Critical Care

Question 1

1. Berapakah umur-paruh dari phenobarbital
A. 6 jam
B. 12 jam
C. 24 jam
D. 100 jam
E. 140 jam

Answer 1

D.
The half-life of phenobarbital is generally between 98 and 120 hours in the average adult. Phenobarbital is largely metabolized by the liver, although 20 to 30% of the drug can be excreted unchanged in the urine. Barbiturates bind the GABAA receptor in the CNS, which facilitates Cl-mediated inhibitory postsynaptic potentials. Phenobarbital is often used in the treatment of partial and generalized tonic-clonic seizures in neonates (Katzung, pp. 3 7 , 358-359, 393-394)

Question 2

2. Terapi awal manakah yang paling dipilih untuk pasien dengan gejala hyperkalemia yang disertai dengan perubahan EKG?
A. Furosemida
B. Insulin/Glukosa
C. Bikarbonat
D. Kayeaksalat
E. Kalsium glukonat

Answer 2

E.
Calcium gluconate is the initial treatment of choice for symptomatic hyperkalemia because it rapidly antagonizes the effects of hyperkalemia directly at the plasma membrane level. The effects of calcium gluconate are short-lived, however, and other therapies should be insti tuted simultaneously. Loop diuretics (furosemide) can i ncrease renal potassium excretion, Kavexalate enhances gastrointestinal potassium excretion, and bicarbonate and insulin/glucose induce intracellular shifts of potassium primarily into muscle cells. Sodium bicarbonate is less effective in patients with renal failure, however, and can actually bind calcium; therefore its utility is limited. The definitive treatment for patients with chronic hyperkalemia is hemodialysis ( M arino, pp. 655-658) .

Question 3

3. Perawatan manakah yang dipilih untuk takikardia supraventrikular paroksimal (SVT)
A. Kardioversi listrik
B. Adenosin
C. Antagonis-antagonis kalsium
D. Bloker β
E. Dogoksin

Answer 3

B.
Paroxysmal supraventricular tachycardia (AV-nodal re-entrant tachycardia) results from re-entry of impulses from an ectopic source. Adenosine blocks the posit.ive inotropic effects of catecholamines, slows conduction at the AV node, and dilates coronary arteries. Additionally, the effects of adenosine are short-lived, so it does not elicit significant myocardial depression. It is these characteristics of adenosine that make it the drug of choice in the treatment of paroxysmal SVT m•er calcium antagonists ( Marino, pp. 329-330)

Question 4

4. Gangguan-gangguan manakah yang paling lazim berasosiasi dengan ‘prominent leucocyt cast’ pada analisa urin secara mikroskopik?
A. Nepritis interstitial akut
B. Nekrosis tubular akut
C. Penyakit perubahan minimal
D. Grioglobulinemia
E. Jawaban A, B, C dan D semuanya salah

Answer 4

A.
Acute interstitial nephritis (AIN) is a common cause of acute renal failure and is usually associated with infections or hypersensiti'ity drug reactions. AIN is characterized by a decrease in the glomerular filtration rate , often with oliguria . Urinalysis often exhibits hematuria, mild proteinuria, an elevated fractional excretion of sodium, eosinophilia, and leukocyte casts with AIN. Acute tubular necrosis (ATN) most commonly result

Question 5

5. Lemah otot, status mental berubah, gelombang U pada EKG
A. Hiponatremia
B. Hipokalsemia
C. Hipomagnesemia
D. Hipokalemia
E. Hipofosfatemia
F. Hipokloremia

Answer 5

D
Symptomatic hyponatremia (usually 120 mEq/L or less) can result in generalized seizures, metabolic encephalopathy, depressed level of consciousness, acute respiratory distress syndrome, muscle weakness, and even cerebral edema and elevated intracranial pressure. Hypokalemia can result in muscle weakness, altered mental status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval) ; however, isolated hvpokalemia does not result in significant cardiac arrhythmias. Hvpomagnesemia is very common in the I C U setting and is often associated with depletion of other electrol

Question 6

6. Berasosiasi dengan kelainan-kelainan elektrolit lainnya dan torsades de pointes
A. Hiponatremia
B. Hipokalsemia
C. Hipomagnesemia
D. Hipokalemia
E. Hipofosfatemia
F. Hipokloremia

Answer 6

C
Symptomatic hyponatremia (usually 120 mEq/L or less) can result in generalized seizures, metabolic encephalopathy, depressed level of consciousness, acute respiratory distress syndrome, muscle weakness, and even cerebral edema and elevated intracranial pressure. Hypokalemia can result in muscle weakness, altered mental status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval) ; however, isolated hvpokalemia does not result in significant cardiac arrhythmias. Hvpomagnesemia is very common in the I C U setting and is often associated with depletion of other electrol

Question 7

7. Lemah otot, cardiac output menurun, anemia hemolitik
A. Hiponatremia
B. Hipokalsemia
C. Hipomagnesemia
D. Hipokalemia
E. Hipofosfatemia
F. Hipokloremia

Answer 7

E
Symptomatic hyponatremia (usually 120 mEq/L or less) can result in generalized seizures, metabolic encephalopathy, depressed level of consciousness, acute respiratory distress syndrome, muscle weakness, and even cerebral edema and elevated intracranial pressure. Hypokalemia can result in muscle weakness, altered mental status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval) ; however, isolated hvpokalemia does not result in significant cardiac arrhythmias. Hvpomagnesemia is very common in the I C U setting and is often associated with depletion of other electrol

Question 8

8. Cardiac output menurun, hiperfleksia, tetani
A. Hiponatremia
B. Hipokalsemia
C. Hipomagnesemia
D. Hipokalemia
E. Hipofosfatemia
F. Hipokloremia

Answer 8

B
Symptomatic hyponatremia (usually 120 mEq/L or less) can result in generalized seizures, metabolic encephalopathy, depressed level of consciousness, acute respiratory distress syndrome, muscle weakness, and even cerebral edema and elevated intracranial pressure. Hypokalemia can result in muscle weakness, altered mental status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval) ; however, isolated hvpokalemia does not result in significant cardiac arrhythmias. Hvpomagnesemia is very common in the I C U setting and is often associated with depletion of other electrol

Question 9

9. Ensepalopati, edema serebral dan kejang‐kejang
A. Hiponatremia
B. Hipokalsemia
C. Hipomagnesemia
D. Hipokalemia
E. Hipofosfatemia
F. Hipokloremia

Answer 9

A
Symptomatic hyponatremia (usually 120 mEq/L or less) can result in generalized seizures, metabolic encephalopathy, depressed level of consciousness, acute respiratory distress syndrome, muscle weakness, and even cerebral edema and elevated intracranial pressure. Hypokalemia can result in muscle weakness, altered mental status, and ECG changes (prominent U waves, T-wave inversion, prolonged QT interval) ; however, isolated hvpokalemia does not result in significant cardiac arrhythmias. Hvpomagnesemia is very common in the I C U setting and is often associated with depletion of other electrol

Question 10

10. Ethosuximide
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 10

A
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 11

11. Asam Valpoat
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 11

F
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 12

12. ACTH
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 12

B
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 13

13. Penitoin
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 13

E
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 14

14. Penobarbital
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 14

D
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 15

15. Karbamasepin
A. Absence
B. Infantile spasms
C. Parsial kompleks
D. Kejang neonatal
E. tonik-klonik umum
F. sindroma LENNOX-GASTAUT
G. Bukan salah satu dari A s/d F

Answer 15

C
Isolated absence seizures (petit mal epilepsy) are generally treated with ethosuximide; however, valproic acid is the agent of choice if the patient also experiences generalized tonic-clonic seizures. LennoxGastaut svndrome is a heterogenous disorder characterized by mental retardation, seizures, and generalized spike-andwave complexes at 1 to 2 l-Iz on EEG. 'alproic acid is the initial treatment of choice for this disorder; howe\•er, less than 1 0% of all patients \“ith Lennox-Gasraut syndrome achieve effecti\•e seizure control \•ith single-agen t anticonvulsant therapy. I nfantile spasms (\‘est S'ndrome) occur in children less than 6 months of age and are associated with tuberous sclerosis, cerebral malionnations. and metabolic disorders. The treatment of choice for infantile spasms is ACTH. Several anticonnllsants are utilized in the treatment of generalized tonic-clonic seizures : hmYe\•er, phenytoin is the traditional first-line agem. Phenobarbital is the drug of choice in the treatment of neonatal seizures, but phenytoin and lorazepam are often added with’ inadequate seizure control. Garbamazepine is the agent of choice in the treatment of complex partial seizures and is particularly effective in preventing secondary generalization (Merritt, pp. 813- 826).

Question 16

16. Ciri-ciri manakah yang TIDAK berlaku bagi synchronize itermittent mandatory ventilation (SIMV)
    A. Beri pernafasan dengan silus volume
    B. Seringkali dipadukan dengan dukungan tekanan untuk mengatasi resistensi ventilator circuit tuning
    C. Memungkinkan pernafasan spontan antara pernafasan melalui ventilator
    D. Berasosiasi dengan menurunnya kerja pernafasan
    E. Berasosiasi dengan pengisian ventricular yang terganggu.

Answer 16

D.
SIIviV was developed secondary to complications (e.g. , hyperinflation and overventilation) that can arise in patients on assist-control ventilation (AGV) with rapid respiratorv rates. SIMV delivers 'Olume-cycled breaths at a preselected rate that are synchronized to the patient’s spontaneous breaths. Additionally, SIMV allows spontaneous breaths to occur between ventilator-delivered breaths. Spontaneous breaths during SIMV occur through a high-resistance circuit with a unidirectional valve, which results in an increased work of breathing and potential for respiratory muscle fatigue. The addition of pressure support facilitates spontaneous breaths and can limit increases in work of breathing (and respiratory muscle fatigue) with SIIvfV. Any form of positive-pressure mechanical ventilation can be associated with impaired ventricular filling and concomitant reductions in cardiac output ( Marino, pp. 434-438) .

Question 17

17. Karakteristik manakah di bawah ini yang TIDAK behubungan dengan extrinsic positive end-respiratory pressure (PEEP)?
    A. Memudahkan pengumpulan alveolar
    B. Menurunkan edema pulmonaris
    C. Meningkatkan tekanan intratorak rata-rata
    D. Menurunkan shunt intrapulmonaris
    E. Menurunkan output jantung

Answer 17

B .
Normally, the alveolar pressure a t the end o f expiration is equal to atmospheric pressure. The addition of PEEP (extrinsic PEEP) results in an elevated alveolar pressure at the end of expiration by stopping exhalation when the preselected pressure is reached. PEEP results in increases in endexpiratory and mean intrathoracic pressures. PEEP tends to prevent alveolar collapse and facilitate alveolar reopening ( recruitment) , which results in improved gas exchange (decreased intrapulmonary shunt) and increased lung compliance. The addition of PEEP can result in decreased cardiac filling and cardiac output, especially in hypovolemic patients; this effect is independent of the absolute value of the extrinsic PEEP. The increases in mean intrathoracic pressure that are secondary to extrinsic PEEP are directlv related to the observed decreases in cardiac output. The application of PEEP does not reduce pulmonary edema and can, in fact, exacerbate pulmonarv edema secondarY to ah•eolar overdistention and impaired pulmonary lvmphatic drainage ( Marino, pp. 382-383, 441-44 5 ) .

Question 18

18. Semua hal di bawah ini berasosiasi dengan sindroma distress pernafasan akut (SDPA),
    KECUALI
    A. Hipoksia
    B. Infiltrasi pulmonaris menyebar
    C. Hiperkapnia
    D. Menambahkan PEEP mencegah keruntuhan alveolar dan memungkinkan penurunan FiO2 ke tingkat non-toksis.
    E. Seringkali menunjukkan rasio PAO2/FiO2 > 200 mmHg

Answer 18

E .
ARDS i s characterized b y the acute onset of diffuse pulmonary infiltrates and hypoxemia that is reiractorv to eJe,•ations in Fi02. Lung-protective ,•entilatorv strategies with ARDS include the utilization of lo\•er tidal ,•olumes ( 7 to 10 cc/kg) than with other traditional forms of ,•entibtion to keep peak inspiratory pressures less than 35 em H20. The addition of PEEP with ARDS prevents ah’colar collapse ( with the lower tidal ,•olumes) and allows the reduction oi the Fi02 to nontoxic levels (

Question 19

19. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang TIDAK berasosiasi dengan auto-PEEP (PEEP intrinsik atau hiperinflasi)?
A. Volume inflasi besar
B. Frekuensi pernapasan rendah
C. Ventilasi rasio terbalik
D. Asma
E. Pneumotoraks

Answer 19

B.
I n trinsic PEEP (occult PEEP) results from incomplete alveolar emptying during expiration. The development of intrinsic PEEP is associated with l arge inflation volumes, rapid respiratory rates, decreases in exhalation time (inverse ratio ventilation), and airway obstruction (e.g., asthma and COPD). High levels of intrinsic PEEP are associated with decreased cardiac output, alveolar rupture (volutrauma) with possible pneumothorax, increased work of breathing, and ele,•ations in plateau pressures ( M a rino, pp. 462-464 ) .

Question 20

20. Di antara perubahan-perubahan EKG di bawah ini, manakah yang dapat diobservasi pada pasien dengan emboli paru?
21. Takikardia
22. Perubahan-perubahan ST non-spesifik
23. Gelombang Q besar pada lead III
24. Gelombang T terbalik pada lead III

Answer 20

E.

EGG changes in acute pulmonary emboli include sinus tachycardia (most common), inverted T waves in !

Question 21

21. Di antara agen-agen di bawah ini, manakah yang merupakan agen baris-pertama yang
    terpilih dalam perawatan takikardia atrial multifokal?
    A. Magnesium IV
    B. Verapamil
    C. Netoprolol
    D. Lidokain
    E. Kardioversi elektrik

Answer 21

A.
Multifocal atrial tachycardia ( l'lA T) exhibits multiple P-wave morphologies and variable PR intervals on EGG, with an irregular ventricular rate. l\fAT is associated with chronic lung disease and theophylline, and has been associated with hypokalemia, acute mvocarclial infarction, pulmonary embolism, and congestive heart failure. l\tlAT should initially be treated with IV magnesium; theophylline should be discontinued and any underlying hypokalemia corrected. If these therapies are ineffective, verapamil or metoprolol should be administered ( Marino, pp. 328-329 ) .

Question 22

22. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang berasosiasi dengan tamponade jantung?
23. Distensi Venus jugular
24. Hipotensi
25. Bunyi jantung lemah
26. Kenaikan dalam tekanan darah stoik (> 10 mmHg) dengan onset inspirasi

Answer 22

A .
Cardiac tamponade i s associated with Beck’s triad (jugular venous distention, m uffled heart sounds, hypotension) and pulsus paradoxus (drop in systolic blood pressure of at least 10 mm Hg with the onset of inspiration) . Diastolic pressures (GVP, PGWP, pulmonary artery diastolic pressure) are often equalized with cardiac tamponade, and the diagnosis is often confirmed with transesophageal echocardiography. The treatment of cardiac tamponade entails emergent pericardiocentesis (Marino, pp. 255-256 ) .

Question 23

23. Perempuan berusia 48 tahun dengan tiga anak mengalami onset demam akut tiga jam
    setelah menerima transfusi darah, Tindakan pencegahan manakah yang seharusnya
    diambil sebelum pemberian transfusi yang kedua?
    A. Berikan sel-sel merah yang telah dibersihkan
    B. Berikan sel-sel merah kadar leukosit rendah
    C. Pra perawatan dengan Tylenol
    D. Selidiki adanya defisiensi IgA
    E. Jawaban A, B, C dan D semuanya salah.

Answer 23

C
Febrile nonhemolytic reactions are extremely common and accompany approximately 1 % of all transfusions. These reactions are secondary to antibodies in the recipient blood that react to donor leukocytes and are more common in multiparous women and a history of prior transfusions. The fever usually occurs between 1 and 6 hours after the transfusion and is not associated with other symptoms. The majority of patients who experience a febrile nonhemolytic reaction will not experience a second fever with repeat transfusion; however, leukocyte-poor red cells can be utilized 220 Intensive Neurosurgery Board Review in patients with repetitive febrile nonhemolytic reactions. Patients with lgA deficiency can exhibit more severe hypersensitivity reactions to transfusions, including rash and anaphylaxis ( Marino, p p . 702-703).

Question 24

24. Di antara test-test laboratorium di bawah ini, manakah yang abnormal memanjang pada penyakit Willebrand ?
25. waktu protrombin
26. Waktu trombioplastin parsial (PTT)
27. Dilusi Protrombin 1 : 1
28. Waktu pendarahan

Answer 24

C.
Von \Villebrand’s disease results in prolongations of the partial thromboplastin time ( PTT) and bleeding time because von \Villebrand factor stabilizes factor VIII and mediates platelet adhesion (Cecil, pp. 993 ) .

Question 25

Jodohkanlah sindroma kejut di bawah ini dg pengukuran-pengukuran/tanda-tanda vital
kateter Swan-Ganz, Catatan – tenakan vena CVP-sentral (mm Hg), PCWP – tekanan pantek
kapilaris pulmonaris (mm Hg), CI – Indeks jantung (L/ mnt/m2 ) SVR – resistensi vaskular sistemik (Dine/cm2 )
A. Kejut hipovolemik
B. Kejut kardiogenik
C. Kejut septic
25. CPV 16, PCWP 20, CI 1.2, SVR 1250

Answer 25

B
Hypovolemic shock i s characterized by decreased central 'enous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1 200 dynes/cm2) , and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1 .8 L/min/m2) , elevated PCWP (> 18 mm J-Ig) and CVP, elevated SVR, and decreased systolic blood pressure (

Question 26

Jodohkanlah sindroma kejut di bawah ini dg pengukuran-pengukuran/tanda-tanda vital
kateter Swan-Ganz, Catatan – tenakan vena CVP-sentral (mm Hg), PCWP – tekanan pantek
kapilaris pulmonaris (mm Hg), CI – Indeks jantung (L/ mnt/m2 ) SVR – resistensi vaskular sistemik (Dine/cm2 )
A. Kejut hipovolemik
B. Kejut kardiogenik
C. Kejut septic
26. CPV 4, PCWP 6, CI 4.5, SVR 350

Answer 26

C
Hypovolemic shock i s characterized by decreased central 'enous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1 200 dynes/cm2) , and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1 .8 L/min/m2) , elevated PCWP (> 18 mm J-Ig) and CVP, elevated SVR, and decreased systolic blood pressure (

Question 27

Jodohkanlah sindroma kejut di bawah ini dg pengukuran-pengukuran/tanda-tanda vital
kateter Swan-Ganz, Catatan – tenakan vena CVP-sentral (mm Hg), PCWP – tekanan pantek
kapilaris pulmonaris (mm Hg), CI – Indeks jantung (L/ mnt/m2 ) SVR – resistensi vaskular sistemik (Dine/cm2 )
A. Kejut hipovolemik
B. Kejut kardiogenik
C. Kejut septic
27. CPV 2, PCWP 5, CI 2.0, SVR 1400

Answer 27

A
Hypovolemic shock i s characterized by decreased central 'enous and intracardiac pressures, decreased cardiac output, elevated SVR (> 1 200 dynes/cm2) , and concomitant hypotension and tachycardia, with a dampened Swan-Ganz catheter waveform. Cardiogenic shock is characterized by a decreased cardiac index (less than 1 .8 L/min/m2) , elevated PCWP (> 18 mm J-Ig) and CVP, elevated SVR, and decreased systolic blood pressure (

Question 28

28. Di antara karakteristik di bawah ini, manakah yang TIDAK berasosiasi dengan multipel neoplasia endokrin tipe-2 (Sindroma Sipple)?
A. Keturunan dominan autosomal
B. Peokromositoma
C. Adenoma Hipofise
D. Karsinoma tiroid medularis
E. Hiperplasia paratiroid

Answer 28

C.
Multiple endocrine neoplasia ( li ‘IEN ) tYpe 2 ( Sipple syndrome) is an autosomal dominant disorder that localizes to chromosome 10 and is characterized by the development pheochromocytomas and medullar

Question 29

29. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang berasosiasi dengan embolisme udara pada vena saat operasi ?
30. Kejadian tinggi pada posisi duduk
31. Modalitas diagnostik yang paling peka adalah ekokardiografi trenasesopageal
32. Berasosiasi dengan penurunan pada end tidal CO2
33. Pasien perlu segera ditempatkan pada posisi dekubitus lateral kanan.

Answer 29

A.
Intraoperative venous air embolism (VAE) has a high incidence during procedures performed in the sitting position (up to 25 to 45% of all case s ) . VAE is characterized by the development of bronchoconstriction, hypoxia, hypercarbia, hypotension, shock, cardiac arrhythmias, increased airway pressures, and decreased end-tidal C02 (secondary to increased dead space) . Transesophageal echocardiography is the most sensitiYe diagnostic modality for VAE, detecting volumes as small as 0.02 mL!kg of air entering the venous S'Stem. The immediate treatment of suspected VAE entails rapid hemostasis \Yith concomitant irrigation of the surgical field, lo\Yering of the patient’s head with left lateral decubitus positioning. increasing the FiO” to 1 00%, stopping any concomi tant nitrous oxide administration, manual occlusion of the j ugular veins. and aspiration of air from a multiorifice C'P catheter ( Greenberg, p . 602 ; Youmans, pp. 614-615; Wilkins, pp. 409-410)

Question 30

Pilihlah karakteristik-karakteristik di bawah ini yang paling lazim tampak dengan CSW/sindroma sekresi ADH yang tidak tepat (SIADH)
A. Pembuangan garam serebral (CSW)
B. SIADH
C. A dan B
D. Bukan A, B atau C

30. Hipovolemia

Answer 30

A
Cerebral salt wasting ( CSW) is characterized bY hYponatremia ( 20 mEq/L ) , elevated urine osmolality, decreased PCWP and CVP (hypovolemia ) , and normal or elevated serum potassium levels. SIADJ-1 is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion. SIADH is associated with a decreased serum osmolality (

Question 31

Pilihlah karakteristik-karakteristik di bawah ini yang paling lazim tampak dengan CSW/sindroma sekresi ADH yang tidak tepat (SIADH)
A. Pembuangan garam serebral (CSW)
B. SIADH
C. A dan B
D. Bukan A, B atau C

31. Hipervolemia

Answer 31

B
Cerebral salt wasting ( CSW) is characterized bY hYponatremia ( 20 mEq/L ) , elevated urine osmolality, decreased PCWP and CVP (hypovolemia ) , and normal or elevated serum potassium levels. SIADJ-1 is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion. SIADH is associated with a decreased serum osmolality (

Question 32

Pilihlah karakteristik-karakteristik di bawah ini yang paling lazim tampak dengan CSW/sindroma sekresi ADH yang tidak tepat (SIADH)
A. Pembuangan garam serebral (CSW)
B. SIADH
C. A dan B
D. Bukan A, B atau C

32. Kenaikan osmolalitas serum

Answer 32

D
Cerebral salt wasting ( CSW) is characterized bY hYponatremia ( 20 mEq/L ) , elevated urine osmolality, decreased PCWP and CVP (hypovolemia ) , and normal or elevated serum potassium levels. SIADJ-1 is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion. SIADH is associated with a decreased serum osmolality (

Question 33

Pilihlah karakteristik-karakteristik di bawah ini yang paling lazim tampak dengan CSW/sindroma sekresi ADH yang tidak tepat (SIADH)
A. Pembuangan garam serebral (CSW)
B. SIADH
C. A dan B
D. Bukan A, B atau C

33. Hipourisemia

Answer 33

B
Cerebral salt wasting ( CSW) is characterized bY hYponatremia ( 20 mEq/L ) , elevated urine osmolality, decreased PCWP and CVP (hypovolemia ) , and normal or elevated serum potassium levels. SIADJ-1 is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion. SIADH is associated with a decreased serum osmolality (

Question 34

Pilihlah karakteristik-karakteristik di bawah ini yang paling lazim tampak dengan CSW/sindroma sekresi ADH yang tidak tepat (SIADH)
A. Pembuangan garam serebral (CSW)
B. SIADH
C. A dan B
D. Bukan A, B atau C

34. Perlakuan berakibat Restriksi air bebas

Answer 34

B
Cerebral salt wasting ( CSW) is characterized bY hYponatremia ( 20 mEq/L ) , elevated urine osmolality, decreased PCWP and CVP (hypovolemia ) , and normal or elevated serum potassium levels. SIADJ-1 is characterized by the presence of hyponatremia and hypervolemia secondary to plasma volume expansion. SIADH is associated with a decreased serum osmolality (

Question 35

35. Di antara agen-agen di bawah ini, agen manakah yang berasosiasi dengan perkembangan “tension pneumocephalus’ ?
A. Propolol
B. Isoflurane
C. Etomidate
D. Oksida Nitrus
E. Lorazepam

Answer 35

D.
Nitrous oxide increases cerebral blood flow and thus intracranial pressure when intracranial compliance is altered. Nitrous oxide can also diffuse into i ntracranial air faster than nitrogen can escape, which can contribute to the development of tension pneumocephalus ( Greenberg, p. 2; You mans, p. 1508; Wil kins, p. 405) .

Question 36

36. Semua karakteristik di bawah ini berasosiasi dengan barbiturat, KECUALI
    A. Supresi letupan EEG tergantung dosis
    B. Berasosiasi dengan penurunan aliran darah serebral
    C. Efek berhenti terutama karena redistribusi
    D. Dapat menyebabkan vasokonstriksi periferal prominen
    E. Supresi miokardial tergantung dosis

Answer 36

D .
Barbiturates are anticonvulsants that result in prominent decreases in CBF and CMR02, dose-dependent EEG burst suppression, dose-dependent myocardial suppression, and peripheral vasodilation. Barbiturates are lipid-soluble and their CNS effects are primarily terminated by redistribution. At higher dosages, barbiturates can actually result in decreases i n cerebral perfusion pressure if decreases in mean arterial pressure exceed the decrease in intracranial pressure ( Katzung, p . 410; Youmans, pp. 1508, 1521; Greenberg, pp. 2, 7 76-7 7 7 ; Wilkins, p. 404).

Question 37

37. Di antara agen-agen di bawah ini, agen manakah yang menunjukkan selektivitas
tertinggi untuk reseptor β1?
A. Dobutamin
B. Dopamin
C. Epineprin
D. Penileprin
E. Isoproterenol

Answer 37

A

Question 38

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

38. Ensepalopati, neuropati periferal, anemia hipokromis

Answer 38

B
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 39

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

39. Gingivostomatitis, neuropati periferal, gangguan kejiwaan

Answer 39

C
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 40

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

40. Perlakuan yang terpilih untuk keracunan besi

Answer 40

H
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 41

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

41. Perlakuan terpilih untuk keracunan lead pada anak-anak

Answer 41

E
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 42

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

42. Kardiomiopati, pansitopenia, renjatan hipotensif

Answer 42

A
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 43

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

43. Perlakuan terpilih untuk penyakit Wilson

Answer 43

F
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 44

Jodohkanlah Intoksikasi logam di bawah ini dengan karakteristik-karakteristik/terapi-terapinya yang tepat.
A. Keracunan arsenik
B. Keracunan Lead
C. Keracunan Mercuri
D. Keracunan besi
E. Succimer (DMSA)
F. Penisilamin
G. Talium
H. Deferoksamin
I. Keracunan mangan
J. Bukan salah satu dari A sampai dengan I

44. Kadang-kadang dirawat dengan L-DOPA

Answer 44

I
Refer t o Table 7.38- 7 . 44A. Arsenic neuropathy is the most common of all the heavy metal-induced neuropathies. Gastrointestinal ( G I ) symptoms such as nausea, vomiting, and diarrhea occur when large quantities are ingested, but these symptoms are often absent if arsenic is taken parenterally or taken in small amounts over a protracted period of time. In acute poisoning, the onset of symptoms usually takes 4 to 8 weeks to de,•elop, but the evolution of polyneuropath

Question 45

45. Berapakah koreksi maksimum yang diharapkan dari seorang pasien dengan hiponatremia simtomatis selama 24 jam (mEq/L)?
A. 4
B. 6
C. 12
D. 16
E. 20

Answer 45

C .
Symptomatic hyponatremia (generally < 1 2 5 mEq/L) should be corrected at a maximal rate of 0 . 5 mEq/L/h ( thus 1 2 mEq/L/24 h) to avoid central pontine myelinolysis ( Ma rino, p . 644; Greenberg, pp. 15-16).

Question 46

46. Berapa lama setelah cedera luka yang telah sembuh akan mengandung kandungan kolagen maksimum?
A. Dua hari
B. Dua minggu
C. Dua bulan
D. Dua tahun
E. Jawaban A, B, C dan D semuanya salah

Answer 46

C.
Wound healing occurs in primarily three phases: the intlammatory, the proliferative, and the remodeling phases. The int1ammatory phase occurs during the first week and is characterized by hemostasis as well as neutrophil and macrophage infiltration . The proliferative phase occurs irom approximately 5 clays to 3 \;eeks and consists of neo\•ascularization, wound contraction (myofibroblasts ) , extracellular matrix synthesis (fibroblasts ) , and cellular migration ( epithelialization) . The third phase (remodeling) occurs from approximately 4 weeks to 2 years and consists of the aggregation and alignment of collagen fibers, 1\•ith a progressi\•e increase in \Youncl tensile strength for the first 6 to 8 months until it plateaus. The wound contains the maximum collagen content approximately 2 to 3 months after injur\•, during theearly portion of the proliferative phase (Robbins, pp. 7 4-76; Wilki ns, pp. 519-520; Youmans, pp. 564-56 5 ) .

Question 47

47. Di antara anestesi-anestesi di bawah ini, manakah yang memiliki ambang minimum kejang yang rendah
48. Enflurane
49. Propolol
50. Metoheksital
51. Diazepam

Answer 47

B.
Enflurane i s a n inhaled general anesthetic that actually lowers seizure threshold; methohexital is a barbiturate that also lowers seizure threshold. This property renders these two agents unsuitable for most neurosurgical procedures (Greenberg, pp. 2, 4 7; Katzung, p. 4 1 7 ; Youmans, pp. 1508-1512) .

Question 48

48. Seorang perempuan berusia 38 tahun dibawa dengan amenorea sekunder, bidang visual normal dan kadar prolaktin 560 ng/mL. Hasil MRI pasien menunjukkan bukti adanya makroadenoma pituitaris yang menyangat, dan pasien segera diberi terapi bromokriptin oral. Setelah beberapa bulan kemudian, kadar prolaktin pasien menunjukkan kembali ke normal, ukuran makroadenoma menurun drastis, dan pada akhirnya pasien bisa mengandung. Pasien kemudian menghilang dan tidak mengikuti prosedur tindak lanjut, sampai lima tahun kemudian datang kembali dengan keluhan kehilangan penglihatan akut. MRI ulangan menunjukkan kambuhnya kembali makroadenoma, dan pasien dilaporkan menderita amenorea dan Galaktorea. Kadar prolaktin serum rutin pasien adalah 39 ng/mL. Penjelasan manakah yang paling mungkin untuk kadar prolaktin pasien kali ini?
    A. Efek Stalkh
    B. Makroadenoma tidak lagi mensintesis prolaktin
    C. Efek Hook
    D. Terapi bromokriptine sebelumnya menunjang pertumbuhan sel-sel pituitaris neopastik yang tidak menghasilkan hormon (adenoma sel-nol)
    E. Jawaban A, B, C,\ dan D salah semua

Answer 48

C .
The Hook effect resul t s i n false-negative lab assays for prolactin in the presence of extremely high prolactin levels. This is secondary to i nhibition of formation of the normal prolactin-antibod,• complexes due to the presence of extremely high prolactin le,•els. In these cases, a 1 : 100 prolactin dilution should be obtained to effectively rule out a prolactinoma. Stalk effect results from compression of the adjacent hypothalamus or pituitary stalk by nonprolactin- secreting macroadenomas and commonly results in prolactin le,•els of 25 to 150 ng!mL. Pituitary adenomas are typically monoclonal neopl:lsms; thus it is unlikelv that a null cell adenoma has arisen in a patient with a prior known prolactinoma. The diagnosis of a prolactinoma generallyrequires a serum prolactin level of > 200 ng/mL (Greenberg, pp. 420-426; Kaye and Laws, pp. 206-210)

Question 49

49. Semua karakteristik di bawah ini sejalan dengan test Supresi deksametason dosis tinggi ( 2mg q 6 h x 8 dosis), KECUALI
    A. Membedakan penyakit Cushing dari adenoma adrenal penghasil kortisol
    B. Kadar kortisol bebas urin yang menunjukkan Supresi 90% dari baseline dengan penyakit Cushing
    C. 17-hidroksisteroid ditekan menjadi

Answer 49

D.
The high-dose dexamethasone suppression test helps distinguish Cushing’s disease (ACTH-secreting pituitary adenoma) from ectopic sources of ACTH and cortisolproducing adrenal adenomas. Pituitary adenomas will exhibit suppression with this test, \Yith concomitant decreases in 17 -hvdroxvsteroids to

Question 50

50. Di antara karakteristik di bawah ini, manakah yang sejalan dengan koma barbiturat pada pasien dengan cedera kepala tertutup? (E)
51. Supresi letupan sedang pada EEG berasosiasi dengan penurunan maksimal dalam metabolisme serebral (CRMO2)
52. Barbiturat meningkatkan perfusi serebral global
53. Barbiturat dapat menyebabkan depresi miokardial
54. Barbiturat berasosiasi dengan imunosupresi

Answer 50

E.
H igh-dose barbiturates uncouple cerebral blood flow and cerebral metabolism, thus resulting in decreases in Clvi R02 and increases in C B F . Burst suppression on EEG results i n maximal reductions in C!IIRO, \Yith continuous barbiturate infusions. High-dose barbiturate t herapy i s associated with myocardial depression and hypotension, and patients often require concomitant ,•asopressor therapy to maintain an adequate mean arterial pressure during barbiturate infusions . O ther effects of high-dose barbiturate infusion include immunosuppression, impaired gastric motility, increased lysosomal stability

Question 51

51. Manakah diantara hal-hal berikut ini yang harus digunakan dalam perawatan
koagulopati akibat penyakit Willebrand?
1. Plasma beku segar (FFP)
2. Desmopresin
3. Platelet
4. Kripopresipitat

Answer 51

C .
Von Willebrand’s disease (VWD) resulrs i n prolongation of the partial thromboplastin time (PTT) and bleeding time. Coagulopathy resulting from VWD is typically treated with cryoprecipitate, which is rich in both factor VII I and von Willebrand factor as well as desmopressin ( D DAVP), which facilitates the release of von Willebrand factor from epithelial cells (Cecil, p. 994 ) .

Question 52

52. Di antara ciri di bawah ini, manakah yang TIDAK berasosiasi dengan pendarahan gastrointestinal perioperatif?
    A. Pasien dengan cedera memar kepala parah
    B. Pasien dengan luka bakar > 30% dari permukaan tubuh.
    C. Kejut hipotensi
    D. Asupan dini makanan enteral pasca-operasi
    E. Tingkat kejadiannya menurun dengan pemakaian penghambat H2 dan sukralfat

Answer 52

D.
Superficial stress ulcers in the gastric/duodenal mucosa are a result of regional decreases in blood flow and are exacerbated by the presence of H+. P atients in the highest risk category for GI hemorrhages are those with severe closed head injuries (Cushing’s ulcer) and those with burns over > 30% body surface area (Curling’s ulcer) . Superficial stress ulcers can lead to nosocomial sepsis and occult GI bleeding, although overt hemorrhage occurs in only 5% of all cases of s tress ulcers. The risk of perioperative GI bleeding can be decreased with the administration of I -I” blockers and sucralfate, maintenance of adequate systemic blood pressure and oxygen transport, and initiation of early enteral feedings ( Marino, p p . 94-101) .

Question 53

53. Reaktan fase akut manakah yang biasanya naik selama masa-masa peradangan sistemik akut?
54. Protein C-reaktif
55. Fibrinogen
56. Haptoglobin
57. Albumin

Answer 53

A. 1,2,3

Superficial stress ulcers in the gastric/duodenal mucosa are a result of regional decreases in blood flow and are exacerbated by the presence of H+. P atients in the highest risk category for GI hemorrhages are those with severe closed head injuries (Cushing’s ulcer) and those with burns over > 30% body surface area (Curling’s ulcer) . Superficial stress ulcers can lead to nosocomial sepsis and occult GI bleeding, although overt hemorrhage occurs in only 5% of all cases of s tress ulcers. The risk of perioperative GI bleeding can be decreased with the administration of I -I” blockers and sucralfate, maintenance of adequate systemic blood pressure and oxygen transport, and initiation of early enteral feedings ( Marino, p p . 94-101) .

Question 54

54. Diantara agen-agen di bawah ini, agen manakah yang bertindak sebagai pirogen pada hipotalamus?
55. Interleukin-6
56. Faktor nekrosis tumor
57. Interleukin-1
58. Prostaglandin E2

Answer 54

E .
There are several different proteins that act at the anterior hypothalamus to induce a systemic fe\•er (pyrogens) , including i nterleukin - 1 , interleukin-6, tumor necrosis factor, interferon-a, and some bacterial toxins . .’\ II of these substances induce local increases in prostaglandin E2 le\•els in the anterior hypothalamus to increase the temperature set point (Cecil, pp. 1533-153 5 )

Question 55

55. Diantara parameter-parameter di bawah ini, parameter manakah yang merupakan indikator terbaik perfusi jaringan yang cukup?
A. Tekanan darah sistolik
B. Output urine
C. rate jantung
D. pH gastrointestinal
E. Kejenuhan oksigen

Answer 55

D.
In shock states, blood is selectively shunted away from the GI tract, which results in decreases in the local gastric pH. GI p H normalizes after adequate resuscitation and is thus an excellent indicator of regional perfusion. CHAPTER 7 Critical Care and Clinical Skills Answers 223 Normal systolic blood pressure, heart rate, and even urine output can all be observed in inadequately resuscitated patients who are i n states of compensated shock ( Marino, p p . 198-200; B rown et a l . , p p . 569-58 5 ) .

Question 56

56. Fitur manakah yang TIDAK biasanya berasosiasi dengan septik shok?
A. Perubahan status mental
B. Asidosis pernafasan
C. Hiperglikemia
D. Naiknya tekanan pulsa
E. Naiknya hitung sel darah putih

Answer 56

B.
Septic shock is usually a result of bacteremia with gram-positive or gram-negative organisms, although it can also occur with fungal and anaerobic infections. Septic shock often exhibits fever, mental status changes, tachypnea, tachycardia, an increased pulse pressure, hyperglycemia, and an elevated whi te blood cell count. Septic shock results in tachypnea and a concomitan t respiratory alkalosis early in the disease course, although late in the disease course a concomitant metabolic acidosis can occur from lactate accumulation ( hypoperfusion) . Septic shock i s also accompanied by tachycardia and an increased cardiac output initially, although cardiac output and stroke volume ar" often decreased in the la ter stages of septic shock. lllost patients with sepsis exhibit an ele,•ated white blood cell count and hyperglycem i a (glucocorticoid release ) , although marked decreases i n the \Yhite blood cell count and hypoglycemia (with prominent bacteremia) are also occasionally observed ( Marino, p p . 505- 510 ) .

Question 57

57. Diantara komplikasi-komplikasi metabolis di bawah ini, komplikasi manakah yang TIDAK biasanya berasosiasi dengan pemberian nutrisi parenteral total?
A. Hiperglikemia
B. kekurangan asam lemak esensial
C. Alkalosis metabolis
D. Hipofosfatemia
E. Kolestasis hepatic

Answer 57

C.
Mletabolic complications of total parenteral nutrition _ ( T PN) include \•olume m•erload, hyperglycemia, hypophosphatemia, hvperchloremic metabolic acidosis, hypomagnesemia, hypokalemia, trace element deficiency, and essential fattv acid deficiency. Patients on long-term TPN are also at risk to develop hepatic cholestasis and vitamin deficiencies. Other complications of TPN include complications related to central line placement (e.g. , pneumothorax, hemothorax) and the presence of a n indwelling central catheter (e.g. , venous thrombosis and sepsis) (Marino, pp. 759- 763).

Question 58

58. Di antara ciri-ciri di bawah ini, karakteristik manakah yang sejalan dengan kolitis pseudomembranus?
59. Pemberian sebelum antibiotika
60. Berkembangnya megakolon toksik
61. Diare berair
62. Enzyme-linked immunosorbent assays (ELISA) untuk toksin C-difficile mencerminkan standar emas dalam diagnosis laboratorium

Answer 58

A .
Pseudomembranous colitis ( PMC) i s a relatively common cause of severe diarrhea and colitis i n the ICU population and results from toxins produced by Clost1idium dij{ici/e. PMC is usually associated w i th prior exposure to third-generation cephalosporins, clindamycin, or one of the penicillins, although many different antibiotics have been implicated in the development of this disorder. C. dif./icile produces two different toxins (toxin A and toxin B) that ultimately result in disruption of colonic mucosal integrity, \Yith subsequent fluid secretion, inflammation, and edema. Findings of PJ\IC include fever, leukocytosis, watery diarrhea, abdominal pain/cramping, dehydration, hypoalbuminemia. and e\•en the development of sepsis and toxic megacolon (with colonic perforations) . The "gold s tandard" laboratory studv for the diagnosis of PMC is direct cytotoxic assay of stool filtrate for C. difficile toxi n . ELISA tests for C. difficile toxin are also available; however, they exhi b i t low sensiti\ •it:•. Direct culture of the bacterium is the most sensiti\•e laboratorv assay, but it is rarely performed due to time andcost constraints and the inability to differentiate between normal and toxic strains of C. difficile. The treatment of PMC includes discontinuation of causative antibiotics, fluid and electrolyte repletion, and the administration of oral metronidazole (Flagyl) (Marino, pp. 534-537 ) .

Question 59

59. Diantara pemeriksaan-pemeriksaan di bawah ini, pemeriksaan manakah yang memiliki nilai prediktif positif tertinggi untuk diagnosis embolisme pulmonaris akut?
    A. Angiogram pulmoner
    B. Angiografi tomografis hitung helikal resolusi tinggi
    C. Scan paru-paru ventilasi-perfusi skintigrafis nuklir
    D. Ultrason dupleks Venus
    E. Jawaban A, B, C dan D semuanya salah

Answer 59

A .
Pulmonary angiography continues t o b e the gold standard in the diagnosis of acute pulmonary embolism (PE), with close to a 100% positive predic ti\•e value and 90% negati\ •e predictive ,•alue. High-resolution helical CT angiography is evolving as a more accurate diagnostic modalitv for acute pulmonary embolism, although its sensiti,•ity and specificity are not as well defined. Nuclear scintigraphic ventilationperfusion (V/Q) lung scan is often the initial diagnostic study of choice in patients with small pulmonary emboli, although approximately 40% of all patients with an acute PE will exhibit a nondiagnostic (indeterminate) V/Q scan. Lower extremity duplex ultrasound can ofren confirm the source of a PE, although a negative result does not significantly reduce the likelihood of a PE ( Marino, pp. 112-115).

Question 60

60. Pemberian walfarin (Coumadin) menghambat sintesis protein faktor-faktor/antikoaguilan pengumpul mana?
61. Faktor VII
62. Faktor II
63. Faktor IX
64. Protein C

Answer 60

E.

Warfarin (Coumadin) inhibits the svnthesis of the vitamin !-dependent clotting factors (f:-

Question 61

61. Obat-obatan manakah yang dapat menyebabkan menurunnya keberadaan hayati warfarin selama pemberiannya?
62. Barbiturat
63. Cimetidine
64. Rimfampin
65. Metronidazole

Answer 61

C.
Barbiturates, rifampin, a n d cholestyramine administration can all result in decreased levels of warfarin (and thus decreases in lN R ) . Cimetidine, metronidazole, trimethoprim-sulfamethoxazole, fluconazole, amiodarone, and disulfiram all result in increased levels of coumadin ( and thus increases in INR) (Katzung, p. 554 ) .

Question 62

62. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang TIDAK tampak pada aldosteronisme primer (Sindroma Conn)?
A. Hipertensi
B. Hiperkalemia
C. Aktivitas renin plasma rendah
D. Alkalosis metabolis
E. Hipomagnesemia

Answer 62

B .
Primary aldosteronism ( Conn's syndrome) i s characterized b

Question 63

63. Laki-laki usia 22 tahun dibawa ke UGD setelah mengalami cedera karena tabrakan kendaraan bermotor. Tekanan jantung pasien adalah 122. Tingkat pernafasan 28, tekanan darah sistolik 86, saturasi oksigen 88% dan mengalami deviasi trakeal ke sebelah kiri. Manakah langkah manajemen berikutnya yang harus segera dilakukan untuk kondisi ini?
A. Torakosentesis jarum darurat
B. Penempatan tabung torakostomi
C. X-ray dada portabel
D. Ambil gas darah arteri
E. CT scan pada dada.

Answer 63

A.
Tension pneumothorax is a life-threatening condition that often exhibits tracheal de\•iation to the side opposite the pneumothorax. The marked increases in intrathoracic pressure that accompan,• tension pneumothorax can result in prominent decreases in \•enous blood return to the heart, with concomitant h,•potension and shock, as in this case. ATLS guidelines recommend immediate empiric treatment of suspected tension pneumothorax with needle thoracocentesis. follo\•ed ]),• placement of a definitive thoracostomy tube (American College of Surgeons Committee on Trauma, pp. 128-129 )

Question 64

Tn. X, 46 tahun tanpa riwayat bedah sebelumnya, diintubasi dan ditempatkan pada bius umum untuk disektomi dan fusi servikal anterior. Beberapa saat setelah intubasi, pasien menunjukkan kenaikkan prominen pada CO2 end tidal, tacikardia, dan suhu tubuh naik

64. Langkah manajemen berikutnya yang haruis segera ditempuh adalah:
A. Rontgen dada portabel STAT
B. Hentikan segera bius inhalasional
C. Antikoaguilan heparin
D. Naikkan tingkat ventilatris
E. A, B, C dan D salah

Answer 64

B

Question 65

Tn. X, 46 tahun tanpa riwayat bedah sebelumnya, diintubasi dan ditempatkan pada bius umum untuk disektomi dan fusi servikal anterior. Beberapa saat setelah intubasi, pasien menunjukkan kenaikkan prominen pada CO2 end tidal, tacikardia, dan suhu tubuh naik

65. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang kemungkinan berkembang karena terlambatnya diagnosis dan perawatan masalah di atas?
66. Hipoksia
67. Rabdomiolisis
68. Asidosis Metabolis
69. Koagulasi intravaskular menyebar

Answer 65

E

Malignant hyperthermia is a heritable disorder

Question 66

Tn. X, 46 tahun tanpa riwayat bedah sebelumnya, diintubasi dan ditempatkan pada bius umum untuk disektomi dan fusi servikal anterior. Beberapa saat setelah intubasi, pasien menunjukkan kenaikkan prominen pada CO2 end tidal, tacikardia, dan suhu tubuh naik

66. Pemberian obat manakah yang efektif dalam menghentikan perkembangan gangguan di atas pada mayoritas kasus?
    A. Propofol B. Etomidate C. Lorazepam D. Dantrolene E. Heparin

Answer 66

D

Malignant hyperthermia is a heritable disorder

Question 67

67. Perawatan manakah yang efektif dalam merawat Hiperkalsemia
68. Furosemida
69. Saline isotonic
70. Kalsitonin
71. Pamidronate

Answer 67

E.
Hypercalcemia is quite rare in the ICU setting and is usually secondary to the presence of hyperparathyroidism, thyrotoxicosis, or malignancy. Medications that are effective in the treatment of hypercalcemia include furosemide (promotes urinary excretion ) , isotonic saline ( corrects hvpovolemia and promotes calcium excretion) , calcitonin (inhibits bone resorption), hydrocortisone, bisphosphonates (e .g. , pamidronate) , and plicamycin (mithramycin ) . Hemodialysis i s also an effective treatment for hypercalcemia ( Marino, pp. 679-681).

Question 68

68. Di antara ciri-ciri di bawah ini, ciri-ciri manakah yang sejalan dengan embolisme lemak?
69. Disfungsio serebral global
70. Gagal ginjal
71. Petechiae Konjuktival
72. Perawatan meliputi Dihindarinya ventilasi tekanan positif

Answer 68

A .
Fat embolism is characterized by pulmonary, cerebral, hepatic, and renal involvement. Cerebral symptoms are usually global, and pulmonary symptoms usually dominate the clinical presentation. Occasionally petechiae of the chest and conjunctivae are observed. Treatment entails aggressive oxygenation with positive-pressure ventilation, volume resuscitation, and the administration of corticosteroids ( Robbins, pp. 1 10-111; Wi l kins, pp. 2 704-2705).

Question 69

69. Diantara patogen di bawah ini, manakah yang paling mungkin menyebabkan infeksi shunt dini (kurang dari 2 minggu) dan lambat (lebih dari 6 bulan)?
    A. staph, aureus, staph. epiderminis
    B. staph. epidermidis, strep. pneumonia
    C. staph. epidermidis, staph. epidermidis
    D. staph. epidermidis, P. acnes
    E. staph. epidermidis, staph aureus

Answer 69

C.
Staphylococcus epidenniclis is the most common pathogen to result in shunt infections in both an early and late fashion (Greenberg, p . 214).

Question 70

70. Meningkatkan metabolisme serebral maupun aliran darah serebral.
A. Etomidate
B. Propofol
C. Lorazepam
D. Halotane
E. Isoflurane
F. Oksida nitrous
G. Fentanil
H. Pentobarbital
I. Bukan salah satu dari A s/d H

Answer 70

F
Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and lCP. Etomidate can also suppress cortisol SYnthesis with prolonged infusions. Halothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation . all of \•h ich can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneumocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g. , ‘ pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CBF. Barbiturates also exhibit minimal diecrsupon evoked potentials (Greenberg, p p . 1-3; Katzung, pp. 417’ 420-42 2 ) .

Question 71

71. Meningkatkan sekali CBF dan dapat merusak autoregulasi
A. Etomidate
B. Propofol
C. Lorazepam
D. Halotane
E. Isoflurane
F. Oksida nitrous
G. Fentanil
H. Pentobarbital
I. Bukan salah satu dari A s/d H

Answer 71

D
Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and lCP. Etomidate can also suppress cortisol SYnthesis with prolonged infusions. Halothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation . all of \•h ich can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneumocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g. , ‘ pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CBF. Barbiturates also exhibit minimal diecrsupon evoked potentials (Greenberg, p p . 1-3; Katzung, pp. 417’ 420-42 2 ) .

Question 72

72. Menurunkan metabolisme serebral dan meningkatkan absorbsi CSF.
A. Etomidate
B. Propofol
C. Lorazepam
D. Halotane
E. Isoflurane
F. Oksida nitrous
G. Fentanil
H. Pentobarbital
I. Bukan salah satu dari A s/d H

Answer 72

G
Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and lCP. Etomidate can also suppress cortisol SYnthesis with prolonged infusions. Halothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation . all of \•h ich can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneumocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g. , ‘ pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CBF. Barbiturates also exhibit minimal diecrsupon evoked potentials (Greenberg, p p . 1-3; Katzung, pp. 417’ 420-42 2 ) .

Question 73

73. Menurunkan CBF dan ICP, menekan produksi kortisol dengan infus-infus lama
A. Etomidate
B. Propofol
C. Lorazepam
D. Halotane
E. Isoflurane
F. Oksida nitrous
G. Fentanil
H. Pentobarbital
I. Bukan salah satu dari A s/d H

Answer 73

A
Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and lCP. Etomidate can also suppress cortisol SYnthesis with prolonged infusions. Halothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation . all of \•h ich can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneumocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g. , ‘ pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CBF. Barbiturates also exhibit minimal diecrsupon evoked potentials (Greenberg, p p . 1-3; Katzung, pp. 417’ 420-42 2 ) .

Question 74

74. Membelah CBF dan metabolisme serebral, pada potensi-potensi yang terpicu minimal
A. Etomidate
B. Propofol
C. Lorazepam
D. Halotane
E. Isoflurane
F. Oksida nitrous
G. Fentanil
H. Pentobarbital
I. Bukan salah satu dari A s/d H

Answer 74

H
Etomidate is often used for induction or cerebral protection during aneurysm surgery; it is a potent cerebral vasoconstrictor that reduces CBF and lCP. Etomidate can also suppress cortisol SYnthesis with prolonged infusions. Halothane is an inhalational anesthetic that increases CBF (often as high as 100%), decreases CSF absorption, and disrupts autoregulation . all of \•h ich can contribute to elevated ICP. Nitrous oxide increases both CBF and cerebral metabolism and increases the risk of developing tension pneumocephalus in patients with underlying pneumocephalus. Narcotics (e.g. , fentanyl) in general increase CSF absorption and decrease cerebral metabolism. Barbiturates (e.g. , ‘ pentobarbital) uncouple cerebral metabolism from CBF, as they decrease cerebral metabolism and increase CBF. Barbiturates also exhibit minimal diecrsupon evoked potentials (Greenberg, p p . 1-3; Katzung, pp. 417’ 420-42 2 ) .

Question 75

75. Seorang laki-laki berumur 18 tahun menderita cedera memar kepala sedang dengan retak pada landas tengkorak. Pasien menunjukkan tanda-tanda meninggal prominen dengan demam dan leukositosis seminggu setelah cedera. Organisme-organisme manakah yang paling mungkin dapat teridentifikasi melalui kultur CSF?
A. Haemuphilus influenzae
B. Moraxella catarrhalis
C. Strep. pneumoniae
D. Klebsiella pneumonia
E. Staph. epidermidis

Answer 75

C.
StTeptococcus pneumoniae is associated with approximately 50 to 70% of all cases of meningitis occurring after traumatic skull fractures. After the appropriate antibiotics are administered and the patient recovers from meningitis, a thorough evaluation for the presence of a CSF fistula, with possible surgical repair, should be entertained (Wi l kins, p . 3305; Greenberg, p . 2 13).

Question 76

76. Efek samping manakah yang TIDAK biasanya berasosiasi dengan pemberian BCNU (carmustine)?
A. Pneumonitis interstitial
B. Hepatitis
C. Supresi sumsum tulang
D. Mual-mual
E. Cistitis hemorargis

Answer 76

E .
BCNU is associated with alopecia, bone marrow suppression, dysphagia, encephalopathy, nausea, diarrhea, hepatitis, and renal failure. Some of the most important side effects of BCNU are dose-dependent pulmonary complications, including interstitial pneumonitis and pulmonary fibrosis ( Katzung, p p . 888-889) .

Question 77

77. Diantara agen-agen di bawah ini, agen manakah yang paling tepat untuk perawatan retensi urine
A. Oxybutinin
B. Bethanecol
C. Imipramin
D. Atropin
E. Metakolin

Answer 77

B .
Bethanechol is a muscarinic agonist that facilitates detrusor contraction and inhibits contraction of the bladder sphincter and trigone, thus effectively treating urinary retention . lvfethacholine is also a muscarinic agonist, however, it is typically used to facilitate the diagnosis of hyperactive aim•ay disease (e.g. , asthma) due to its potent bronchoconstricti, •e effects (Greenberg, p . 1 16; Katzu ng, pp. 94, 96, 100 ) .

Question 78

78. Manakah yang paling mungkin menyebabkan kasus pneumonia nosocomial pada pasien dengan ventilasi mekanis
A. Cocci gram-positif
B. Rod gram-positif
C. Cocci Gram-negatif
D. Rod gram-negatif
E. Jawaban A, B, C dan D semuanya salah

Answer 78

D.
While gram-positive cocci (e.g. , StTeptococcus pneum o n iae) account for the majority of cases of communityacquired pneumonias, gram-negative rods account for the majority of cases of nosocomial pneumonia. Gram-negative rods account for 46% of all cases of nosocomial pneumonia in ward patients and 83% of all patients on mechanical ventilation. Pseudomonas species are the most common bacteria to account for ventilator-associated nosocomial pneumonia (30% of all cases) ( M a rino, pp. 516-517).

Question 79

79. Di antara ciri-ciri di bawah ini, ciri manakah yang sejalan dengan DIC?
80. Berasosiasi dengan trombosis mikrovaskular difusa
81. Berasosiasi dengan pelepasan besar-besaran faktor jaringan
82. Seringkali menyebabkan ARDS fulminant
83. Heparin ber kontraindikasi dengan onset dari DIC

Answer 79

A .
DIC is often a result of sepsis and severe systemic trauma, which results in endothelial cell damage and release of tissue factor. The presence of large amounts of tissue factor can result in the diffuse activation of both the fibrinolytic and coagulation pathways. Clinically, DIC is characterized by diffuse microvascular thrombosis, thrombocytopenia, and hemorrhage (especially GI bleeding) . As DIC progresses, oliguric renal failure, ARDS, and even death from multiple organ failure can ensue. DIC often exhibits elevations of fibrin split products (n-dimer), decreases in fibrinogen, prolongations of the PT and PTT, and thrombocvtopenia. Although not contraindicated, heparin is often ineffecti\•e in controlling the diffuse microvascular thrombosis that is inherent to D I C because antithrombin I I I levels are concomitantly decreased ( Marino, pp. 7 12-7 13).

Question 80

80. Diantara agen-agen di bawah ini, agen manakah yang berasosiasi dengan tirotoksikosis presipitasi (efek Jodbasedow)?
A. zat kontras radiografis iodinasi
B. Profiltiourasil
C. Hidrokortison
D. Propanolol
E. Jawaban A, B, C dan D semuanya salah

Answer 80

A .
The Jodbasedow effect refers to the precipitation of thyrotoxicosis in patients with toxic nodular goiter (or occasionally Graves’ disease) who are exposed to large Je,•els CHAPTER 7 Critical Care and Clinical Skills Answers 225 •of iodine acutely. Common precipitating agents include iodinated radiographic contrast dye and amiodarone (Cec i l , p p . 123 5 - 1236) .

Question 81

81. Paralitik manakah yang berasosiasi dengan perkembangan hyperkalemia?
A. Rokuronium
B. Vekuronium
C. Pankuronium
D. Sukinilkolin
E. Jawaban A, B, C dan D semuanya salah

Answer 81

D.
Succinylcholine usually results in mild elevations in serum potassium levels and is rarely associated with severe hyperkalemia (Greenberg, p. 49; Katzung, p . 444).

Question 82

82. Diantara vitamin-vitamin di bawah ini, vitamin manakah yang seringkali diberikan bersama-sama dengan pemberian isoniazid untuk mencegah defisiensi relatif?
A. Tiamin
B. Vitamin K
C. Pirodoksin
D. Vitamin B12
E. Vitamin D

Answer 82

C.
Isoniazid is associated with the development of peripheral neuropathy that occurs secondary to a relative pyridoxine deficiency ( excessi,•e excretion) . Administration of pyridoxine during isoniazid therapy is effective in preventing the development of peripheral neuropathy ( Katzung, p . 773).

Question 83

83. Manakah diantara hal-hal di bawah ini yang BUKAN merupakan ciri toksisitas atropin?
A. Midriasis
B. Kserostonia
C. Delirium
D. Bradikardia
E. Cutaneous flushing

Answer 83

D.
Atropine is an antimuscarinic agent that blocks almost all parasympathetic effects at high concentrations. Symptoms of atropine toxicity include deli . rium , mydriasis, cycloplegia, xerostomia, tachycardia, cutaneous flushing, and fever. Treatment of atropine toxicity involves the judicious use of physostigmine ( Katzung, pp. 113- 114 ) .

Question 84

84. Tn. X, 56 tahun mengeluh sakit dada berat pada hari 1 pasca-bedah setelah menjalani Mikrodisektomi lumbar selektif. Tekanan darah pasien adalah 163/82 dengan denyut 48,tingkat
    pernafasan 18, dan saturasi oksigen 98% pada oksigen 2 L melalui nasal cannula. EKG pasien menunjukkan bukti elevasi ST 0.5 s/d 2.0 mm pada tiga lead berturut-turut. Obat manakah yang seharusnya diberikan ( dalam hal ini TIDAK kontraindikasi ) pada sat itu?
85. Aspirin
86. Penghambat β
87. Nitrogliserin
88. Aktivator plasminogen jaringan (t-PA)

Answer 84

B.
Morphine, nitroglycerin, aspirin, oxygen , and beta blockers are often administered in the setting of an acute myocardial infarction (IVH ) . The administration of thrombolytics have been shown to improve outcome in patients with acute !VII who exhibit chest pain (for > 30 minutes and

Question 85

85. Agen inotropik terpilih untuk merawat gagal jantung parah akut
A. Isoprotenerol
B. Dopamin
C. Dobutamin
D. Epineprin
E. Norepineprin
F. Bukan salah satu dari A s/d E

Answer 85

C
Isoproterenol is a potent agonist that results in prominent increases in cardiac output and decreases in diastolic blood pressure (peripheral vasodilation, . Isoproterenol promotes both positi,•e inotropic and chronotropic actions. Dopamine primarilY activates dopaminergic receptors in the renal. mesenteric, and cerebral vasculature at low dosages. augmenting tlow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, acti,•ating peripheral a. receptors. Dobutamine is primarily an agonist that is the inotropic agent of choice in acute, severe systolic heart fail ure. Epinephrine stimulates both a. and receptors. At Jo”• dosages. epinephrine stimulates primaril receptors: at high dosages, a. receptors are primarilY stimulated. As opposed to dopamine. howe,•er, epinephrine is a potent renal ,.oconstrictor, e,•en at low dosages. Norepinephrine is ana-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Mari no, pp. 281-286, 295-296).

Question 86

86. agonis reseptor α primer untuk keadaan syok
A. Isoprotenerol
B. Dopamin
C. Dobutamin
D. Epineprin
E. Norepineprin
F. Bukan salah satu dari A s/d E

Answer 86

E
Isoproterenol is a potent agonist that results in prominent increases in cardiac output and decreases in diastolic blood pressure (peripheral vasodilation, . Isoproterenol promotes both positi,•e inotropic and chronotropic actions. Dopamine primarilY activates dopaminergic receptors in the renal. mesenteric, and cerebral vasculature at low dosages. augmenting tlow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, acti,•ating peripheral a. receptors. Dobutamine is primarily an agonist that is the inotropic agent of choice in acute, severe systolic heart fail ure. Epinephrine stimulates both a. and receptors. At Jo”• dosages. epinephrine stimulates primaril receptors: at high dosages, a. receptors are primarilY stimulated. As opposed to dopamine. howe,•er, epinephrine is a potent renal ,.oconstrictor, e,•en at low dosages. Norepinephrine is ana-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Mari no, pp. 281-286, 295-296).

Question 87

87. Mempertahankan aliran darah serebral, pada dosis rendah.
A. Isoprotenerol
B. Dopamin
C. Dobutamin
D. Epineprin
E. Norepineprin
F. Bukan salah satu dari A s/d E

Answer 87

B
Isoproterenol is a potent agonist that results in prominent increases in cardiac output and decreases in diastolic blood pressure (peripheral vasodilation, . Isoproterenol promotes both positi,•e inotropic and chronotropic actions. Dopamine primarilY activates dopaminergic receptors in the renal. mesenteric, and cerebral vasculature at low dosages. augmenting tlow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, acti,•ating peripheral a. receptors. Dobutamine is primarily an agonist that is the inotropic agent of choice in acute, severe systolic heart fail ure. Epinephrine stimulates both a. and receptors. At Jo”• dosages. epinephrine stimulates primaril receptors: at high dosages, a. receptors are primarilY stimulated. As opposed to dopamine. howe,•er, epinephrine is a potent renal ,.oconstrictor, e,•en at low dosages. Norepinephrine is ana-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Mari no, pp. 281-286, 295-296).

Question 88

88. Terutama aktivitas α1
A. Isoprotenerol
B. Dopamin
C. Dobutamin
D. Epineprin
E. Norepineprin
F. Bukan salah satu dari A s/d E

Answer 88

F
Isoproterenol is a potent agonist that results in prominent increases in cardiac output and decreases in diastolic blood pressure (peripheral vasodilation, . Isoproterenol promotes both positi,•e inotropic and chronotropic actions. Dopamine primarilY activates dopaminergic receptors in the renal. mesenteric, and cerebral vasculature at low dosages. augmenting tlow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, acti,•ating peripheral a. receptors. Dobutamine is primarily an agonist that is the inotropic agent of choice in acute, severe systolic heart fail ure. Epinephrine stimulates both a. and receptors. At Jo”• dosages. epinephrine stimulates primaril receptors: at high dosages, a. receptors are primarilY stimulated. As opposed to dopamine. howe,•er, epinephrine is a potent renal ,.oconstrictor, e,•en at low dosages. Norepinephrine is ana-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Mari no, pp. 281-286, 295-296).

Question 89

89. Terutama agonis reseptor β yang meningkatkan output jantung dan menurunkan tekanan darah diastolic
A. Isoprotenerol
B. Dopamin
C. Dobutamin
D. Epineprin
E. Norepineprin
F. Bukan salah satu dari A s/d E

Answer 89

A
Isoproterenol is a potent agonist that results in prominent increases in cardiac output and decreases in diastolic blood pressure (peripheral vasodilation, . Isoproterenol promotes both positi,•e inotropic and chronotropic actions. Dopamine primarilY activates dopaminergic receptors in the renal. mesenteric, and cerebral vasculature at low dosages. augmenting tlow to these regions. At high dosages, dopamine acts primarily as a vasoconstrictor, acti,•ating peripheral a. receptors. Dobutamine is primarily an agonist that is the inotropic agent of choice in acute, severe systolic heart fail ure. Epinephrine stimulates both a. and receptors. At Jo”• dosages. epinephrine stimulates primaril receptors: at high dosages, a. receptors are primarilY stimulated. As opposed to dopamine. howe,•er, epinephrine is a potent renal ,.oconstrictor, e,•en at low dosages. Norepinephrine is ana-receptor agonist that results in prominent vasoconstriction (Katzung, pp. 127-128; Mari no, pp. 281-286, 295-296).

Question 90

90. Tn. X, 62 tahun dimasukkan ke ICU untuk penatalaksanaan hipertensi berat
    setelah infark miokardial subendokardial. Hipertensi penderita tersebut refrakter terhadap pemberian labetalol, hidralazin, dan nitrogliserin i.v. Meskipun demikian memberi respon baik terhadap pemberian infus kontinyu nitroprusside. Pengobatan diteruskan dengan pengobatan antihipertensi oral. Pada hari berikutnya penderita mengalami akut onset berupa bingung, tinnitus, mual, takikardia, nyeri abdomen, dan pandangan kabur. Tindakan apakah yang paling tepat untuk penderita ?
    A. Periksa Gas darah Arteri.
    B. Perksa Kadar serum Natrium.
    C. Berikan lorazepam i.v.
    D. Berikan Methylen Blue i.v.
    E. Berikan hematin

Answer 90

D.
Prolonged nitroprusside infusions are associated with the accumulation of cyanide, which gradually exhausts thiosulfate and methemoglobin reserves and can result i n cyanide toxicity. Cyanide accumulation can result i n delirium, ataxia, tinnitus, abdominal pain, blurry vision, muscle spasms, nausea, emesis, and dyspnea. Vv’ithout treatment, cyanide toxicity can progress to metabolic acidosis, hypotension, coma, and death. Treatment of n itroprusside-induced cyanide toxicity i ncludes cessation of the medication and IV methylene blue. Sodium n itrite, sodium thiosulfate, and hemodialysis are also effective therapies ( Marino, pp. 838- 841).

Question 91

91. Berikut ini manakah yang paling bermanfaat untuk pengobatan SIADH ?
92. Restriksi cairan
93. Pemberian infus NaCl 3 %
94. Demeclocycline
95. Hemodialisis

Answer 91

E.
First-line therapy for asymptomatic patients with hyponatremia secondary to SIADH entails fluid restriction. The treatment of severe, symptomatic hyponatremia ( typically Na < 120 m Eq/L) secondary to SIADH involves more aggressive correction with 3% saline infusions, which are generally discontinued when the patient’s symptoms resolve o r the serum sodium reaches 1 28 to 130 mEq/L. The treatment of chronic SIADH often involves demeclocycline; the treatment of SIADH in association with congestive heart failure or renal failure often involves hemodialysis (Green berg, p p . 17-19; Mahno, p . 643 )

Question 92

92. Berapakan defisit cairan dari seorang laki-laki berat 80 kg dengan serum
Natrium 148 mEq/L ?
A. 1,4 L
B. 2,7 L
C. 3,5 L
D. 4,8 L
E. 6,0 L

Answer 92

B.
To calculate free water deficit, total body water (TBW) must be calculated i n itially. TBW is 0.5 t i mes lean body mass ( i n kilograms) for a female and 0 . 6 times lean body mass for a male. Free water deficit is then calculated by multiplying TBW by (SNa-140)/140. Thus, the free water deficit in this patient is 2. 7 L (Greenberg, p. 19).

Question 93

93. Berikut ini manakah yang merupakan kofaktor pembentukan kolagen?
A. Vitamin D
B. Thiamine
C. Vitamin B 12
D. Vitamin C
E. Pyridoksin

Answer 93

D.
Vitamin C is a necessary cofactor i n the synthesis of collagen. Vitamin C is important i n the intracellular hydroxylation of proline and lysine residues in the procollagen molecule ( Robbins, pp. 456-459; Wilkins, pp. 519-520).

Question 94

94. Vitamin manakah yang bilamana keracunan akut menimbulkan gejala sakit kepala, gangguan penglihatan, mual, muntah dan papil edema ? (peninggian tekanan intrakranial)
A. Vitamin A
B. Vitamin D
C. Vitamin E
D. Thiamine
E. Folat.

Answer 94

A.
Acute vitamin A toxicity can result in symptoms of elevated intracranial pressure ( h eadache, nausea, emesis, blurry vision, papilledema). hepatomegaly, and ascites. These symptoms are usuall\• transient and typically resolve after discontinuing the excessi\•e i n ta ke of vitamin A; however, severely symptomatic patients occasionally require serial lumbar punctures ( to t reat the ele'ated intracranial pressure) and restoration ot any underlying electrolyte abnormalities (e.g. , hypercalcemia) ( Robbins, p. 441).

Question 95

95. Karakteristik manakah yang BUKAN merupakan sindroma Cushing ?
    A. Kelemahan Otot
    B. Plethora
    C. Kehilangan irama diurnal sekresi kortisol.
    D. Nilai serum ACTH tinggi.
    E. Adenoma adrenal soliter.

Answer 95

D.
Cushing’s syndrome usually results from iatrogenic steroid administration o r adrenal adenomas. Under these circumstances, the diurnal rhythm of cortisol secretion is lost and serum ACTH levels are markedly depressed. Rarely, ectopic ACTH production by a malignant tumor occurs (e.g. , oat cell carcinoma of the lung); this can result in Cushi ng’s syndrome with concomitant high serum ACTH levels. Cushing’s disease results from an ACTH-producing pituitary adenoma. The clinical symptomatology of Cushing’s syndrome and Cushing’s disease is similar and consist of truncal obesity, abdominal striae, acne, muscle weakness, hirsuitism, depression, lethargy, “moon facies,” and plethora (Greenberg, pp. 420-42 1).

Question 96

96. pH 7,27, PaCO2 52 mmHg, HCO3- 23 m Eq/L
    A. Asidosis respiratorik
    B. Alkalosis respiratorik
    C. Asidosis Metabolik
    D. Alkalosis Metabolik
    E. Kombinasi asidosis respiratorik dan asidosis metabolik.
    F. Kombinasi alkalosis respiratorik dan alkalosis metabolik

Answer 96

A
The normal range is 7.36 to 7 .44; for PC02 36 to 44 mm I Tg; and for I-ICO, 22 to 26 mEq/L. The initial step i n the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory o r metabolic. With primarv metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction_ With primary respiratory disorders, the changes i n pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the p!-I are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as wel l . The expected compensatory change in PC02 for metabolic acidosis is 1 . 5 HC03 + ( 8 ± 2 ) . The expected compensatory change in PCO: for metabolic alkalosis i s 0 . 7 HC03 + ( 2 1 ± 2)_ I f the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value, a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in p!-I can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pl-I is 0.008 x ( PC02 - 40). With acute respiratory alkalosis, the expected change in p!-I is 0 . 008 x ( 40 - PC02) . If the change in pH exceeds 0 .008 times the change i n PC02, a superimposed metabolic acid-base disorder exists. In addition, with chronic ( fully compensated) respiratory disorders, the change in p!-I i s 0 . 003 times the change i n PC02. I n question 96, the ndues are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fullY compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 1 00 is combined respiratory and metabolic acidosis ( Marino, pp. 581-586) .

Question 97

97. pH 7,48 , PaCO2 45 mmHg, HCO3- 32 m Eq/L
    A. Asidosis respiratorik
    B. Alkalosis respiratorik
    C. Asidosis Metabolik
    D. Alkalosis Metabolik
    E. Kombinasi asidosis respiratorik dan asidosis metabolik.
    F. Kombinasi alkalosis respiratorik dan alkalosis metabolik

Answer 97

D
The normal range is 7.36 to 7 .44; for PC02 36 to 44 mm I Tg; and for I-ICO, 22 to 26 mEq/L. The initial step i n the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory o r metabolic. With primarv metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction_ With primary respiratory disorders, the changes i n pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the p!-I are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as wel l . The expected compensatory change in PC02 for metabolic acidosis is 1 . 5 HC03 + ( 8 ± 2 ) . The expected compensatory change in PCO: for metabolic alkalosis i s 0 . 7 HC03 + ( 2 1 ± 2)_ I f the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value, a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in p!-I can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pl-I is 0.008 x ( PC02 - 40). With acute respiratory alkalosis, the expected change in p!-I is 0 . 008 x ( 40 - PC02) . If the change in pH exceeds 0 .008 times the change i n PC02, a superimposed metabolic acid-base disorder exists. In addition, with chronic ( fully compensated) respiratory disorders, the change in p!-I i s 0 . 003 times the change i n PC02. I n question 96, the ndues are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fullY compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 1 00 is combined respiratory and metabolic acidosis ( Marino, pp. 581-586) .

Question 98

98. pH 7,35 , PaCO2 48 mmHg, HCO3- 28 m Eq/L
    A. Asidosis respiratorik
    B. Alkalosis respiratorik
    C. Asidosis Metabolik
    D. Alkalosis Metabolik
    E. Kombinasi asidosis respiratorik dan asidosis metabolik.
    F. Kombinasi alkalosis respiratorik dan alkalosis metabolik

Answer 98

A
The normal range is 7.36 to 7 .44; for PC02 36 to 44 mm I Tg; and for I-ICO, 22 to 26 mEq/L. The initial step i n the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory o r metabolic. With primarv metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction_ With primary respiratory disorders, the changes i n pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the p!-I are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as wel l . The expected compensatory change in PC02 for metabolic acidosis is 1 . 5 HC03 + ( 8 ± 2 ) . The expected compensatory change in PCO: for metabolic alkalosis i s 0 . 7 HC03 + ( 2 1 ± 2)_ I f the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value, a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in p!-I can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pl-I is 0.008 x ( PC02 - 40). With acute respiratory alkalosis, the expected change in p!-I is 0 . 008 x ( 40 - PC02) . If the change in pH exceeds 0 .008 times the change i n PC02, a superimposed metabolic acid-base disorder exists. In addition, with chronic ( fully compensated) respiratory disorders, the change in p!-I i s 0 . 003 times the change i n PC02. I n question 96, the ndues are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fullY compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 1 00 is combined respiratory and metabolic acidosis ( Marino, pp. 581-586) .

Question 99

99. pH 7,31 , PaCO2 34 mmHg, HCO3- 19 m Eq/L
    A. Asidosis respiratorik
    B. Alkalosis respiratorik
    C. Asidosis Metabolik
    D. Alkalosis Metabolik
    E. Kombinasi asidosis respiratorik dan asidosis metabolik.
    F. Kombinasi alkalosis respiratorik dan alkalosis metabolik

Answer 99

C
The normal range is 7.36 to 7 .44; for PC02 36 to 44 mm I Tg; and for I-ICO, 22 to 26 mEq/L. The initial step i n the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory o r metabolic. With primarv metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction_ With primary respiratory disorders, the changes i n pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the p!-I are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as wel l . The expected compensatory change in PC02 for metabolic acidosis is 1 . 5 HC03 + ( 8 ± 2 ) . The expected compensatory change in PCO: for metabolic alkalosis i s 0 . 7 HC03 + ( 2 1 ± 2)_ I f the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value, a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in p!-I can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pl-I is 0.008 x ( PC02 - 40). With acute respiratory alkalosis, the expected change in p!-I is 0 . 008 x ( 40 - PC02) . If the change in pH exceeds 0 .008 times the change i n PC02, a superimposed metabolic acid-base disorder exists. In addition, with chronic ( fully compensated) respiratory disorders, the change in p!-I i s 0 . 003 times the change i n PC02. I n question 96, the ndues are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fullY compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 1 00 is combined respiratory and metabolic acidosis ( Marino, pp. 581-586) .

Question 100

100. pH 7,28 , PaCO2 40 mmHg, HCO3- 19 m Eq/L
     A. Asidosis respiratorik
     B. Alkalosis respiratorik
     C. Asidosis Metabolik
     D. Alkalosis Metabolik
     E. Kombinasi asidosis respiratorik dan asidosis metabolik.
     F. Kombinasi alkalosis respiratorik dan alkalosis metabolik

Answer 100

E
The normal range is 7.36 to 7 .44; for PC02 36 to 44 mm I Tg; and for I-ICO, 22 to 26 mEq/L. The initial step i n the interpretation of acid-base disorders involves determining whether the disorder is primarily respiratory o r metabolic. With primarv metabolic acid-base disorders, the changes in pH and PC02 occur in the same direction_ With primary respiratory disorders, the changes i n pH and PC02 occur in opposite directions. The absolute value of the PC02 and the change in the p!-I are then used to determine whether there is a superimposed respiratory or metabolic acid-base disorder as wel l . The expected compensatory change in PC02 for metabolic acidosis is 1 . 5 HC03 + ( 8 ± 2 ) . The expected compensatory change in PCO: for metabolic alkalosis i s 0 . 7 HC03 + ( 2 1 ± 2)_ I f the PC02 is normal, higher (respiratory acidosis) or lower (respiratory alkalosis) than the expected value, a superimposed respiratory acid-base disorder is also present. With primary respiratory acid-base disorders, the expected change in p!-I can be calculated to determine whether a metabolic acid-base disorder is also present. With acute respiratory acidosis, the expected change in pl-I is 0.008 x ( PC02 - 40). With acute respiratory alkalosis, the expected change in p!-I is 0 . 008 x ( 40 - PC02) . If the change in pH exceeds 0 .008 times the change i n PC02, a superimposed metabolic acid-base disorder exists. In addition, with chronic ( fully compensated) respiratory disorders, the change in p!-I i s 0 . 003 times the change i n PC02. I n question 96, the ndues are consistent with an acute respiratory acidosis without renal compensation. Question 97 represents metabolic alkalosis with partial respiratory compensation. Question 98 is fullY compensated respiratory acidosis. Question 99 is metabolic acidosis with partial respiratory compensation. Question 1 00 is combined respiratory and metabolic acidosis ( Marino, pp. 581-586) .