ischemic cardiomyopathy
  2. Constitutes post-infarction cardiac decompensation (owing to exhaustion of compensatory hypertrophy of noninfarcted viable myocardium)
A

Chronic IHD

174
Q

The ff are gross features of which syndrome of IHD?

  1. Hypertrophy (enlarged and heavy) secondary to LVH and dilatation
  2. Moderate to severe stenosing atherosclerosis, sometimes total occlusion
  3. Mural endocardium have patchy fibrous thickening
  4. Mural thrombi may be present
A

Chronic IHD

175
Q

The ff are microscopic features of which syndrome of IHD?

  1. Interstitial fibrosis (Discrete gray-white scars) of healed infarcts
  2. Myocardial hypertrophy
  3. Diffuse subendocardial vacuolization
  4. Mural endocardium: patchy fibrous thickening, mural thrombi may be present
A

Chronic IHD

176
Q
  1. Unexpected death in asymptomatic patients
  2. IHD –> fatal arrhythmia/massive pump failure –> cardiogenic shock –> ____
  3. It’s most common trigger is ACUTE MYOCARDIAL ISHEMIA
A

Sudden cardiac death

177
Q

Th ff are a causes of which syndrome of IHD?
1. Atherosclerosis (major)

The ff occur in 10-20% of cases only)

  1. Congenital structure or coronary arterial abnormalities
  2. Aortic valve stenosis
  3. Mitral valve prolapse
  4. Dilated or hypertrophic cardiomyopathy
  5. Myocarditis
  6. Pulmonary HPN
  7. Hereditary or acquired abnormality of a cardiac conduction system
  8. Isolated hypertrophy
A

Sudden cardiac death

178
Q

What is ultimate mechanism of SCD?

A

Lethal arrhythmia

179
Q

The ff are consistent morphological findings in which syndrome of IHD?

  1. 80-90% of cases: marked coronary atherosclerosis
  2. 50%: acute plaque disruption
  3. 40%: healed or old MI
  4. 25%: acute MI changes
180
Q

Most SCD is not associated with AMI but is a result of?

A 
Myocardial ischemia (induced irritability that initiates mal
If ant ventricular arrhythmias)
181
Q

What gross and microscopic findings are indicative of severe chronic ischemia? (2)

A
  1. Scars of previous infarcts

2. Subendocardial myocyte vacuolization

182
Q

What markedly improves the prognosis of patients vulnerable to SCD?

A

Implantation of pacemaker or automated cardioverter defibrillator (senses and electrically counteracts an episode of ventricular fibrillation)

Pathology (10 decks)

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