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133 Cards in this Set
- Front
- Back
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What are some effects of aging on the heart? |
increased epicardial fat, calcifation of mitral annulus and aortic valve (can cause stenosis), stiffenening of aorta, fewer myocytes, atherosclerosis.
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There are 6 principal mechanisms of heart failure
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ok |
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Name some adapations to increased cardiac workload, or diminished cardiac function that maintain perfusion |
Frank starling (intrinsic). Hypertrophy with/without chamber dilation, neurohumoral adaptation (NE/ Renin/AT/ ANP…etc…)
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What are some metabolic consequences of cardiac hypertrophy.
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Increased metabolic demand of the heart without subsaquent expansion of capillary beds.
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What are primary causes of left sided heart failure?
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Ischemic heart disease, HTN, Mitral, Aortic valve deficiencies, myocardial disease.
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What is orthopnea and PND?
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orthopnea is a difficulty breathing associated with left heart failure mediated pulmonary edema. PND is dyspnea during nighttime. Also associated with Left heart failure/ fluid in lungs.
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What worsens pulmonary edema in left heart failure?
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reduced CO leads to activation of Renin/AT… fluid retention…..worse edema.
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What is systolic left sided failure?
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insufficent ejection fraction
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What is diastolic left sided failure?
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A stiffning of the left ventricle ccauses inability to relax during contraction. It cant expand properly either. This increases filling pressure and that reverbates back to pulmonary system poducing rapid onset pulmonary edema when there is an increase in demand on the heart.
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What casues right sided heart failure
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left sided heart failure
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What causes cor pulmonale?
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isolated right sided failure, due to disorders of the lungs. This can include pulmonary HTN, PE, and stenosis. Congestion is minimal in the pulmonary circuit but systemic and portal engorgement is pronounced
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What causes nutmeg liver?
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right heart failure leading to congestion within the liver.
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What is ancarasa?
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generalized massive edema.
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When do major cardiac structures develop and begin to function
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Weeks 3-8
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Where do the earliest cardiac precursors appear?
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lateral mesoderm.
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what type of shunting causes a dusky blueness?
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right to left
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When may a patient with a left to right shunt become cyanotic ?
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Volume and pressure overload from the shunt in the pulmonary right heart and pulmonary system can lead to pressure reaching systemic levels, this can reverse the shunt
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What is an obstructive congential heart disease? Example?
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Stenosis of pulmonary artery seen in TOF, Coarctation of the aorta. Blockage or narrowing of chambers, valves, or vessels.
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What is the most common type of CHD?
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L to R shunts.
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Is patent foramen ovale an ASD? Why?
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no. the hole was supposed to be there, it just didn’t close.
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what is the septum primum?
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crescent shaped ingrowth that partially separates the R and L atrium, the Ostium primum is the hole that allows R to L shunting in utero
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what is the ostium secundum?
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remaining opening after the growing septum primum obliterates the ostium primum.
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What is the septum secundum.
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another ingrowth, this one leaves the foramen ovale.
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What are the clinical patterns associated with ASDs
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increasesd pulmonary blood flow, murmur due to excessive pulmonary valve flow
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What do VSD's almost always lead to?
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irreversable pulmonary vascular damage, resulting in reversal of shunt, cyanosis….and death.
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When may closure of the ductus arteriosis be delayed? Why?
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When the infant is hypoxic? Vasoconstriction in the DA from adaquate oxygenation that usually occurs does not due to lack of oxygenation.
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What produces a harsh, machinery like murmur?
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PDA
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What are the 4 clinical observations seen in TOF?
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1. VSD 2. RVH 3. Renal artery stenosis (proximal) 4. aorta overides the VSD
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What malformation causes the 4 clincial observations seen in TOF?
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anterosuperior displacment of the infundivular septum
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What is the most common cause of a blue baby?
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TOF
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What is TGA? Is this compatable with life?
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Transposition of the great arteries. Not long term, but VSDs can create a stable shunt and are seen in some patients. PFO, PDA is responsible for shunting early in life but surgical intervention is required if the child is to survive long term.
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What is tricuspid atresia? What maintains circulationn in these patients?
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complete occlusion of the tricuspid orifice. Circulation is maintained through R to L shunting. Not good outlook.
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What is a common obstructive CHD seen in many turner syndrome pts.
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Coarctation of the aorta
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What accompanies 50% of coarctation cases?
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bicuspid aortic valve.
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What is the difference in clinical presentation of coarctation w/wo PDA?
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with PDA you will have worse symptoms and earlier. There is early onset cyanosis localized to the bottom half of the body. Without PDA patinets can be asymptomatic until adult hood.
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Why are there BP differences in pts with coarctation.
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high BP in upper body and low BP in lower due to area of occlusion
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When might you asculatate a murmur and thrill present throughout systole?
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coarctation of the aorta or subaortic stenosis
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What usually develops with pulmonary stenosis?
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RVH
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What molecules bring cholesterol to the peripheral tissues?
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LDL. Conversely, HDL takes lipids from the periphery back to the liver for excretion.
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What molecules take cholesterol from peripheral tissues and deliver them to the liver for bile excretion?
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HDL
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How do statins work?
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Statins inhibit HMG-CoA reductase. This is the RLS of cholesterol synthesis. Lack of cholesterol synthesis within the cell increases expression of LDL receptors and increases uptake from the blood, lowering serum LDL.
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What is the most common cause of LV Hypetrophy?
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Chronic hypertension
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What does CRP indicate? What does elevated CRP indicate risk for?
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CRP is a marker of systemic inflammation. It is increased by inflammatory mediators, increased CRP is a marker for MI, stroke, PAD, and sudden cardiac death,
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What is the effect of homocystine on the development of coronary and peripheral artery disease? What elevates homocystine?
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Homostine levels correlate with increased coronay atherosclerosis as well as peripheral vascular disease. Low folate and B12 can increase homocystine due to an inability to regenerate methionine in the remethylation pathway.
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What is "metabolic syndrome?"
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Combined metabolic disease requiring a combonition of insulin resistance, central adiposity, HTN, dyslipidemia, hypercoaguability, pro-inflammatory state
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What is Lipoprotein-A?
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This is an altered form of LDL that contains ApoB100 linked to apolipoprotein-A. Lp(A) is associated with increased risk for coronary/cerebrovascular risk independent of LDL.
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explain the steps that result in the pathogenesis of atherosclerosis?
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Endothelial injury causes increased vascular adherance and leukocyte adhesion. This leads to accumulation of lipoprotiens (LDL) in the vessel wall. Monocytes adhere and become macrophages which take up the lipids and become foam cells. Platlets adhere to the lesion and activate, releasing factors that induce smooth muscle recruitment and proliferation, as well as increased deposition of matrix. The excess lipids continue to accumulate
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What are the 2 most important causes of endothelial dysfunction?
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Hemodynamic disturbances and hypercholesterolemia
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Plaques occur at the ostia of exiting vessels, branch points, and along the posterior wall of abdominal aorta. What do these points have in common?
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All are areas of disturbed flow patterns. Areas of laminar flow are less susceptable to atherosclerosis
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What is the highest risk lipid profile for the development of atherosclerosis?
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High LDL, Triglycerides, Total Cholesterol, and Lp(a) and low HDL
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What is a foam cell?
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A macrophage that has penetrated the endothelium, entered the intima and accumulated lipids. Smooth muscle cells can also take in LDL and become foam cells as well. Oxidized LDL can be taken into the macrophage by a scavenging receptor. This receptor does not internalize when the o-LDL is taken in, allowing for massive accumulation of oxidized LDL and foam cell progression.
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What is the difference between an intimal smooth muscle cell and a smooth muscle cell of the media? How do intimal cells contribute to the progression of atherosclerosis?
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Intimal smooth muscle cells have a proliferative and snythetic phenotype…ie they divide and excrete tons of matrix.
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What artery(ies) are most extensively involved in athersclerosis? List the top 5.
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Lower abdominal aorta, coronary arteries, popliteal ateries, internal carotid, circle of willis
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What are the 3 principal components of an atherosclerotic plaque?
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1. smooth muscle, macrophage, T cells. 2. ECM (including collagen, elastic fibers). 3. Intracellular/extracellular lipids
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Rupture, ulceration and erosion at the surface of a plaque will lead to __________?
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Thrombosis which can lead to partial or complete vessel occlusion. Additionally this can lead to hemorrhage, emboolism, or aneurysm formation.
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What are the major clinical concequences of artherosclerotic disease (4)?
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MI, Cerebral Infarct, Aortic Aneurysm, and Peripheral Vascular Disease
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What is critical stenosis? When does it occur in the coronary artery?
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This is the stage where occlusion of the artery is sufficent to produce tissue ischemia. IN coronary arteries this is usually 70%. Angina on exertion (stable) may be seen when critical stenosis is reached one or several coronary arteries.
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What is the role of collagen, MMPs and TIMPS in the development of acute/ long term outcome plaques?
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Collagen is the major component of the fibrous cap of a plaque. It is frequently remodeled as the plaque grows. MMP's increase collagen breakdown, TIMPS stabilize collagen. If the fibrous cap of an atheroma is thin then it is more prone to rupture.
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What controls collagen turnover? What inhibits it?
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MMP's increase collagen turnover, these are exaserbated by the macrophage response. Macrophages also affect the balace of TIMP's. Generally speaking, plaque inflammation encourages collagen breakdown and destabilizes the plaque.
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What is the worst thing that happens when a plaque ruptures?
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Total occlusion of an artery or thrombosis and embolisim of a distal artery. This can lead to infarct of tissues supplied by these arteries.
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What is an aneurysm?
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localized, abnormal dilation of a blood vessel. Can be acquired or congenital.
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What is the difference between a true and false aneurysm? |
A true aneurysm is a weakening of the wall that leads to dilation but the layers of the vessel remain unbroken. In a false aneurism, the blood vessel wall ruptures but extravascular CT forms a hematoma which while not actively bleeding into the interstitium is not a true aneurysm.
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What is a dissecion?
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A dissection is when blood enters a defect in the arterial wall and splits layers of the vessel.
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What is marfan syndrome? What is loyes-dietz syndrome? What do these contribte to?
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A genetic condition where the fibrillin genee is defective. This leads to impaired collagen synthesis and aberant TGF-B activity. This comprimises elastic tissue. Aortic dissection is common. Loyez-dietz syndrome is another collagen synthesis disease that results in defective synthesis of elastin, Collagen I and III. These patients have a high incidense of aneurysms
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would an increase in MMP or a decrease in MMP activity be more likely to contribute to aneurysm? What about TIMPS?
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increased MMP contributes to aneurysm development. Decreased TIMPS can also contribute to aneurysm progression.
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What contributes to medial ischemia?
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Systemic hypertension can lead to constriction of the vasa vasorum. This causes ischemia in the outer media. In the inner media, ischemia is caused when intimal thickening limits the diffusion of Oxygen to the media.
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What is cystic medial degeneration?
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This is the histologic appearance of medial ischemia caused by intimal thickening and loss of blood flow to the vasa vasorum. It is also seen in Marfan syndrome and scurvy as well.
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What are the 2 most important causes of aortic aneurysms?
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Atherosclerosis and Hypertension. Atherosclerosis is a greater factor for Abdominal aortic aneurysms but HTN contributes more to Ascending aortic aneurysms
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How does an aortic dissection develop?
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Blood separates the laminar planes of the media forming a channel of blood within the aortic wall.
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What is a type A aortic dissection? Type B? Which is worse?
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Type A are the most common and dangerous dissections. They involve the asceding and descending aorta (or just ascending) Thye B are distal to the subclavian artery are less dangerous and common than type A
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What 2 principal mechanisms underlie vascular disease?
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Stenosis or complete obstruction and wall weakeaning leading to dilation or rupture.
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What separates the intima from the media?
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The internal elastic lamina
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What do you see a lot of in the media of elastic arteries such as the aorta? How does this compare to muscular arteries?
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Lots of elastic fibers are found in the media of elastic arteries and lots of smooth muscle cells are found in the media of muscular arteries.
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What is the prinicpal point of physiologic resistance to blood flow. Why?
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Arterioles. Resistance to flow increases to the 4th power when you half diameter of a vessel. The structure of arterioles allows them to control their dimeters and closely regulate both total and regional resistance to flow.
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What and where is the vasa vasorum.
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These are smaller blood vessels that supply the periphery of larger vessels, found in the adventicia of these vessels
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Wht is a berry aneurysm? Where are you likely to see one?
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These are develompental aneurysms that are often found in the cerebral vessels.
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What are some of the effects of fibromuscular dysplasia?
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Thickening of the arteries which can result in luminal stenosis and renovascular hypertension if the thickening occurs in a renal artery (like our renal artery stenosis patient)
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What are some changes that occur when an endothelial cell is activated? What may cause activation of an endothelial cell?
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Hypertension, turbulant flow, cytokine, compliment, AGCEs, hypoxia, cigarettes, etc… can cause endothelial activation. The activated endothelial cell will express adhesion molecules which can lead to procoagulant and proinflammatory conditions.
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What is a common result of endothelial cell dysfunction or loss?
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"Intimal thickening is the stereotypical response of a vessel wall to any insult". This is caused by smooth muscle in the media proliferating and secreting additional matrix materials. The result is similar to what you see when fibroblasts repair a wound in the skin.
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What is secondary hypertension? Do more people with high blood pressure have this or primary?
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Hypertension as a result of an underlying disease or condition such as an adrenal tumor or renal artery stenosis. Most patients have primary hypertension that is idiopathic (95%).
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If untreated what kills roughly half of hypertensive patients?
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Ischemic heart disease.
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What are the 2 primary determinants of blood pressure?
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Cardiac output (stroke volume x heart rate) and peripheral resistance.
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Which of the following humoral factors vasoconstrict/vasodilate? AT-II, Endothelin, Catecholamines, Kinins, Leukotrienes, NO, Prostaglandins, Thromboxine
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Constrictors: AT2, Endothelin, Catecholamines, Leukotrienes, Thromboxine ;;; Dilators: NO, Kinins, Prostaglandins
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What is the purpose of myocardial natriuretic peptides?
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In response to volume expansion in atria/ventricles (stretch) these peptides are released and work to inihbit sodium resorption in the distal tubules, leading to increased Na+ excretion, water follows, lowering BP. These peptides also induce vasodilation.
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Why is renin increased in renal artery stenosis?
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Increased BP is due to retention due to renin release. Renin is released because the stenosed kidney sees a BP that is much lower than in the rest of the body (because of the blockage). Low BP induces renin release, renin further raises BP further worsening the hypertension.
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What are some contributions that may lead to essential hypertension?
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Genetics, reduced renal sodium excretion vasoconstrictive influences and environmental influences (lifestyle)
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What is the most common (90%) cause of myocardial ischemia?
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Reduced blood flow to coronary arteries due to atherosclerotic lesions
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There are 4 major presentations of ischemic heart disease. Name them.
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MI, Angina pectoris, Chronic IHD, Sudden cardiac death.
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What is the threshold of occlusion for significant coronary artery disease?
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a fixed lesion which occludes >75% of the coronary artery
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90% occlusion of a coronary artery can lead to ________________
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inadaquate blood flow even at rest
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Is myocardial ischemia associated with angina pectoris sufficent to induce myocyte necrosis?
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No
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Is stable angina associated with a plaque disruption? What about unstable?
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No. Yes.
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What is the cause of prinzmetal variant angina?
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Coronary artery spasm. Anginal attacks are unrelated to physical activity.
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What is crescendo angina?
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This is unstable angina. It is a frequent, prolonged, or severe angina that occurs at very low levels of activity or even at rest. Often due to disruption of a plaque by a thromus, embolization, or vasospasm.
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Explain the basic pathogenesis of a MI.
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Coronary plaque undergoes an acute change, exposure of subendothelial collagen to blood causes thrombosis, vasospasm, occlusion.
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What is the first biochemical consequence of myocardial ischemia?
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The cardiac myocytes cease aerobic metabolism almost immediately, reducing ATP levels and increasing lactic acid production.
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When does myocaridal contractility begin to decrease after onset of ischemia?
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Within a minute of severe ischemic onset myocardial contractility can cease. This is before irreversible damage has occurred.
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How long after ischemia onset does irreversable injury occur?
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Irreversable damage will occur between 20-30 minutes following onset of ischemia.
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What is the pattern of cell death with prolonged ischemia?
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Will occur first at subendocardium and proceed in a wavelike fashion across the myocardium toward the affected vessel.
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How long after onset of MI do you see half thickness necrosis of the myocardium? Transmural?
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Necrosis will engulf roughly half of the myocardial thickness within 2-3 hours and will become transmural within 6 hours.
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Why is an occlusion in the LAD so bad?
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The LAD supplies the apex of the heart which encompasses the anterior wall of the left ventricle as well as the anterior 2/3 of the ventricular septum.
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What is a right/left dominant circulation pattern? How will this relate to possible outcomes of occlusion in the RCA/LCX
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The posterior IV septum can receive its blood from the RCA or LCX. Individuals (80%) are right dominant. The RCA is especially important in these individuals. Occlusion of the RCA will affect the entire R ventricular free wall, posteriobasal left entricle and posterior IV septum.
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What is a transmural infarction pattern? What is it associated with?
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Complete wall infarcts. These are associated by a permanent occlusion of the LAD, LCX, or RCA (or posterior descending branch)
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What is the infarction pattern that can result in subendocardial damage in a circumfrential pattern?
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Non-transmural infarct due to global hypotension. Since the subendocardium is the least perfused and most vulnerable area for ischemia, hypotension can cause infarct of this tissue.
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When do you see multifocal microinfarcts?
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These are seen when pathology affects the smaller intramural vessels. These can occur if there is vasculitis, spasm, or elevated catecholamines.
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What type of infarct is sometimes refered to as a STEMI?
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Transmural infarcts are refered to as STEMI's due to their effect on the EKG.
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What areas of the heart are affected by a LAD occlusion?
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An infarct of the LAD will involve the anterior all of the left ventricle, the anterior septum and the apex of the heart.
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What areas of the heart are affected by a RCA occlusion?
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RCA infarcts involve the posterior and inferior wall of the left ventricle, the posterior 1/3 of the intraventricular septum, and the right ventricular free wall (in some cases)
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What areas of the heart are affected by a LCX occlusion?
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Infarct of the LCX will involve the lateral wall of the left ventricle sparing the apex.
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Why might a reperfused infarct be hemmorhagic?
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Vasculature is damaged during ischemia and upon restoration of blood flow bleeding can occur.
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What are the common clinical symptoms of MI? What may vomitting/nausea indicate?
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vomiting and nausea suggest that the posterior inferior ventricle can be involved and that secondary vagal stimulation may be occuring.
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What enzymes and proteins are useful for diagnosing MI?
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Cardiac troponins T and I as well as creatine kinase MB are useful. IN the blood you will begin to see these circulate post MI. You see these begin to rise in 3-12 hours, with CKMB and cTnI peaking at 24 hours. CK-MB will return to normal within 48-72 hours but tropinins can persist for 5-14 days.
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What are the 3 types of creatine kinase? Where are they found?
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Creatine kinase is a dimer enzyme that consists of isoforms M and B. MM are found in skeletal and cardiac muscle, BB is in brain and lung, and MB is cardiospecific.
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When may an infarct cause more severe arrythmias?
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myocardial irritibility following MI can cause arrythmias including sinus brady, a fib, heart block, v tach, or v fib. If the infarct affects the bundle of his or conduction pathways there can be heart block or more lethal rhythyms
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What is the most common rupture seen in transmural MI's? How long after onset of MI does the rupture usually occur?
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Rupture of ventricular free wall occuring within 2-4 days post infarct due to coagulative necrosis.
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What is a false aneurysm? How is it different from a true ventricular aneurysm?
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A false aneurysm occurs when complete tear of myocardium has occurred but pericardium is adherent enough in the area to trap blood in a hemotoma, still prone to rupture. A true ventricular aneurysm is bounded my scarred myocardium.
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What is a mural thrombus?
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Infarcted tissue is prone to coagulation due to stasis and inflammation. This can lead to thrombosis and embolism.
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What will ischemic damage to a papillary muscle(s) cause?
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Valvular incompetance and regurgitation.
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Who is at the greatest risk for a free wall rupture?
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a patient with an anterior transmural infarct
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Who is at the greatest risk for conduction block and RV involvment?
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a patient with a posterior transmural infarct
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What a cardioprotective effect of ACE inhibitors post MI?
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lessening of ventricular remodeling
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Briefly explain the events that lead to the development of Chronic IHD?
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Accumulated myocardial damage leading to decompensated heart functioning. This is due to hypertrophy, progressive remodeling, and vessel occlusion.
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What would you call an arrhythmia originating from the atrium
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supraventricular
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Explain the difference between ventricular fibrilation and asystole.
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asystole is lack of electrical activity. V fib is erratic electrical activity but without any functional contraction.
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Wht is the most common cause of a rhythm disorder?
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Ischemic injury
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If the SA node is damaged what takes over? How does this effect HR?
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The AV node takes over at a lower rate of firing (sinus bradycardia)
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What causes heart block. What is 1st, 2nd, 3rd degree heart block?
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Heart block is caused by a dysfunction in the AV node. 1st would be a simple elongation in PR interval, or intermittent rtransmission (2nd) or complete faiulre (3rd).
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Why is reentry bad?
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Abnormal firing to the ventricular muscle can lead to v fib.
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What is long QT syndrome?
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Long QT is caused by a mutation in ionchannels which conduct electrial currents in the heart. Prolonged QT can predispose a patient to malinant ventricular arrythmias. Some causes are a loss of function in K+ channels or a GOF function in Na+ channel. QT elongation is associated with prolongation of cariac repolarization (which makes sense because if the K+ channels dont work it will take longer to repolarize)
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What is the leading cause of SCD?
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Coronary Artery disease
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If many patients who die from SCD are undergoing an Acute MI, why are there few diagnostic changes in the heart?
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They die of a lethal arrythmia before necrosis can occur.
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What is cor pulmonale? What causes it? |
Cor pulmonale is right sided heart failure caused by R ventricular pressure overload. It often follows massive PE but more often left sided heat failure.
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How does the heart respond to chronic hypertension?
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Increased wall thickness and stiffness to move blood at sustained high pressures. |
