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