Cardiovascular System Pathology Flashcards
1
Q
Vascular damage
A
- Weakening of vessel walls
- Narrowing of lumen
- Damage to endothelium
2
Q
Artery layers
A
- Intima (endothelium to internal elastic lamina)
- Media (internal elastic lamina to external elastic lamina)
- Adventitia (external elastic lamina onward)
3
Q
Endothelial cell activators
A
- Cytokines
- Bacterial products
- Hemodynamic stress
- Lipid products
- Advanced glycosylation end products
- Viruses
- Complement proteins
- Hypoxia
- Inflammatory mediators
4
Q
Endothelial cell induced genes
A
- Adhesion molecules
- Cytokines/chemokines
- Growth factors
- Vasoactive mediators
- Coagulation proteins
- MHC molecules
- Others
5
Q
Endothelial response
A
- Elaborate (adhesion molecules, chemokines, growth factors)
- MHC molecule expression
- Vasoconstriction and vasodilation
6
Q
Intimal response to injury
A
- Smooth muscle cell migration
- Synthesis/deposition of extracellular matrix
- Multiplication of intimal cells
7
Q
Arteriosclerosis (hardening of arteries) is the generic name for
A
- Atherosclerosis
- Monckeberg medial calcific sclerosis
- Arteriolosclerosis
8
Q
Arteriosclerosis
A
- Atherosclerosis
- Arteriolosclerosis
- Aneurysms
9
Q
Atherosclerosis
A
- Characterized by intimal lesions called fibrofatty plaques or atheromas
10
Q
Atheromatous plaque components
A
- Lumen
- Fibrous cap
- Cholesterol clefts
11
Q
Atherosclerosis primarily affects
A
- Elastic arteries, large and medium sized arteries
12
Q
Atherosclerosis etiologic and injurious factors
A
- Hyperlipidemia
- Hypertension
- Cigarettes
- Diabetes Mellitus
- Homocysteine
- Personality
- Sex (M>F)
13
Q
Pathogenesis of atherosclerosis
A
- Chronic inflammatory response of the arterial wall initiated by some form of injury to the endothelium
14
Q
Multifactorial endothelial cell injury (pathogenesis of atherosclerosis)
A
- Lipids
- Toxins
- Hemodynamic
15
Q
Etiology of atherosclerosis
A
- Endothelial injury
- Lipid insudation
- Macrophage uptake (Foam cells)
- Smooth muscle cell migration to intima
- Proliferation of smooth muscle cells
- ECM synthesis
- Debris accumulation
16
Q
Atheromatous plaque
A
- Located in the intima
- Fibrous cap
- Necrotic center
- Consequences: rupture, thrombosis
17
Q
Hypertension accelerates
A
- Atherogenesis
- Affects structure and function of muscular arteries and arterioles
18
Q
Hypertension is associated with 2 forms of small vessel disease
A
- Hyaline Arteriolosclerosis
- Hyperplastic Arteriolosclerosis
19
Q
Hyaline Arteriolosclerosis
A
- Encountered in the elderly
- Common in diabetes
- Hyaline thickening/narrowing of lumen
20
Q
Hyaline Arteriolosclerosis findings
A
- Hyalinized arteriole wall
- Narrowed lumen
21
Q
Hyperplastic Arteriolosclerosis
A
- Acute or severe increases in blood pressure
- Malignant hypertension
22
Q
Hyperplastic Arteriosclerosis findings
A
- Onion skinning
- Lumen obliteration
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
Diabetes mellitus
- High circulating levels of glucose
| - Non-enzymatic glycosylation of proteins, macromolecules, and lipids (LDL)
26
Non enzymatic glycosylation of lipids (LDL) and proteins traps or retards efflux
- Enhances cholesterol deposition
27
Aneurysm
- A localized abnormal dilation of a blood vessel
| - Occurs most commonly in the aorta or the heart
28
Most common causes of aneurysms
- Atherosclerosis
| - Medial cystic degeneration
29
True aneurysm
- Blood remains in the confines of the circulatory system
30
Pseudoaneurysm
- An extravascular hematoma that communicates with the intravascular space
31
Types of aneurysms
- True aneurysm
- Pseudoaneurysm
- Berry aneurysm
- Abdominal
- Syphilitic
- Dissecting (hematoma)
32
Atherosclerotic aneurysms most frequent location
- Abdominal aorta
| - Major cause = atherosclerosis
33
Clinical course of abdominal aneurysm
- Rupture into peritoneal cavity
- Occlusion of a branch by pressure or thrombus
- Embolism
- Compression of adjacent structure
34
Syphilitic aneurysm
- Ascending aorta
| - Inflammation of the vasa vasorum
35
Syphilitic aneurysm pathology
- Obliterative Endarteritis
36
Syphilitic aneurysms cause
- Medial destruction secondary to disruption of blood supply
| - Ischemia
37
Dissecting aneurysm (hematoma)
- Catastrophic illness
- Dissection of blood in between and along the laminar planes of the media
- Blood filled channel within the aortic wall
38
Dissecting aneurysm (hematoma) epidemiology
- Men 40 to 60 years old with long standing hypertension
| - Younger patients with a connective tissue disorder
39
Dissecting aneurysm (hematoma) etiology
- Superficial transverse intimal tear (cause unknown)
| - Dissection can extend proximally or distally
40
Types of dissecting aneurysms (hematomas)
- Type A (DeBakey I, DeBakey II)
| - Type B (DeBakey III)
41
Dissecting aneurysm (hematoma) clinical
- Confused with Myocardial Infarction
- Sudden onset excruciating pain
- Rupture
- Death in seconds
42
Diseases of the heart
- Acute coronary syndromes (Ischemic Heart Disease)
| - Myocardial Infarction
43
Ischemic Heart Disease (IHD)
- A consequence of atherosclerosis of the coronary arteries
| - Develops when blood flow is inadequate to provide for oxygen demands of the heart
44
Manifestations of IHD
- Angina Pectoris:
- Substernal chest discomfort
- Transient cardiac ischemia
- Cellular necrosis does not occur
45
Types of angina pectoris
- Stable
- Unstable
- Prinzmetal
46
Stable angina pectoris
- Reduction in coronary perfusion
- Chest pain develops with increased O2 demand
- Relieved by rest
47
Unstable angina pectoris
- Disruption of an atherosclerotic plaque
- Superimposed thrombosis
- Occurs at rest
48
Prinzmetal angina pectoris
- Occurs at rest
| - Coronary artery spasm
49
Types of myocardial infarction
- Transmural
| - Subendocardial
50
Pathogenesis of myocardial infarction
- Coronary artery occlusion
| - IHD transitions to MI
51
Subendocardial myocardial infarction (NSTEMI)
- Ischemic necrosis limited to the inner 1/3 to ½ of the ventricular wall
52
Transmural myocardial infarction (STEMI)
- Full thickness of the ventricular wall
| - Coronary artery is completely obstructed
53
Evolution of morphological changes in MI
- ½ -4hr ; waviness of fibers
- 4-12hr ; coagulation necrosis
- 1-3days ; phagocytosis, neutrophil infiltrate
- 7-10days ; fibrovascular, granulation tissue
- 10-14days ; collagen deposition
54
MI clinical laboratory findings
```
- CK - MB (elevated)
Troponin T (elevated)
Troponin I (elevated)
```
55
MI clinical presentation
- SOB
- Diaphoresis
- Chest pressure / pain
- Pain radiation to left arm
- N/V
- Stomachache
- Dizziness
- Overwhelming fatigue
- ***Diabetics may have no symptoms***
56
Acute MI complications
- Contractile dysfunction
- Arrhythmias
- Myocardial rupture
- Pericarditis
- Mural thrombus formation
- Papillary muscle dysfunction
