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Pathology I > Cardiovascular System Pathology > Flashcards

Cardiovascular System Pathology Flashcards

1
Q

Vascular damage

A
  • Weakening of vessel walls
  • Narrowing of lumen
  • Damage to endothelium
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2
Q

Artery layers

A
  • Intima (endothelium to internal elastic lamina)
  • Media (internal elastic lamina to external elastic lamina)
  • Adventitia (external elastic lamina onward)
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3
Q

Endothelial cell activators

A
  • Cytokines
  • Bacterial products
  • Hemodynamic stress
  • Lipid products
  • Advanced glycosylation end products
  • Viruses
  • Complement proteins
  • Hypoxia
  • Inflammatory mediators
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4
Q

Endothelial cell induced genes

A
  • Adhesion molecules
  • Cytokines/chemokines
  • Growth factors
  • Vasoactive mediators
  • Coagulation proteins
  • MHC molecules
  • Others
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5
Q

Endothelial response

A
  • Elaborate (adhesion molecules, chemokines, growth factors)
  • MHC molecule expression
  • Vasoconstriction and vasodilation
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6
Q

Intimal response to injury

A
  • Smooth muscle cell migration
  • Synthesis/deposition of extracellular matrix
  • Multiplication of intimal cells
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7
Q

Arteriosclerosis (hardening of arteries) is the generic name for

A
  • Atherosclerosis
  • Monckeberg medial calcific sclerosis
  • Arteriolosclerosis
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8
Q

Arteriosclerosis

A
  • Atherosclerosis
  • Arteriolosclerosis
  • Aneurysms
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9
Q

Atherosclerosis

A
  • Characterized by intimal lesions called fibrofatty plaques or atheromas
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10
Q

Atheromatous plaque components

A
  • Lumen
  • Fibrous cap
  • Cholesterol clefts
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11
Q

Atherosclerosis primarily affects

A
  • Elastic arteries, large and medium sized arteries
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12
Q

Atherosclerosis etiologic and injurious factors

A
  • Hyperlipidemia
  • Hypertension
  • Cigarettes
  • Diabetes Mellitus
  • Homocysteine
  • Personality
  • Sex (M>F)
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13
Q

Pathogenesis of atherosclerosis

A
  • Chronic inflammatory response of the arterial wall initiated by some form of injury to the endothelium
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14
Q

Multifactorial endothelial cell injury (pathogenesis of atherosclerosis)

A
  • Lipids
  • Toxins
  • Hemodynamic
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15
Q

Etiology of atherosclerosis

A
  1. Endothelial injury
  2. Lipid insudation
  3. Macrophage uptake (Foam cells)
  4. Smooth muscle cell migration to intima
  5. Proliferation of smooth muscle cells
  6. ECM synthesis
  7. Debris accumulation
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16
Q

Atheromatous plaque

A
  • Located in the intima
  • Fibrous cap
  • Necrotic center
  • Consequences: rupture, thrombosis
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17
Q

Hypertension accelerates

A
  • Atherogenesis

- Affects structure and function of muscular arteries and arterioles

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18
Q

Hypertension is associated with 2 forms of small vessel disease

A
  • Hyaline Arteriolosclerosis

- Hyperplastic Arteriolosclerosis

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19
Q

Hyaline Arteriolosclerosis

A
  • Encountered in the elderly
  • Common in diabetes
  • Hyaline thickening/narrowing of lumen
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20
Q

Hyaline Arteriolosclerosis findings

A
  • Hyalinized arteriole wall

- Narrowed lumen

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21
Q

Hyperplastic Arteriolosclerosis

A
  • Acute or severe increases in blood pressure

- Malignant hypertension

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22
Q

Hyperplastic Arteriosclerosis findings

A
  • Onion skinning

- Lumen obliteration

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23
Q

Type I diabetes

A
  • Destruction of Beta islet cell

- No insulin production

24
Q

Type II diabetes

A
  • Multifactorial

- Decreased insulin secretion and/or decrease response to insulin

25
Q

Diabetes mellitus

A
  • High circulating levels of glucose

- Non-enzymatic glycosylation of proteins, macromolecules, and lipids (LDL)

26
Q

Non enzymatic glycosylation of lipids (LDL) and proteins traps or retards efflux

A
  • Enhances cholesterol deposition
27
Q

Aneurysm

A
  • A localized abnormal dilation of a blood vessel

- Occurs most commonly in the aorta or the heart

28
Q

Most common causes of aneurysms

A
  • Atherosclerosis

- Medial cystic degeneration

29
Q

True aneurysm

A
  • Blood remains in the confines of the circulatory system
30
Q

Pseudoaneurysm

A
  • An extravascular hematoma that communicates with the intravascular space
31
Q

Types of aneurysms

A
  • True aneurysm
  • Pseudoaneurysm
  • Berry aneurysm
  • Abdominal
  • Syphilitic
  • Dissecting (hematoma)
32
Q

Atherosclerotic aneurysms most frequent location

A
  • Abdominal aorta

- Major cause = atherosclerosis

33
Q

Clinical course of abdominal aneurysm

A
  • Rupture into peritoneal cavity
  • Occlusion of a branch by pressure or thrombus
  • Embolism
  • Compression of adjacent structure
34
Q

Syphilitic aneurysm

A
  • Ascending aorta

- Inflammation of the vasa vasorum

35
Q

Syphilitic aneurysm pathology

A
  • Obliterative Endarteritis
36
Q

Syphilitic aneurysms cause

A
  • Medial destruction secondary to disruption of blood supply

- Ischemia

37
Q

Dissecting aneurysm (hematoma)

A
  • Catastrophic illness
  • Dissection of blood in between and along the laminar planes of the media
  • Blood filled channel within the aortic wall
38
Q

Dissecting aneurysm (hematoma) epidemiology

A
  • Men 40 to 60 years old with long standing hypertension

- Younger patients with a connective tissue disorder

39
Q

Dissecting aneurysm (hematoma) etiology

A
  • Superficial transverse intimal tear (cause unknown)

- Dissection can extend proximally or distally

40
Q

Types of dissecting aneurysms (hematomas)

A
  • Type A (DeBakey I, DeBakey II)

- Type B (DeBakey III)

41
Q

Dissecting aneurysm (hematoma) clinical

A
  • Confused with Myocardial Infarction
  • Sudden onset excruciating pain
  • Rupture
  • Death in seconds
42
Q

Diseases of the heart

A
  • Acute coronary syndromes (Ischemic Heart Disease)

- Myocardial Infarction

43
Q

Ischemic Heart Disease (IHD)

A
  • A consequence of atherosclerosis of the coronary arteries

- Develops when blood flow is inadequate to provide for oxygen demands of the heart

44
Q

Manifestations of IHD

A
  • Angina Pectoris:
  • Substernal chest discomfort
  • Transient cardiac ischemia
  • Cellular necrosis does not occur
45
Q

Types of angina pectoris

A
  • Stable
  • Unstable
  • Prinzmetal
46
Q

Stable angina pectoris

A
  • Reduction in coronary perfusion
  • Chest pain develops with increased O2 demand
  • Relieved by rest
47
Q

Unstable angina pectoris

A
  • Disruption of an atherosclerotic plaque
  • Superimposed thrombosis
  • Occurs at rest
48
Q

Prinzmetal angina pectoris

A
  • Occurs at rest

- Coronary artery spasm

49
Q

Types of myocardial infarction

A
  • Transmural

- Subendocardial

50
Q

Pathogenesis of myocardial infarction

A
  • Coronary artery occlusion

- IHD transitions to MI

51
Q

Subendocardial myocardial infarction (NSTEMI)

A
  • Ischemic necrosis limited to the inner 1/3 to ½ of the ventricular wall
52
Q

Transmural myocardial infarction (STEMI)

A
  • Full thickness of the ventricular wall

- Coronary artery is completely obstructed

53
Q

Evolution of morphological changes in MI

A
  • ½ -4hr ; waviness of fibers
  • 4-12hr ; coagulation necrosis
  • 1-3days ; phagocytosis, neutrophil infiltrate
  • 7-10days ; fibrovascular, granulation tissue
  • 10-14days ; collagen deposition
54
Q

MI clinical laboratory findings

A 
- CK - MB (elevated)
Troponin T (elevated)
Troponin I  (elevated)
55
Q

MI clinical presentation

A
  • SOB
  • Diaphoresis
  • Chest pressure / pain
  • Pain radiation to left arm
  • N/V
  • Stomachache
  • Dizziness
  • Overwhelming fatigue
  • Diabetics may have no symptoms
56
Q

Acute MI complications

A
  • Contractile dysfunction
  • Arrhythmias
  • Myocardial rupture
  • Pericarditis
  • Mural thrombus formation
  • Papillary muscle dysfunction

Pathology I (9 decks)

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