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Sem 4-Path-CVS1+2
Sem 4 - Path - CVS Pathology (HTN and AS)
| Question | Answer |
|---|---|
| What are the branches of the LCA? What areas do they supply? | LCA branches into 1) LAD and 2) LCX (Left ant. Descending and Left Circumflex). LAD: Most of apex, LV anterior wall, and anterior 2/3 of interventricular septum. LCX: Supplies LV lateral wall. |
| What artery supplies the anterior 2/3 of IV septum | LAD (branch of LCA) |
| What artery supplies most of the apex? | LAD (branch of LCA) |
| What artery supplies the anterior wall of the LV | LAD (branch of LCA) |
| What artery supplies the lateral wall of the LV | LCX (branch of LCA) |
| What artery supplies the free wall of the RV | RCA (right coronary a.) |
| What artery supplies the posterior wall of the LV | RCA |
| What artery supplies the posterior 1/3 of the IV septum?` | RCA |
| What does the RCA supply? | RV free wall, LV post. wall, Post 1/3 of IV septum |
| Differentiate a hypertensive crisis from hypertensive urgency. | Hypertensive crisis (aka hypertensive emergency) is when there is *acute end-organ damage* (heart: MI, brain:TIA or stroke, Kidneys: ARF, eye: papilledema. Urgency is when there is a sudden BP spike with no end organ damage |
| What are the two major types of htn? Which is more prominent? | Essential hypertension and secondary hypertension. Essential (idiopathic) hypertension is most come (95% of all cases). Secondary htn (htn due to underlying disease s/a renal, endocrine, or CV dz) accounts for 5% of cases |
| Major causes of death in pt with benign htn | Renal failure, benign nephrosclerosis, lv hypertrophy --> heart failure |
| Benign hypertension is associated with what type of arteriosclerosis? | Hyaline arteriosclerosis. |
| What type of arteriosclerosis is most commonly seen in patients with DM | Hyaline arteriosclerosis. |
| What type of arteriosclerosis is seen in both benign htn as well as hypertensive crisis? | hyperplastic arteriosclerosis. |
| Necrotizing arteriolitis is considered the hallmark of what type of htn? | hypertensive crisis (malignant htn). |
| What vascular change is most associated with hypertensive crisis (malignant htn)? | Necrotizing arteriolitis |
| What is the hyaline (in hyaline arteriosclerosis) made of? | it is a translucent highly eosinophilic proteinacious substance that forms as the result of endothelial damage. It forms when plasma components react with collagen. ONLY SEEN IN BENIGN HTN, DM, and NORMOTENSIVE PTS |
| What type of arteriosclerosis does not occlude the blood vessel? | Hyaline arteriosclerosis. |
| Describe the mechanism of necrotizing arteriolitis. | When endothelial permeability is too high, fibrinogen infiltrates vascular wall, where it is then converted to fibrin, and then to fibrinoid. Resulting in fibrinoid necrosis. Mostly effects the kidneys |
| Necrotizing arteriolitis effects what organ the most? | The glomeruli of the kidneys. |
| What type of arteriosclerosis is associated with the histological finding of arteriolar/arterial thickening w/o occlusion? | Hyaline arteriosclerosis. |
| What cardiac changes are associated with hypertension? | LV hypertrophy ‡ hypertensive heart disease |
| Describe the vascular changes seen in benign htn compared to malignant htn. | Benign: Hyaline arteriosclerosis and hyperplastic arteriosclerosis. Malignant: Hyperplastic arteriosclerosis and necrotizing arteriolitis. |
| What is binswanger disease? | Brain damage associated with htn. (Covered later in semester) |
| What are boxcar nuclei? | Large, hyperchromatic, and rectangular nuclei seen in cardiomyocyte hypertrophy caused bypertensive heart disease. |
| “Flea-Bitten kidneys” are a feature of what type of hypertension? | Malignant htn. |
| What is the cause of the appearance of kidney in pts with “flea bitten kidneys”? | microhemorrhages due to vascular death in renal parenchyma in malignant htn |
| What causes the granules seen in granular contracted kidneys | hemorrhages in renal parenchyma due to vascular death. |
| What stain is used for dx of hyaline arteriosclerosis? | Fuschin stain. Shows hyaline deposition in kidneys. |
| What stain used for dx of hyperplastic arteriosclerosis? | PAS stains carbohydrates, basement membrane, etc pink, demonstrating proliferation of vascular wall |
| Gross appearance of Granular contracted kidney is caused by what disease? | What are the granules made of? Benign htn. Granules are hypertrophied glomeruli. |
| Compare flea bitten kidney to granular contracted kidney. | Flea bitten kidney is the result of microhemorrhages in the renal parenchyma due to malignant htn. Granular contracted kidney is caused by benign htn. Granules form as the result of hypertrophied glomeruli. |
| Familial hypercholesterolemia is caused by…? | a mutation in the gene that encodes for the LDL receptor. LDLs can no longer be bound a transported |
| What is acquired dyslipoproteinemia? Lab findings? | Increased LDL, Cholesterol, and decreased HDL. Can be caused by obesity, diet, htn, DM, smoking, physical inactivity. |
| List the major endothelial injury inducing factors. | *The big H’s* - Htn, Hemodynamic stress (ie turbulent flow), hypercholesterolemia, hyperhomocysteinemia, hypoxia. Also, smoking, endotoxins, viruses, etc |
| What are foam cells? | Foam cells are oxidized LDLs that have been engulfed by macrophages causing the macrophage to die. This leads to fatty streaks and atheroma. |
| What cells produce the ECM that leads to fibrosis in arteriosclerosis? | Subendothelial smooth muscle cells. |
| The formation of the plaque of arteriosclerosis is formed by what two contributors? | 1) atheroma leads to fatty plaque (central necrosis) and promotes 2) the migration and proliferation of subendothelial smooth muscles cells which produce ECM leading to fibrosis. Fatty plaque + fibrosis. |
| What is atheroma? | the plaque formed as a result of central necrosis (macrophagic engulfment of oxidized LDL |
| What is the cause of the central necrotic core seen in arteriosclerosis? | Macrophage engulfment of oxidized LDLs |
| Where are arteriosclerotic plaques most likely to be found? | branch points / bifurcation of medium and large arteries. |
| Arteriosclerosis primarily effects what size arteries? Htn? | AS -> large arteries, htn -> small arteries/arterioles. |
| What macroscopic changes can be seen in neonates as the result of arteriosclerosis? | Fatty streaks. These regress and can reappear later in life |
| Artheromatous plaques can begin to appear at what age? | 40 and up. |
| What are the possible complication are AS plaque? | Calcification, mural thrombosis, embolism, intramural hemorrhage, rupture, ulceration, and aneurysm. Plaques can also destabilize and cause luminal occlusion (mural thrombosis) -> acute coronary syndrome. |
| What is the mechanism by which AS causes acute coronary syndrome? | Arteriosclerotic plaque destabilizes and forms a mural thrombosis which then leads to lumen occlusion. |
| What is the histological finding of arteriosclerosis? | Cholesterol clefts: empty spaces that conained cholesterol when tissue was still in body. |
| What are the function of natriuretic peptides? | Inhibition of Na resorption. |
| What is PTCA? | Percutaneous Transluminal Coronary Angioplasty; dilation of a stenotic artery by a percutaneously inserted balloon catheter which results in luminal expansion, plaque rupture, medial dissection and stretching of the vascular wall. |
| What are the potential complications associated with PTCA? | 1) Abrupt reclosure due to dissection, thrombosis, and atheromatous emboli. 2) Proliferative restenosis (thickening of the intima) |
| What complication of PTCA is most likely to occure within 4-6 months of the procedure? | Proliferative restenosis (thickening of the intima). |
| What is the advantage of coronary stenting? | Better results / prognosis. 70% of all PCTA are followed by stenting due to the higher success rate. A PCTA must be performed in order to put a stent in. |
| What are 2 potential complications of coronary stenting? | In-stent restenosis leading to 1) early thrombosis and 2) late intimal thickening ( re-endotheliazation, SMC proliferation, and ECM production) |
| What is CABG? | Coronary Artery Bypass Graft surgery. AKA aortocoronary bypass. Occluded area is bypassed to bring blood from the aorta to area distal to occluded segment. Radial a. used as graft has shown been prognosis. |
| Potential complications of CABG? | Mainly with saphenous graft… Thrombosis, intimal hyperplasia, AS with complicated plaques. |
| What are the constitutional risk factors for arteriosclerosis? | familial hypercholesterolemia, old age, male gender. |
| What causes the oxidation of LDL in AS plaque formation (what event leads to it) ? | Endothelial damage leads to infiltration and oxidation of LDLs. Which is then followed by macrophage engulfment and resulting foamy cell formation. Fibrosis from smoth muscle cells then surrounds these foamy cells. |
| What is the key distinction of malignant htn | Papilledema. Malignant htn is a type of hypertensive emergency. |
| What is the key distinction of a hypertensive emergency (aka htn crisis) | end organ damage |
| What is the most preferable method of interventional tx for coronary AS?????? @ | PCTA + stenting or CABG with internal mammary/thoracic artery (or radial a.) |
Created by:
rkirchoff
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