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Step 1 Cardio2Testwe
| Question | Answer |
|---|---|
| What are the 5 T's causing R to L shunt in CHD "blue babaies"? | Tetrology of Fallot, transposisition of great vessels, truncus arteriosus, Tricuspid atresia, TAPVR (totoal |
| What is a persistent truncus arteriosus? | failure of truncus to divide into pulmonary trunk and aorta |
| What is tricuspid atresia? What does it require for viability? | absence of tricuspid valacve and hypoplasia of RV. nneds ASD and VSD for viabilitity |
| What is total anomalous pulmonary venous return? | pulmonary veins drain into RH circulation |
| What are 3 causes of a L to R shunt in CHD? | VSD, ASD, PDA |
| What heart sounds are observed in an ASD? | loud S1, fixed split of S2 |
| What is used to close a patent ductus arteriosus? | indomethacin |
| What is Eisenmenger's syndrome? | uncorrected VSD or ASD or PDA causes compensatory pulmonary vasculature hypertrophy= progressive PHTN |
| How does Eisenmenger's cause a shunt reversal? What Sx will it cause? | due to incr Pulmonary reistance, shunt reverse from L to R to R to L= late cyanosis and clubbing. |
| What is the tetrology of Fallot? | 1. pulmonary Stenosis 2. RVH 3. overriding aorta 4. VSD |
| How does a patient typically compensate for Tetrology of Fallot and what is the mech? | Patient learns to squat, which compresses the femoral arteries and incr TPR which will decrease the R to L shunt directing more blood to lungs |
| What is the mechanism of cyanosis and shunt in tetrology of Fallot? | early cyanosis by R to L shunt across VSD because of stenotic pulmonic valve |
| What does a Tetrology of Fallot heart look like on CXR? | boot shaped heart due to RVH |
| What causes Tetralogy of Fallot? | anterosuperior displacement of infundibular septum |
| What is is D transposition of the great vessels and what is the only way it is compatible with life? | Aorta leaves RV, pulmonary trunk leaves LV (separation of systemic and pulmonic circulations). Not compatible with life unless a VSD, PDA, patent foramen ovale exists |
| What causes a transpositon of the great vessels? | failure of aorticopulmonary septum to spiral. infants die without surgical correction |
| What is infantile type of coarctation of the aorta? | aortic stenosis proximal to insertion of ductus arteriosus (preductal). |
| What CHD is Turner Syndrome associated with? | infantile (preductile) coarctation of the aorta |
| What is the adult type of coarctation of the aorta? | stenosis distal to ligamentum arteriosum (post ductal). |
| What are the major associated Sx of adult coarctation of the aorta? | associated with notching of ribs due to notching of ribs, HTN in uppe extermiteis with diminshed pulses in lower extremities. can get aortic regurgiation |
| What is a key physical exam toll to use in evaluation for aortic coarctation? | checking femoral pulses |
| What other CHD is a coarctation of the aorta associated with? | congenital bicuspid aortic valve |
| What is the mech and shunt of a patent ductus arteriosus? | shunt is R to L in fetal period, but when lung R decr with birth it becomes L to R = RVH and failure |
| What murmur is hear in PDA and how is its patency maintained? | machine like continuous murmur. patency maintained by PGE2 and low O2 tension |
| What type of cyanosis might be seen in an uncorrected PDA? | late cyanosis of lower extremitites (differential cyanosis) |
| When might maintainig a PDA be neccessary for life? | in transposistion of the great vessels |
| What CHD are 22q11 syndromes associated with? | Truncus arteriosus, tetralogy of Fallot |
| What CHD is Down syndrome associated with? | ASD,VSD, AV septal defect (endocardial cushion) |
| What CHD is congenital rubella associated with? | septal defects, PDA, pulmonary artery stenosis |
| What CHd is Turner syndrome associated with? | coarctation of aorta (preductal) |
| What CHD is Marfan's syndrome associated with? | aortic insufficiency |
| What CHD is an infant of a mother with DM at risk for? | transposition of great vessels |
| How is HTN defined? | BP >140/90 |
| What are the major RF for high BP? | incr age, obesity, DM, smpoking, black>white>asian |
| What is the mech of primary HTN? | either incr CO or incr TPR |
| What does chronic HTN expose you to ? | atherosclerosis, LVH, stroke, CHF, renal failure, retinopathy, aortic dissection |
| What are atheromas and what are they a sign of? | plaques in BV walls. sign of hyperlipidemia |
| What are xanthomas and what are they a sign of? | plaques or nodules composed of lipid laden histiocytes in skin esp in eyelids. sign of hyperlipidemia |
| What is a tendinous xanthoma and what is it a sign of? | lipid deposit in tendon, especially achilles. hyperlipidemia |
| What is corneal arcus and what is it a sign of? | lipid deposit in cornea, nonspecific (arcus senilis). |
| What is Monckeberg atherosclerosis? Does it obstruct blood flow? | calcification in media of arteries esp radial or ulnar. Usually benign; "pipestem arteries. doesnt obstruct blood flow because intima isnt involved. |
| What is arteriolosclerosis, where is it seen and how might it appear in malignant HTN? | hyaline thickening of small a in HTN or DM. see hyperplastic onion skinning in malignant HTN |
| What is atherosclerosis? | fibrous plaques and atheromas forming in intima of arteries |
| What are the major RF for atherosclerosis? | smoking, HTN, DM, hyperlipidemia, FHx |
| What is the usually progression of atherosclerotic plaque? | Endothelail cell DysFx-->macrophage and LDL accumulation-->foam cell formation-->fatty streaks-->SMM migration (PDGF and TGF beta)--->fibrous plaque--->complex atheroma |
| What are some major complications of atherosclerosis? | aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli |
| What are the major locations of atherosclerosis? | abdominal aorta>coronary a>popliteal a>carotid a |
| What are some Sx of atherosclerosis? | angina, claudication, but can be Asx |
| What is an abdominal aortic aneurysm and who gets them? | associated with atherosclerosis. occurs more frequently in male than female. also smokers, >50 y/o |
| What are 2 things associated with a thoracic aortic aneurysm? | associated with HTN, cystic medial necrosis(Marfan's) |
| What is the tear in an aortic dissection and how does it present? | longitunial intraluminal tear forming a false lumen associated with HTN and cystic medial necrosis (MArfans). Get tearing chest pain radiating to the back |
| What does the CXr show in an aortic dissection? | mediastinal widening |
| How much must a CAD be occluded to cause angina? | 75% |
| What is stable angina, how does it present? | mostly secondary to atherosclerosis; ST depression on ECG. retrosternal CP with exertion |
| What is Prinzmetal's variant angina and how does it present ? | occurs at rest secondary to coronary artery spasm. ST elevation on ECG |
| What is unstable/crescendo angina and how does it present? | thrombosis but no necrosis. ST depression on ECG. worsening CP at rest or with minimal exertion |
| What is coronary steal syndrome? | vasodilator may aggrivate ischemia by shunting blood from area of critical stenosis to area of higher perfusion |
| What is the usualy cause of an MI? | most often acute thrombosis due to coronary artery atherosclerosis, resulting in myocyte necrosis |
| What is sudden cardiac death and the most common cause? | death from cardiac causes within 1 hr of Sx onset. commonly due to lethal arrythmia like V fib |
| What is the presentation of chronic ischemic HD? | progressive onset of CHF over years doe to chronic ischemia of myocardium |
| What is the order of likelihood for coronary artery occlusion? | LAD>RCA>Circumflex |
| What are some acute Sx of MI? | diaphoresis, n/v, severe retrosternal pain, pain in left arm or jaw, SOB, fatigue, adrenergic Sx |
| What is the major complication risk risk in an MI 0-4 days? | arrythmia |
| What are the gross changes observed in an MI 4-24hrs old? | dark mottling pale with tetrazolium stain |
| What are the microscopy findings in an MI 4-12 hrs old? | early coagulative necrosis, edema, hemorrhage, wavy fibers |
| What are the microscopy findings 12-24 hrs post MI? | contraction bands, release of necrotic cell content into blood. see beggining of neutrophil emigration |
| What gross changes are seen in the heart 2-4 days post MI? | hyperemia |
| What microscopy changes are seen 2-4 days post MI? | extenisve coagulative necrosis, tissue around infarct with acute inflammation, n eutrophil emigration |
| What gross changes are seen in the heart 5-10 days post MI? | hyperemic border with central yellow softening |
| What microscopy changes are seen 5-10 days post MI? | appearance of granulation tissue |
| What are the major complication risks for an MI 5-10 days post MI? WHy? | free wall rupture, tamponade, papillary muscle rupture, IV septal rupture sue to macrophage degrading of structural components |
| What gros changes are seen in the heart 7 weeks post MI? | recanalized artery and a gray white area |
| What microscopy changes are seen 7 weeks post MI? | completeion of contracted scar |
| What is the major complication risk 7 weeks post MI? | ventricular aneurysm |
| What is the gold standard for MI Dx in the 1st 6 hrs? | ECG |
| What protein markers is the most specific for an MI confirmation and when does it appear? | cardiac troponin I, rises after 4 hrs and elevated for 7-10 days |
| What is CK-MB and what is its usefulness for MI Dx? | found in myocardium but can also be released by skeletal muscles. useful to Dx an reinfarction on top of acute MI |
| What is the use of ASt for MI Dx? | nonspecific can also be found in liver and SM |
| What ECG changes are seen in a transmural infarct? | ST elevation, pathological Q waves |
| What ECG changfes are seen in an subendocardial infarct? | ST depression |
| What are some general properties of transmural infarcts? | incr necrosis, affects whole wall, ST elevation and Q waves on ECG |
| What are some general characterisitcs of a subendocardial infarct? | due to ischemic necrosis of <50% of ventricular wall.. subendocardium is especiually vulnerable to ischemia, ST depression on ECG |
| What leads have Q waves or other abnormaility in an anterior wall infarct? Which CA? | LAD. V1-V4 |
| What leads have Q waves or other abnormality in an anterospetal infarct and what CA? | LAD. V1-V2 |
| What leads have Q waves or other abnormalities in anterolateral infarct and what CA? | LCX. V4-V6 |
| What leads have Q waves or other abnormalities in lateral wall infarct and what CA? | LCX. I, aVL |
| What leads have Q waves or other abnormalities in inferior wall infarct and what CA? | RCA. II, III, aVF |
| What complication of MI might cause death before reaching the hospital? when is it most common? | cardiac arrythmias, seen most in first few days |
| What is the major complication of a ventricular free wall rupture? | cardiac tamponade |
| What are the major Sx of an papillary muscle rupture post MI? | severe mitral regurgiation, pulmonary edema |
| What are the complications that could happen in an aneurysm formas post MI? | decr CO, risk of arrythmias, embolus from mural thrombus |
| What might be seen and when in a post infarction fibrinous pericarditis? | friction rub (3-5 d post MI) |
| What is Dressler's Syndrome? | autoimmune phenomenon resulting in fibrinous pericarditis several weeks post MI |
| What are some major presenting Sx of bacterial endocarditis? | fever, Roth spots on retina, Osler's nodes (raised lesion on finge or toe pads) new murmur, Janeway lesion (palm or sole), splinter hemorrhages on nail bed |
| What is a common pathogen for accute endocarditis and what is seen? | S. aureus, large vegetations on a previously normal valve |
| What are some common pathogens for subacute endocarditis and what is seen? | viridans strep. smaller vegetations on congentially abnormal or disease valves. sequela of dental procedures |
| When might endocaridits be secondary? | malignancy, hypercoagulable state, lupus. S bovis in colon cancer, S epidermidis in prosthetic valves |
| What valve is most frequently invovled in bacterial endocarditis? | mitral valve |
| When is the tricuspid valve invovled in endocarditis? What pathogens? | IVDA. S. aureus, Pseudomonas, Candida. |
| What are some major complications of bacterial endocarditis? | chordae rupture, glomerular nephritis, suppurative pericarditis, emboli |
| What is a mnemonic for the Sx of bacterial endocarditis? | FROM JANE: fever, Roth spots, Oslers nodus, murmur, Janeway lesions, Anemia, Nail bed hemmorrhage, emboli |
| What cuases rheumatic HD? | pharyngeal infection with beta hemolytic strep |
| What are the early and late problems caused by rheumatic fever? | early death due to myocarditis. late valve disease (mitral>aortic>>tricuspid) which goes from mitral valve prolaspe to mitral stenosis |
| What is seen pathoglogyically in rheumatic HD, and what titers might be elevated? | Aschoff bodies (granuloma with giant cells), Anitschkow's cells ( histiocytes), elevated ASO titers |
| What mediates Rheumatic fever? | immune mediate, type II hypersensitivty, not direct effect of bacteria. Anitbodies to M protein of beta hemolytic strep |
| What is the mnemonic for the presentation of rheumatic fever? | FEVERSS: fever, erythema marginatum, valvular damage (vegetation and fibrosis, incr ESR, Red-hot joint(migratory polyartritis), subcutaneous nodules, St. Vitus's dance (chorea) |
| How does acute pericarditis present? | sharp pain. aggrevated by inspiration and relieved by sitting up and leaning forward |
| What is fibrinous pericarditis? How does it present and what might cause it? | most frequent type. caused by dressler's syndrome, uremia, radiation. loud friction rub |
| What is serous pericarditis, and what causes it? | noninfectious inflammatory disease (rheumatic fever, SLE) |
| What cuases suppurative/purulent pericarditis? | infectious agents |
| What is the mech of cardiac tamponade? | compression of heart by fluid in pericardium, leading to decr CO |
| What happens to pressures in all 4 heart chambers in cardiac tamponade? | all 4 chambers diastolic P is eequal |
| What are the major findings seen in cardiac tamponade? | hypotension, incr venous P (JVD), distant heart sounds, incr HR, pulsus paradoxus |
| What is pulsus paradoxus? | decr in amplitude of systolic BP by 10mmHg during inspiration. Seen in tamponade, astma, sleep apnea, pericarditis, croup |
| What is the mechanism and complication risk of syphilitc HD?> | tertiary syphilisdisrupts the vasa vasorum with dialtion of aorta and valve ring. can lead to aneurysm of ascending aorta and aortic valve incompetence |
| What happens pathologically to the arota in syphilitic Hd? | calcification of aortic root, tree bark appearance of the aorta |
| What is the most common primary tumor in adults of the heart and where does it occur? | myxomas, ball valve obstruction in LA (associated with multiple syncopal episodes) |
| What is the most frequent primary cardiac tumor in children? | rhabdomyomas associted iwht tuberous sclerosis |
| What is Kussmaul's sign? | incr in JVP on inspiration |
| What are varicose veins? | dilated, tortuous superficial veins due to chronically elevated venous P. |
| What are 2 things that a varicose vein could predispose one to? | poor wound healing and varicose ulcers. thromboembolism is rare. |
| What is Raynaud's disease? | decr blood flow to skin due to arteriolar vasospasm in response to cold temp or stess. most often in fingers |
| What is Raynaud's phenomenon? | when Raynaud's disease is secondary to mixed CT disease like SLE or CREST syndrome |
| What is the epidemiology of Temporal arteritis? | elderly females. unilateral HA, jaw cladication. may cause irreversible blindness sue to occlusion of opthalmic a. |
| What disease is temporoal (giant cell) arteritis associated with? | polymyalgia rheumatica |
| What is the pathology labs, and Tx for Temporal (giant cell arteritis)? | affects branches of carotid a. focal granulatomous inflammtion, incr ESR. tx: high dose steroids |
| What is the epidemiology and presentation of takayasu's arteritis? | Asian females <40. Pulseless disease (weak upper extermity pulses), fever, night sweats, artritis, myalgia, skin nodules, ocular disturbances |
| What are the pathology and labs of takayasu's arteritis? | granulatomous thickening of aortic arch and proximal great vessels. incr ESR |
| What is the epidemiology and presentation of polyarteritis nodosa? | young adults. HepB positive in 30%. get fever, wt loss, malaise, HA, GI: abd pain, melena. HTN neuro dysfx, cutaneous disruptions |
| What vessels are most commonly invovled in polyarteritis nodosa? | renal and visceral vessles. NOT pulmonary a. |
| What mediates polyarteritis nodosa and what pathology is seen? | immune complex mediated. get transmural fibrinoid necrosis with lesions of different ages |
| What might you see on an arteriogram of polyarteritis nodosa? | multiple aneurysms and constrictions |
| How do you Tx polyarteritis nodosa? | corticosteroids, cyclophosphamide |
| What is the epidemiology/presentation of Kawasaki disease? | Asian children<4 y/o. fever, lymphadenitis, conjunctivits, changes in lips/oral mucosa (strawberry tongue). hand foot erythema, desquamation |
| What is the major danger of kawasaki disease and what is the tx? | can develop coronary aneurysms, Tx: IV immunoglbulin and aspirin |
| What is the epidemiology and presentation of Buerger's disease (thromangitis obliterans)? | heavy smokers, males <40 y/o. intermittent claudication may lead to gangrene, digit autoamputation, superficial nodular phlebitis |
| What other disease phenomena is Bueger's disease (thrombangitis obliterans) associated with? | Raynaud's phenomenon (cold sensitivity) due to neural invovlement |
| What is the pathology and Tx for Buerger's disease (thrombangitis obliterans)? | segmental thrombosing vascultis. tx: smoking cessatiuon |
| What is the epidemiology/presentation of microscopic polyangitis? | pauci-immunie glomerular nephritis. palpable purpura |
| What is the pathology and key lab of microscopic polyangitis? | no granulomas. +pANCA |
| What 3 body parts are most typically affected by Wegener's granulomatosis? | URT, LRT, Renal |
| What does Wegener's granulomatosis present like in the URT? | upper RT: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis |
| What does Wegener's granulomatosis present like in the LRT? | Lower RT: hemoptyisis, cough, dyspnea |
| What does Wegener's granulomatosis present like in the kidney? | Renal: hematuria, red cell clasts? |
| What is the key pathological triad of Wegener's granulomatosis? | 1. focal necrotizing vascultis 2. necrotizing granulomas in lung and upper airways 3. necrotizing glomerular nephritis |
| What is the key lab finding and CXR in Wegener's gramulomatosis? | c-ANCA. CXR: large nodular densities |
| How do you Tx Wegener's granulomatosis? | cyclophosphamide, corticosteroids |
| What is the epidemioloy/presentation of Churg-Strauss syndrome? | ASTHMA, sinusitis, palpable purpura, peripheral neuropathy (wrist/foot drop). can also involve heart, GI , kidneys |
| What is the pathology and key lab seen in Churg-strauss syndrome? | pauci-immune. granulomatous vasculitis with eosinophilia. p-ANCA |
| What is Henoch-Schonlein purpura, How does it present? | childhood systemic vasculitis following URIs. Triad: 1. skin: palpable purpura or buttocks/legs 2. arthralgia 3. GI: abdominal pain, melena, multiple lesions of same age |
| What causes Henoch-Schonlein purpura? | IgA immune complexes. associted wiht IgA nephropathy |
| What is the presentation of Sturge-Weber disease? | congenital vascular disorder affecting capillary BV. port wine (nevus flammeus) stain on face, ipsilateral leptomeningial angiomatosis (intracerbral AVM), seizures, early onset glaucoma |
| What vessels are most affected in Sturge-Weber disease? | small ones |
| What is a strawberry hemangioma? | benign capillary hemangioma of infancy. appears in first few weeks of life. grows rapidly and regresses at 5-8 y/o |
| What is a cherry hemangioma? | benign capillary hemangioma of elderly. doesnt regress |
| What is a pyogenic granuloma? | polypoid capillary hemangioma that can ulcerate and bleed. associted with trauma and pregnancy |
| What is a cystic hygroma? what is its associted with? | cavernous lymphangioma of neck. associted with Turner syndrome |
| What is a Glomus tumor? | beingn, patinful, red blue tumor under fingernails. arises from midifes SMM of glomus body |
| What is bacillary angiomatosis? When are they seen, What causes them, and what might it be confused for? | benign capillary skin papules found in AIDs pt. caused by bartonella hensale. can be mistake for Karposi's sarcoma |
| What is anm angiosarcoma? | highly lethal malignancy of liver. associted with vinyl choloride, arsenic, ThO2(throtrast exposure) |
| What is an lymphangiosarcoma? | lymphatic malignancy associted with lymphedema (post radical mastectomy) |
| What is Kaposi's sarcoma? What causes it? | endothelial malignancy of skin associted with HHV-8 and HIV. can be mistake for bacillary angiomastosis |
| What is the tx for essential HTN? | diuretics, ACE I, angiotensin II receptor blockers, Ca++ channel blockers |
| What is used to treat HTN in CHF? | diuretics, ACEI/ARBs, beta blocerks(if compensated, contra if cardiogenic shock), K+ sparing diuretics |
| What is used for HTN in DM? | ACE I/ARB, Ca++ channel blockers, diuretics, Beta blockers, alpha blockers |
| Why are Ace I particulary useful in DM HTN management? | they are protective against diabwetic neuropathy |
| What is the mech of hydralizine? | incr cGMP--> SMM relaxation. vasodiates arterioles > veins. reduces afterload |
| What is the clinical use of hydralizine? | severe HTN, CHF. 1st linefor HTN in pregnancy with methyldopa. adminstered with Beta blocker to prevent relfex tachy |
| What are the major SE of hydralizine? | reflex tachy (so contraind in angina and CAD), fluid retention, nausea, HA, angina, lupus like syndrome |
| What is the mech of nifedipine, verapamil, diltiazam, amlodipine? | Ca++ channels blockers, which block L type channels of CM and SMM reducing contractility |
| Which clacium channel blockers acts most on vascular SMM? | nifedipine>diltiazem>verapamil |
| Which Ca++ channel blockers acts most on the heart? | verapamil>diltiazem>nifedipine |
| What is the clinical use of nifedipine, verapamil, diltiazem, amlodipine? | HTN, angina, arrythmia (NOT nifedipine), prinzmetal's variant angina, Raynaud's syndrome |
| What are the major SE of nifedipine, verapamil, diltiazem, amlodipine? | cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
| What can nitroprusside, fenoldopam, and diazoxide all be used for? | malignant HTN |
| What is the mech and major SE of mitroprusside? | short acting incr cGMP via release of NO. can cause cyanide toxicity(releases cyanide) |
| What is the mech of fenoldopam? | dopamine D1 receptor agonist which relaxes renal vascular SMM |
| What is the mech and major SE of diazoxide? | K+ channel opener, hyperpolarizes and relaxes vascular SMM. can cause hyperglycemia (reduce insulin release) |
| What is the mech of nitroglycerine, isosorbide dinitrate? | vasodilate by releasing NO in SMM causing incr cGMP and SMM relaxion. work veins>>arteries. decr afterload |
| What is the clionical use of nitroglycerin, isosorbide dinitrate? | angina, pulmonary edema. used also as aphrodesiac and erection enhancer |
| What are the major SE of nitroglycerin, isosorbide dinitrate? | reflext tachycardia, hypoTN, flushing, HA. |
| What is Monday disease in assocition with nitroglycerin and isorbide dinitrate? | industrial exposure develops tolerance over week and on weekedn gets tachycardia, dizziness, HA on rexposure after tolerance drops on weekends |
| What are the overall goals of antiangina therapy? | reduce myocardial O2 consumption, by decr EDV, BP, HR, contractility, ejectionm time |
| What is the effect of nitrates on the variables in angina therapy? | decr EDV, BP, ejection time, MVo2. incr HR and contractivitly via reflex response |
| What uis the effect of beta blockers on the variables targeted in angina? | incr EDV, ejection time. decr BP, contractilty, HR, MVO2 |
| What is the effect on the target variable in angina by a combined Nitrate and beta blocker? | none or decr EDV, decr BP, HR. little to no effect on contractilty and ejection time. very decr MVO2 |
| Which drugs are nifedipine and verapamil similar to in anginal mechanisms? | Nifedipine similar to nitrates, verapamil to Beta blcokers |
| What 2 partial beta agonists are contra indicated in angina? | pindolol, acebutolol |
| What is the mech of lovastatin, pravastatin, simvastain, atrovastatin, rosuvastatin? | HMG-CoA reductase inhibitors. inhibit cholesterol precursor mevalonate |
| What cirulating lipid do statins have the most effect on? | vastly decr LDL, also decr Tg, incr HDL |
| What are the major SE of the statins? | hepatotoxicity (incr LFTs), rhabdomyolysis |
| What is the lech of niacin? | inhibits lipolyisis in adipose tissue, reduces hepatic VLDL secretion into circulation |
| What is the major effect of niacin on circulating lipids? | best at incr HDL, also decr LDL, TGs |
| What are the major SE of Niacin? | red, flushed face (decr by aspirin), long term use hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbating gout) |
| What is the class and mech of cholestyramine, colestipol, colesevalam? | bile acid resins. prevent intestinal reabsrobtion of bile acids, forcing the liver to use cholesterol to make more? |
| What are the effects of cholestyramine, colestipol, colesevalam on circulating lipids? | decr LDL and slightly incr HDL and TGs |
| What are the major SE of cholestyramine, colestipol, colesevalam? | pt hate it. tastes bad, cuases GI discomfort, decr absrobtion of fat soluble vitamins, cholesterol gallstones |
| What is the class and mech of ezetimibe? | cholesterol absorbtion blocker, prevents cholesterol reabsorbtion at small intestine brush border |
| What is the major effect on circulating lipids by ezetimibe? | decr LDL |
| What are the SE of ezetimibe? | rarely incr LFTs |
| What is the class and mech of gemfibrozil, clofibrate, bezafibrate, fenofibrate? | fibrates, upregualte LPL increasing TG clearance |
| What are the major effects of gemfibrozil, clofibrate, bezafibrate, fenofibrate on circulating lipids? | most effective at decr TGs, also incr HDL, decr LDL |
| What are the major SE of gemfibrozil, clofibrate, bezafibrate, fenofibrate? | myositis, hepatotoxicity(incr LFTs), cholesterol gallstones |
| What is the mech and T 1/2 of digoxin? | direct inhibiton of Na+/K+ ATPase leads to direct inhibition of Na+/Ca++ exhanger causeing incr Ca++ and positive inotropy. stimulates vagus n. |
| What is the clinical use of digoxin? | CHF (incr contractility), atrial fib (decr condcution at AV node |
| What are the major SE of digoxin? | Cholinergic: n/v, diarrhea, blurry yellow vision (van Gogh). |
| What effects would digoxin have on the ECG? | incr PR, decr QT, scooping, T wave inversion, arryhtmia, hyperkalemia |
| What conditions might worsen the effects of digoxin? | renal failure ( decr excretion), hypokalemia (digoxin can bin to K+ site on ATPase), quinidine (decr digoxin clearance, displaces digoxin from tissue-binding sites) |
| What is the antidote to digoxin OD? | slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragment,Mg2+ |
| What is the mech of nesiritide? | recombinant B-type natriuretic peptide. causes incr cGMP and vasodilation |
| What is the clinical use of nesiritide? | acute decompensated HF |
| What is the major SE of nesiritide? | hypoTN |
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tjs2123
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