Test 1 study guide Flashcards
The “response to injury” model is the most commonly accepted model for atherogenesis. - describe it
Oxidized LDL and hyperglycemia are big culprits among contributors to endothelial injury.
Remember that M0 enter the intima of the vessel wall and ingest oxidized LDL to become “foam cells” (all the fat they eat makes them look foamy).
Oxidized LDL can induce the overlying endothelium to express adhesion molecules and increase the secretion of chemotactic factors, which facilitate the homing of monocytes and lymphocytes to the localized and activated endothelial area. Under ordinary homeostatic circumstances, the endothelial monolayer is resistant to prolonged contact with blood leukocytes. However, in the presence of adhesion molecules, blood monocytes adhere to the endothelial layer and penetrate between intact ECs to the intima.
The “response to injury” model is the most commonly accepted model for atherogenesis. - describe it
Oxidized LDL and hyperglycemia are big culprits among contributors to endothelial injury.
Remember that M0 enter the intima of the vessel wall and ingest oxidized LDL to become “foam cells” (all the fat they eat makes them look foamy).
Oxidized LDL can induce the overlying endothelium to express adhesion molecules and increase the secretion of chemotactic factors, which facilitate the homing of monocytes and lymphocytes to the localized and activated endothelial area. Under ordinary homeostatic circumstances, the endothelial monolayer is resistant to prolonged contact with blood leukocytes. However, in the presence of adhesion molecules, blood monocytes adhere to the endothelial layer and penetrate between intact ECs to the intima.
CAD
Reduction in blood flow to cardiac muscle.
IHD
inadequate supply to demand ratio by heart muscle.
Myocardial infarction (MI)
Angina pectoris (stable, variant, and unstable angina)
Chronic IHD with heart failure (pump is not meeting demand)
Sudden cardiac death.
Subendothelial
(non-transmural) (some percentage of the wall is affected).
- Coronaries narrowed but patent
- Thrombotic occlusion -> thrombolysis
- Limited period of time of increased oxygen demand and/or decreased oxygen delivery.
-Hypotension/ Hypertension.
Anemia
Subendothelial
(non-transmural) (some percentage of the wall is affected).
Coronaries narrowed but patent
Thrombotic occlusion [Symbol] thrombolysis
Limited period of time of increased oxygen demand and/or decreased oxygen delivery.
Hypotension/Hypertension.
Anemia
Labs for MI
High WBC
High LDH
High cardiac enzymes (Creatine phosphokinase, troponin)
MI’s resulting from subtotal occlusion result in more heterogeneous damage, which may be evidenced by a non Q-wave M.I. pattern on the ECG.
how are most infarcts caused
Most infarctions are caused by the disruption of an atherosclerotic plaque.
Gross changes to myocardium following MI
Histopathology by light microscopy s/p MI
0-0.5 hours – No visible changes
0.5-4 – Glycogen depletion, as seen with PAS stain and Poss. Waviness of myocardial fibers at borders
4-12 – Initiation of coagulation necrosis, edema, hemorrhage
12-24 – Ongoing coagulation necrosis, hypereosinophilia, contraction band necrosis in margins, beginning of neutrophils infiltration
1-3 days – Continued coagulation necrosis, loss of myocardial cell nuclei and striations, increased infiltration of neutrophils to interstitium.
3-7 days – Beginning of disintegration of dead muscle fibers, necrosis of neutrophils, beginning of macrophage removal of dead cells at border.
7-10 days – Increased phagocytosis of dead cells at border, beginning of granulation tissue formation at margins.
10-30 days – Mature granulation tissue with type 1 collagen.
2-8 weeks – Increased collagen deposition, decreased cellularity.
>2 months – Dense collagenous scar formed.
Hemopericardium
Blood trapped in the pericardium leads to massive hemorrhage and cardiac tamponade.
Tamponade
Compression of the heart by an accumulation of fluid in the pericardial sac.
Most common rupture following MI
Rupture of the ventricular free wall with hemopericardium and cardiac tamponade. Usually fatal.
Pericarditis
Often develops on the second, third, or fourth day after an MI. Usually resolves over time. Happens about 17-25% of the time.
Dressler’s Syndrome
occurs weeks to months after injury to the heart. Low fever, chest pain, friction rub and/or pericardial effusion. May be an autoimmune response to myocardial antigens
HTN
90-95% of HTN is primary and idiopathic. Most of the secondary is caused by renal failure/renal artery stenosis.
Marfans
• noted in5-9% of all individuals who develop aortic dissection.
o Tend to develop aneurysms that localize to the aorta.
o Abnormal fibrillin-1 protein increases risk of dissection.
o Also high risk for cystic medial necrosis, which is pretty much just a genetic predisposition to dissecting aortic aneurysms.
CHF:
• The heart is unable to pump enough blood to meet the body’s metabolic requirements for oxygen and nutrients.
o Over time, chronic cardiac failure will result in the development of increased ventricular wall thickness or ventricular hypertrophy.
o Stasis of fluid within the lungs gives rise to heart failure cells, which are hemosiderin containing macrophages in the aleoli.
o Left sided CHF can lead to pulmonary congestion due to increased left ventricular pressure and increased left arterial pressure.
o The most common cause of right side CHF is left side CHF!
o Cor pulmonale = heart failure that occurs as a direct result of pulmonary disease such as emphysema, chronic bronchitis, pulmonary embolus or pulmonary HTN.
o The first manifestation of CHF is usually tachycardia.
o High output failure: warm extremities.
Low output failure: cold extremities.
• Compare and contrast the different types of cardiomyopathies
o Dilated (90% of cases of non-ischemic cardiomyopahty)
♣ Enlargement and dilation of all four chambers of the heart.
♣ Most common cause is alcoholism (DT vitamin deficiency).
♣ Next most common is viral myocarditis.
o Hypertrophic
♣ Myocardial hypertrophy, abnormal diastolic filling, and, in 1/3 of cases, intermittent ventricular outflow obstruction.
♣ Genetic disease caused by a mutation in one of several genes that encode sarcomere proteins.
o Restrictive
♣ The myocardium is usually infiltrated with abnormal tissue that results in impaired ventricular filling.
♣ The most common causes are amyloidosis and hemochromatosis.
Endocarditis
♣ Defined as the invasion of heart valves or heart muscle by microbial agents.
♣ The microbes can build up and form vegetations, which can lead to the destruction of the underlying tissue.
♣ Vegetations can also embolize and spread.
♣ Risks
• Artificial heart valves (staph epidermitis)
• Immunocompromised
• Alcoholics (anaerobes and oral cavity bugs)
• Vascular grafts
• Poor dental hygene/pharyngeal infection
• GU infections/In dwelling catheters (E.Coli, other Gm-)
• Skin infections (impetigo)
• Pulmonary infections
• IV drug use (staph aureus)
♣ Acute endocarditis
• Rapidly developing, destructive infection, often of a previously normal heart valve. Usually due to very virulent infection and can lead to death within days to weeks in 50% of cases.
