Internal Medicine Form 2:

Answers with explanations from UpToDate

1. PREDNISONE THERAPY.
myopathy, a well-recognized side effect of glucocorticoid (corticosteroid) therapy, can occur with any
of the glucocorticoid preparations. The risk may be increased in older or malnourished patients and in
those with cancer.
Glucocorticoid-induced myopathy can occur with the initiation of systemic therapy as well as in
chronic maintenance therapy when the dose is increased. Affected patients typically present with
gradual onset over several weeks of proximal muscle weakness accompanied by muscle wasting. A
common manifestation is difficulty getting up from a chair or climbing stairs. Myalgias and muscle
tenderness are not observed. Although there is wide variation in the dose and
duration of treatment prior to the onset of muscle weakness, there is a general dose relationship with
systemic glucocorticoid therapy. Daily doses in excess of 40 to 60 mg/day can induce clinically
important weakness within two weeks and almost always result in some degree of muscle weakness
when continued for more than one month. By comparison, glucocorticoid myopathy is unusual in
patients treated with less than 10mg/day of prednisone or its equivalent. Inhaled glucocorticoids are
rarely associated with muscle weakness
The diagnosis of glucocorticoid-induced myopathy is one of exclusion, being based upon the history
and timing of glucocorticoid exposure and upon the absence of other causes of myopathy. The
diagnosis is generally established by demonstrating improved strength within three to four
weeks after appropriate dose reduction. There are two settings in which the diagnosis may be
particularly difficult: in patients with an underlying inflammatory myopathy, and in those treated with
neuromuscular blocking agents.
Muscle strength begins to improve within three to four weeks after appropriate dose reduction and
eventually resolves in virtually all patients if glucocorticoid therapy can be discontinued.

2. C, Assess patients decision making capacity .

3. E. Renal Failure.
4. C. Decreased synaptic activity of cholinesterase.
Organophosphorus compounds contain carbon and phosphorous acid derivatives . These agents
are well absorbed through the skin, lungs, and gastrointestinal tract. They bind to
acetylcholinesterase (AChE), also known as red blood cell (RBC) acetylcholinesterase, and
render this enzyme non-functional. AChE is the enzyme responsible for hydrolysis of
acetylcholine to choline and acetic acid, and inhibition leads to an overabundance of
acetylcholine at the neuronal synapses and the neuromuscular junction.
5. 5.B Glucose concentration equal to that of serum glucose concentration.
The pleural fluid is next characterized as either a transudate or an exudate

Transudates Transudates result from imbalances in hydrostatic and oncotic pressures in the chest, as
occur with CHF and nephrosis, or conditions external to the pleural space. Examples of the latter include
movement of fluid from the peritoneal, cerebrospinal, or retroperitoneal spaces, or from iatrogenic causes,
such as crystalloid infusion through a central venous catheter that has migrated into the mediastinum or
pleural space.

Exudates In contrast, exudative effusions present more of a diagnostic challenge. Disease in virtually
any organ can cause exudative pleural effusions by a variety of mechanisms, including infection,
malignancy, immunologic responses, lymphatic abnormalities, noninfectious inflammation, iatrogenic
causes, and movement of fluid from below the diaphragm

Exudates result primarily from pleural and lung inflammation (resulting in increased capillary and pleural
membrane permeability) or from impaired lymphatic drainage of the pleural space (resulting in decreased
removal of protein and other large molecular weight constituents from the pleural space). Exudates can
also result from movement of fluid from the peritoneal space, as seen with acute or chronic pancreatitis,
chylous ascites, and peritoneal carcinomatosis

Diagnostic criteria The Light's Criteria Rule is a traditional method of differentiating transudates and
exudates that measures serum and pleural fluid protein and LDH

According to the traditional Light's Criteria Rule, if at least one of the following three criteria (ie,
component tests of the rule) is fulfilled, the fluid is defined as an exudate [

Pleural fluid protein/serum protein ratio greater than 0.5, or

Pleural fluid LDH/serum LDH ratio greater than 0.6, or

Pleural fluid LDH greater than two-thirds the upper limits of the laboratory's normal serum LDH

.)

Glucose A low pleural fluid glucose concentration (less than 60 mg/dL [3.33 mmol/liter], or a
pleural fluid/serum glucose ratio less than 0.5) narrows the differential diagnosis of the exudate to the
following possibilities [32]:

Rheumatoid pleurisy
Complicated parapneumonic effusion or empyema
Malignant effusion
Tuberculous pleurisy
Lupus pleuritis
Esophageal rupture

All transudates and all other exudates have pleural fluid glucose concentration similar to that of blood
glucose.

The mechanism responsible for a low pleural fluid glucose depends upon the underlying disease. Specific
examples include:

Decreased transport of glucose from blood to pleural fluid with rheumatoid pleurisy or malignancy]
Increased utilization of glucose by constituents of pleural fluid, such as neutrophils, bacteria
(empyema), and malignant cells [36
lowest glucose concentrations are found in rheumatoid pleurisy and empyema, with glucose being
undetectable in some cases. In comparison, when the glucose concentration is low in tuberculous
 pleurisy, lupus pleuritis, and malignancy, it usually falls into the range of 30 to 50 mg/dL (1.66 to
2.78 mmol/liter)
6. 6.A, AMBULATORY ECG
Sudden onset of syncope without a prodrome is more common among patients with cardiac syncope
(arrhythmic or mechanical cardiac etiology) than among patients with non-cardiac syncope.

Ambulatory ECG monitoring is the most widely employed technology to evaluate a patient with symptoms
suggestive of a cardiac arrhythmia or a conduction abnormality. The 1999 American College
of Cardiology/American Heart Association (ACC/AHA) guidelines on ambulatory electrocardiography
recommended only two indications for this approach

Unexplained syncope, near syncope, or episodic dizziness ()

Unexplained recurrent palpitations (
7. G. VARIANT ANGINA PECTORIS.
8.D. Surgical Drainage.
Intergluteal pilonidal disease is an infection of the skin and subcutaneous tissue at or near the upper part
of the natal cleft of the buttocks. An acute pilonidal abscess is managed with an incision and drainage
(I&D) procedure at the time of presentation, usually under local anesthesia.
9. B.
Idiopathic central diabetes insipidus.
central diabetes insipidus (CDI) is characterized by decreased release of antidiuretic hormone (ADH, also
called arginine vasopressin or AVP), resulting in a variable degree of polyuria.
The most common causes of central diabetes insipidus (CDI), accounting for the vast majority of cases,
are idiopathic diabetes insipidus (DI) [1,3,4], primary or secondary tumors or infiltrative diseases (such as
Langerhans cell histiocytosis) [5], neurosurgery, and trauma

10. e.zinc
Numerous signs and symptoms have been associated with zinc depletion (table 3). Mild zinc deficiency is
associated with depressed immunity, impaired taste and smell, onset of night blindness, and decreased
spermatogenesis. Severe zinc deficiency is characterized by severely depressed immune function,
frequent infections, bullous pustular dermatitis, diarrhea, and alopecia .

11. a. Fluid restriction.

12. c empyema.
13. D. MONOSPOT TEST.
Ebstein-Barr virus (EBV)-induced infectious mononucleosis (IM) should be suspected when an
adolescent or young adult complains of sore throat, fever, and malaise and also has lymphadenopathy
and pharyngitis on physical examination [8,81].

Supportive evidence of EBV infection is derived from the observation of lymphocytosis and increased
circulating atypical lymphocytes along with a positive heterophile antibody test. Occasionally EBV-specific
antibodies are warranted.
Heterophile antibodies Heterophile antibodies react to antigens from phylogenetically unrelated
species. They agglutinate sheep red blood cells (the classic Paul-Bunnell test), horse red blood cells
(used in the "Monospot" test), and ox and goat erythrocytes. The Monospot is a latex agglutination assay
using horse erythrocytes as the substrate [85,86]. Other rapid diagnostic tests use ELISA (enzyme-linked
immunosorbent assay) techniques. The sensitivity and specificity of the rapid kits approach 85 and 100
percent, respectively .

14. A. OSTEONECROSIS.
Osteonecrosis (also called avascular, aseptic, or ischemic necrosis) in patients with systemic lupus
erythematosus (SLE) is most common in the femoral head, although the humeral head, tibial plateau, and
scaphoid navicular can also be affected [1,44-46]. Osteonecrosis is usually bilateral and is often
asymptomatic. When symptoms occur, femoral head involvement usually manifests as pain in the groin,
especially with weightbearing.

Osteonecrosis begins by interruption of blood supply to the bone. Subsequently, the adjacent area
becomes hyperemic, resulting in demineralization, trabecular thinning, and, if stressed, collapse [13].
(See "Osteonecrosis (avascular necrosis of bone)".)

Patients with SLE who have taken glucocorticoids are at greatest risk, although occasional cases have
been noted in the absence of glucocorticoid therapy [46]. Osteonecrosis often develops a relatively short
time after the onset of glucocorticoid therapy, within a month in some patients who receive high doses
[45,53-56]. One prospective study, for example, evaluated 60 patients with SLE over a period of five
years [57]. In that study, patients who had no MRI abnormalities in the femoral head during the first year
of follow-up were unlikely to develop osteonecrosis at a later date [57]. Glucocorticoid dose and duration
of therapy seem to be important factors in the development of osteonecrosis, although there is some
controversy about this issue [

15.J PANCREATITIS.
16. E. VACCINE.
17.D. OXYBUTYNIN.
18.C. DECREASED MYOCARDIAL CONTRACTILITY.
19. F , H/O MI IN PAST 6MNTHS.
20.A ,50% IN EACH CHILD, ITS AUTOSOMAL DOMINANT

21. D. ASPIRATE THE JOINT.

22. A PPD SKIN TEST
All CD4 counts

Tuberculosis All HIV-infected individuals, regardless of CD4 count, should be screened for latent
tuberculosis using either tuberculin skin testing or an interferon gamma release assay. Therapy for latent
infection should be administered to those who test positive and are without evidence of active disease.
(See "Treatment of latent tuberculosis infection in HIV-infected adults".)

CD4 counts 250 cells/microL

Coccidioidomycosis We perform annual IgG and IgM serologic screening for coccidiomycosis in
asymptomatic patients with CD4 counts 250 cells/microL who live in endemic regions (eg, Arizona or
California). We administer pre-emptive therapy with fluconazole therapy to such patients if they have a
newly positive serologic test. We discontinue therapy in patients receiving antiretroviral (ART) when their
CD4 count is >250 cells/microL for at least six months [25]. (See "Coccidioidomycosis in compromised
hosts", section on 'Patients with HIV/AIDS'.)

CD4 counts 200 cells/microL

Pneumocystis We recommend trimethoprim-sulfamethoxazole (TMP-SMX) to prevent PCP for

patients with a CD4 count 200 cells/microL. For patients who cannot take TMP-SMX, alternative agents
include dapsone, atovaquone suspension, or aerosolized pentamidine. Antimicrobials may be
discontinued when ART therapy results in an increase in the CD4 count to >200 cells/microL for more
than three months. (See "Treatment and prevention of Pneumocystis infection in HIV-infected patients",
section on 'Preventing initial infection'.)

CD4 counts 150 cells/microL

Histoplasmosis In general, we do not administer antifungal prophylaxis with itraconazole to prevent

primary infection with histoplasmosis since there are limited data to suggest the efficacy of prophylaxis,
and most patients will have immune recovery (ie, increased CD4 count) on antiretroviral therapy.
However, in areas where histoplasmosis is hyperendemic (>10 cases/100 patient-years), such as certain
parts of South America and French Guiana, some providers administer itraconazole (200 mg daily) to
patients with CD4 counts 150 cells/microL. For such patients, antimicrobials can be discontinued when
the CD4 cell count is >150 cells/microL for more than six months after initiation of ART [1].
(See "Diagnosis and treatment of histoplasmosis in HIV-infected patients", section on 'Prevention'.)

CD4 counts 100 cells/microL

Toxoplasma We administer suppressive therapy with TMP-SMX to prevent reactivation of T. gondii in

patients with a CD4 count 100 cells/microL and a positive toxoplasmosis IgG serology (see "Initial
evaluation of the HIV-infected adult"). For patients who have contraindications to TMP-SMX, we
use dapsone plus pyrimethamineand leucovorin. If the patient is intolerant or allergic to the above two
regimens, we administer atovaquone with or without pyrimethamine/leucovorin. Monotherapy with
dapsone, pyrimethamine, azithromycin, or clarithromycin should not be used. Among patients receiving
ART, we discontinue suppressive therapy when the CD4 count is >200 cells/microL for at least three
months. (See "Toxoplasmosis in HIV-infected patients".)

Cryptococcus Preventive therapy for cryptococcal disease is generally not recommended because of
drug interactions, adverse effects, potential for antifungal drug resistance, cost, and the lack of overall
survival benefit [1,10]. However, for certain patients with a CD4 count <100 cells/microL, especially those
in resource-limited settings, screening for serum cryptococcal antigen and pre-emptive therapy for those
who test positive may be useful to prevent symptomatic infection. The use of pre-emptive therapy is
discussed in detail elsewhere. (See "Treatment of Cryptococcus neoformans meningoencephalitis in HIV-
infected patients", section on 'Screening and treatment of early infection'.)

CD4 counts 50 cells/microl

Mycobacterium avium complex (MAC) Primary prophylaxis against MAC infection should be given to
all HIV-infected patients with a CD4 count 50 cells/microL[1]. Blood cultures for MAC isolation should be
obtained before prophylaxis is initiated if there is any suspicion of clinical disease; the treatment regimen
is different if blood cultures are positive (ie, the patient has active disease). For prophylaxis, we prefer the
macrolide antibiotic azithromycin; clarithromycin and rifabutin are alternative options. However, if rifabutin
is used, a chest x-ray should be obtained to rule out active tuberculosis. Primary prophylaxis may be
discontinued when effective ART is associated with an increase in CD4 count to >100 cells/microL for
more than three months [1]. (See "Mycobacterium avium complex (MAC) infections in HIV-infected
patients".)

23. E, IV FUROSEMIDE.

24. E, IV 0.9% SALINE

Severe hypercalcemia Patients with calcium >14 mg/dL (3.5 mmol/L) require more aggressive
therapy. The acute therapy of such patients consists of a three-pronged approach [1,2,4]:

Volume expansion with isotonic saline at an initial rate of 200 to 300 mL/hour that is then adjusted
to maintain the urine output at 100 to 150 mL/hour. (See 'Saline hydration' below.)
In the absence of renal failure or heart failure, loop diuretic therapy to directly increase calcium
excretion is not recommended because of potential complications and the availability of drugs that
inhibit bone resorption, which is primarily responsible for the hypercalcemia.
Administration of salmon calcitonin (4 international units/kg) and repeat measurement of serum
calcium in several hours. If a hypocalcemic response is noted, then the patient is calcitonin-sensitive
and the calcitonin can be repeated every 6 to 12 hours (4 to 8 international units/kg). We typically
administer calcitonin (along with a bisphosphonate) in patients with calcium >14 mg/dL who are also
symptomatic. (See 'Calcitonin' below.)
The concurrent administration of zoledronic acid (ZA; 4 mg intravenously [IV] over 15 minutes)
or pamidronate (60 to 90 mg over two hours), preferably ZA, because it is superior to pamidronate in
reversing hypercalcemia related to malignancy. (See 'Bisphosphonates' below.)

The administration of calcitonin plus saline should result in substantial reduction in serum calcium
concentrations within 12 to 48 hours. The bisphosphonate will be effective by the second to fourth day,
thereby maintaining control of the hypercalcemia.
 25. C DEFECIENT MINERALISATION OF OSTEOID.

26. D, SCLERODERMA

27. C. ABNORMALITY OF ANTIPROTEINASE.

28. E FELTY SYNDROME:

Felty described a syndrome characterized by the triad of rheumatoid arthritis (RA), neutropenia, and
splenomegaly, with the following features [1]:

Rheumatoid arthritis The arthritis is typically severe, erosive, and seropositive for rheumatoid
factor (RF) and/or anti-citrullinated peptide antibodies (ACPA). (See'Rheumatoid arthritis' below.)
Neutropenia Neutropenia is present in all patients, with absolute neutrophil counts
below 2000/microL. (See 'Neutropenia' below.)
Splenomegaly Splenomegaly is present in most patients, although infrequently splenomegaly is
undetectable in RA despite marked neutropenia; spleen size does not correlate with the degree of
neutropenia or clinical cours

29. D, ORAL H2 RECEPTOR BLOCKING AGENT.

30. G, REASSURANCE ONLY.
31. B. BRONCHITIS
Acute bronchitis is one of the most common conditions encountered in clinical practice. It is a self-
limited inflammation of the bronchi due to upper airway infection. Patients with acute bronchitis
present with a cough lasting more than five days (typically one to three weeks), which may be
associated with sputum production. Acute bronchitis should be distinguished from chronic bronchitis,
a condition in patients with chronic obstructive pulmonary disease distinguished by a cough for at
least three months in each of two successive years.

Acute bronchitis is characterized by self-limited inflammation of the bronchi and clinically expressed as
cough, which may include sputum production. Acute bronchitis cannot be distinguished from upper
respiratory infections in the first few days of illness, but acute bronchitis should be considered when
cough persists for more than five days [21]. Since treatment for either viral upper respiratory infection or
acute bronchitis is directed toward symptom control, making the distinction between these diagnoses is
not critical. Furthermore, acute bronchitis is often associated with viral upper respiratory infection.

It is important, however, to distinguish acute bronchitis from pneumonia, which usually indicates need for
antibiotic therapy. Fever is an unusual sign in patients with acute bronchitis and suggests the presence of
either influenza or pneumonia. Patients with the combination of cough, fever, sputum production, and
constitutional symptoms are more likely to have influenza or pneumonia. Patients with acute bronchitis
have few systemic symptoms. They may have chest wall tenderness related to muscle strain from
coughing. Wheezing may also occur.

32. F, INCREASED VASCULAR PERMEABILITY.

[Dinesh Devareddy] F. Diffuse crackles - point to pulmonary edema. 2 causes of pulmonary edema - 1)
Cardiogenic 2) Non-cardiogenic. PCWP is normal - s0 cardiogenic pulmonary edema is excluded. The
only other cause is ARDS. Sepsis induced ARDS

33. B, CML

Chronic myeloid leukemia (CML) is suspected in a patient with some or all of the following:

Systemic complaints (fatigue, malaise, sweating, weight loss).

Early satiety
Tenderness over the lower sternum
Varying degrees of hepatosplenomegaly
Laboratory findings of an elevated white blood cell count with a peripheral smear demonstrating
increased numbers of immature cells of the granulocytic series with a "myelocyte bulge" associated
with mild anemia, thrombocytosis, and basophilia.

Although the diagnosis can be made fairly accurately by morphologic features in the blood and marrow,
the "gold standard" for the diagnosis of CML is either the demonstration of the Philadelphia chromosome
or the underlying t(9;22) translocation by conventional cytogenetic techniques (figure 1), or the
demonstration of the BCR-ABL1 fusion gene or mRNA fusion product (figure 2) by fluorescence in situ
hybridization (FISH) analysis, or reverse transcription polymerase chain reaction (RT-PCR).
34. B. BICUSPID AORTIC VALVE.
35. C. S.CREAT MEASUREMENT.
36. B.

37. B, ENALAPRIL,

MAINTAIN HTN HERE , USE ACE INHIBITORS.

38. C, AVOIDANCE OF WEED.?? HAVE A DOUBT HERE !!

39. D, Carotid duplex ultrasound (CDUS) uses B-mode ultrasound imaging and Doppler
ultrasound to detect focal increases in blood flow velocity indicative of high grade carotid stenosis [15-17].

40. A, ADENO CA OF LUNG. MARY

 Although most cases of lung cancer are due to tobacco smoking, lung cancer among never-
smokers is an important problem, with the age-adjusted incidence rate for lung cancer in never-
smokers aged 40 to 79 years ranging from 11.2 to 13.7 per 100,000 person-years for men and from
15.2 to 20.8 per 100,000 person-years for women. (See 'Incidence' above.)
Although the etiology for lung cancer among never-smokers is not always clear, risk factors include
second hand tobacco smoke, radon, and other environmental exposures. (See 'Risk factors' above
and "Cigarette smoking and other risk factors for lung cancer".)
Adenocarcinoma is the most common pathology among never-smokers and is more common than
among ever smokers. (

41. F, ABDOMINAL PARACENTESIS.

42.B CLINDAMYCIN

LUNGABCESS .

43. D, KARYOTYPE ANALYSIS.

44. E, PACKED RED BLOOD CELLS

45. E, MEASURE TSH CONC.

[Dinesh Devareddy] E. Nice scenario of hypothyroidism.

Periorbital edema,
Menorrhagia,
Proximal muscle weakness and tenderness
Weight gain
Hyponatremia
Hypercholesterolemia
Mild elevation in Creatine Kinase

46. A, DEC MEAN RED CELL VOLUME

47. C, IPRATROPIUM THERAPY.
[Dinesh Devareddy] C. Considering that she is not any medication. We will start first with an inh anticholinergic.
Home 02 therapy indications:
1) Sa02 <88 %
2) Pa02 <65 %
3) Signs of cor pulmonale, pulmonary HTN

48. C, IV 0.9%SALINE .
49. E, VARICELLA ZOSTER VIRUS.
50. B, AMIKACIN