Term
| How far occluded do the coronary arteries need to be occluded before angina is present? What is the time at which we start to get permanent damage? |
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Definition
>70%
-After about 20min of reduced blood to heart we can start to get some permanent damage
-These means that in IHD, the angina last less than 20min |
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Term
| Define and compare stable angina, unstable angina, and prinzmetal angina in terms of causes, EKG signs, & treatment? |
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Definition
Stable angina; pain with exertion
-From atherosclerosis with >70% occlusion
-EKG shows ST-segment depression from subendocardial ischemia
-Relieved by rest and nitroglycerine
Unstable angina; pain at rest
-From thrombosis formation or embolization with incomplete occlusion
-Also get ST depression from subendocardial ischemia
-Relieved with nitroglycerin
Prinzmetal angina; episodic pain unrelated to exertion
-From coronary artery vasospasm (complete clamp-down)
-This time we get ST elevation because of TRANSMURAL (entire wall) ischemia
-Relieved by nitroglycerine and CALCIUM channel blockers |
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Term
| What is nitroglycerin and what does it do? |
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Definition
-Belongs to a group of drugs called nitrates which are converted to nitric oxide by mitochondrial aldehyde dehydrogenase
-NO is a potent natural vasodilator |
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Term
| What are causes of MI? What part is involved? |
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Definition
-Most typical is rupture of an atherosclerotic plaque with thrombosis and complete occlusion of the coronary a.
-Also can be from an emboli, vasospasm (from prinzmetal or cocaine use), or vasculitis
-Typically effects the left ventricle and spares the rest |
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Term
| What are the three common occluded arteries in MI? |
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Definition
-Ant. interventricular (aka left anterior descending artery, or LAD) is the most common at 40%
-Right coronary, or RCA (wraps all the way to back)
-Left circumflex artery goes over lateral wall of the LV |
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Term
| What are the blood markers for MI and their time frames? |
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Definition
-Troponin I is the gold standard; rises 2-4 hours after infarction, peaks at 24 hours, and lasts 7-10 days
-CK-MB is good for detecting reinfarction occurring days after original; rises 4-6 hours after infarction, peaks at 24, but lasts only for 3 days |
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Term
| What are six common treatments for MI? |
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Definition
1. Aspirin and/or heparin; limits thrombosis
2. Supplemental O2; minimize ischemia
3. Nitrates; vasodilatation
4. β-blocker; slows heart rate lowering O2 demand
5. ACE inhibitor; lowers blood pressure
6. Fibrinolysis or angioplasty; opens vessel |
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Term
| What are results that can arise from angioplasty? |
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Definition
-Contraction band necrosis occurs from calcium influx into irreversibly-damaged cells (can see fibers and no nucleus)
-Reperfusion injury can result from return of oxygen and inflammatory cells leading to free radical generation and further myocyte damage |
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Term
| What are time stages after infarct in terms of what we see grossly and microscopically along with complications? |
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Definition
<4hours;
-No visible changes
-May have cardiogenic shock, congestive heart failure, arrhythmia*
4-24 hours;
-We see dark discoloration from coagulative necrosis
-We see pyknosis>karyorrhexis>karyolysis
-Again major complication is arrhythmia
1-7 days;
-Grossly we see a yellow pallor
-Microscopically we will first see neutrophil (1-3 days) and then macrophage (4-7 days) infiltrate
-Complications of neutrophils is fibrinous pericarditis, which causes a friction rub
-Complications of macrophages is rupture of structures due to weakness (macs are eating up debris)
1-3 weeks;
-We see a red boarder of granulation tissue entering infarct with fibroblasts, collagen, and blood vessels
Months;
-White scar from fibrosis
-Complications can be an aneurisms from weakness of wall, leading to mural thrombus
-Another possible long-term complication is Dressier syndrome
Overall;
CN ||DAY|| inflammation ||WEEK|| GT ||MONTH|| scar |
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Term
| What is Dressier syndrome? |
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Definition
| -It is autoimmune pericarditus that is rare, but can occur 6-8 weeks after an infarct from sensitization of immune system to pericardial antigens |
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Term
| What are the systemic effects of left vs. right-sided heart failure? What about signs and treatment? |
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Definition
Left-sided will give pulmonary congestion
-Presents with dyspnea and or orthopnea (dyspnea when laying down) along with hemosiderin-laiden macrophages in lungs from intraalveolar hemorrhage
-Also get decrease flow to kidneys leading to activation of renin-angiotensis system, exacerbating CHF
Right sided failure will cause systemic congestion
-Is usually due to left-sided failure first, but can also be from things that increase right side load (like L>R shunt)
-Will present with jugular venous distention, painful hepatosplenomegaly with "nutmeg" liver, and pitting edema from increased hydrostatic pressure
-Could treat either with ACE inhibitor |
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Term
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Definition
-Angiotensin converting enzyme
-Makes angiotensin I -----> angiotensin II (active)
-Angiotensin I is, in turn, made by RENIN
-System acts to increase BP |
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