Cardiovascular USMLE

Frage	Antworten
What are the five dilatations of the primitive heart tube?	Truncus arteriosus Bulbus cordis Primitive ventricle Primitive atrium Sinus venosus
Name the structures in the mature heart that are derived from the following embryonic structures:	Truncus arteriosus: Ascending aorta and pulmonary trunk Bulbus cordis: Smooth parts of left (aortic vestibule) and right (conus arteriosus) ventricle Primitive ventricle: Trabeculated parts of left and right ventricle Primitive atria: Trabeculated parts of left and right atria Left horn of sinus venosus: Coronary sinus Right horn of sinus venosus: Smooth part of right atrium (sinus venarum) Transient common pulmonary vein: Smooth part of left atrium Right common cardinal vein and right anterior cardinal vein: Superior vena cava.
What embryonic layer gives rise to most of the cardiovascular system?	Mesoderm
What structure divides the truncus arteriosus and bulbus cordis?	Aorticopulmonary septum
Name the structure between the atria that develops from the walls of the septum primum and septum secundum.	Foramen ovale.
Name three physiologic shunts in the fetal circulation and the structures they shunt between	Foramen ovale (right to left atrium) Ductus arteriosus (pulmonary artery to aortic arch) Ductus venosus (umbilical vein to IVC)
What are the two anatomic divisions of the pericardium?	Serous pericardium (made of visceral epicardial layer and parietal layer) Fibrous pericardium.
Which nerve lies between the fibrous pericardium and mediastinal pleura?	Phrenic nerve (runs with pericardiophrenic vessels)
Name the chamber associated with each heart surface:	Sternocoastal surface: Right ventricle Posterior surface (base)- Left atrium Diaphragmatic surface- Right and left ventricles. Pulmonary surface and apex- Left ventricle
Name the structures that compose each heart border:	Right border: right atrium Left border: Left ventricle, left auricle Inferior border: Right ventricle Superior border: Right and left auricles, great vessels.
Name the event associated with each heart sound:	S1: Closure of the AV (tricuspid, mitral) valves. S2: Closure of semilunar (aortic, pulmonary) valves S3: Flow of blood from atria into ventricles during diastole (often seen with large ventricular volumes, ie CHF, often benign in youth and trained athletes.) S4: Flow of blood from atria into ventricles during atrial systole (often present in patient with stiffened ventricle)
Describe the best location for auscultation of the following cardiac valves:	Tricuspid valve- Left sternal border, fifth intercostal space Pulmonary valve- Left sternal border, second intercostal space. Mitral valve- Apex of heart, fifth intercostal space. Aortic valve- Right sternal border, second intercostal space.
What are the most common sites for coronary occlusion?	Left anterior descending (LAD) >RCA > circumflex
Trace the general pathway of venous drainage from myocardium.	Great, middle, and small cardiac veins -> coronary sinus -> right atrium.
Describe the function of each myocardial cellular component:	Sacromere: Contractile unit Intercalated disks: Cell adhesion Gap junction: Electrochemical communication between myocardial fibers T tubules: carry action potentials into the cell interior Sarcoplasmic reticulum: Storage and release of calcium.
What congenital valvulvar defect is associated with aortic stenosis?	Bicuspid aortic valve
What are two common manifestations of aortic stenosis?	Angina and syncope
Which disorder results from myxomatous degreneration of the mitral valve?	Mitral valve prolapse
Patients with mitral valve prolapse are at increased risk of which infection?	Infective endocarditis
Name the valvular defect causing each murmur described below:	.
Harsh midsystolic murmur in the left second intercostal space at the left sternal border.	Pulmonic stenosis
Harsh midsystolic murmur in the right second intercostal space at the right sternal border, radiating to the neck (carotid arteries) and apex	Aortic stenosis
Harsh midsystolic murmur at the left third and fourth interspaces radiating down the left sternal border, murmur louder with decreased preload (ie, on Valsalva), S4 and biphasic aphical impulse often present	Hypertrophic cardiomyopathy
Blowing holosystolic murmur at apex radiating to the left axilla with increased apical impulse	Mitral regurgitation.
Blowing holosystolic murmur at the lower left sternal border radiating to the right of the sternum, may increase with inspiration	Tricuspid regurgitation
Soft, late systolic murmur at the left sternal border or apex, accompanied by mid systolic click	Mitral valve prolapse
Harsh holosystolic murmur at the lower left sternal border, accompanied by a thrill	Ventricular septal defect (VSD)
Blowing, high pitched diastolic murmur at the left second to fourth interspaces radiating to the apex	Aortic regurgitation.
Low-pitched diastolic murmur at the apex that gets louder prior to S1 and opening snap is often present just after S2	Mitral stenosis
Systolic flow murmur at left upper sternal border, fixed splitting of S2	Atrial septal defect (ASD
Name four important manifestations of ischemic heart disease	Angina, myocardial infarction, Lethal arrhythmia causing sudden cardiac death, Chronic CHF
What are two major etiologies of myocardial ischemia?	Decreased coronary perfusion, Increased myocardial O2 demand.
What conditions compound the consequences of impaired myocardial perfusion?	Anemia, advanced lung disease, cigarette smoking, congenital heart disease.
name the type of angina	Pain precipitated by exertion, relieved by rest/vasodilators-Stable angina Paroxysmal chest pain at rest in patient with or without coronary risk factors- Prinzmetal angina Severe substernal pain/pressure at rest- Unstable angina.
Describe the underlying pathology for each type of angina	Stable angina: Greater than 75% occlusion of coronary artery Prinzmetal angina: Coronary vasospasm Unstable angina: Plaque disruption with resulting occlusive thrombosis within a coronary artery
Name the type of myocardial damage described below:	Full thickness infarction caused by complete occlusion of a coronary artery: Transmural infarction Infarction of the inner half (or less) of the ventricular wall supplied by a partially occluded coronary artery: Subendocardial infarction T wave inversion on ECG: Transmural ischemia ST depression on ECG: Subendocardial injury ST elevation on ECG: Transmural injury Q waves present on ECG: Transmural infarction
What is the initial event in the development of a transmural infarction?	Acute plaque disruption.
What are the most common symptoms of a myocardial infarct?	Crushing retrosternal chest pain or pressure, dyspnea, pain radiating into left arm or neck, diaphoresis, nausea
What type of necrosis is seen in myocardium within 24 hours of infarction?	Coagulative necrosis
What type of inflammatory cells are seen in the myocardium within 24 hours of infarction?	Neutrophils
What is the most common type of inflammatory cell seen in myocardium from the 2nd to 10th day after an infarction?	Macrophages
When is the risk of myocardial rupture greatest and why?	At 4 to 7 days. Tissue is weakest following phagocytosis of debris by macrophages and prior to growth of granulation tissue.
How many days does it take to form granulation tissue in a region of infarcted myocardium?	7 to 10 days.
How many days does it take to form granulation tissue in a region of infarcted myocardium?	7 to 10 days.
How many weeks does it take to form contracted scar tissue in a region of infarcted myocardium?	7 weeks
What is the diagnostic test of choice in a patient with suspected MI?	ECG
What two classic ECG changes are seen during an MI?	Q waves, ST elevation.
When does CK-MB being to rise, peak and return to normal?	Rise- 3 to 8 hours Peak- 10 to 24 hours Return to normal- 2 to 3 days.
When does troponin I begin to rise, peak and return to normal?	Rise: 3 to 8 hours Peak: 24 to 48 hours Return to normal: 5 to 10 days.
What are the advantages and disadvantages of the CK-MB serum cardiac marker?	Allows diagnosis of re-infarction as levels quickly return to normal; may be falsely elevated with skeletal muscle injury.
What are the advantages of the troponin test?	Very specific to cardiac injury, allows diagnosis of late presenting MI
What are the two most common complications of MI?	Cardiac arrhythmia, CHF
List five less common but severe complications of MI?	Cardiogenic shock Ventricular aneurysm or rupture. Papillary muscle rupture Mural thrombosis with resulting peripheral embolism Dressler syndrome.
How does the left ventricle respond to long-standing HTN?	Concentric hypertrophy
What are the three types of cardiomyopathy?	Dilated or congestive Hypertrophic Restrictive
What are the most common nongenetic etiologies of dilated cardiomyopathy?	Alcohol abuse Beriberi (thiamine deficiency) Coxsackie B myocarditis, Cocaine, Chagas disease Doxorubicin toxicity Pregnancy.
For each antiarrhythmic agent, name the unique toxicity/toxicities?	.
Quinidine	Cinchonism-headache, tinnitus, thrombocytopenia, torsades de pointes.
Procainamide	Reversible drug-induced lupus
Lidocaine	CNS depression, cardiac depression, local anesthetic
Flecainide	Proarrhythmic
Propanolol	Sedation and fatigue, erectile dysfunction, exacerbation of asthma and COPD, masks effects of hypoglycemia
Bretylium	Severe postural hypotension
Amiodarone	Interstitial pulmonary fibrosis, thyroid dysfunction, hepatotoxicity, tremor, ataxia, neuropathy, bluish discoloration of skin, corneal deposits.
What is the drug of choice for abolishing acute supraventricular tachycardia (SVT)?	Adenosine
Most common tumor of infancy	Port wine stain birthmark
Cutaneous vascular tumor commonly seen in patients with end-stage liver disease (hyperestrinism)	Spider telangiectsia
Which vessels are most commonly involved in temporal arteritis?	External carotid artery and its branches
What is the triad of Wegener granulomatosis?	Focal necrotizing vasculitis of upper airways and lungs Necrotizing granulomas of upper and lower respiratory tract Necrotizing glomerulitis
Name the type of vasculitis associated with the following clinical and pathologic features:	Presence of C-ANCA- Wegener granulomatosis Presence of P-ANCA- Microscopic Polyangiitis, PolyArteritis Nodosa (PAN), and Churg-Strauss syndrome.
Fibrous thickening of origins of the great vessels leading to absent pulses.	Takayasu arteritis
Well-demarcated, segmented fibrinoid necrosis of the arterial wall and diffuse neutrophilic infiltrates in medium-sized arteries	PAN

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