Internal Medicine Form 1: Answers with explanations from UpToDate 1. E. Vancomycin : here ceftazidime covers gm -ve & vanco will do gm +ve. EXP: Central venous catheter (CVC) use has increased substantially, and associated infections have become a frequent complication of catheter use. CVC infection rates are highest with short-term noncuffed, nontunneled hemodialysis and multilumen catheters, and lowest with subcutaneous central venous ports. catheter-related bacteremia can arise from one of two sources [13]: ●Migration from the skin along the outside of the c atheter into the bloodstream. The Dacron cuff in
tunneled catheters typically incites an inflammatory response with fibrosis that, in t urn and in time, may create a mechanical barrier to migration of bacteria from the skin along the outside of the catheter. ●Direct inoculation from a biofilm containing pathogenic micro-organisms that may form on t he inner
surface of the catheter Most catheter-related infections are caused by staphylococci and gram -negative bacilli; therefore, antibiotics commonly used in antibiotic lock therapy (ALT) include vancomycin, cefazolin, ceftazidime, ciprofloxacin, and gentamicin.(UPTODATE).
2. (A) ALS: AMYOTROPIC LATERAL SCLEROSIS: The diagnosis of ALS is suggested when t here are progressive symptoms consistent with upper and lower motor neuron dysfunction that present in one of four body segments (cranial/bulbar, cervical, thoracic, and lumbosacral) followed by spread to other segments over a period of months to years. The course is not relapsing and remitting, but rather is insidiously progressive. Involuntary weight loss and muscle wasting unrelated to nutrition may also occur. Physical examination — Lower motor neuron signs include weakness, atrophy and fasciculations. Upper motor neuron signs include the following:
●Increased
tone and increased extremity deep tendon reflexes .
●The presence of any reflexes re flexes in muscles that are profoundly weak and wasted
●Pathologic reflexes such as crossed adductors, a
jaw jerk, or Hoffman sign .
●The syndrome of pseudobulbar affect, which consists of inappropriate laughing, crying, and/or forced
yawning The Babinski sign (reflex great toe extension, often with fanning of the small toes, with lateral plantar stimulation) is present in about one-half of patients with ALS , but is a definitive indicator of upper motor neuron pathology when present . Lateral plantar stimulation normally produces reflex toe flexion without other leg or foot movement. Triple flexion occurs when plantar stimulation produces reflex great toe extension, flexion of the knee, and flexion of the hip.
3.(A) Ig A defeciency : Recurrent sinopulmonary infections ●Autoimmune disorders ●Gastrointestinal infections and other intestinal disorders ●Allergic disorders ●Anaphylactic transfusion reactions
4.
c. obtain CT without consent.
5. Warfarin : Anticoagulant therapy is effective in reducing the risk of systemic embolization in patients with nonvalvular atrial fibrillation (AF). Anticoagulation with warfarin, dabigatran, rivaroxaban, apixaban, or edoxaban reduces this risk by almost 70 perce nt, and should be considered for most nonvalvular AF patients. recommendations for anticoagulant therapy in patients with nonvalvular AF are as follows
●For
patients with a CHA2DS2-VASc score ≥2
●For patients with a CHA2DS2-VASc
chronic anticoagulation (Grade 1A).
score of 1,The risk factor present may influence decision making.
Age 65 to 74 years is a stronger risk factor than the other features conferring a CHA2DS2-VASc score of 1. ●For patients with a CHA2DS2-VASc o f 0 =we suggest no anticoagulant therapy (Grade
2C). Patients
who are particularly stroke averse and who are at low bleeding risk may r easonably choose anticoagulation.
6. a. ACTH STIMULATION TEST
adrenal insufficiency : Pt has hypotension, hyponatremia, hyperkalemia.
most patients with adrenal insufficiency have the following: Chronic malaise,Lassitude,Fatigue that is worsened by exertion and improved with bed rest
Weakness that is generalized, not limited to particular muscle groups,Anorexia Weight loss, hypotension,
7.E LACTIC ACID .
8.H RHABDOMYOLYSIS : HERE IT’S THE ONLY OPTION I THINK WOULD LEAD TO BLOOD IN URINE.
9. E, GIVE IV 0.9%SALINE 10. C, INDOMETHACIN, acute gout here treat most patients able to take an oral medication with a nonsteroidal antiinflammatory drug (NSAID). ● An oral low-dose colchicine regimen may be used in patients who are able to take an oral medication but who have contraindications to NSAIDs (eg, moderate or more severe chronic kidney disease [CKD], active peptic ulcer disease, or a history of NSAID-intolerance ●In patients with contraindications to the use of both NSAIDs and colchicine, we prefer intraarticular, oral, or parenteral glucocorticoids, depending upon the number of involved joints, the experience of the clinician with joint injection techniques, and the need, if present, for parenteral rather than orally administered.
11. B Drug reaction is the only option left here as rest all are negative. Drug fever: Clinicians are universally aware of t he common occurrence of fever caused by drugs, although reliable data on incidence are not available. Fever c an be the sole manifestation of an adverse drug reaction in 3 to 5 percent of cases. The risk of developing drug fever increases with the number of drugs prescribed, especially in elderly patients. Patients with HIV infection also appear to have an increased susceptibility to drug reactions of all types, including fever. Failure to recognize the etiologic
relationship between a drug and fever ofte n has undesired consequences including extra testing, unnecessary therapy, and longer hospital stays.(See 'Introduction' above).
●Drug fever can be defined as "a disorder characterized by fever c oinciding with administration of a drug and disappearing after the discontinuation of the drug, when no other cause for the fever is evident after a careful physical examination and laboratory investigation." (See 'Definition' above ).
●The mechanisms of drug fever are multiple and, in many cases, are poorly or incompletely understood. However, most authorities classify drug-related fevers into five broad categories: •Hypersensitivity reactions, including the drug r eaction with eosinophilia and systemic symptoms (DRESS) syndrome
•Altered thermoregulatory mechanisms •Reactions that are directly related t o administration of the drug •Reactions that are direct extensions of the pharmacologic action of the drug •Idiosyncratic reactions (see 'Mechanisms' above ) ●Drug fever is usually a diagnosis of exclusion. The first assumption of most clinicians is that fever is due to infection, which may not always be easy to exclude. Connective tissue diseases or malignancy, which are other causes of fever of unknown origin, are also often difficult to exclude. (See 'General clinical issues' above).
●Rash, when present, may be a valuable clue to the presence of drug fever, but its absence should not deter the clinician from suspecting the diagnosis. (See 'Presence of rash' above). ●The timing of the onset of fe ver in relation to beginning the drug and t he pattern of fever are frequently not helpful in making a diagnosis. The median time to onset is about eight days but varies from less than 24 hours to many months. S imilarly, the pattern of fever may vary from a low-grade fever without other associated symptoms to a "hectic" pattern with chills and rigors. (See 'Fever patter ns' above).
●The white blood cell count can be elevated with accompanying eosinophilia in drug fever, but these findings occur in less than 20 perce nt of cases. The erythrocyte sedimentation rate is usually increased, but this is a nonspecific finding. Unexplained disturbance of liver function and/or renal impairment can provide clues to the diagnosis. If urine microscopy reveals pyuria, a stain for eosinophils can be performed and may be positive, especially in interstitial nephritis caused by beta-lactam antibiotics. (See 'Laboratory investigations' above). ●In the majority of patients, the only w ay to know if a patient has a drug fever is by stopping the drug(s).
The usual approach is to discontinue the most probable offending drug first, followed se quentially by cessation of other drugs if fever persists. Discontinuing all medications at once may eliminate the fever but may also put the patient at some risk from the underlying disease and prevent identification of the
causative drug. In most but not all cases, resolution of drug fever will occur w ithin 72 to 96 hours of discontinuing the offending drug. (See 'Cessation of the drug(s)' above.)
12. a. Barium swallow. Suspect zenkers diverticulum here…
Zenker's diverticula are usually discovered in older adults, although they have been described in children. Most patients present after the age of 60 (often above age 75), having had symptoms ranging from weeks to years. For unclear reasons, the majority of patients are male . Transient oropharyngeal dysphagia may be noted early in the course. The openings of large ZD are often aligned with the axis of the pharynx such that food is preferentially diverted into the diverticulum. When the pharyngeal sac becomes large enough to retain contents such as mucus, pills, sputum, and food, the patient may complain of pulmonary aspiration, foul breath, gurgling in the throat, appearance of a mass in the neck, or regurgitation of food into the mouth. Marked weight loss and malnourishment can occur in patients with longstanding dysphagia. The ZD may become so large that its retained contents may push anteriorly and completely obstruct the esophagus.
13.b oral corticosteroids.
If after initial home treatment the patient has symptoms or signs suggestive of a severe exacerbation (eg, marked breathlessness, inability to speak more than short phrases, use of accessory muscles) or a peak flow less than 50 percent of baseline, he or she should seek urgent medical attention. Patients may be advised by their clinician to take a dose of oral glucocorticoids (eg, prednisone 40 mg) on route to the emergency department.
14. D. OSMOTIC DIURESIS. 15.B. GLUTEN SENSITIVE ENTEROPATHY. The classic definition of celiac disease or gluten-sensitive enteropathy includes the following three features: villous atrophy; symptoms of malabsorption such as steatorrhea, weight loss, or other signs of nutrient or vitamin deficiency [7]; and resolution of the mucosal lesions and symptoms upon withdrawal of gluten-containing foods, usually within a few weeks to months. Patients with classic disease present with diarrhea, weight loss, or malabsorption, and possess antibodies against gliadin and especially tissue transglutaminase. Gastrointestinal manifestations — Patients may present with classic signs, including diarrhea with bulky, foul-smelling, floating stools due to steatorrhea and flatulence.
16. E .DO NOT ADMINISTER, MEDICALLY CONTRAINDICATED. 17. A. 0 %. 18. D sarcoidosis Hilar adenopathy + uveitis + ppd negative .
19. e. weight reduction. 20.Mineralocorticoid Excess
Nonsuppressible (primary) hypersecretion of aldosterone is an underdiagnosed cause of hypertension. The classic presenting signs of primary aldosteronism are hypertension and hypokalemia. The most common subtypes of primary aldosteronism are: ●Aldosterone-producing adenomas (APAs) ●Bilateral idiopathic hyperaldosteronism (IHA; bilateral adrenal hyperplasia)
21. D. Kallamans Syndrome.
Congenital GnRH deficiency primarily is a disease of males, with the male-to-female ratio being approximately 5:1, and can present at any age. The presenting signs and symptoms are a function of the age-related period of reproductive activity.
During the neonatal period, boys with GnRH deficiency can present with micropenis and/or cryptorchidism due to the silence of their hypothalamic-pituitary-gonadal axis during this period; approximately one-half of boys with microphallus have isolated GnRH deficiency as the underlying diagnosis. In comparison, newborn girls have no obvious abnormal findings that might provide clues to the diagnosis. During childhood, which is physiologically characterized by a latency period of reproductive activity, the lack of sense of smell in some patients (anosmia) or the presence of skeletal abnormalities such as cleft lip/cleft palate or syndactyly (in patients with mutations in the FGF signalling pathway) generally are the only way the diagnosis can be made. This association of IHH with anosmia is referred to as Kallmann Syndrome. At puberty, patients of both sexes can present with a variable failure to undergo sexual maturation and establish a clear-cut growth spurt (eg, primary amenorrhea in girls Physical findings — The body habitus of adolescent patients failing to undergo puberty often is eunuchoidal, with arm span exceeding height by 5 cm or more. This finding reflects the delayed closure of the epiphyses of long bones caused by hypogonadism during puberty. In women, secondary sexual characteristics are often completely absent, with little or no breast development or axillary hair. Men have little or no beard and body hair development, no increase in bulk of the muscles, and failure of the voice to deepen. In both sexes, some pubic hair can be present because adrenarche, with its concomitant small amounts of adrenal androgen and estrogen secretion, is characteristically normal
22. Paradoxical Pulse:
Systemic blood pressure is not constant but varies slightly from heart beat to heart beat and between inspiration and expiration. Normally, the systolic blood pressure decreases by less than 10 mmHg during inspiration, but a decline of this magnitude is not detectable on examination of the peripheral pulse. Moderate to severe cardiac tamponade, and occasionally constrictive pericarditis, induce hemodynamic changes that enhance the inspiratory fall in systolic blood pressure. This exaggerated drop in systemic blood pressure during inspiration is termed pulsus paradoxus
23. B. Chronic
volume overload on right ventricle. Pulmonary Hypertension .
he initial symptoms of PH are the result of an inability to adequately increase cardiac output during exercise [2,3]. These include exertional dyspnea, lethargy, and fatigue. Additional symptoms emerge as the PH progresses and right ventricular hypertrophy and failure developThese include the following: ●Exertional chest pain (ie, angina) is usually due to subendocardi al hypoperfusion caused by increased right ventricular wall stress and myocardial oxygen demand. However, it is occasionally caused by dynamic compression of the left main coronary artery by an enlarged pulmonary artery; this risk is greatest for patients with a pulmonary artery trunk at least 40 mm in diameter [4-6]. ●Exertional syncope is due to the inability to increase cardia c output during activity or reflex bradycardia that is secondary to mechanoreceptor activation in the right ventricle. ●Peripheral edema is due to right ventricular failure, increased right sided filling cardiac pressures, and extracellular volume expansion. ●Anorexia and/or abdominal pain in the right upper quadrant due to passive hepatic congestion. Uncommon symptoms include cough, hemoptysis, and hoarseness (Ortner's syndrome). The hoarseness is caused by compression of the left recurrent laryngeal nerve by a dilated main pulmonary artery. Examination — Patients with PH may develop the following physical signs as they progress from PH alone to PH associated with right ventricular failure: ●The initial physical finding of PH is usually increased intensity of the pulmonic component of the second heart sound, which may become palpable. The second heart sound is narrowly split or single in patients with preserved right ventricular function ●As right ventricular hypertrophy develops, a prominent A wave may emer ge within the jugular venous pulse. This may be accompanied by a right-sided fourth heart sound and either a left parasternal heave or a downward subxiphoid thrust. ●Right ventricle failure (or a right bundle branch block) widens the splitting of the seco nd heart sound. Auscultation may reveal a holosystolic murmur of tricuspid regurgitation and,
occasionally, systolic ejection murmur and, in more severe disease, a diastolic pulmonic regurgitation murmur.
24. A CT Scan of abdomen. 25. A activation of renin angiotensin system
The presence of an upper-abdominal bruit with a diastolic component that lateralizes toward one side is highly suggestive of renal artery stenosis.
26. E Biopsy and culture of lung mass .Have a doubdt here I think this would be right if we want to confirm m.avium here.
27. D. Administer 50% dextrose in water : as hypoglycemic episode here. 28. F Gilbert’s Syndrome - Clinical manifestations of Gilbert's syndrome include icterus secondary to a mild, predominantly unconjugated hyperbilirubinemia (normal levels in these patients are < 3 mg/dl). Those patients who are symptomatic tend to have nonspecific complaints, including malaise, fatigue, or abdominal discomfort. Certain events, such as hemolysis, fasting or consuming a fat-free diet, physical exertion, febrile illness, stress, or fatigue are thought to be triggers for hyperbilirubinemia in patients with Gilbert's syndrome.
29. A acute hepatitis 30. c. ciprofloxacin : 31.A. Aortic Dissection : 32. Intravenous acyclovir therapy. 33. A . Alveolar arterial Mismatch. 34. A. Bone metastasis. 35. D Increased bone turm over : pagets here. PDB is characterized by abnormalities of the osteoclast [38]; there are accelerated bone turnover and abnormal bone remodeling. Both genetic and environmental causes are thought to contribute to its pathogenesis. Inheritance appears to be autosomal dominant with variable penetrance, and multiple genetic loci have been associated with PD B. The majority of patients with PDB are asymptomatic. Symptoms are usually due to overgrowth of the affected bone. Pain may arise directly, from a paget ic lesion in bone, or from secondary causes, including osteoarthritis, fracture, nerve impingement, or,
rarely, tumor. Osteosarcoma is a rare, usually fatal complication of PDB, which typically presents in t hose with longstanding skeletal disease. Such patients may report increased bone pain that is poorly responsive to medical therapy, local swelling, and, less often, a pathologic fracture. Giant cell tumors may arise in pagetic bone and are usually benign. Laboratory findings, which reflect increased bone turnover and are typical of untreated disease, include elevated levels of se rum alkaline phosphatase (sAP) and bone-specific alkaline phosphatase (bAP). The degree of elevation generally reflects the extent and activity of the disease, although this is not always the case. A normal or minimally elevated AP may be seen in more limited disease.
Plain radiographs reflect the abnormal bone turnover character istic of disease. A predominantly osteolytic lesion may be seen early in disease. Over time, however, there is evidence of an osteoblast response, and the bone thickens and enlarges, with thickened cortices marked by tunneling and accentuated trabeculae at one or more affected skeletal sites. In late disease, there may be dense bone by plain film, with little evidence of remodeling by biochemical parameters. Increased uptake is seen focally at the sites of active pagetic bone lesions on radionuclide bone scanning. Bone scintigraphy is more sensitive than plain radiography, particularly in early disease.
. We obtain a baseline radionuclide bone scan to document the extent and locations of skeletal involvement; we perform radiographs of affected sites to identify impending fractures, potential malignant lesions, osteoarthritis, or other bone abnormalities.
36.B Cardiomyopathy 37. E. Recurrent pulmonary emboli here ..there are subsegmental perfusion defect seen. 38. Pyelonephritis acute uncomplicated pyelonephritis is suggested by fevers, chills, flank pain, costovertebral angle tenderness, and nausea or vomiting, with or without the typical symptoms of cystitis
39. E Renal tubule. 40. a. Observation only 41. B. Give isoniazid in asymptomatic tb with negative cxr findings. 42. E aortic valve replacement . 43. B. Measurement of Serum Cholestrol. 44. c. 7Measurement of Serum Ferritin Conc , Hemochromatosis here Dark brown color - Mild elevation in liver e nzymes - S3 - hyperglycemia. All these manifestations point toward Hemochromatosis Also, about the OA UTD
"One report noted an increased frequency of heterozygous carriage of the hemochromatosis HFE gene allele (C282Y) in older people with OA of the hands compared with healthy young controls"
45.C, Malignant Transformation of epithelial cells 46.D.Fat embolism. 47. E, Ventricles , VT is common after MI. 48.E, Ingested spores ,C difficile is highly transmissible via the fecal-oral route by ingestion of spores. 49. B. oral acyclovir, Herpetic whitlow. 50.D. Sytemic broad spectrum antibiotics.
