1、Cardiology 1题库,Q 21,A 56-year-old man comes to the cardiology clinic because of fatigue, palpitations, and exertional dyspnea over the last several weeks. On physical examination, his heart rate is irregular and measures 122 beats per minute, while his blood pressure is 110/70 mm Hg. The patient und
2、ergoes further work-up, including ECG, radiographic studies, and laboratory studies. His ECG shows atrial fibrillation and trans-esophageal echocardiography reveals a thrombus in a dilated left atrium. In the event of an interruption of blood flow secondary to arterial occlusion, which of the follow
3、ing organs would be least vulnerable to infarction?A.SpleenB.BrainC.KidneyD.LiverE.Heart,A 21,Correct answer:DInfarcts in an otherwise normal liver are rare because it has a dual blood supply: the portal vein and hepatic artery. Should the hepatic artery become occluded, the portal venous supply and
4、 retrograde arterial flow through accessory vessels (e.g., from the inferior phrenic, adrenal, intercostal arteries, etc.) is typically sufficient to sustain the liver parenchyma. The notable exception is when a transplanted liver undergoes hepatic artery thrombosis. In this case, the liver can deve
5、lop biliary tree infarction and organ failure because the collateral blood supply is severed during transplantation.(Choice A) The spleen is relatively vulnerable to infarction because the perfusion via the splenic artery is end-arterial. Wedge-shaped, capsule-based splenic infarcts occur and are a
6、known complication of sickle cell anemia, infective endocarditis, and cardiac mural thrombosis.(Choice B) Irreversible damage appears to occur in the most vulnerable of neurons after approximately 5 minutes of complete ischemia.(Choice C) The kidney, similar to the spleen, has an end-arterial blood
7、supply, and is generally able to tolerate warm ischemia for at least 30 minutes. Longer periods of complete ischemia result in immediate functional loss; late recovery of renal function is incomplete or absent.(Choice E) The myocardium can endure complete arterial ischemia for twenty or thirty minut
8、es without severe consequences. Briefer periods of ischemia do not result in necrosis, but rather myocardial stunning. Coronary artery embolism is an uncommon cause of myocardial infarction; nonetheless, it should be considered in myocardial-infarcted patients with atrial fibrillation, infective end
9、ocarditis, left atrial or ventricular thrombus, and in patients undergoing cardiac catheterization.,Q 22,Autopsy of an 86-year-old Caucasian male shows localized amyloid deposition in the cardiac atria. No other organs are involved. The amyloid is most likely composed of which of the following polyp
10、eptide fragments?A.Calcitonin B. Prolactin C. AmylinD- (3-amyloid protein E. Immune globulin light chain F. Natriuretic peptide,A 22,Correct answer:FLocalized amyloidosis confined to the cardiac atria (isolated atrial amyloidosis, or IAA) is due to deposition of abnormally folded -pleated sheet conf
11、ormation) atrial natriuretic peptide-derived proteins. The incidence of IAA increases with age, reaching 90% in the ninth decade. This is a form of senile cardiac amyloidosis which may increase the risk of atrial fibrillation.(Choice A) Deposition of abnormally folded calcitonin-derived peptides is
12、responsible for localized amyloidosis of the thyroid gland in patients with medullary carcinoma of the thyroid.(Choice B) Deposition of abnormally folded prolactin-derived proteins may be responsible for localized amyloidosis of the pituitary gland.(Choice C) Islet amyloid protein (amylin) is usuall
13、y found in patients with localized pancreatic amyloidosis. It is detected in the pancreatic islets of more than 90% of patients with type 2 diabetes.(Choice D) (3-amyloid protein is the 4000 Dalton peptide found in the core of the cerebral plaques of Alzheimer disease, -amyloid protein is also found
14、 in localized amyloid deposits in the walls of cerebral blood vessels of Alzheimer patients as well as in patients with cerebral amyloid angiopathy (CAA).(Choice E) Deposition of immune globulin light chains，especially -light chains and their fragments,is responsible for primary systemic (not locali
15、zed) amyloidosis. Primary systemic amyloidosis arises in association with monoclonal B-cell proliferations (e.g multiple myeloma) and causes systemic amyloid deposition involving the heart, as well as the skin, tongue, gastrointestinal tract, kidney, and peripheral nerves. Immunoglobulin light chain
16、s of either the or the variety (Bence Jones proteins) may also be found in the serum and urine.,Q 23,A 21-year-old Caucasian male presents to the emergency department following an episode of syncope. The syncopal episode was not provoked by any activity or circumstance, nor was it preceded by lighth
17、eadedness. The patient has no significant past medical history and he is not taking any medications. An ECG obtained in the ER reveals QT-interval prolongation but is otherwise unremarkable. Assuming this is an inherited condition, the relevant mutation most likely affects which of the following str
18、uctures? Cardiac cell cytoskeleton proteins B. Cardiac cell sarcomere proteinsMitochondrial enzymes of oxidative phosphorylation Calcium-binding sarcoplasmic reticulum protein Membrane potassium channel proteins,A 23,Correct answer:EThis patients sudden-onset syncopal episode suggests a sudden cardi
19、ac arrhythmia. QT prolongation in an otherwise healthy young individual is usually congenital. The mutation most likely to cause QT-interval prolongation can be determined based on an understanding of cardiac electrophysiology. On an ECG tracing, the QT interval begins at the start of the QRS comple
20、x and ends at the end of the T wave. Thus, the QT-interval reflects the cardiac myocyte action potential duration, which is determined in part by K+ currents through channel proteins. The mutations listed in the other answer choices would be less likely to directly affect the cardiac cell action pot
21、ential duration.There are two important congenital syndromes that cause QT prolongation: Jervell and Lange-Nielsen syndrome (autosomal recessive, with neurosensory deafness) and the more common Romano-Ward syndrome (autosomal dominant, no deafness). Both may predispose to torsades de piontes ventric
22、ular tachyarrhythmia) at a young age, causing syncopal episodes and possible sudden cardiac death.(Choices A and C) Mutations affecting cardiac cell cytoskeletal proteins or the mitochondrial enzymes of oxidative phosphorylation are thought to cause the genetic form of dilated cardiomyopathy (DCM).
23、DCM usually presents with gradual onset of left-sided heart failure (with symptoms like dyspnea on exertion initially), as opposed to the sudden syncopal episode in a previously asymptomatic patient described above.(Choice B) Mutations in cardiac cell sarcomere proteins (e.g. beta-myosin heavy chain
24、) underlie hypertrophic cardiomyopathy (HCM). Although HCM may present as syncope in a previously asymptomatic young person, the syncope of HCM is typically provoked by exertion. Additionally, QT prolongation is not generally found in HCM.(Choice D) Mutations of a calcium-binding sarcoplasmic reticu
25、lum protein might underlie some cases of arrhythmogenic right ventricular cardiomyopathy (ARVC), a progressive fibrofatty replacement of the right ventricular myocardium of uncertain pathogenesis. QT prolongation is not generally seen with ARVC.,Q 24,A 10-year-old Caucasian male is brought to your o
26、ffice complaining of occasional headaches and nose bleeds, as well as difficulty walking or running uphill due to muscle weakness. Pulsatile vessels are palpable along the patients ribs. He most likely suffers from:Primum-type atrial septal defect B. Secundum-type atrial septal defect C. Ventricular
27、 septal defect D. Patent ductus arteriosus E. Coarctation of the aorta F. Tetralogy of Fallot,A 24,Correct answer:EHeadaches and epistaxis may be caused by hypertension in the arteries supplying the head and neck. Lower extremity muscle weakness or fatigue with exercise may be caused by inadequate l
28、ower body perfusion. In adult-type aortic coarctation, the stenosis is post-ductal (in contrast to the infantile form, where the coarctation is generally preductal and fatal soon after birth without surgical repair). Adult-type aortic coarctation can produce hypertension in the upper aortic circulat
29、ion and simultaneously low perfusion in the distal aorta supplying the legs. The likelihood of an adult-type, postductal coarctation in this patient is greatly increased by the finding of enlarged, palpable intercostal vessels, which indicate the development of a collateral arterial circulation to t
30、he region of the aorta distal to the coarctation. On radiographic exam, patients with adult-type aortic coarctation often have notching of the ribs as a result of the enlarged, tortuous intercostal arteries.(Choice D) The initial left-to-right shunt of an isolated patent ductus arteriosus generally
31、does not result in poor exercise tolerance until the persistent pulmonary hypertension causes pulmonary vascular sclerosis and shunt flow reversal (Eisenmenger syndrome). One would not expect to find epistaxis or enlarged intercostal arteries in these patients.(Choice F) Tetralogy of Fallot could de
32、crease exercise tolerance via increased right-to-left shunting and hypoxemia in response to vasodilation in active skeletal muscles. However, one would not expect epistaxis or enlarged intercostal arteries in these patients.,Q 25,A 45-year-old man comes to the emergency department because of severe
33、chest pain, diaphoresis, and palpitations. The patient dies two hours after the onset of his symptoms. Autopsy reveals 100% occlusion of the left anterior descending artery. At the time of the patients death, light microscopy of the affected myocardium would most likely demonstrate which of the foll
34、owing? Edema and punctate hemorrhages Myocyte hypereosinophilia Dense interstitial neutrophil infiltrate Extensive macrophage phagocytosis of the dead cells Fibrovascular granulation tissue with neovascularization Dense collagen scar Normal myocardium,A 25,Correct answer:GThe cause of death was most
35、 likely an acute myocardial infarction. In myocardial infarction，changes on light microscopy are usually not apparent until 4 hours after the onset of severe ischemia. Although a variable waviness of myofibrils at the border of the infarct (due to myofibril relaxation) might be observed before this,
36、 more definite signs of early coagulative necrosis, such as cytoplasmic eosinophilia and nuclear pyknosis, take at least 4 hours to develop.Other potentially lethal causes of chest pain, diaphoresis, and palpitations/tachycardia include aortic dissection and/or rupture, massive pulmonary embolism, a
37、nd tension pneumothorax. The chest pain of aortic dissection is typically tearing in nature and often radiates to the back. Dyspnea is typically the most prominent symptom in the event of a pulmonary embolus or tension pneumothorax.(Choices A & B) Cytoplasmic hypereosinophilia on light microscopy is
38、 one of the earliest signs of coagulative necrosis of cardiac myocytes. It begins approximately 4 hours after the onset of lethal ischemia. Light microscopy may also reveal edema and punctate hemorrhages in infarcted myocardium starting also at about 4 hours after the ischemic event.(Choice C) An in
39、terstitial infiltrate of neutrophils around a zone of myocardial infarction is not seen until 1 to 3 days after the onset of severe ischemia.(Choice D) Extensive macrophage phagocytosis of the dead cells generally does not develop until at least 5 days after myocardial infarction, and is most promin
40、ent during post-infarction days 7 to 10.(Choice E) Fibrovascular granulation tissue with neovascularization generally begins to develop 7 days after myocardial infarction, and is most prominent on post-infarction days 10 to 14.(Choice F) Increased collagen deposition and decreased cellularity in a z
41、one of infarcted myocardium is not generally evident until 2 weeks post-infarction. Fibrosis continues during weeks 2 to 8, producing a dense collagenous scar by two months post-infarction.,Q 26,In experiments, transient myocardial ischemia causes myocardial cells to increase in size. This effect is
42、 due in part to which of the following?A. Intracellular K+ accumulation B. Intracellular Ca2+ accumulation C. High cellular HC3- contentD. Cascade protein phosphorylation E. Net cellular solute loss,A 26,Correct answer:BWhen blood flow cannot meet myocardial demands, cardiac myocytes transition from
43、 aerobic to anaerobic metabolism. However, anaerobic metabolism cannot maintain proper intracellular ATP levels, and ADP, AMP and adenosine accumulate. Without ATP, the membrane Na+/K+-ATPase and the sarcoplasmic reticulum Ca2+ ATPases fail, leading to increased intracellular Na+ and Ca2+ and increa
44、sed intramitochondrial Ca2+ concentrations. These increased concentrations attract free water, causing cellular and mitochondrial swelling. Failure of the sarcoplasmic reticulum to resequester Ca2+ leads to cessation of contraction within ischemic zones of myocardium.(Choice A） The cell membrane Na+
45、/K+-ATPase pump normally brings K+-into the cell in exchange for Na+ .Thus, in ischemic tissue, intracellular K+ is decreased.(Choice C) Cellular HC3- is not elevated in cardiac ischemia. Anaerobic metabolism leads to lactic acid production and a decrease in pH. Tissue C2, the conjugate acid of HC3-
46、 ，is thus elevated in ischemic myocardium.(Choice D) Protein phosphorylation cascades play a role in a variety of processes including second messenger signaling and regulation of apoptosis. The cells response to ischemia does involve initiating certain metabolic processes through protein phosphoryla
47、tion, but this does not cause cell swelling.(Choice E) Ischemia causes a net solute gain within cardiac myocytes. Elevated concentrations of Na+ and Ca2+ draw free water into the cells, causing edema.,Q 27,A 10-year-old Caucasian boy is referred to the physician due to restlessness and sudden jerkin
48、g movements of his extremities. The patient does not take any medications and his vaccinations are up-to-date. He does not recall any recent infections other than a sore throat three months ago. This patient is at risk of developing:A. Valvular heart disease B. Parkinson disease C. Early dementiaD.
49、Deforming polyarthritis E. Renal failure,A 27,Correct answer:AThe patient is described as having purposeless extremity movements and restlessness three months after having a sore throat. It is possible that he has a focal seizure disorder or attention deficit hyperactivity disorder, but the temporal
50、 relationship of these symptoms to his sore throat suggests that this may be the hyperkinetic extrapyramidal movement disorder, Sydenham chorea. Sydenham chorea is the most common acquired chorea of childhood, and is the sole neurologic manifestation of acute rheumatic fever. Sydenham chorea is thou
51、ght to be a CNS autoimmune reaction precipitated by a group A P-hemolytic streptococcal sore throat after a latency of 2-3 months. Anti-neuronal antibodies binding to the caudate and subthalamic nuclei may be involved. Since Sydenham chorea is a manifestation of acute rheumatic fever, a patient with
52、 this disorder would be at risk for chronic rheumatic heart disease, including mitral and aortic valve involvement.(Choice B) Parkinson disease is an extrapyramidal hypokinetic movement disorder, consisting of tremor, rigidity, akinesia, and postural instability. Jerking extremity movements are gene
53、rally not seen in a patient with Parkinsons disease, unless the patient has been given an overdose of levodopa.(Choice C) Early onset (presenile) dementia, particularly Alzheimer dementia, is associated with Down syndrome. Currently, it is thought that the type 4 allele of apolipoprotein E (ApoE eps
54、ilon-4) may be a risk factor.(Choice D) Although acute rheumatic fever can also produce a migratory polyarthritis as its first manifestation, this is generally transient and rarely, if ever, deforming.(Choice E) Diagnosis of acute rheumatic fever requires either two major Jones criteria or one major
55、 and two minor Jones criteria, with supporting evidence of an antecedent group A streptococcal infection. The Jones criteria are:Major Criteria: Carditis, polyarthritis, chorea, erythema marginatum, subcutaneous nodules Minor Criteria: Fever, arthralgia, elevated acute-phase reactants (erythrocyte sedimentation rate or C-reactive protein), prolonged PR-interval,
