Term
| In atheroscl, LDL accumulates to fatty streaks and induce monocytes to enter the streak. Describe how this is possible. |
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Definition
| Endothelial cells display increased adhesion molecules and chemotactic factors. VCAM-1, MCP-1, IL-8. Monocytes become more adhesive for endothelium. Only specific monocyte types enter |
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Term
| Sphingomyelinase modified LDL-taken up by scavenger receptors do cause foam cells. What inhibits their for formation? |
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Definition
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Term
| Describe the formation of fibrous plaques. |
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Definition
| Oxidized Lipids induce macrophages lead to SMC proliferation, proteases digest elastic lamina to aid migration. SMC synthesize collagen and specific proteoglycans, take up lipid forming foam cells, necrosis liberating cell contents. Th 1 Tcells produce ifn gamma and Bcells make antibodies to oxidized lipids. |
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Term
| The following are the characterisitics of type of plaque - Accelerated cell death and growth of necrotic core, Angiogenesis, Formation of small thrombi on lumenal surface, Hemorrhage from newly formed vessels, Incorporation of thrombi and clots into vessel wall. |
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Definition
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Term
| When the fibrous cap to a plaque ruptures and spills necrotic core what is the result and what genes regulate it? |
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Definition
| Thrombus formation due to metalloproteinase, apop factors, regulators of clotting. |
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Term
| T or F: exposure of oxidized lipids to platelts actiates them. |
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Definition
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Term
| Which of the following gene polymorphisms are associated with lipid oxidation - CD36, Paraoxonase, Platelet activating factor, HO-1, Glutathione Transferrase, Glutathione Synthase. |
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Definition
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Term
| How do the following affect a thrombus - plasminogen activator inhibitors, lipoprotein A, decreased protein C,S? |
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Definition
| they inhibit thrombolysis |
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Term
| What chem. from monocytes in plaques induces extrinsic clotting of platelets? |
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Definition
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Term
| What two chems in the blood are the greatest predictors of cardiac events? |
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Definition
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Term
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Definition
| Ischemia without infarction |
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Term
| Post MI cellular necrosis start from the __________ surface. |
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Definition
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Term
| In reperfusion injury what is diff btw stunned and hibernating myocardium? |
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Definition
| Stunned is calcium overloaded cells, hibernating is downregulated cells to match O2 supply |
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Term
| Acute coronary syndrome is the sudden formation of thrombi in the coronary arteries due to plaque rupture. So in this phase what is the diff btw NSTEMI and STEMI? |
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Definition
| NSTEMI is only partial occlusion from thrombus tx with antithrombin/platelets and is less severe than STEMI which is total occlusion and you use fibrinolytics in addition |
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Term
| Name a drug for fibrinolysis, thrombolysis, and antiplatelet therapy for post MI. |
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Definition
| Lytics = Streptokinase, tPA, Tenektaplase; Thrombolytics = Heparin; platelets = ASA, Clopidogrel, G2a3b inhibs |
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Term
| Fibrinolytics like tenectaplase catalyze the formation of serine plasmin from plasminogen but what are complications? |
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Definition
| Bleeding, microemboli, doesnt attack platgelets or thrombin which are now rushing into blood |
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Term
| What is the diff mech of Heparin, Low molec heparin, and direct antithrombins? |
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Definition
| Heparin binds to the thrombin complex, LMH binds to Xa complex, and direct drugs bind to thrombin itself. |
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Term
| What is a major complication of unfractionated heparin? |
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Definition
| Heparin-induced thrombocytopenia causes platelet agg. And thromboembolism |
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Term
| What are important things to monitor in antiplatelet drugs? |
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Definition
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Term
| Which mechanical revasculartization post MI is better than fibinolytics like tPA? |
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Definition
| PCI- percutaneous coronary intervention via ballon angio and stenting |
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Term
| Since post MI patients are still at risk after mechanical treatment what drugs should they be on? |
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Definition
| B-blocker, ACEi, fish oil (targets arrythmias), ASA/Clopidogrel, statins; NOT nitrates or CaCB |
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Term
| LDL is cleared from the the blood by the liver via receptors that recognize which molecule on the low density lipoprotein? |
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Definition
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Term
| HMG-CoA reductase inhibitors statins lower LDL, up HDL, down TAGs, by preventing the production of malevonate and thus cholesterol. What are the important side effects since there is a limit on how much LDL stopped with a max dose? |
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Definition
| Preggers! Gi upset, hepatotoxic, death from rhabdomyolysis, and some induce CYP3a4 |
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Term
| If a patient has high LDL you can use cholesterol abs inhibs. They block abs at the brush border of intestine without blocking fat sol vitamins. Name a drug in this class and describe some risks. |
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Definition
| Ezetimibe, has minimal system exposure and 3 fold increase in LFTs with statins |
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Term
| Use of bile acid resins like cholestyramine, colestipol, and colesevelam bring down LDL. But cause GI upset, impairs fat sol vitamins, and has DD rxns. How do they work? |
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Definition
| they bind bile from intestinal lumen causing to excrete it, causes liver to increase LDL receptors to absorb choles from blood to make more bile |
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Term
| Niacin can cause flushing, rash, GI, acanthosis nig, but it is drug of choice for down LDL, VLDL, and up HDL. How does it work? |
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Definition
| suppresses liver creation of VLDL and apolipoprotein B, while stop catabolism of HDL |
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Term
| Fibrates like gemfibrozil and fenofibrate reduce TAGs dramatically (HDL some) but cause rash, GI, gallstones, or warfarin related myopathy. How do they work? |
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Definition
| fibrates act as PPARa ligands that cause up LPL by increase clearance of TAG/VLDL and decrease synthesis; HDL via increasing Apo A1 secretion |
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Term
| Anatommic reentry is an anatomic pathway that guides a reentrant cardiac wave. Give examples and therapy. |
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Definition
| Infarcted tissue circumvention, Wolf-Parkinson-White syndrome, typical A. Fib - treat with surgical ablation |
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Term
| Funciton cardiac wave reentry is an open field reentry with no anatomical pathway, give examples and treatment. |
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Definition
| V. fib, some a fib,- treat with drugs or implant defib device |
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Term
| What is the difference between A. fib and a. flutter on ECG? |
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Definition
| A fib is no discrete p waves in between irregularly spaced QRS complexes treat with warfarin, whereas a flutter is sawtooth appearance with back-back atrial p waves treat with antiarrhythmics |
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Term
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Definition
| Completely errativ rhytym with no id able waves. |
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Term
| Name this artial conduction syndrome - accessory conduction pathway from atria to ventricles bypoassing AV node, ventricles partially depolarize early resulting in wide QRS complex (delta wave), may results in supraventricular tachy. |
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Definition
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Term
| Amiodarone is an important antiarry drug, class 3, but acts on all channels. What are its deadly side effects? |
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Definition
| Pulmonary fibrosis, hepato, hypo/hpyerthyoidism |
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Term
| Whether the atrial fibrillation is chronic, intermittent (so-called paroxysmal atrial fibrillation), or requires medication for rhythm control, the risk of stroke is ____________ and justifies the use of warfarin in the high risk population. |
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Definition
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Term
| In a. fib, symptoms are due to ventricular rate. But what test should you order from this list - history, ecg, cxr, thyroid function, echo, consider stress test. |
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Definition
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Term
| What is the acute management of a fib? |
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Definition
| Control ventricular rate (via AFFIRM trial) with b-blockers, CCB, digoxin and consider cardioversion with K/Na channel blockers |
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Term
| When cardioverting a. fib what are the risks with K and Na channel blockers? |
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Definition
| K risks polymorphic ventricular tachy, Na risks ventricular arrys |
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Term
| Do not cardiovert if patient known to be in atrial fibrillation for longer than __ hours without first getting transesophageal echocardiogram (TEE) to verify there is no clot. |
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Definition
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Term
| The CHADS score assess stroke risk in non-valvular a fib. What does it stand for? |
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Definition
| CHF history, HTN, Age>75, DM, secondary prevention |
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Term
| ID this ECG abnormality - macro-reentrant rhytym, sawtooth pattern, waves at 300 bpm, ventricular variable depending on AV node block, symptoms are rate dependent. |
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Definition
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Term
| If all drug therapy and cardioversion fail in a fib, what to do? |
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Definition
| Ablate AV node and place pacemaker |
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Term
| Atrial flutter has similar risks and management as A fib, with two exceptions, which are? |
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Definition
| Easier to cardiovert, AV nodal ablation much more likely to be successful |
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Term
| Name this type of cardiac conduction abnormality - most common parox supraventricular tachy, more in women, palpitations, chest pain, dyspnea, onset starts with PAC. |
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Definition
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Term
| When treating AVNRT you want to block the conduction pathway with vagal maneuvers like valsalva, or use adenosine. How does adenosine work? |
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Definition
| It increases K+ current out of cells and hyperpolarizes cell and downs Ca currents - so it increases AV nodal refractory period and PR interval. Very short acting, toxicity is flushing, hypotension, chest pain |
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Term
| Conduction bypass tracts like WPW syndrome is most well known. What is the major risk in a WPW patient with A. fib and what is treatment? |
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Definition
| The atrium can reach >300 bpm the pulse may travel down to ventricles which cannot be sustained. Tx with ablation or cardioversion (Na/K channel blockers). |
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Term
| The mechanism of PVC is not understood and is uaually asymptomatic, but benignly presents with skipped beats, palpitations, chest pain, irregular rhytym. What is the treatment for symptoms? |
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Definition
| Usually not indicated, avoid stims. But Na channel blocker flecainide can be used after stress echo test. |
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Term
| Name this arrhythmia - monomorphic stable spiral wave, but can degenerate to V. fib, electrical cardioversion if hypotensive, amiodarone is the IV drug of choice if patient has blood pressure, b-blockers help to suppress it, usually in patient with heart disease like acute ischemia and dilated cardiomyopathy/HF. |
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Definition
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Term
| Sometimes the wave pattern of v. tachy is polymorphic, how do you treat it? |
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Definition
| Just like monomorphic - shock it if no BP, give 1-2mg of Mg, look for underlying cause like lytes and drugs and prolonged QT |
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Term
| Ventricular fibrillation can be caused by ischemia, metabs, drugs, and degeneration from VT. How should you treat it? |
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Definition
| Treat like a polymorphic VT - shock if no BP, treat ischemia if present, treat cause like metabs, drugs, prolonged QT |
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Term
| 25-35% of sudden cardiac deaths are due to VF and VT with early VF(<4 hours) becing the majority and both of which occurred within the first 48 hours. What is the long term management for early VT/VF (<48/<4) and late VT/VF (>48/>4)? |
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Definition
| No treatment because patients have no further risks, late needs defib implated unless cause is clearly reversible like ischemia |
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Term
| Why dont you put post-MI V.tach patients on antiarrythmics? |
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Definition
| Trial shows they killed patients |
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Term
| With defibrillators, slower monomorphic rhythyms use synchronous low energy shock while fast rhytyms use asynchronous high energy shock. But why are biphasic units better than monophasic units? |
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Definition
| Lower energy needed and better at delivering shock with transthoracic impedance |
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Term
| AICDs are very effective in treating patients with ischemic cadiomyopathy or EF<35%, but if all else fails and you still have recrruent arrys then what? |
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Definition
| Catheder ablation to let pacemaker work solely |
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Term
| Which of the following are options for managing a AV block - eliminate rate slowing meds, bedrest and waiting, temp pacemaker, chronotropic drugs like isoproteranol, vagolytic drugs like atropine. |
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Definition
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Term
| T or f, Isoproteranol vasodilates so it can reduce BP. |
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Definition
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Term
| A temp pacemaker may be turned on due to symptomatic hypotension with slow ventricular ate or v. arrys with slow ventric rate. What are the indications for palcing it in first place? |
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Definition
| AV block 2nd degree with asymptomatic mobitz 2 or asymp Type 3 block |
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Term
| In a bradyarry patient which of the following are indications for temp transvenous pacing - patient is hypotensive because of slow HR, atropine failed, isoporteranol failed or provokes ventricular arrys, permanent pacemaker not available at time. |
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Definition
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Term
| Name this AV block - PR interval is prolonged >200msec. asymp. |
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Definition
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Term
| Name this AV block - progressive lengthening of PR interval until a beat is dropped (P wave without QRS), usually asym. |
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Definition
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Term
| Name this AV block - dropped beats not preceded by lengthing PR interval, results in pathologic condition that may progress, often found with 2:1 P:QRS waves. |
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Definition
| 2nd, mobitz 2 can progress to type 3 |
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Term
| Name this AV block - Both P waves and QRS waves have no relation to each other, atrial rate is faster than ventricular, beat independently, treat with pacemaker, can be due to lyme disease. |
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Definition
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Term
| T or F, sick sinus syndrome is fast rhythyms followed by abrupt onset of lowng pauses with no P waves activity, can be due sclerodegenerative change of AV node. |
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Definition
| False, the chages are to SA node |
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Term
| Pacemakers pace from the RV apex. Why does this create dyssynchorny? |
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Definition
| The impulse is not in physiological place and RV beats before LV. So bi-ventricular pacemaker placed. |
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Term
| What maternal diseases can result in congential heart defects? |
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Definition
| Rubella= septal defects or PDA, T2DM= transposition of great vessels |
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Term
| In CHD the risk for flow lesions is familial but what about CHD other than flow lesions? |
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Definition
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Term
| Flow lesions are the largest category of CHD, with 25% having a deleted 22q11 syndrome such as Digeorge or Velocardiofacil syndrome (both have cardio/facial probs). It is the result of homologous recombo errors. What is the inheritance and major defects that result? |
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Definition
| AD, bootshaped tetraology of Fallot or truncus arteriosus; side note - 22q11 high correlation with schizophrenia |
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Term
| In the typically deleted regions of 22q11 syndromes (Digeorge) there is a defect in pharaygneal arch developemtn and cell apoptosis in heart development. What is the gene name? |
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Definition
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Term
| Name this CHD syndrome - patent ductus arteriosis, 2:1 females, facial and finger dimorphism, Auto dom, linked to chrome 6p12, caused by mutation of AP-2b transcription factor needed for neural crest cell development |
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Definition
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Term
| What are the sign of shock? |
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Definition
| Hypotnsion, tachy, ab mental status, oliguria, sweating |
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Term
| Which of the following patient are prone to cardiogenic shock - old, women, prior MI, diabetes, anterior MI location. |
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Definition
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Term
| The leading cause of death of acute MI is cardiogenic shock (pump failure) with half of deaths in 48 hours. What is the most common etiology? |
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Definition
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Term
| What is the strongest predictor of survival of cardiogenic shock? |
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Definition
| Cardiac power which is cardiac index times MAP |
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Term
| Which of the following labs are elevated due to ischemia from cardiogenic shock - BUN/creatinine, liver transaminases, WBC, lactic acid, metabolic acidosis, cardiac biomarkers. |
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Definition
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Term
| Medical treatment of cardiogenic shock is not a solution just a means to transport patient for operation. What is the best treatment for acute MI? |
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Definition
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Term
| After acute MI and cardiogenic shock what two molecules compete against compensatory vasoconstriction (which makes cardiogenic shock better then hypotensive shock)? |
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Definition
| NO and Peroxynitrite - they inhibit contractility, suppress mitochondrial respiration, reduce catechol responses, inflammatory, vasodilate |
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Term
| What ist eh effect of oral inotropes in treating Heart failure? |
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Definition
| Higher risk of death like antiarry drugs; short term use only |
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