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Barry Patho II

6-19-10 Patho II CAD

What percent of all deaths in western society are caused by CAD 33%
How do you know if your old All elderly have at least some impairment of CAD
How many ml/min is resting coronary flow 225ml/min (8ml of o2/100g of tissue/min)
What percent of cardiac output becomes coronary blood flow 4-5 % of total CO
Exercise can increase coronary demand by ? many times (in relation to CO) 4 times
How many ml of O2 is required to maintain cell life 1.3 ml of O2/100g of tissue/min
Coronary blood flow is controlled by the local metabolism
What is the most important factor in local blood flow regulation of the coronary perfussion O2 demand
What does stimulation of the SNS have on the heart increase HR, strength, and vasoconstriction
What does PNS (parasymp) stimulation do to the heart decreases strength and HR
70% of the metabolism of the cardiac muscle uses what as its energy source Fatty acids, but in emergencies glycolysis is used
Death due to CAD is the result of (2 things) Acute occlusion or Cardiac Fibrillation
The most frequent cause of decreased coronary flow is Atherosclerosis
Atherosclerosis starts at what age childhood
Atherosclerosis causes - besides lipid accumulation, what are 3 other causes necrotic debis, proliferation of internal vessel (intimal) smooth muscle cell, the formation of large amounts of connective tissue matrix (collagen and elastic fibers) by proliferated cells
Proliferated cells form large amounts of Connective tissue matrix (collagen and elastic fibers
Name 3 independant predictors for the development of athrosclerosis cigarett smoking, High BP, plasma cholesterol
What Theory is this: some form of injury in the endothelium will trigger the events by changing the fx activity of the endothelium which combined with incr. cholest, smooth muscle prolif. and platlet activity lead to the atherosclerosis plaque Response-To-Injury theory
What theory is this: each lession of athrosclerosis is originated from a single smooth muscle cell that serves as a source of all of the cells within a lesion - each lesion is a benign neoplasm - caused by viruses, chemicals, or mutants Monoclonal
??? is when coronary demand is greater than supply Coronary insufficiency
Adequate perfussion with decreased O2 supply is called Hypoxia
Zero O2 supply with adeqate perfusion is called Anoxia
Ischemia is the result when what 3 things decrease O2 supply, perfusion, removal of metabolic waste
Angina Pectoris is pain felt due to Ischemia (not necrosis, no pain with necrosis)
Angina Pectoris is describes as hot, pressing, and constricting
Per slide 13, which of the following 2 are not related to myocardial ischemia pain: [Throat, neck jaw][shoulder][retrosternal][epigastric][right chest pain][left chest pain][back pain] left chest pain and right chest pain (per the slide)
T/F: there is necrosis in angina Give Fernandez's cell phone a ring and get the scoop (IN BOLD LETTERS, NO!!!!)
What are the classes of angina (3 of them) Chronic (or Stable), Acute (or Unstable), and Variant (Prinzmetal's angina)
Angina that starts gradually and gets worse over minutes than dissipates after trigger is gone is classified as ? angina Chronic or Stable angina
Chronic or stable angina is caused by Increase O2 demand over supply (physical activity, emotions, eating, Mary Beth, hurrying, fever, chills, tachycardia, motion of hands over head)
In chronic or stable angina there is a "fixed coronary occlusion" which means The O2 "flow" to the heart(coronaries) is max'd out but is not meeting the O2 demand
T/F: "Angina Of Effort" is caused by decreased O2 flow False, it results from increased demand with fixed supply
T/F: Chronic angina disappears with rest True
Other diagnosis that could mimic angina (MI)- (6 of them) Esophagus dz, biliary colic, GI syndrome, cervical radiculitis, PE (dyspnea), Acute pericarditis
Chronic angina findings include (3 things) HTN, non-specific S-T and T changes, left bundle branch blocks
What is the name of the cardiac diagnostic test that injects a radionuclide and compares peak exercise to rest periods Stres thalium 201 Myocardial perfusion imaging - it shows defects
A defect found in a stress test that last 2-3 hrs in consistant with the diagnosis of MI
Name a definative coronary diagnostic test Coronary arteriography with left ventricular arteriography
Management of an MI (3 things) Lifestyle changes, drug tx, revascularization
Four types of revascularization PTCA, CABG, Laser angioplasty, Coronary atherectomy
What is the difference between Acute (unstable) Angina and Chronic (Stable) Angina Acute (unstable) angina happens at rest or with minimal effort, Chronic (stable) needs significant trigger event
T/F: Acute (unstable) angina is when O2 demand is increased with a fixed O2 supply False (that is the definition of Chronic/Stable angina). A true statement would be: fixed O2 demand with decreased O2 supply
What are the clinical symptoms that differ between Acute and Chronic angina Acute symptoms include more intense pain and longer duration and usually while the patient is resting
What things (2 of them ) do not relieve symptoms in Acute angina but do in Chronic angina Bed rest and nitroglycerin cannot eliminate acute pain completely or permanently
What are clinical findings that differ between Acute and Chronic Angina In acute angina there is less collateral flow, higher number of vessles dz (more than one), increased incidence of coronary thrombi, faster progression of atherosclerosis, increased platlet aggregation, and thrombosis + coronary spasms
What are the different diagnosive test between Acute and Chronic angina None
Management of Acute angina (8 of them) Hospitalization, Quietness, keeping cardiac O2 demand down (no fevers, anemia, infections, arrhythmias), drug tx (beta blockers, nitrates, anticoagulants), thrombolitic tx, ballon pump, PTCA, and Surgical intervention
What is the difference between Ischemia and Infarction (MI) Dead tissue (from prolonged ischemia)
Transmural infarction includes The whole thickness of the ventricular wall
Sub-endocardial infarction includes the subendocardium, the intramural myocardium or both --does not extend into the epicardium
What is the most common cause of transmural infarction Acute coronary thrombosis
What are the variables with Acute coronary occlution that determine whether the damage will be transmural, subendocardial or no damage How fast the onset of the occlution occurs, and the number and quality of distal collaterals involved
Enzymes tested related to MI (4 of them) Troponin, Creatine Kinase, Lactic Dehydrogenase, and Glutamic-Oxalacetic Transaminase (GOT)
MI management includes (4 things) Drugs (b-blockers, nitrates, analgesics, and O2), Controll of physical activity, Thrombolitics (intracoronary and intravenously), and PTCA (easier through fresh thrombus)
T/F: In a CABG, the harvested vessle can be from either a venous or arterial source True
In a CABG, revascularization occurs by connecting the harvested vessle distal to the coronary blockage and into the ? or the ? Subclavian artery or the Aorta
What makes a CABG the treatment of choice When the PTCA was not successful (or could not be performed), or multiple vessles need intervention
CABG is containdicated in what patients Patients with uncomplicated Transmural infarcts more than 6 hours after the onset
How many hours after an AMI should a CABG be performed to be most successful. 4-6 hours (before 2 hours should be the goal)
The pain associated with Variant Angina Pectoris is related to Coronary artery spasm
T/F: Variant Angina is like Acute angina, it can occur at rest True - occurs almost exclusively at rest
T/F: Varient angina is like Chronic angina, it is related to physical exertion or emotion stress False, Varient angina does is not related to physical activity or emotional stress; Chronic angina is
Does anything happen with the ST segment with Variant Angina Yes, it is associated with ST elevation
T/F: Variant angina is like Acute angina, the onset of pain gets progressively worse with time False, Variant angina pain does not get worse (Acute angina pain gets worse)
The key component to diagnosing Variant angina is the development of ST segment elevation with pain
What oxytocic drug in give to diagnose Variant angina Ergonovine
What will the administration of Ergonovine cause in a patient with Variant angina ST elevations
What is the best management treatment for patients with Variant angina The best treatment is to combine nitrates and Ca++ antagonists (calciun channel blockers)
What circumstance makes it appropriate to perform a PTCA or CABG on a Variant angina patient When the spasm is present with obstruction (PTCA and CABG are contraindicated in Variant angia without obstruction)
Created by: smorrissey1



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