MDE CVS 2008

Rabu, 16 Juni 2010

1. Jawaban : D. Mesoderm
Alasan : keseluruhan jantung dibentuk dari splanchnic mesoderm (Moore embryology hlm 286)
2. Jawaban : E. Carniocaudal folding of the embryo
Alasan : Moore embryology hlm 292
3. Jawaban : C. Right ventricle
Alasan : bisa dilihat di gambaran anatomi jantung  right ventricle ada di anterior surface (Moore anatomy hlm 146)
4. Jawaban : D. Membranous VSD
Alasan : Moore embyology hlm 312
5. Jawaban : E. TGA
Alasan : pada TGA letak aorta dan pulmonary trunk jadi terbalik (Moore embryology hlm 314)
6. Jawaban : A. CKMB
Alasan : kelainan pada jantung yang biasanya diperiksa adalah CKMB dan cardiac specific troponin
7. Jawaban : A. Apolipoprotein A1
Alasan : Apo-A1 adalah penyusun utama HDL  semakin ↑ HDL  semakin ↓ risk for CAD yang ditanya : inverse/berbanding terbalik (harusnya Harper ada tapi males buka buku jadi dari inet...^_^)
8. Jawaban : B. AST peak in 24-48 hours after AMI and return to normal in 4-6 days
Alasan : Mild to moderate increases may be seen with vigorous excercise and muscle injury or in conditions such as acute pancreatitis and heart attacks
9. Jawaban : B. Troponin
Alasan : sama dengan no 6
10. Jawaban : B. Ckmb levels are normal in cases of cardiac ischemia
Alasan : CKMB akan naik bila terjadi infarct (penjelasan waktu lab act + Lilly hlm 183)
11. Jawaban : C. LDH pericardial fluid/serum ratio > 0.6
Alasan : ciri exudate  pericardial protein/serum >0.5 atau pericardial LDH/serum > 0.6 (Lilly hlm 344)
12. Jawaban : B. Therapy of amiodarone
Alasan : untuk menjaga stabilitas meskipun sudah sinus rhytm tetap perlu diberikan antiarrhytmia  amiodaron  ↓ sinud firing (Lilly 296, 428)
13. Jawaban : B. Loud 1st heart sound
Alasan : Lilly hlm 202
14. Jawaban : C. Janeway lesion
Alasan : Lilly hlm 220
15. Jawaban : E. Mitral Regurgitation
Alasan : MR bisa disebabkan oleh rupture chordae tendinae akibat blunt chest trauma (Baraunwald ch 62)
16. Jawaban : ???
Alasan : It is a consequence of shortening, rigidity, deformity, and retraction of one or both mitral valve cusps and is associated with shortening and fusion of the chordae tendineae and papillary muscles (Braunwald ch 61)  ini dr Braunwald tapi ga ada pilihan spesifik, kayaknya sih B
17. Jawaban : A. Thickening of chordae / leaflets
Alasan : Lilly hlm 199
18. Jawaban : B. Pulmonary hypertension
Alasan : Lilly hlm 216
19. Jawaban : E. Pericardial friction rub
Alasan : chest pain saat posisi tidur dan hilang saat duduk  tanda pericarditis (Lily hlm 337)
20. Jawaban : C. Coagulation
Alasan : Lilly hlm 177

21. C
Risk factor yang paling tinggi menyebabkan mortalitas: rokok, DM, alcohol, obesity
22. A
23. A
* 4-12 hours – 1-3 days = terjadi neutrophilic infiltrates
* 3-7 days – 7-10 days = well developed macrophage
* 10-14 days – 2-8 weeks = fibrous tissue formation
25. C. sebenernya bingung karena dari semua sumber, aschoff bodies itu bisa melibatkan semua lapisan cardium.. tapi kalo kita belajar dari tutorial, komplikasi tersering dari RHD tu kan valve stenosis ato regurgitant (dlm case ini diduga mitral involvement = karena ada dyspnea) jadi mikirnya kalo kena disitu, berarti lapisan endocardium..
26. A. Aschoff bodies = swollen eosinophilic collagen yang dikelilingi T lymphocyte
27. C.. uda jelas ya.
28. C
29. A. di robin hal 216,,epitheloid cells itu merupakan manifestasi dari hypersensitivity type 4 karena non degradable product seperti tubercle bacilli. Disekitarnya dikelilingi oleh collar lymphocyte.
30. b
31. C. pada orang DM, terdapat abnormalitas fungsi metabolism lipid juga dan enzim pemecah seperti Lipoprotein lipase.. hasilnya menunjukan increasing LDL dan VLDL, decreasing HDL, dsb.
32.d.
33. B. statin merupakan obat HMG CoA reductase..
34. E. berdasarkan alur produksi hormonal.. reninANG 1  ANG2  Aldosteron
35. B. salah satu indicator dari pelepasan renin adalah penurunan perfusi dan tekanan darah ke ginjal yang dalam hal ini bisa karena penurunan BP.. tapi jika BP sudah mendapat batas, maka terjadi feedback negative ke ginjal untuk stop produksi dari RAA system.
36.
37. D.
38. B. efeknya oleh Endothelin isoform 1 (ET-1), dan endothelin ini juga bisa dihasilkan selain oleh endothelium, juga oleh cardiac myocyte.
39.
40.?
61. -
62. -
63. -
64. B
65.-
66. E
67. C
68. B
69. B
70. B
71. A
72. A
73. D
74. B
75. B
76. -
77.-
78. D
79. A
80. C
81. C. anterior interventricular branch of coronary artery
Distribution of anterior IV branch: right and left ventricle and anterior two third of IVS
Moore,158

82. C. Left side in midclavicular line in the 5th ICS
Auscultation area of mitral valve is 5LICS(5th left intercostals space)
Moore, 168

83. E. in the wall of the RA near the opening of the superior vena cava
Normal heart rate controlled by SA node. This is location of SA node
Moore, 162

84. C. activate guanilate cyclase
Lily, 414

85. B. Captopril
The drug to prevent ventricular remodeling process: captoril. Karena obat ini akan menghambat produksi aldosterone sehingga efek bahayanya bisa terhindari. Efek buruk dari aldosterone adalah provoking hypertrophy and fibrosisi within myocardium

86. A. decreased potassium level
MOA Furosemide adalah loop diuretic yaitu menghambat NKCC2, the luminal Na/K/Cl transporter in thick ascending limb of Henle’s loop.
Transporter ini normalnya akan menyerap Na,K,dan Cl searah dari lumen ke sel-sel ascending limb,sekaligus menyerap air. Ketika traspoter ini dihambat tidak ada penyerapan air(dan Na,Cl, serta K)pembuangan K tinggihypokalemia
(katzung 10th,243)

87. D. Captoril
Kontra Indikasi Captopril:.
-Penderita yang hipersensitif terhadap captopril atau penghambat ACE lainnya (misalnya pasien mengalami angioedema selama pengobatan dengan penghambat ACE lainnya)
-Wanita hamil atau yang berpotensi hamil.
-Wanita menyusui
-Gagal ginjal

88. B. Increased of bradykinin level
Ingat penjelasan salah seorang dokter waktu lecture. Untuk mekanisme lebih jelasnya baca lagi ya

89. C. Digoxynpositive inotropic drug
90. B. Heparinanticoagulant effect
91.
92. E. Nifedipineblockage of Ca channel
93. D. Propanololcompetitive B-antagonist
94. E. Pulsatile arterial trauma

96. E. Thromboangitis Obliterans
Ciri khas: Heavy smoker dan painful ulcer in distal extremities
Lily, 361

97. C. Ischemia
Thromboangitis obliteran muncul dengan Triad Symptom:
-Distal arterial occlusionmenghasilkan claudication,yaitu exertional limb fatigue and pain cause by ischemia(inadequate supply to of blood to affected muscle)
-Raynold’s phenomenon
-Migrating superficial vein thrombophlebitis
Lily,361

98. E. Phlebitis
Lihat penjelasan nomor 97

99. D. Hemosiderin deposit

100. E. Angiography
Left arm hypertension and claudication in her limb masalah pada pembuluh darah extremitas pemeriksaannya adalah angiography

100)E claudication is a classic symptom of exertional limb fatigue and pain.usually occur in peripheral aterial disease(PAD),which may result in chronic occlusive arterial disease,with progressive stenosis & obstruction of blood flow.evaluation : duplex USG-assess the extent of arterial stenoses & corresponding reduction in blood flow.other imaging-MRA,CT-angiography-are obtained when revascularization procedure are planned (lilly;4th ed,pg 356-359)

101)E  Tuberculous pericardial effusions are typically exudative and characterized by a high protein content and increased leukocyte count, with a predominance of lymphocytes and monocytes.(American Heart Association-Circulation. 2005;112:3608-3616).
Nontuberculous bacterial(suppurative) pericarditis-fluid is a turbid exudates characterized by PMN leukocytes,increased LDH & decreased glucose.(braunwald;6th ed;pg 1854)

102)

103)A ECG pattern-diffuse ST segment elevation in most of ECG leads,usually with exception of aVR & V1.PR segment depression in several leads is often evident,reflecting abnormal atrial repolarization related to atrial epicardial inflammation.(lilly;4th ed;pg 338)

104) B most frequent symptoms of acute pericarditis are chest pain & fever-pain may be severe..pain typically sharp & pleuritic & positional(sitting & leaning forward often lessen the discomfort).dyspnea is common during acute pericarditis but is not exertional & probably result from a reluctance of patient to breath deeply because of pleuric pain.(lilly,4th ed;pg 337)

105)

106)A idiopathic/viral pericarditis is a self limited disease-runs in course in 1-3weeks-management-rest,analgesic & NSAIDs.recurrent pericardial pain-oral corticosteroid.(lilly,4th ed;pg 339)

107)E an intravenous drip containing isotonic saline or dextrose in water can be used to deliver supporting therapy (braunwald,6th ed,pg 1840)

108)may be B or CECG,always nonspecifically abnormal,T wave-low/flat/have general /local inversion.QRS n T wave voltage may be normal or reduced,interatrial block is common-P waves wider than 100ms n usually notched.
Constriction (especially chronic) may present deceptively as congestice failure,pleural effusion,RA thrombosis,even hepatic coma.CP resembles ,but is not HF;venous congestion resembles right-sided HF with appropriate compensatory response.
All cardiac diastolic pressures are nearly equilibrated as in cardiac temponade (braunwald,6th ed,pg 1850-1852)

109)

110) C ELECTROCARDIOGRAPHY-In acute pericarditis, the ECG typically shows ST-segment elevation in all leads, with an upward concavity of the elevation (so-called “smiling face”). The PR segment is depressed. Unlike myocardial infarction, there is no reciprocal change, and T waves are not inverted.12–15
In this situation, the differential diagnosis includes acute myocardial infarction and normal-variant repolarization abnormality. It is particularly important to distinguish pericarditis from acute myocardial infarction, because thrombolytic therapy could have disastrous effects in patients with pericarditis. Characteristic features of acute pericarditis, acute myocardial infarction, and early repolarization are summarized in Table 3. Examples illustrating the ECG differentiation of the three conditions are provided in Figure 2.16

Electrocardiographic Differentiation of Pericarditis
________________________________________
Acute pericarditis Acute myocardial infarction Early repolarization
ST-segment elevation in many leads, with no ST-segment depression Upward concave ST-segment elevation No T-wave inversion in leads with ST-segment elevation PR-segment depression Q waves during evolution ST-segment elevation in anatomically contiguous leads, with possible reciprocal ST-segment depression Upward convex ST-segment elevation T-wave inversion in leads with ST-segment elevation as myocardial infarction evolves No PR-segment depression May have Q waves during evolution ST-segment elevation in middle and left precordial leads, but may be widespread Upward convex ST-segment elevation May have T-wave inversion in leads with ST-segment elevation No PR-segment depression No Q waves


A. Acute pericarditis. The ST segment (long arrows) is elevated in all leads (universal elevation in contrast to the focal elevation in acute myocardial infarction), with no reciprocal change. The ST-segment elevation shows upward concavity (so-called "smiling face"). The PR interval (short arrow) is depressed because of inflammatory changes involving the atrial wall.

B. Acute myocardial infarction. The ST segment (long arrow) is elevated in leads II, III, and aVF, and depressed (short arrow) in leads I, aVL, and V1, V2, and V3 (focal elevation in segment of injury, with reciprocal ST-segment depression). The ST elevation is convex upward (tomb shape or so-called "sad face").

C. Early repolarization. ST-segment elevation (long arrow) is present in all leads, with no reciprocal depression. Peaked T waves (short arrow) are seen in the middle precordial leads. No Q waves are present
In cardiac tamponade, the ECG shows electrical alternans as the heart “floats” in relation to the recording leads. Chronic constrictive pericarditis presents with low voltage of the QRS complex and diffuse flattening or inversion of the T waves. Atrial fibrillation occurs in one third of patients with pericardial disease.
LABORATORY TESTS
Laboratory studies are useful for excluding other possible causes of symptoms and clarifying the underlying cause of pericarditis. Testing is individualized but frequently includes a complete blood cell count (CBC), an erythrocyte sedimentation rate (ESR), cardiac enzyme levels, and serum chemistries. Non-specific elevations in the CBC and ESR are common in patients with pericarditis. (American Academy of Family Physicians)
111)A a sharp early diastolic thrust is common especially in chronic constriction,corresponding to ventricular rapid filling.it coincides with loud,often palpable,abnorlmal S3,which sometimes has a ‘knocking’ quality.CP resembles,but is not HF.(braunwald,6th ed,pg 1851-1852)
112)A hypothesis-COPD,diagnosis:chest radiograph,ECG,echoCG,MRI,CT scan,radionuclide ventriculography(braunwald,6th ed,pg 1938)

113)B dilation of RV gives the heart a globular appearance,but right ventricular hypertrophy or dilation is not easily discernible on a plain chest radiograph.pulmonary arterial hypertension in patient with COPD has been shown to be related to width of right descending pulmonary artery.although there are numerous disorders that fall under the heading of COPD,the 2 largest components are emphysema and chronic bronchitis.(braunwald,6th ed,pg 1938-1939)

114)D management goals in COPD are ameliorate air flow obstruction and improve symptos,toavoid 2ndry complications,to maintain functional capacity & to improve the quality of life.drugs:anticholinergics,beta-blocker agonist,rheophylline,corticosteroids,digitalis,vasodilators,NO,ACE inhibitors,noninvasive ventilation(braunwald,6th ed,1941-1943)

115)

116)C PAH in COPD is due to multiple factors,include pulmonary vasoconstriction caused by alveola hypoxia,academia,and hypercarbia;the mechanical effects of high lung volume on pulmonary vessels;the loss of small vessels in vascular bed in regions of emphysema & lung destruction;ang increased of CO n blood viscosity from polycythemia secondary to hypoxia.of these causes,hypoxia is undoubtedly the most important & is associated with pathological changes that occur characteristically in peripheral pulmonary arterial bed.(braunwald,6th ed,pg 1940)

117)D pulmonary thromboembolism,as a single event or as repeated events,rarely leads to development of chronic pulmonary hypertension(braunwald,6th ed,pg 1949)

118)D vasodilators produced by endothelium include NO,prostacyclin,& EDHF(LILLY,4TH ED,144)

119)A lec note

120)C lecture note(cardiac rehabilitation)

161. Which of the following is the most likely diagnosis?
A. VSD
B. ASD
C. Aortic stenosis
D. Tricuspid regurgitation
E. Mitral valve prolapsed
Jawab: E
Pembahasan:
Karakteristik bunyi jantung pada penyakit-penyakit di atas adalah sbb:
Ventricular septal defect: harsh systolic murmur, middiastolic rumble
Atrial septal defect: RV heave, widened-splitted S2, middiastolic murmur at left lower sterna border
Aortic stenosis: coarse late-peaking systolic ejection murmur, parvus-tardus carotid pulse, S4, attenuated S2
Tricuspid regurgitation: systolic murmur at lower left sterna border which is augmented by inspiration
Mitral valve prolapse: midsystolic click, late systolic murmur

162. Which of the following is the most appropriate management for the patient?
A. Cardiac catheterization
B. Penicillin prophylaxis for dental procedure
C. Avoidance of strenuous activity
D. Beta blocker
E. Digitalis
Jawab: B
Pembahasan:
Mitral valve prolapse secara umum kondisinya benign sehingga kebanyakan pasien akan asymptomatic untuk sebagian besar masa hidupnya.
Komplikasi utama adalah endocarditis. Sehingga opsi B adalah jawaban paling tepat.

163. The heart disease that is present at the time of birth is known as …
A. congenital heart disease
B. cardiogenic shock
C. cardiovascular disease
D. coronary heart disease
E. acquired heart disease
Jawab: A
Pembahasan: jelas :-)

164. A 45-year-old man is admitted to the hospital with low grade fever, night sweat, fatigability, malaise, weight loss, and valvular insufficiency. There is also erythematous subcutaneous nodules about the tips of the digits and hemorrhagic retinal lesion. After examining the patient, the doctor in charge thought that the man suffered from subacute bacterial endocarditis. What is the common cause of the disease?
A. Staphylococcus aureus
B. Staphylococcus epidermidis
C. Streptococcus viridans
D. Streptococcus non hemolyticus
E. Streptococcus gamma haemolyticus
Jawab: C
Pembahasan:
Etiologi utama acute infective endocarditis adalah Staphylococcus aureus.
Etiologi utama subacute infective endocarditis adalah Streptococcus viridans, enterococci, fastidious gram negative bacteria. Yang ada di pilihan hanya Streptococcus viridans.

165. Blood culture of suspected subacute infective endocarditis patients is performed on blood agar and after incubation in 37 C for 24 hours, growth of some bacterial colony is observed. What is the colony morphology of such bacteria?
A. Diameter is 3 mm, non hemolytic
B. Diameter is 3 mm, hemolytic
C. Pinpoint colony, non hemolytic
D. Pinpoint colony, alpha hemolytic
E. Pinpoint colony, beta hemolytic
Jawab: D
Pembahasan:
Kemungkinan besar, bakteri yang ditemukan pada kultur adalah Streptococcus viridans (karena subacute infective endocarditis). Bakteri ini termasuk golongan alpha-hemolytic. Jadi jawabnya D.

166. To confirm an infective endocarditis, the doctor usually must have three positive blood cultures of the patient. From three blood samples drawn from three different venipuncture, except for a certain bacterium, only one positive sample is needed. What is the name of the bacterium?
A. Mycobacterium tuberculosis
B. Pseudomonas aeruginosa
C. Streptococcus pneumonia
D. Coxiella burnetti
E. Eikenela corrodens
Jawab: D
Pembahasan:
Criteria for Diagnosis of Infective Endocarditis
Major Criteria
Positive blood culture
Typical microorganism for infective endocarditis from two separate blood cultures
Viridans streptococci, Streptococcus bovis, HACEK group or
Staphylococcus aureus or community-acquired enterococci in the absence of a primary focus, or
Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from:
Blood cultures (≥2) drawn more than 12 hr apart, or
All of three or a majority of four or more separate blood cultures, with first and last drawn at least 1 hr apart
Single positive blood culture for Coxiella burnetii or antiphase I IgG antibody titer >1:800
Evidence of endocardial involvement
Positive echocardiogram (TEE advised for PVE or complicated infective endocarditis)
Oscillating intracardiac mass, on valve or supporting structures, or in the path of regurgitant jets, or on implanted material, in the absence of an alternative anatomical explanation, or
Abscess, or
New partial dehiscence of prosthetic valve, or
New valvular regurgitation (increase or change in preexisting murmur not sufficient)
Minor Criteria
Predisposition: predisposing heart condition or intravenous drug use
Fever ≥38.0°C (100.4°F)
Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
Immunological phenomena: glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
Microbiological evidence: positive blood culture but not meeting major criterion as noted previously or serologic evidence of active infection with organism consistent with infective endocarditis
Sumber: Braunwald hal. 1718

For question no. 167-168, see the scenario below
Most of the bacteria adhere to the damaged endothelium and cause endocarditis. There is also a kind of bacteria that can cause endocarditis on intact endothelium.

167. What is the name of such bacteria?
A. Coxiella burnetti
B. Haemophilus influenza
C. Streptococcus alpha hemolyticus
D. Pseudomonas aeruginosa
E. Staphylococcus aureus
Jawab: E
Pembahasan:
Mekanisme terjadinya endocarditis pada endothelium utuh (intact) adalah sbb:
1. Pada orang yang tua (elderly), terjadi proses degenerasi pada katup, sehingga ada inflamasi. Inflamasi ini akan menginduksi terbentuknya berbagai adhesion molecules yang dapat membantu pelekatan leukosit ke katup; namun juga dapat membantu pelekatan mikroorganisme ke katup.
2. Pada intravenous drug users (IDU), hal yang sama terjadi.
Mikroorganisme yang mampu berlekatan dengan adhesion molecule yang diekspresikan adalah Staphylococcus aureus, karena bakteri ini memiliki microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). Selain itu, S. aureus memiliki keunikan mampu membuat sel endothel menginternalisasi S. aureus sehingga di dalam sel endothel, S. aureus dapat melakukan multiplikasi. Akibatnya, sel endothel akan mengalami kematian, sehingga tidak lagi intact. Ketika endothel tidak lagi intact, sementara bakteri sudah berkumpul di sekitarnya, maka terjadi endocarditis.
Sumber Braunwald hal 1719

168. What is the bacterial product that facilitate bacteria adherence to the endothelium of the endocardium?
A. LPS
B. Hyaluronidase
C. Hemolysin
D. Clumping factors
E. Streptokinase
Jawab: D
Pembahasan:
Secara kolektif, molekul-molekul pada permukaan bakteri yang dapat membantu perlekatan ke endothelium disebut dengan microbial surface components recognizing adhesive matrix molecules (MSCRAMMs). Molekul ini ada beberapa jenis:
1. Glucan atau dextran, diproduksi oleh Streptococci. Fungsinya memediasi penempelan dengan fibrin, katup yang terluka, dan memfasilitasi perkembangan endocarditis.
2. Fim A protein, diproduksi oleh Streptococcus parasanguis, membantu penempelan dengan fibrin dan memfasilitasi perkembangan endocarditis.
3. Fibronectin receptor, diproduksi oleh Staphylococcus aureus, Streptococcus viridans, Streptococcus Group A, C, dan G, Enterococi, Streptococcus pneumonia, dan Candida albicans. Receptor ini akan berikatan dengan Fibronectin yg secara alami diekspresikan oleh sel endothel. Pelekatan akan memediasi pembentukan endocarditis.
4. Clumping factor, diproduksi oleh Staphylococcus aureus, akan memediasi penempelan bakteri ke thrombi yang dibentuk, dan, pada eksperimen, ke katup aorticus.
5. Glycocalyx dan slime (lendir) di permukaan S. epidermidis tidak membantu pelekatan, namun dapat membuat S. epidermidis lebih virulen dan menghindari host defense.
Sumber: Braunwald

169. A 15-year-old boy is admitted to the hospital because of fever, malaise, and migratory polyarthritis. After examining the patient, the doctor in charge suspected that the boy suffered from rheumatic fever. What is the bacteria most likely responsible for such disease?
A. Staphylococcus epidermidis
B. Staphylococcus aureus positive coagulase
C. Streptococcus beta haemolyticus group A
D. Streptococcus alpha haemolyticus
E. Haemophilus influenza
Jawab: C
Pembahasan:
Cukup jelas. Etiologi dari rheumatic fever adalah group A beta-hemolytic streptococci (GABHS).

170. A doctor in charge in Cardiology Ward performs pericardiocentesis to a patient suspected of chronic infective pericarditis and takes out some bloody fluid. What bacteria is the most likely cause?
A. Pseudomonas aeruginosa
B. Mycobacterium tuberculosis
C. Streptococcus pneumonia
D. Haemophilus influenza
E. Staphylococcus aureus
Jawab: B
Pembahasan:
Pilihan-pilihan lainnya adalah bacterial pericarditis, yang kemungkinan menunjukkan pus pada pericardial fluid-nya.




For question number 171 and 172, refer to the scenario below
A 62-year-old man comes to your clinic with exercise-induced angina. His serum cholesterol is 277 mg/dL, LDL 157, HDL 43, and triglyceride 170. He is overweight and has two risk factors for CAD. On cardiac catheterization, there is occlusion of left anterior descending and the origin of right coronary artery.

171. Which of the following process cause the disease above?
A. adventitial proliferation
B. injury to endothelium
C. formation of an intimal plaque
D. proliferation of smooth muscle cells
E. attraction of platelet to collagen microfibrils
Jawab: C
Pembahasan:
Berdasarkan keluhan (exercise-induced angina), anamnesis (2 faktor risiko untuk CAD), pemeriksaan fisik dan lab (overweight, hypercholesterolemia, dyslipidemia, hyperlipidemia), maka pasien mengalami CAD.
Pada CAD, terbentuk atherosclerosis pada dinding arteri koroner pada jantung. Proses pembentukannya diawali oleh kerusakan pada endothelium yang menyebabkan LDL dapat masuk ke dalam jaringan subintima. Ketika LDL masuk, ia akan dimodifikasi menjadi modified LDL melalui proses oksidasi atau glikasi. Modified LDL akan menginduksi pembentukan reseptor scavenger pada leukosit yang masuk ke dalam tunica intima sehingga leukosit akan meng-engulf modified LDL. Engulfment ini akan mengubah leukosit (macrophage) menjadi foam cells. Foam cells sendiri mampu mensekresikan cytokine dan growth factor. Cytokine akan menginduksi migrasi sel otot polos dari tunica media ke intima. Growth factor akan menginduksi proliferasi sel otot polos tsb. Sel otot polos akan mensekresikan extracellular matrix (ECM). Proliferasi sel otot polos dan sekresi ECM akan menyebabkan penebalan lokal dari dinding pembuluh darah, menyebabkan oklusi.
Jadi, kesimpulannya, proses yang menyebabkan CAD adalah pembentukan plaque pada tunica intima.
Opsi yang lain tidak cukup untuk secara mandiri menyebabkan CAD.

172. Which of the type of arteries involved in the above condition?
A. Conducting
B. Distributing
C. Arterioles
D. Metarterioles
E. Capillaries
Jawab: B
Pembahasan:
Histologi Arteri
Arteri ada 3 macam:
1. Elastic/conducting artery
a. Diameter > 1 cm
b. Contoh: aorta, bracicephalic artery, common carotid artery, subclavian artery, pulmonary artery, common iliac artery
c. Fungsi utamanya adalah membantu mendorong darah ketika ventricle sedang relaksasi.
d. Tunica intima terdiri atas endothel, basal membrane, dan internal elastic lamina yang tidak utuh.
e. Tunica media terdiri atas smooth muscle, banyak elastic fibers, dan external elastic lamina yang tipis.
f. Tunica adventitia terdiri atas collagen dan elastic fibers.
2. Muscular/distributing artery
a. Diameter 0.1 – 1 cm
b. Contoh: brachial artery, radial artery
c. Fungsi utamanya untuk menentukan kecepatan aliran darah karena kemampuan konstriksi dan dilatasinya sangat tinggi
d. Tunica intima terdiri atas sel endothel, basal membrane, dan internal elastic lamina yang tipis
e. Tunica media terdiri atas banyak smooth muscle cells, sedikit elastic fibers, dan external elastic lamina yang tebal
f. Tunica adventitia terdiri atas collagen fiber dan elastic fibers.
3. Arteriole
a. Diameter 10-100 μm
b. Tunica intima terdiri atas endothel, basal membrane, dan internal elastic lamina
c. Tunica media terdiri atas smooth muscle cells, sedikit elastic fibers, tanpa external elastic lamina.
d. Tunica adventitia terdiri atas collagen dan elastic fibers.
Arteri koroner memiliki diameter < 1 cm, namun masih dapat terlihat jelas. Selain itu, kemampuan vasokonstriksi dan dilatasinya tinggi, sehingga termasuk muscular/distributing artery.

173. A 45-year-old woman came with painful, tender, cord-like structure with associated redness and swelling as chief complaint. Which of the following normal structures from damaged organ above?
A. Tunica intima has pericytes
B. Tunica intima has thick internal elastic lamina
C. Tunica media has reticular and elastic fibers
D. Tunica media has thick external elastic lamina
E. Tunica adventitia has smooth muscle cells
Jawab: kurang tahu, tapi kalau di buku 2006, dijawab D
Pembahasan:
Pembahasan 2006 juga:
Kemungkinan besar, arteri yang dimaksud adalah arteri muscular karena berada di antara jantung dan organ yang akan divaskularisasi.
Opsi A salah, karena pericyte hanya dimiliki oleh kapiler
Opsi B salah, karena tunica intima dari muscular artery memiliki internal elastic lamina yang tipis.
Opsi C salah, karena tunica media dari muscular artery hanya dibentuk oleh elastic fiber dan otot polos.
Opsi E salah, karena (di vaskular jenis apa pun) adventitia hanya terdiri atas collagen dan elastin
Opsi D benar, karena pada muscular artery, tunica medianya memiliki external elastic lamina yang tebal.

For question number 177 and 178, refer to the options below.
A. Decrease pulmonary vascular markings
B. Hilar alveolar infiltrats and widening of hilum
C. Cephalization
D. Revised comma sign

177. A man with a history of cardiac enlargement was confined for 7 days. Today, he is complaining of dyspnea again and chest X-ray reveals pulmonary congestion.

178. A middle-aged man smoker admitted to the hospital due to setting or worst chest pain. Based on x-ray, doctors’ conclusion was pulmonary edema.

Pembahasan tentang radiografi (dari jawaban 2006, maaf saya g nemu..):
- Decreased pulmonary vascular markings disebabkan oleh penurunan aliran darah pada arteri pulmonalis, biasanya karena ada block pada arteri tersebut. Contoh penyakitnya adalah pulmonary stenosis, TOF (karena ada pulmonary stenosis), pulmonary atresia.
- Hilar alveolar infiltrates disebabkan adanya alveolar edema karena congestive heart failure.
- Cephalization adalah redistribusi aliran darah dari vena pulmonalis untuk paru-paru lobus inferior ke lobus yang superior (normalnya, lobus yang inferior mendapat lebih banyak aliran). Ini biasa ditemukan pada congestion juga, namun tipe congestion yang lebih berat daripada hilar alveolar infiltrate.
Pada no. 177, jawabnya kemungkinan C, karena pada kasus ada cardiac enlargement, yang mengindikasikan gagal jantung confestif yang sudah lebih parah.
Pada no. 178, jawabnya kemungkinan B, karena ada pulmonary edema yang belum terlalu parah.

For number 179 and 183, refer to the options below.
A. MRI
B. CT scan
C. Nuclear medicine
D. Echocardiography
E. Conventional radiography of the chest

179. Abnormal of the costa sternum
180. Evaluation of hemodynamics of the heart

Pembahasan modalitas imaging untuk jantung (dari 2006 juga):
MRI digunakan untuk melihat jaringan lunak (darah maupun jaringan) pada berbagai bidang.
CT scan digunakan untuk melihat jaringan pada sumbu melintang tubuh.
Nuclear medicine berkaitan dengan penyuntikan zat radioaktif (kontras) untuk melihat uptake dari jaringan yang ditarget. Pada jantung, bisa digunakan untuk melihat fungsi myocardium.
Echocardiography paling baik digunakan untuk meng-assess fungsi jantung. Biasa melihat fungsi hemodinamik jantung jika dikombinasikan dengan Doppler, bisa melihat pergerakan katup, kontraksi jantung, dll.
Radiography thorax dapat melihat siluet jantung dan paru, vaskular markings, serta tulang-tulang pada thorax.
Jadi, jawaban no. 179 adalah E dan jawaban no. 180 adalah D.

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