Datasets:

ridhomhd

/

MedMCQA-filtered

like 0

05e92aa4-f149-49d2-bfb3-48263f7de421

Regarding vaginal candidiasis which one of the following is false:

Cottage cheese like secretions are seen

Intense pruritus

Most common in non-pregnant women

Buds and hyphae seen in KOH preparation

multi

Ans. C. Most common in non-pregnant womenCandidiasis is caused by Candida albinism which thrives in an acidic medium with an abundant supply of carbohydrates. It is found commonly in pregnancy, and in patients on oral contraceptives, antibiotics and. corticosteroids. It is also seen in patients with diabetes. It causes a profuse discharge and intense pruritus with soreness of vagina and dysuria. Vagina and vulva are edematous and excoriated and the white patches of cheesy material on the vagina and vulva can be easily identified. A 10%KOH smear shows the buds and hyphae of the Candida organism. Nystatin or ketoconazole vaginal tablets used for one week are curative when used along with a cream of the same medication for External use.

Gynaecology & Obstetrics

Miscellaneous (Obs)

836756cc-2b92-483b-a8cc-302b578a9eaa

For TOF management in antenatal period includes ?

Balloon valvotomy

Open hea surgery

Karyotyping

Aspirin

multi

Ans. is 'c' i.e., KaryotypingTOF has been associated with untreated maternal diabetes, phenylketonuria, and intake of retinoic acid.Associated chromosomal anomalies occur in 30% cases and include trisomies 21, 18, 13 and 22q11 microdeletion, especially in pulmonary atresia and absent pulmonary valve syndrome (APVS).There is also a high association with extra - cardiac anomalies in paicular, abdominal and thoracic abnormalities.When a TOF is diagnosed during fetal life, karyotyping and targeted morphologic ultrasound examination should be offered.Isolated TOF - Good prognosis in TOF with pulmonary stenosis (>90% survival after surgery).However, other forms of TOF such as pulmonary atresia and absent pulmonary valve syndrome do not have a good prognosis (moderate prognosis for pulmonary atresia and bad prognosis for APVS).

Pediatrics

d1fd564a-489c-4075-9f2d-fe1fcf5a93b3

Which of the following vitamin reduces the risk of insulin resistance, obesity, and the metabolic syndrome?

Vitamin A

Vitamin C

Vitamin D

Vitamin B12

single

Higher Intakes of Vitamin D May Be Beneficial There is evidence that Vitamin D intake considerably higher than that required to maintain calcium homeostasis reduce the risk of insulin resistance, obesity, and the metabolic syndrome, as well as various cancers. There is growing evidence that higher vitamin D status is protective against various cancers, including prostate and colorectal cancer, and also against prediabetes and the metabolic syndrome. Desirable levels of intake may be considerably higher than current reference intakes, and ceainly could not be met from unfoified foods. While increased sunlight exposure would meet the need, it carries the risk of developing skin cancer. Reference: Harper; 30th edition; Page no: 552, 553

Biochemistry

vitamins

a90571f1-9a01-4477-ab8a-5613d6dd48f9

Which of the following is not a component of transpo system?

Receptor activation

Selective gate

Non-selective channel

Energy coupling system

single

Functions: Transpo Systems An essential role of biomembranes is to allow movement of all compounds necessary for the normal function of a cell across the membrane barrier. These compounds include a vast array of substances like sugars, amino acids, fatty acids, steroids, cations and anions to mention a few. These compounds must enter or leave the cells in an orderly manner for normal functioning of the cell. A. 1. Ion Channels Ion channels are transmembrane channels, pore-like structures composed of proteins. Specific channels for Na+, K+, Ca++, and Cl- have been identified. Cation conductive channels are negatively charged within the channel and have an average diameter of about 5 to 8 nm. All ion channels are basically made up of transmembrane subunits that come together to form a central pore through which ions pass selectively. All channels have gates and are controlled by opening and closing. Types of Gates Two types of gated channels. They are a. Ligand-gated channels: In this, a specific molecule binds to a receptor and opens the channel. Example: Acetylcholine receptor is present in the postsynaptic membrane. It is a complex of five subunits, having a binding site for acetylcholine. Acetylcholine released from the presynaptic region binds with the binding site of the postsynaptic region, which triggers the opening of the channel and influx of Na+. b. Voltage-gated channels: These channels open or close in response to changes in membrane potential. Some propeies of ion channels * Composed of transmembrane protein subunits. * Highly selective. * Well regulated by the presence of "gates". * Two main types of gates: Ligand-gated and voltage-gated. * Activities are affected by ceain drugs. * Mutations of genes encoding transmembrane proteins can cause specific diseases. 2. Ionophores Ceain microorganisms can synthesize small organic molecules, called ionophores, which function as shuttles for the movement of ions across the membrane. Structure: These ionophores contain hydrophilic centres that bind specific ions and are surrounded by peripheral hydrophobic regions. Types: Two types: (a) Mobile ion carriers: Like valinomycin (Refer uncouplers of oxidative phosphorylation). (b) Channel formers: Like gramicidin. 3. Water Channels (Aquaporins) In ceain cells, e.g. in red blood cells, and cells of the collecting ductules of the kidney, the movement of water by simple diffusion is enhanced by movements of water through water channels, composed of tetrameric transmembrane proteins called aquaporins. About five distinct types of aquaporins have been recognised. CLINICAL ASPECT Recently mutations in the gene encoding AP-2 (Aquaporin 2) protein, have been shown to be the cause of one type of nephrogenic diabetes insipidus. 4. Gap Junction Ceain cells develop specialized regions on their membranes for intercellular communications which are in close proximity. Function: They mediate and regulate the passage of ions and small molecules upto 1000 to 2000 mol wt, through a narrow hydrophilic core connecting the cytosol of adjacent cells. Structure: They are primarily composed of protein, called connexon which contains four membrane-spanning a-helices. the mitochondrial membrane also has paicularly energy coupling mechanism.Ref: MN Chatterjea Textbook of Medical Biochemistry, 8th edition

Biochemistry

Respiratory chain

de848149-c145-4341-95fd-5e7fb647e705

Antibodies associated with GTCS in SLE :

Anti neuronal ab

Anti-Ro ab

Anti-Sm ab

multi

Ans.A Anti neuronal ab (Ref: Harrison's Internal medicine 18th/Table 319-1; 17th edition, P. 2076). Autoantibodies in Systemic Lupus Erythematosus (SLE) Antibody Prevalence, % Antigen Recognized Clinical Utility Antinuclear antibodies 98 Multiple nuclear Best screening test; repeated negative tests make SLE unlikely Anti-dsDNA 70 DNA (double-stranded) High titers are SLE-specific and in some patients correlate with disease activity, Anti-Sm 25 Protein complexed to 6 species of nuclear U1 RNA Specific for SLE; no definite clinical correlations; most patients also have anti Anti-RNP 40 Protein complexed to U1 RNA Not specific for SLE; high titers associated with syndromes that have overlap blacks than whites Anti-Ro (SS-A) 30 Protein complexed to hY RNA, primarily 60 kDa and 52 kDa Not specific for SLE; associated with sicca syndrome, predisposes to subacute cutaneous with decreased risk for nephritis Anti-La (SS-B) 10 47-kDa protein complexed to hY RNA Usually associated with anti-Ro; associated with decreased risk for nephritis Antihistone 70 Histones associated with DNA (in the nucleosome, chromatin) More frequent in drug-induced lupus than in SLE Antiphospholipid 50 Phospholipids, 2 glycoproteins 1 cofactor, prothrombin Three tests available ELISAs for cardiolipin and 2G1, sensitive prothrombin Antierythrocyte 60 Erythrocyte membrane Measured as direct Coombs' test; a small proportion develops overt hemolysis Antiplatelet 30 Surface and altered cytoplasmic antigens on platelets Associated with thrombocytopenia but sensitivity and specificity are not good; Antineuronal (includes anti-glutamate receptor) 60 Neuronal and lymphocyte surface antigens In some series a positive test in CSF correlates with active CNS lupus. Antiribosomal P 20 Protein in ribosomes In some series a positive test in serum correlates with depression or psychosis Also remember: Antibody Best screening test for Antibody ANA SLE Anti-Histone Drug-induced lupus Antinuclear antibodies SLE, nonspecific Anti-dsDNA; Anti-Sm Specific for SLE Anti-sm (Nelson's Paediatric Textbook) Marker of CNS lupus Anti-DNA Level of which correlates with disease activity Anti-Ro (SS-A) SACL, neonatal lupus Anti-Ro and Anti-La ie risk of nephritis (protective against nephritis) Antiphospholipid Hematological and Fetal Loss Antiribosomal protein Depression and Psychosis Anti-basement membrane Goodpasture syndrome Anticardiolipin, lupus anticoagulant SLE, antiphospholipid syndrome Anticentromere Limited scleroderma (CREST syndrome) Anti--Scl--70 (anti--DNA topoisomerase 1) Scleroderma (diffuse) Anti--SSA, anti--SSB (anti-Ro, anti--La) Sjogren syndrome Anti--Jo--1, anti--SRP, anti--Mi--2 Polymyositis, dermatomyositis Anti--TSH receptor Graves disease Anti--U1RNP (ribonucleoprotein) Mixed connective tissue disease c-ANCA (PR3-ANCA) Granulomatosis with polyangiitis (Wegener) IgA antiendomysial, IgA anti--tissue transglutaminase Celiac disease p-ANCA (MPO--ANCA) Microscopic polyangiitis, Churg--*JStrauss syndrome Anti--ACh receptor Myasthenia gravis Rheumatoid factor (antibody, most commonly IgM, specific to IgG Fc region), anti--CCP Rheumatoid arthritis Anti--glutamate decarboxylase Type 1 diabetes mellitus Anti--desmoglein Pemphigus vulgaris Anti--hemidesmosome Bullous pemphigoid Antimicrosomal, antithyroglobulin Hashimoto thyroiditis Antimitochondria! 1*< biliary cirrhosis Anti--smooth muscle Autoimmune hepatitis ALSO KNOW: LE cells Neutrophils with LE bodies seen in SLE, RA Penicillamine drug induced Hematoxilin bodies SLE endocarditis (Libmann-Sack) 'Wire-loop' lesions SLE type IV nephritis

Unknown

b9799e1c-a706-43df-8a51-7f1fa165d79c

National program for prevention and control of Cancer, Diabetes, Cardiovascular disease and stroke (NPCDCS), true is -

Separate centre for stroke, DM, cancer

Implementation in some 5 states over 10 districts

District hospital has specialised facilities

Subcentre has facility for diagnosis and treatment

multi

Ans. is 'c' i.e., District hospital has specialised facilities Sational program for prevention and control of cancer, diabetes, cardiovascular diseases and stroke (NPCDCS1 Introduction Single centre fi- cancer, diabetes, cardiovascular disease, stroke. 100 districts in 21 states being covered in 1 1 th live year plan. 20,000 subcentres and 700 community health centres (CHCs) covered. o Activities as sub-centres Health promotion for behaviour and lifestyle change. Oppounistic screening of BP. blood glucose (strip method) in age > 30 years. Referral to CHC of cases of DM, HT. o Activities at CHCs : Diagnosis and management at NCD clinic. Home visits by nurse for bedridden cases. Referral to district hospital for complicated cases. o Activities as District hospital : Health promotion Screening of population > 30 years. Diagnosis and management of cardiovascular disease. Home-based palliative care for chronic, debilitating progressive patients. Specialized facilities. Urban health check-up shceme JOr diabetes and high BP : Screen urban slum population. Screen population > 30 years and pregnant females. Cancer control in NPCDCS : Regional cancer control scheme : Regional cancer centres to act as referral centres for complicated cases. Oncology wing development scheme. Decentralized NGO scheme : IEC activities and early cancer detection. lEC at central level. Research and mining.

Social & Preventive Medicine

b83ec510-9c3f-4f3c-ae71-6cad16b917ea

In a young female of reproductive age an absolute contraindication for prescribing oral contraceptive pills is:

Diabetes

Hypertension

Obesity

Impaired liver function

single

Ans-D i.e., Impaired liver function Repeat Q No 173 (Nov. 2004)Absolute contraindications include:A personal h/O thromboembolic venous, arterial or cardiac disease or severe or multiple risk factor for these. Transient cerebral ischaemic attacks without a headache.Infective hepatitis, until 3 months after liver function tests has become normal, and another liver disease including disturbances of hepatic excretion e.g. cholestatic jaundice, Dubin Johnson and Rotor syndromes.A migraine, if there is a typical aura, focal features or if it is severe and lasts > 72 hours despite t/t or is treated with an ergot derivative.Carcinoma of the breast or the genital tractOther conditions including SLE, porphyria, following the evacuation of a hydatidiform mole (until urine and plasma gonadotropin concentrations are normal), undiagnosed vaginal bleeding.Relative contraindications of OCP'sThe family history of venous thromboembolism, arterial disease or a known prethrombotic condition e.g. Factor V Leiden (pretreatment coagulation investigation is advised).Diabetes mellitus which may be precipitated or become more difficult to control (avoid if there are diabetic complications).Hypertension (avoid if B.P. exceeds 160/100)Smoking > 40 Cigarettes per day (15 Cigarettes/day enhances the risk of circulatory disease and constitutes an absolute contraindication for women over 35 years.Long-term immobility (e.g. due to Leg plaster, confinement to bed.Breastfeeding (until weaning or for 6 months after birth).Obesity

Unknown

44c444b1-70f2-4e52-94f0-78544786ed41

Which of these following statements is wrong about Tacrolimus?

It is one of the macrolide antibiotic

It can be safely administered with any nephrotoxic drug

Glucose intolerance is a well known side effect

It is used as prophylaxis for transplant rejection

multi

The side effects of Tacrolimus includes, nephro and hepato toxicity. It can also cause hypeension, tremors, seizure, diabetes mellitus and blurred vision. It should be better avoided with other hepato and renal toxicity drugs. Ref: Manzoor M. Khan (2008), Chapter 4 "Immunesupressive Agents", In the book, "Immunopharmacology", Springer Publications, USA, Page 91 ; Katzung, 9th Edition, Pages 941, 942

Pharmacology

e828463d-f844-4e66-acb8-7b75e9733df4

Macrosomia is a

Large size baby

Big mouth

Large head

Large tongue

single

Macrosomia:- A condition where a baby is large before bihFactors causing macrosomia:Mother having diabetesMother having gestational diabetesObese mother(Refer: Nelson's Textbook of Pediatrics, SAE, 1st edition, pg no. 777, 897 - 899)

Pediatrics

All India exam

c51ac107-3607-4bb8-8ed2-f6b8984f2cd1

Urine osmolality in Diabetes insipidus is

<150 mmol/L

<300 mmol/L

<600 mmol/L

<900 mmol/L

single

Diabetes insipidus is condition characterised by excessive thirst excretion of large amounts of severely diluted urine Those with diabetes insipidus continue to uinate large amount of urine in spite of water deprivation.Ref: DM Vasudevan, 7th edition, page no: 373

Biochemistry

Endocrinology

7ae4d04b-7e5e-4455-abcb-068b61031179

Starvation and diabetes mellitus can lead on to ketoacidosis which of the following features is in our of ketoacidosis due to diabetes mellitus.

Increase in glucagon/insulin ratio, increased CAMP and increased blood glucose

Decreased insulin, increased free fatty acid which is equivalent to blood glucose

Decreased insulin, increased free fatty acid which is not equivalent to blood glucose

Elevated insulin and free fatty acid, equivalent to blood glucose

single

A i.e. Increase in glucagons/ insulin ratio, increased C- AMP & increased blood sugar.In diabetes little glucose is oxidized as fuel, except by the brain. The rest of tissues burn a large amount of fat, paicularly the liver where the amount of acetyl COA formed from fatty acids exceeds the capacity of the tricarboxylic acid cycle to oxidize it. The excess acetyl COA is conveed to ketone bodies l/t ketonemia, ketonuria & ketoacidosisDiabetics not only have a defect in the tissue utilization of glucose but also appears to be metabolically poised to produce maximum amount of glucose from amino acids (gluconeogenesis) and to prevent glucose from being utilized to to form fat. (fat synthesis)Insulin is decreased & glucagons is increased 1/t Dglucagon/ insulin ratioQ. Glucagon acts elevation in C- AMPQ

Biochemistry

8b1e7f01-b79f-4f24-a759-3f3fed9c1978

Which of the following drugs used to treat type II diabetes mellitus causes weight loss:

Metformin

Glimepiride

Repaglinide

Gliclazide

single

Pharmacology

0fe4c348-ea07-4893-836e-83b4fccf6b45

Which of the following is not a cause of glomerular proteinuria?

Diabetes Mellitus

Amyloidosis

Multiple myeloma

Nil Lesion

single

Multiple myeloma is characterized by tubular proteinuria. The Bence Jones proteins induce tubular damage Increased beta-2-microglobulin levels in urine is an prognostic indicator of Multiple myeloma Diabetes Mellitus and amyloidosis lead to damage to basement membrane of the kidney leading to glomerular proteinuria in form of albuminuria Nil Lesion is also called as minimal change disease and presents as glomerular cause of proteinuria leading to nephrotic presentation . Multiple Myeloma: SPEP will demonstrate a sharp peak ("church spire" orM band) in the gamma globulin region as shown below:

Medicine

Nephrology

67ceb846-ab6f-411b-8c28-d9e47f0fe14d

Most common cause of Papillary necrosis is

Diabetes Mellitus

Sickle cell anaemia

Analgesics

Pyelonephritis

single

Major causes of Papillary Necrosis1. Analgesic nephropathy2. Sickle cell nephropathy3. Diabetes with UTI4. Prolonged NSAID use Reference: Harrison&;s Principles of Internal Medicine; 19th edition; Chapter 340; Tubulointerstitial Diseases of the Kidney

Medicine

Kidney

78647e01-58cb-4288-98b9-1044314042fb

What is an ideal method to prevent aspiration pneumonia?

Cuffed endotracheal tube

Inhalational anaesthesia

Increased intra abdominal pressure

Full stomach

single

Ans: A (Cuffed endotracheal tube) Ref: Bailey, 24th ed, p. 46; Ajay Yadav, p. 101A cuffed endotracheal tube is used to:1. Facilitate artificial airway ventilation or surgery around face or airway.2. Protection of lung if there is a risk of pulmonary aspiration.Predisposing factors for aspiration:1. Full stomach-- single, most important factor.2. | Level of consciousness.3. Conditions which reduce the tone of LES:Pregnancy (acid aspiration in late pregnancy- Mendelson syndrome)Abdominal tumorsObesity, hiatus herniaPresence of nasogastric tubeDrugs-Atropine, glycopyrrolate, opioids, thiopentone.4. Conditions delaying gastric emptyingDiabetes, hypothyroidism, pain, anxiety, anticholinergics, opium.Management:Prevention:Management - full stomach patients:1. Empty stomach2. H2blockers- to reduce acid production.3. Metoclopramide4. Neutralisation of gastric contents by antacids1. Regional anesthesia is preferred2. Awake intubation3. Rapid sequence intubation- Sellick maneuver

Unknown

0255b23e-45f6-4f9a-a407-cc8bcbc85cd3

The diagnosis of diabetes mellitus is ceain in which of the following situations?

Abnormal oral glucose tolerance in a 24-yrs-old woman who has been dieting

Successive fasting plasma glucose concentrations of 8, 9, and 8.5 mmol/L in an asymptomatic, otherwise healthy businesswoman

A serum glucose level >7.8 mmol/L in a woman in her twenty-fifth week of gestation after a 50-g oral glucose load

Persistent asymptomatic glycosuria in a 30-yrs-old woman

single

The occurrence of hyperglycemic ketoacidosis or hyperglycemic hyperosmolar coma is diagnostic of diabetes mellitus. Similarly, persistent fasting hyperglycemia , even if it is asymptomatic, has been recommended by the National Diabetes Data Group as a criterion for the diagnosis of diabetes. However, abnormal glucose tolerance-whether after eating or after a standard "glucose tolerance test" -can be caused by many factors (e.g., anxiety, infection or other illness, lack of exercise, or inadequate diet). Similarly, glycosuria may have renal as well as endocrinologic causes. Therefore, these two conditions cannot be considered diagnostic of diabetes. Gestational diabetes is diagnosed in women between the twenty-fouh and twenty-eighth weeks of gestation, first using a 50-g oral glucose load if the I-h glucose level >7.8 mmol/L (140 mg/dL); a 100-g oral glucose test is performed after an overnight fast. Gestational diabetes is initially treated with dietary measures; if the postprandial glucose level remains elevated, insulin therapy is often staed. About 30% of women with gestational diabetes will eventually develop true diabetes mellitus.

Medicine

Endocrinology

0ff5d474-8b83-4e08-a720-1546fc5dee6f

NOT a cause of granular contracted kidney ?

Diabetes mellitus

Chronic pyelonephritis

Benign nephrosclerosis

Chronic glomerulonephritis

single

Ans. is 'a' i.e., Diabetes mellitusCauses of Granular contracted kidney ?Chronic glomerulonephritis (symmetric)Chronic pyelonephritis (asymmetric) o Benign Nephrosclerosis (Symmetric) Sometimes, Diabetes too can cause granular contracted kidney

Pathology

5333eaa6-744a-45de-a1ff-a03c87ffd2e0

Devic's disease is associated with

Aquaporin 0

Aquaporin 1

Aquaporin 2

Aquaporin 4

single

(D) Aquaporin 4 # NEUROMYELITIS OPTICA (NMO) or Devic's disease or Devic's syndrome, is a heterogeneous condition consisting of recurrent and simultaneous inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis).> Currently at least two different causes are proposed based on the presence of autoantibodies against AQP4.> Autoimmune reactions against aquaporin 4 produce Devic's disease Mutations in the aquaporin-2 gene cause hereditary nephrogenic diabetes insipidus in humans. Mice homozygous for inactivating mutations in the aquaporin-0 gene develop congenital cataracts.> A small number of people have been identified with severe or total deficiency in aquaporin-1. Interestingly, they are generally healthy, but exhibit a defect in the ability to concentrate solutes in the urine and to conserve water when deprived of drinking water.

Medicine

Miscellaneous

cf7902f7-2a01-458c-ae6c-4b7ddf126c00

True about diabetic nephropathy -

Microalbuminiuria is not an indicator of long term cardiovascular morbidity.

Strict glycemic control cannot prevent microalbuminuria

b-islet cell\/pancreatic transplantation can improve the proteinuria in early stage.

Angiotensin receptor blockers have no additive advantage over other drugs except B.P. control.

multi

Beta islet cell/ pancreatic transplantation can improve proteinuria in early stages.. Strict control of blood glucose retards the progression of any diabetes related complication Early pathological change and albumin excretion abnormalities is reversible with normalization of plasma glucose Administration of ACE inhibitors or ARB&;s, is also effective in slowing progression from Microalbuminuria to ove nephropathy Ref Harrison 17/e p 2287-88

Medicine

Endocrinology

68b5caed-e01f-4385-aff7-44808d77250a

Diabetic neuropathy is a

Distal symmetric sensory polyneuropathy

Mononeuritis

Autonomic neuropathy

All of the above

multi

Diabetic neuropathy causes substantial morbidity and increases moality. It is diagnosed on the basis of symptoms and signs, after the exclusion of other causes of neuropathy . Depending on the criteria used for diagnosis, it affects between 50% and 90% of patients with diabetes, and of these, 15-30% will have painful diabetic neuropathy (PDN). Like retinopathy, neuropathy occurs secondary to metabolic disturbance, and prevalence is related to the duration of diabetes and the degree of metabolic control. Pathological features can occur in any peripheral nerves. They include axonal degeneration of both myelinated and unmyelinated fibres, with thickening of the Schwann cell basal lamina, patchy segmental demyelination and abnormal intraneural capillaries (with basement membrane thickening and microthrombi). Ref - Davidsosn 23e p780

Medicine

Endocrinology

a5b2e089-3e8a-490a-9387-74687302149f

ACE inhibitor contraindicated in which of the following condition:

Bilateral renal artery stenosis

Chronic kidney disease

Post myocardial infarction

Diabetes mellitus

single

Ans. (a) Bilateral renal artery stenosisRef. Katzung's pharmacology 10th ed. Ch 11* ACEI inhibits the converting enzyme peptidyl dipeptidase that hydrolyzes angiotensin I to angiotensin II and (under the name plasma kininase) inactivates bradykinin, a potent vasodilator, which works at least in part by stimulating release of nitric oxide and prostacyclin.* Drugs under this class are: Captopril, Enalapril, Lisinopril, Benazepril, fosinopril, moexipril, perindopril, quinapril, ramipril, and trandolapril.* ACE inhibitors have a particularly useful role in treating patients with chronic kidney disease because they diminish proteinuria and stabilize renal function (even in the absence of lowering of blood pressure).* ACE inhibitors have also proved to be extremely useful in the treatment of heart failure, and after myocardial infarction, and* There is recent evidence that ACE inhibitors reduce the incidence of diabetes in patients with high cardiovascular risk.

Pharmacology

ACE Inhibitors

5f4b4e34-a0b0-4a8f-a266-03dc79aaa72c

renal papillary necrosis is caused by ?

alcohol

cocaine

heroin

morphine

single

Etiology # Pyelonephritis # Obstruction of the urinary tract # Sickle cell hemoglobinopathies, including sickle cell trait # Tuberculosis # Cinhosis of the liver, chronic alcoholism # Analgesic abuse # Renal transplant rejection, Radiation, Renal vein thrombosis # Diabetes mellitus # Systemic vasculitis Renal papillary necrosis # Renal papillary necrosis (RPN) is characterized by coagulative necrosis of the renal medullary pyramids and papillae # Renal papillary necrosis generally affects individuals who are in the middle decades of life or older # It is more common in women than in men # 60% of the patients have DM, 30% Urinary tract obsruction, 15% have both. # Renal papillary necrosis is primarily a bilateral process ref : harrisons 21st ed

Medicine

All India exam

6e9d73be-adf4-402b-8c33-4c04fc394a07

Which drug is not used to prevent contrast nephropathy -

Fenoldopam

N-acetylcysteine

Infusion of Hair normal saline

Hemodialysis

single

Ans. is 'a' i.e., Fenoldopam Summary And Recommendations for prevention of contrast induced nephropathy (uptodate recommendation )o Optimal therapy to prevent contrast-induced acute renal failure remains uncertain. Patients with near-normal renal function are at little risk and few precautions are necessary other than avoidance of volume depletion.o We recommend the following preventive measures for patients at increased risk of contrast nephropathy, which is defined a serum creatinine >1.5 mg/dL (132 micromol/L) or an estimated glomerular filtration rate <60 ml/l 73 m2, particularly in those with diabetes.o Use, if possible, ultrasonography, MRI without gadolinium contrast, or CT scanning without radiocontrast agents.o We recommend NOT using high osmolal agents is not recommendedo We recommend the use of iodixanol or nonionic low osmolal agems such as iopamidol or ioversol rather than iohexol.o Use lower doses of contrast and avoid repetitive, closely spaced studies.o Avoid volume depletion and nonsteroidal anti-inflammatory drugs.o If there are no contra indications to volume expansion, we recommend isotonic intravenous fluids prior to and continued for several hours after contrast administration. The optimal type offluid and timing of administration are not well established. We suggest isotonic bicarbonate rather than isotonic saline.o Despite conflicting data, we suggest that acetylcysteine be administered the day before and the day of the procedure, based upon its potentialfor benefit and low toxicity and cost. If acetylcysteine is administered, we suggest giving 1200 mg orally twice daily rather than 600 mg twice daily the day before and the day of the procedure.o Based upon the lack of convincing evidence of benefit and ihe potential risk of anaphylactoid reactions, we suggest not using intravenous acetylcysteine for the prevention of contrast nephropathy. (Note: Oral acetylcysteine is used)o We recommend NOT using mannitol or other diuretics prophytactically.o Among patients with stage 3 and 4 CKD, we recommend NOTperforming prophylactic hemofiltration or hemodialysis after contrast exposure.o Among patients with stage 5 CKD, we suggest prophylactic hemodialysis after contrast exposure if there is already a functioning hemodialysis access.

Medicine

Drugs

2f39ca11-d54f-459e-aee2-7ad761bdc720

An elderly diabetic with excruciating pain in ear, appearance of granulation in meatus, skull base infection with facial paralysis should be treated with

Penicillin

Ciprofloxacin

2nd generation ciphalosporin

Erythromycin

single

All clinical features are suggestive of malignant otitis externa, an inflammatory condition of the external ear. Malignant otitis externa (also k/a Necrotizing external otitis) Malignant otitis externa is an inflammatory condition of the external ear usually spreading deep to cause osteomyelitis of temporal bone and base of skull. It occurs primarily in immunocompromised persons, especially older persons with diabetes mellitus, and is often initiated by self-inflicted or iatrogenic trauma to the external auditory canal [May also be seen in pts. who received radiotherapy to skull base I The most frequent pathogen is Pseudomonas aeruginosa. Others may be S. aureus, Staphylococcus epidermidis, Aspergillus, Actinomyces, and some gram-negative bacterial. One of the hallmarkof malignant otitis externs is granulation tissue in the external auditory canal, especially at the hone-cailage junction. As the infection spreads to the temporal bone, it may extend into the cranium and result in cranial nerve palsies (commonly the facial nerve) Cranial nerve involvement indicates poor prognosis. Death is usually due to intracranial complications such as sigmoid sinus thrombosis. It has high moality rate due to which the name 'malignant' is used for this disease. Treatment Includes correction of immunosuppression (when possible), local treatment of the auditory canal, long-term systemic antibiotic therapy, and in selected patients, surgery. - In all cases, the external ear canal is cleansed and a biopsy specimen of the granulation tissue sent for culture. - IV antibiotics is directed against the offending organism. - For Pseudomonas aeruginosa, the most common pathogen, the regimen involves an antipseudomonal penicillin or cephalosporin (3rd generation-piperacillin or ceftazidime) with an aminoglycoside. A fluoroquinolone antibiotic can be used in place of the aminoglycoside. Ear drops containing antipseudomonal antibiotic e.g. ciproflaxacin plus a glucocoticoid is also used. - Early cases can be managed with oral and otic fluoroquinolones only. - Extensive surgical debridement once an impoant pa of the treatment is now rarely needed.

ENT

d0efa4a0-aeef-4af5-acef-c41cfb68529e

Which of the following drugs is contraindicated along with spironolactone

Chlorothiazide

Beta blockers

ACE inhibitors

Amlodipine

single

CONTRAINDICATIONS / PRECAUTIONS Adrenal insufficiency, anuria, diabetes mellitus, hyperkalemia, renal disease, renal failure, renal impairment. ... Acid/base imbalance, metabolic acidosis, metabolic alkalosis, respiratory acidosis. ... Ascites, biliary cirrhosis, hepatic disease. ... Menstrual irregularity.

Pharmacology

Kidney

8d7ab965-4d7f-4dc9-a4b4-44bbc7334175

Mechanism of action of the sulfonylureas is

K+ ATP channel blocker

Na ATP channel blocker

Cl ATP channel blocker

Ca ATP channel blocker.

single

Ans. is 'a' i.e., K ATP channel blocker * Sulfonylurease provoke a brisk release of insulin from pancreas. They act on the so called "Sulfonylurea receptors" (SUR1) on pancreatic b-cell membrane - cause depolarization by reducing conductance of ATP sensitive K+ channels. This enhances influx of Ca+2 - degranulation. They do not cause hypoglycemia in pancreatectomized animals and type 1 diabetes (Presence of at least 30% of functional b-cells in essential for their action). A minor action reducing glucagon secretion by increasing insulin and somatostatin release has been demonstrated.

Pharmacology

Endocrinology

c2c522e9-595e-4327-a763-7eb93c7fcb88

A 68-year-old male is brought to the outpatient by his wife due to increasing forgetfulness. On taking history in details, wife repoed that for around 6 months patient is having trouble in organising the finances and paying bills, something he has done all his life. He has also become withdrawn and has decreased meeting people. The patient also behaved inappropriately with a female neighbour couple of says back, which is much against his usual nature. The patient denies having any problems and seems indifferent to his wife's concern. He has a medical history of hypeension and type 2 diabetes mellitus There is a family history of Alzheimer disease. On MMSE, score came out to be 23. Which of the following is the most likely diagnosis?

Alzheimer disease

Creutzfeldt-Jakob disease

Dementia with Lewy bodies

Frontotemporal dementia

multi

The history is suggestive of executive dysfunction (trouble in organising the finances and paying bills), apathy and disinhibition (decreased socialisation and inappropriate behaviour with women), lack of insight (denies having any problem) and memory disturbances. This is suggestive of frontotemporal dementia, in which personality changes are prominent, memory disturbances appear later in frontotemporal dementia. In contrast, in alzheimers disease memory disturbances are prominent early in the disorder and personality changes later. Creutzfeldt-Jakob disease which is caused by a prion manifests with rapidly progressive dementia, myoclonus, and cerebellar dysfunction.

Psychiatry

Organic Mental Disorders

b326349f-be05-4904-ad6e-b661620f54e8

A 65yr old male with his of Diabetes and HTN presents Ito OPD with complaints of diplopia and squint on examination secondary detion is seen to be more than primary detion Which of the following is the most probable diagnosis

Paralytic squint

Incomitant squint

Restrictive squint

Pseudo squint

single

ref : ak khurana 7th ed

Ophthalmology

All India exam

1cd6d32e-78c4-4549-b4df-93edb57a3d59

A 7-year-old boy, Manoj underwent successful chemotherapy and cranial radiation for the treatment of acute lymphocytic leukemia. One month after the completion of therapy, the patient presented with excessive thirst and urination plus hypernatremia. Laboratory testing revealed pituitary diabetes insipidus. To corect these problems, this patient is likely to be treated with:

Coicotropin

Desmopressin

hCG

Menotropins

single

(Ref: KDT 6/e p57) Drugs used for the treatment of central (pituitary) diabetes insipidus are: - Desmopressin (selective V2 agonist) - Thiazides - Chlorpropamide - Carbamazepine Drugs used for the treatment of nephrogenic (renal) diabetes insipidus are: - Thiazides - Amiloride (for lithium induced) Thiazides are useful for the treatment of both central as well as nephrogenic diabetes insipidus. Desmopressin is not effective in nephrogenic diabetes insipidus.

Anatomy

Other topics and Adverse effects

99023c78-540d-4c18-bf21-ba0ef9396849

After overnight fasting, levels of glucose transpoers reduced in

Brain cells

RBCs

Adipocytes

Hepatocytes

single

GluT4 is the major glucose transpoer in skeletal muscle and adipose tissue.GluT4 is under the control of insulin.In Type 2 diabetes mellitus, membrane GluT4 is reduced, leading to insulin resistance in muscles and fat cells.Ref: DM Vasudevan, 7th edition, page no: 107

Biochemistry

Metabolism of carbohydrate

0f057ac7-45e6-432d-a7d8-0b01445762a6

Commonest fungal infection of female genitalia in diabetes?

Cryptococcal

Madurmycosis

Candida

Aspergillosis

single

Candida is the commonest infection of female genital tract in diabetes. Candida species are normal commensals of the mouth, GI tract, vaginal mucosa and in the patients with an indwelling catheter. Diabetes is paicularly associated with increased susceptibility to vaginal infections.

Dental

Fungal infections

c926913f-44fb-49f1-a528-88c215b243aa

Fatty liver is caused by all except

DM

Tetracycline

Starvation

Excess iron intake

multi

Fatty change in the liver may result from one of the two types of causes: 1.Conditions with excess fat: i) Obesity ii)Diabetes mellitus iii)Congenital hyperlipidaemia 2.Liver cell damage: i) Alcoholic liver disease (most common) ii)Starvation iii)Protein calorie malnutrition iv)Chronic illnesses (e.g. tuberculosis) v) Acute fatty liver in late pregnancy vi)Hypoxia (e.g. anaemia, cardiac failure) vii)Hepatotoxins (e.g. carbon tetrachloride, chloroform, ether, aflatoxins and other poisons) viii)Drug-induced liver cell injury (e.g. administration of methotrexate, steroids, CCl4, halothane anaesthetic, tetracycline etc) ix) Reye's syndrome. TEXTBOOK OF PATHOLOGY HARSH MOHAN 6TH EDITION PAGE NO:38

Pathology

G.I.T

f0f4b676-ab5a-4469-916c-bdfd4113be62

The adverse effect of clozapine -

Hypertension

Sialorrhea

Extrapyramidal S/E

Neuroleptic malignant syndrome

single

Side effects of clozapine Agranulocytosis Urinary incontinence Unstable BP & Tachycardia Hypersalivation (sialorrhoea) Worsening of diabetes Weight gain Seizures Sedation

Psychiatry

7c021870-c90d-4a27-93c5-e0a629acc78b

Which of the following is present normally in the urine of a pregnant women in the third trimester and lactation?

Glucose

Lactose

Galactose

Fructose

multi

Glucosuria during pregnancy is not necessarily abnormal. The appreciable increase in glomerular filtration, together with impaired tubular reabsorptive capacity for filtered glucose, accounts in most cases for glucosuria. Though glucosuria is common during pregnancy, the possibility of diabetes mellitus should not be Ignored when it is identified.

Gynaecology & Obstetrics

Physiological Changes of Pregnancy

d446048b-0034-4303-8417-5ef013eb95af

Following a myocardial infarct, a 40-year-old man is being treated prophylactically with propranolol. You would be concerned about the use of this drug if the patient also had what comorbid condition

Glaucoma

Essential tremor

Diabetes

Supraventricular tachycardia

multi

Metabolic actions:- Propranolol inhibits glycogenolysis in hea, skeletal muscles and in liver, which occurs due to Adr release during hypoglycaemia--recovery from insulin action is delayed. Warning signs of hypoglycaemia mediated through sympathetic stimulation (tachycardia, tremor) are suppressed in patients taking beta blockers like propranolol, so it should be cautiously used in patients with diabetes. Ref:- kd tripathi; pg num:-145,146

Pharmacology

Autonomic nervous system

8dde9b32-c47d-422e-9720-57c03d99d65c

Chediak-Higashi syndrome is characterized by

Defects in phagolysosome function

Defects in macrophage production

Defects in leukocyte adhesion

Defects in microbicidal activity

single

Ans. a (Defects in phagolysosome function) (Ref. H - 17th/pg. Table 61-4)CHRONIC GRANULOMATOUS DISEASEChronic Granulomatous Disease presents before the age of 2 and can be transmitted through X-linked or autosomal pattern of inheritance. The defect lies in the inability to generate oxidative burst to kill organisms after being phagocytosed. The neutrophils lack enzyme NADPH oxidase, which plays an important role in production of microbicidal oxygen radicles. In the lab, the diagnosis can be confirmed through Nitro blue Tetrazolium reduction dye test, which will be negative. B cell and T cell functions are normal. Recurrent infections with catalase producing organisms are common. The NBT test is a measure of the respiratory burst in neutrophils and is used to screen for CGD. Neutrophils will reduce the dye NBT, a clear yellow water-soluble compound, to formazan upon stimulation of the respiratory burst. Formazan thus forms precipitates as a dark blue granular substance, which remains trapped in the cytoplasm. Patients with CGD lack a component of the oxidase system, which produces super oxide anion and thus cannot reduce NBT to formazan. Results are interpreted as follows: Normal (positive test) - cells with an orange-red nucleus and blue cytoplasm; Abnormal (negative test) - cells with an orange-red nucleus and colorless cytoplasm.Phagocytic cell deficiency:Leukocyte adhesion deficiency syndrome (type 1): Defect in LFA-1 integrin proteins on phagocytes. Presents early with recurrent bacterial infections, absent pus formation, and delayed separation of umbilicus.Chediak-Higashi disease:Autosomal recessive. Defect in microtubular function and lysosomal emptying of phagocytic cells. Presents with recurrent pyogenic infections by staphylococci and streptococci, partial albinism, and peripheral neuropathy.Chronic granulomatous disease:Defect in phagocytosis of neutrophils owing to lack of NADPH oxidase activity or similar enzymes. Presents with marked susceptibility to opportunistic infections with bacteria, especially S. aureus, E. coli, and Aspergillus. Diagnosis confirmed with negative nitroblue tetrazolium dye reduction test. Rx:Gamma Interferon.Inherited Disorders of Phagocyte Function: Differential FeaturesClinical manifestationsCellular or molecular defectsDiagnosisChronic Granulomatous Diseases (70% X-linked, 30% Autosomal Recessive)Severe infections of skin, ears, lungs, liver, and bone with catalase-positive microorganismsSuch as S. aureus, BurkholderiaChromobacterium violaceum; often hard to culture organism; excessive inflammation with granulomas, frequent lymph node suppuration; granulomas can obstruct GI or GU tracts; gingivitis, aphthous ulcers, seborrheic dermatitisNo respiratory burst due to the lack of one of four NADPH oxidase subunits in neutrophils, monocytes, and eosinophilsNBT or DHR test; no superoxide and H2O2 production by neutrophils; immunoblot for NADPH oxidase components; genetic detectionChediak-Higashi Syndrome(Autosomal Recessive)Recurrent pyogenic infections, especially with S. aureus; many patients get lymphoma-like illness during adolescence; periodontal disease; partial oculocutaneous albinism, nystagmus, progressive peripheral neuropathy, mental retardation in some patientsReduced chemotaxis and phagolysosome fusion, increased respiratory burst activity, defective egress from marrow, abnormal skin window; defect in LYSTGiant primary granules in neutrophils and other granule-bearing cells (Wright's stain); genetic detectionSpecific Granule Deficiency(Autosomal Recessive)Recurrent infections of skin, ears, and sinopulmonary tract; delayed wound healing; decreased inflammation; bleeding diathesisAbnormal chemotaxis, impaired respiratory burst and bacterial killing, failure to upregulate chemotactic and adhesion receptors with stimulation, defect in transcription of granule proteins; defect in C/EBPLack of secondary (specific) granules in neutrophils (Wright's stain), no neutrophil- specific granule contents (i.e., lactoferrin), no defensins, platelet granule abnormality; genetic detectionMyeloperoxidase Deficiency(Autosomal Recessive)Clinically normal except in patients with underlying disease such as diabetes mellitus; then candidiasis or other fungal infectionsNo myeloperoxidase due to pre- and posttranslational defectsNo peroxidase in neutrophils; genetic detectionLeukocyte Adhesion DeficiencyType 1: Delayed separation of umbilical cord, sustained neutrophilia, recurrent infections of skin and mucosa, gingivitis, periodontal diseaseImpaired phagocyte adherence, aggregation, spreading, chemotaxis, phagocytosis of C3bi-coated particles; defective production of CD18 subunit common to leukocyte integrinsReduced phagocyte surface expression of the CD18-containing integrins with monoclonal antibodies against LFA-1 (CD18/CD11a), Mac-1 or CR3 (CD18/CD11b), pl50,95 (CD1S/ CD11c); genetic detectionType 2: Mental retardation, short stature, Bombay (hh) blood phenotype, recurrent infections, neutrophiliaImpaired phagocyte rolling along endotheliumReduced phagocyte surface expression of Sialyl-Lewisx, with monoclonal antibodies against CD15s; genetic detectionPhagocyte Activation Defects(X-linked and Autosomal Recessive)NEMO deficiency: mild hypohidrotic ectodermal dysplasia; broad based immune defectrpyogenic and encapsulated bacteria, viruses, Pneumocystis, mycobacteria; X-linkedImpaired phagocyte activation by IL-1, IL-18, TLR, CD40 TNF-leading to problem with inflammation and antibody productionPoor in vitro response to endotoxin;lack of NF-B activation; genetic detectionClinical manifestationsCellular or molecular defectsDiagnosisIRAK4 deficiency: susceptibility to pyogenic bacteria such as staphylococci, streptococci, Clostridia; resistant to mycobacteria; autosomal recessiveImpaired phagocyte activation by endotoxin through TLR and other pathway; TNF-signaling preservedPoor in vitro response to endotoxin; lack of NF-B activation by endotoxin; geneticdetectionHyper IgE-Recurrent InfectionSyndrome (Autosomal Dominant)(Job's Syndrome)Eczematoid or pruritic dermatitis, "cold" skin abscesses, recurrent pneumonias with S. aureus with bronchopleural fistulae and cyst formation, mild eosinophilia, mucocutaneous candidiasis, characteristic facies, restrictive lung disease, scoliosis, delayed primary dental deciduationReduced chemotaxis in some patients, reduced suppressor T cell activityClinical features, involving lungs, skeleton, and immune system; serum IgE > 2000 IU/mL

Pathology

Immunity

c3639327-dc10-4a69-a63c-14cf56b71d72

A 8 years boy with headache, supracellar mass, with bilateral hemianopia, showing the following MRI scan of head. What is the diagnosis

Craniopharyngioma

Pituitary apoplexy

Nasopharyngeal fibroma

Hypothalamic glioma

single

(A) Craniopharyngioma[?]Craniopharyngioma:Craniopharyngioma are pituitary gland tumor develop from the embryogenic remnants in pituitary gland.Present at any time during childhood, tumor is congenital &d arises from squamous epithelial cell rests of the embryonic Rathke's pouch.The neoplasm is usually cystic & benign.Clinical presentation:Headaches and raised ICPVisual symptoms: 20% of children & 80% adults.Hormonal imbalances:Short stature and delayed puberty in childrenDecreased libido; Amenorrhoea; Diabetes insipidusBehavioural change due to frontal or temporal extension.Growth failure; Signs of increased intracranial pressure; Endocrine abnormalities such as diabetes insipidus and delayed puberty (<10% of cases); Retarded Bone age.X-ray of skull may show calcificationMost preferred treatment is micro surgical excision & transcranial route through craniotomy.Tumor cyst can be aspirated or malignant craniopharyngiomas are treated with radiotherapy or implants.Types of Non Cancerous Brain Tumors seen in ChildrenChordomasMeningiomasCraniopharyngiomaPineocytomasGangliocytomasPituitary AdenomaGlomus JugulareSchwannomasOther Options[?]Pituitary apoplexy:Pituitary apoplexy or pituitary tumor apoplexy is bleeding into or impaired blood supply of the pituitary gland at the base of the brain. This usually occurs in the presence of a tumor of the pituitary, although in 80% of cases this has not been diagnosed previously.The most common initial symptom is a sudden headache, often associated with a rapidly worsening visual field defect or double vision caused by compression of nerves surrounding the gland.This is followed in many cases by acute symptoms caused by lack of secretion of essential hormones, predominantly adrenal insufficiency[?]Nasopharyngeal fibroma:Nasopharyngeal fibroma is a benign tumour but locally invasive and destroys the adjoining structures. It may extend into: Nasal cavity causing nasal obstruction, epistaxis and nasal discharge.Cranial cavity: Middle cranial fossa is the most common.There are two routes of entry:-By erosion of floor of middle cranial fossa, anterior to foramen lacerum. The tumour lies lateral to carotid artery & cavernous sinus.-Through sphenoid sinus, into the sella. Tumour lies medial to carotid artery.Surgical excision is now the treatment of choice. Radiotherapy has been used as a primary mode of treatment.Hormonal therapy as the primary or adjunctive treatment.Recurrent and residual lesions have been treated by chemotherapy.[?]Hypothalamic glioma:Rare tumors cause diencephalic syndrome in infants.Fail to thrive, loss of subcutaneous fat & suffer sleep & respiratory disturbances.Precocious puberty seen in older children.Associated histological types include glioma, pinealoma, teratomas & hamartomas.

Pediatrics

Childhood Tumors

103017e3-b606-4e18-8dbf-16bd7144f2a8

A 60-year-old woman with no past medical history has an elevated blood pressure of 165/80 mm Hg on routine evaluation. Repeated measurements over the next month confirm the elevated pressure. Physical examination, routine blood count, and biochemistry are all normalFor patient with high blood pressure, select the most appropriate medication

thiazides

spironolactone

clonidine

prazosin

multi

Thiazides have been a cornerstone in most trials of antihypertensive therapy. Their adverse metabolic consequences include renal potassium loss leading to hypokalemia, hyperuricemia from uric acid retention, carbohydrate intolerance, and hyperlipidemia. The current U.S. Joint National Committee (JNC-7) guidelines suggest starting with thiazide diuretics because of their proven efficacy in lowering mortality and morbidity in large clinical trials. Other agents are considered if there are comorbidities such as diabetes or CAD.

Medicine

C.V.S.

adff28ff-34c2-43af-b347-852c499020d2

A pregnant mother at 32 weeks gestation presents in preterm labour. Therapy with antenatal steroids to induce lung maturity in the fetus may be given in all of the following conditions except:

Prolonged rupture of membranes for more than 24 hours

Pregnancy induced hypertension

Diabetes mellitus

Chorioamnionitis

multi

“Corticosteroids can be given even in presence of maternal hypertension or diabetes mellitus, but should preferably be avoided if PROM is associated with definitive evidence of chorioamnionitis” Meherban Singh 5/e, p 227 “Steroid treatment is contraindicated in presence of overt infection.” Fernando Arias 3/e, p 220 Steroid therapy in preterm labour: Steroids are recommended for all women in preterm labour before 32 weeks with or without membrane ruptures in whom there is no evidence of chorioamnionitis. According to ACOG, single dose steroid injection is recommended between 24 to 32 weeks. There is no concensus regarding treatment between 32-34 weeks. Corticosteroid therapy is not recommended before 24 weeks. Advantage: Steroids reduce the rate of respiratory distress syndrome, intraventricular hemorrhage and necrotising enterocolitis in the newborn. The effect of treatment is maximal between 24 hours of the first dose and uptil 7 days. Earlier it was recommended to give repeated doses weekly till the patient delivers but this practice is associated with significant fetal and neonatal side effects like cerebral palsy and should be abandoned. Betamethasone is the steroid of choice as it also prevents periventricular leukomalacia although dexamethasone can also be used. Dose: Betamethasone = 2 doses of 12 mg, 24 hours apart, Dexamethosane: 4 doses of 6 mg, 12 hours apart.

Gynaecology & Obstetrics

35808bff-963d-4ea2-9406-16b9ad41fe45

Obesity is associated with all of the following except:

Osteoahritis

Hypeension

Gall stones

Pancreatitis

multi

Answer is D (Pancreatitis): Pancreatitis has no association with obesity. RISKS OF OBESITY INCLUDE THE FOLLOWING : A. Cardiovascular disease : -increased risk of atherosclerosis -increased risk of hypeension - increased risk of sudden death B. Pulmonary function : Sleep apnea and Right hea failure C. Gall bladder disease : Increased incidence of Gall stones D. Joint : - Increased risk of osteoahritis Q :paly due to added trauma of increased weight bearing - Increased incidence of Gout 2:due to impairment in urate clearance. E. Diabetes mellitus : Type II diabetes mellitus Q is almost always seen in the obese. F. Cancer : Increased incidence of endometrial carcinoma post menopausal breast cancer prostate cancer Q - colorectal carcinoma G. Skin : Increased incidence of Acanthosis nigricans Q H. Endocrine : Insulin Resistance : leading to Hyperinsulinemia is directly related to degree of obesity. Growth hormone Q :secretions is reduced but IGF-I levels are normal thus growth is not affected. Testosterone level is reduced.Q

Medicine

68ff9908-2480-44a0-b76d-a50dd05032f9

A 60-year-old man with diabetes acutely develops double vision and discomfort in his left eye. On examination, there is ptosis of the left eyelid, the eye is rotated down and out, and the pupil is 3 mm and reactive to light. The right eye is normal. Which of the following is the most likely diagnosis?

fourth nerve palsy

diabetic autonomic neuropathy

third nerve palsy

sixth nerve palsy

single

Third nerve palsy can result in ptosis of the eyelid. There is also loss of the ability to open the eye, and the eyeball is deviated outward and slightly downward. With complete lesions, the pupil is dilated, does not react to light, and loses the power of accommodation. In diabetes, the pupil is often spared. The sixth cranial nerve can also be affected by diabetes, but this is much less common.

Medicine

C.N.S.

1cbc1e30-83a5-441e-88ae-bdbb01c3c049

Most common ophthalmic complication of diabetes mellitus is

Retinopathy

Cataract

Rubeosis iridis

Vitreous hemorrhage

single

(A) Retinopathy # Most common ophthalmic complication of diabetes mellitus is diabetic retinopathy, with diabetic retinopathy being the most common preventable cause of blindness> Ocular features of diabetes mellitus: Blurring of vision Cataract formation Diabetic pupil Diabetic retinopathy Macular edema Retinal neovascularization Vitreous hemorrhage Retinal detachment Neovascularization of the iris (i.e. Rubeosis iridis) Cranial nerveCN III, IV and VI palsy> Blindness is primarily the result of progressive diabetic retinopathy and clinically significant macular edema.> Diabetic retinopathy is classified into two stages: nonproliferative and proliferative. Nonproliferative diabetic retinopathy usually appears late in the first decade or early in the second decade of the disease and is marked by retinal vascular microaneurysms, blot hemorrhages, and cotton wool spots.> Mild nonproliferative retinopathy progresses to more extensive disease, characterized by changes in venous vessel caliber, intraretinal microvascular abnormalities, and more numerous microaneurysms and hemorrhages. The pathophysiologic mechanisms invoked in nonproliferative retinopathy include loss of retinal pericytes, increased retinal vascular permeability, alterations in retinal blood flow, and abnormal retinal microvasculature, all of which lead to retinal ischemia.

Medicine

Miscellaneous

474c328c-5f55-4822-bde3-3c0e167a5281

Absense of taste sensation is termed as:

Hypogeusia

Ageusia

Dysgeusia

Partial ageusia

single

(B) Ageusia # Ageusia is the loss of taste functions of the tongue, particularly the inability to detect sweetness, sourness, bitterness, saltiness, and umami (the taste of monosodium glutamate). It is sometimes confused for anosmia--a loss of the sense of smell. Because the tongue can only indicate texture and differentiate between sweet, sour, bitter, salty, and umami most of what is perceived as the sense of taste is actually derived from smell. True aguesia is relatively rare compared to hypogeusia--a partial loss of taste--and dysgeusia--a distortion or alteration of taste.> Causes of Ageusia:> Neurological damage: Tissue damage to the nerves that support the tongue can cause ageusia, especially damage to the lingual nerve and the glossopharyngeal nerve.> Neurological disorders such as Bell's palsy, Familial dysautonomia, and Multiple sclerosis cause similar problems to nerve dam- age, as do certain infectious conditions like primary amoeboid meningoencephalopathy. The lingual nerve (which is a branch of the trigeminal V3 nerve, but carries taste sensation back to the chorda tympani nerve to the geniculate ganglion of the facial nerve) can also be damaged during otologic surgery, causing a feeling of metal taste.> Problems with the endocrine system:> Deficiency of vitamin B3 (Niacin) and zinc can cause problems with the endocrine system, which may cause taste loss or alteration. Disorders of the endocrine system, such as Cushing's syndrome, hypothyroidism and diabetes mellitus, can cause similar problems.> Ageusia can also be caused by medicinal side-effects from antirheumatic drugs such as penicillamine, antiproliferative drugs such as cisplatin, ACE inhibitors, and other drugs including azelastine, clarithromycin and zopiclone.> Other causes:> Local damage and inflammation that interferes with the taste buds or local nervous system such as that stemming from radiation therapy, glossitis, tobacco abuse, and denture use also cause ageusia. Other known causes include loss of taste sensitivity from aging (causing a difficulty detecting salty or bitter taste), anxiety disorder, cancer, renal failure and liver failure.

Physiology

Misc.

91722c3d-51dc-45b7-88e4-325139b977fe

All of the following can cause osteoporosis, except -

Hyperparathyroidism

Steroid use

Flurosis

Thyrotoxicosis

multi

Osteoporosis It refers to reduction ofbone mass per unit volume (loss of matrix and defective mineralisation) (Fig. 9.47). Aetiology 1.Involutional 2.Endocrinological 3.Gastrointestinal 4.Haematological 5.Rheumatological 6.Collagen vascular Normal bone Type I (postmenopausal) and Type II (senile) Hypehyroidism Hyperparathyroidism Diabetes mellitus Hypogonadism Cushing's syndrome Malnutrition Malabsorption Anorexia nervosa Multiple myeloma Mastocytosis Rheumatoid ahritis Marfan's syndrome Ehler-Danlos syndrome Osteogenesis imperfecta Osteoporosis Fig. 9.47 Anticonvulsants Steroids Vitamin A Alcohol Heparin Furosemide Thyroid hormone in excessive doses Lithium GnRH agonist Cyclosporin Cytotoxic drugs 8.Cigarette smoking 9.Glucocoicoid therapy 10.Hypogonadism 11.Alcoholism 12.Renal disease 13.GI/Hepatic disorders. Bone forming agents a.Fluoride--75 mg/day b.Anabolic steroids: Testosterone is used in the treatment of osteoporotic man with gonadal deficiency. R ALAGAPPAN MANUAL OF PRACTICAL MEDICINE FOUH EDITION PAGE NO-690

Medicine

Endocrinology

befccb93-a1fc-4f0e-a081-96fddab45483

All are hypercoagulable states, except :

Protein C resistance

Factor V Leiden deficiency

Antiphospholipid antibody

Polycythemia

multi

Answer is B (factor V Leiden deficiency) Factor V Leiden mutation (or T Factor V Leiden levels) are associated with a hypercoaguable state and not a Factor V Leiden deficiency. Inherited Defective inhibition of coagulation factors Factor V Leiden (resistant to inhibition by activated protein C) - Antithrombin III deficiency (or resistance) - Protein C deficiency (or resistance) - Protein S deficiency (or resistance) - Prothrombin gene mutation (G20210A) Impaired clot lysis - Dysfibrinogenemia - Plasminogen deficiency - PA deficiency - PAI-I excess Unceain mechanism - Homocystinuria Acquired Diseases or syndromes Lupus anticoagulant/anticardiolipin antibody syndrome Malignancy - Myeloproliferative disorder - Thrombotic thrombocytopenic purpura - Estrogen treatment Hyperlipidemia - Diabetes mellitus Hyperviscosity - Nephrotic syndrome - Congestive hea failure - Paroxysmal nocturnal hemoglobinuria Physiologic states - Pregnancy (especially postpaum) - Obesity - Postoperative state - Immobilization - Old stage

Medicine

3b147043-2a85-4d1b-a67a-a280456bb2f6

Which of the following drugs is used to treat both diabetes mellitus and diabetes insipidus

Chlorpropamide

Glibenclamide

Glicazide

Glipizide

multi

Pharmacology

f4802146-6def-4136-905e-6f2d462b0cf7

A 63-year-old man with insulin-dependent diabetes develops a black, crusting lesion in the nose and left maxillary sinus. Biopsy reveals nonseptate hyphae, which confirms the diagnosis of what? SELECT ONE.

Erysipelas

Eczema

Scarlet fever

Mucor mycosis

single

Mucor is an opportunistic mold that causes mucormycosis. At least 50% of reported cases are associated with uncontrolled diabetes, and many of the remaining patients are immuno- suppressed. It appears as black crusting in the nose and sinuses and spreads rapidly to involve the cerebrum. Biopsy reveals nonseptate hyphae, which confirms the diagnosis. Treatment is directed toward control for diabetic ketoacidosis and use of amphotericin B.

Surgery

Miscellaneous

f0e1adc0-eeb7-43ed-b013-27f0a855961f

A 23-year-old woman is noticed to have irregular pupils on routine examination. She has 1 large pupil, which has minimal response to light stimulation, but it does respond to accommodation. The eye movements are normal and she experiences no double vision.For the above patient with a pupillary abnormality, select the most likely diagnosis.

essential anisocoria

Horner syndrome

tonic pupils (Holmes-Adie syndrome)

Argyll Robertson pupils

multi

The tonic pupil (Holmes-Adie syndrome) is caused by a parasympathetic lesion at or distal to the ciliary ganglion. The pupil is large and usually unilateral, with absent response to light. A bright room, by causing constriction of the normal pupil, accentuates the anisocoria. The tonic pupil can be associated with Shy-Drager syndrome, amyloidosis, or diabetes. However, it is most commonly seen in otherwise healthy young women.

Medicine

C.N.S.

9309b256-ce0c-4567-b8a9-98b29e161a19

A 55 year old diabetic man is brought to the emergency room in an unresponsive state. The following laboratory values are obtained: PCO2 19 mm Hg, HCO3 11 mEq/L, and pH 6.9. The most appropriate immediate treatment of this patient is ?

Administration of an oral hypoglycemic agent

Administration of bicarbonate

Administration of insulin

Close observation only

single

This patient is in a diabetic ketoacidotic coma. The goals in treating such a patient are to increase the rate of glucose utilization by insulin-dependent tissues, to reverse ketonemia and acidosis, and to replenish fluid imbalances. Oral hypoglycemic agents are commonly prescribed for the maintenance of NIDDM patients and would not be appropriate in an acute setting. Treatment with bicarbonate would result in only a transient elevation of pH. Since this is a life-threatening condition, monitoring the patient without treatment is unacceptable. Ref: D'Alessio D. (2011). Chapter 43. Endocrine Pancreas and Pharmacotherapy of Diabetes Mellitus and Hypoglycemia. In B.C. Knollmann (Ed), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e.

Pharmacology

a9bbcbfa-4ce5-4430-9f86-9f855877e4b8

A 50 years old male with type 2 diabetes mellitus is found to have 24-hour urinary albumin of 250 mg. Which of the following drugs may be used to retard progression of the renal disease?

Hydrochlorothiazide

Enalapril

Amiloride

Aspirin

single

Antihypeensive drugs in Diabetes MellitusACE inhibitors (enalapril) or angiotensin receptor blockers are the first line of therapy in hypeensive individuals with type 2 DM.They have no known adverse action on glucose or lipid metabolism.Minimize the development of diabetic nephropathy (by reducing renal vascular resistance and renal perfusion pressure-the primary factor underlying renal deterioration in these patients).(Refer: Harrison's Principles of Internal Medicine, 18th edition, pg no: 2054-2058)

Pathology

All India exam

64258a36-8a3f-4b35-af99-dc8dbc7ab71d

Osteoporosis is seen in all the following except-

Thyrotoxicosis

Rheumatoid ahritis

Hypoparathyroidism

Steroid therapy

multi

Osteoporosis It refers to reduction ofbone mass per unit volume (loss of matrix and defective mineralisation) (Fig. 9.47). Aetiology 1.Involutional 2.Endocrinological 3.Gastrointestinal 4.Haematological 5.Rheumatological 6.Collagen vascular Normal bone Type I (postmenopausal) and Type II (senile) Hypehyroidism Hyperparathyroidism Diabetes mellitus Hypogonadism Cushing's syndrome Malnutrition Malabsorption Anorexia nervosa Multiple myeloma Mastocytosis Rheumatoid ahritis Marfan's syndrome Ehler-Danlos syndrome Osteogenesis imperfecta Osteoporosis Fig. 9.47 Anticonvulsants Steroids Vitamin A Alcohol Heparin Furosemide Thyroid hormone in excessive doses Lithium GnRH agonist Cyclosporin Cytotoxic drugs 8.Cigarette smoking 9.Glucocoicoid therapy 10.Hypogonadism 11.Alcoholism 12.Renal disease 13.GI/Hepatic disorders. Bone forming agents a.Fluoride--75 mg/day b.Anabolic steroids: Testosterone is used in the treatment of osteoporotic man with gonadal deficiency. R ALAGAPPAN MANUAL OF PRACTICAL MEDICINE FOUH EDITION PAGE NO-690

Medicine

Endocrinology

c91799d3-9837-4a4c-8e4d-e2b2976d8e7f

Drug of choice for neurogenic diabetes insipidus

Vasopressin

Terlipressin

Desmopressin

Pralipressin

single

Desmopressin is used to treat neurogenic diabetes insipidus, bedwetting, hemophilia A, von Willebrand disease it acts as an agonist to vasopressin receptor or ADH receptor- produce antidiuresis- less urine production-used in DI, bedwetting, vasoconstriction - used in esophageal varices and produces vwf- used in von Willebrand disease ref KD Tripathi 8th ed

Pharmacology

Kidney

96343aec-f5b4-4eef-8a25-eb597271b931

Hypeonic urine is excreted due to absorption of water in:

Collecting ducts

DCT

Ascending pa of loop of Henley

Descending pa of loop of Henley

single

A i.e. Collecting DuctOsmolality of urine depends on the action of vasopressin on the collecting ductsQ. Alteration in water metabolism by vasopressinUrine isotonic to plasmaGFR (ml/min)% of filteredwaterreabsorbedUrine volume(L/d)Urine concentration(mosm /kg H20)Gain /Loss of water inexcess of solute (L/d)12598.72.4290 Vasopressin present12599.70.51400Q (almost 5 timeof plasma)1.9 gainNo vasopressin (Diabetesinsipidus)12587.123.33020.9 loss

Physiology

b16bee91-a6ce-4cb0-8693-594f08525983

Baby born to DM have following except :

Hypercalcemia

Hypokalemia

Hypoglycemia

Obesity

multi

Ans. is a i.e. Hypercalcemia Neonatal complications of Maternal diabetes : Respiratory distress syndrome (RDS) Hypoglycaemiadeg Hypocalcemiadeg Hypomagnesemia Polycythemia Hyperbilirubinaemia Hyperviscosity syndrome Hyperophic cardiomyopathy Bih trauma - Erb's and Klumpke's paralysis and fractures of the clavicle and humerus due to large size Feeding problems. Late effects : Increased risk of diabetes in children if : If mother is diabetic Risk 1-3% If father is diabetic Risk 6% If both are diabetic - Risk 20% - Self Assessment & Review Obstetrics As far as Hypokalemia is concerned - It is not given anywhere that hypokalemia is seen in neonate of diabetic mother, but we all know that in neonate of diabetic mother hyperinsulinemia is seen. "Insulin causes potassium to shift in to the cells by Na' antipoer and Na' ATPase pump thereby lowers plasma potassium concentration".

Gynaecology & Obstetrics

ea9a7b25-59ee-4f1b-b398-9afb7e6d7373

Earliest clinical indicator of sodium loss is

Altered sensorium

Reduced skin turgor

Arrhythmia

Orthostatic hypertension

single

Ans. a (Altered sensorium) (Ref. Harrison's - 18th/pg. Ch. 45).Hyponatremia may be due to water excess, diabetes, lipidemia etc. Drugs known to release ADH will cause dilutional hyponatremia include morphine, tricyclics, nicotine, NSAIDs, etc. The individual present with confusion, anorexia, lethargy and cramps. When sodium drops abruptly, seizures, hemiparesis and coma can develop.CLINICAL FEATURES OF HYPONATREMIA# The clinical manifestations of hyponatremia are related to osmotic water shift leading to increased ICF volume, specifically brain cell swelling or cerebral edema.# The symptoms are primarily neurologic.# Patients may be asymptomatic or complain of nausea and malaise.# As the plasma Na+ concentration falls, the symptoms progress to include headache, lethargy, confusion, and obtundation.# Stupor, seizures, and coma do not usually occur unless the plasma Na+ concentration falls acutely below 120 mmol/L or decreases rapidly.# Loss of Na+ and K+, followed by organic osmolytes, from brain cells decreases brain swelling due to secondary transcellular water shifts (from ICF to ECF).# The net effect is to minimize cerebral edema and its symptoms.Composition of World Health Organization Oral Rehydration Solution (ORS) A,BConstituentConcentration, mmol/LNa+90K+20Cl-80Citrate10Glucose110Also know:*SLADH is characterized by hypotonic hyponatremia with euvolemia. Low plasma osmolality (<280 mOsm/Kg) with high urine osmolality (>100-150 mOsm/Kg) in suspected patients is diagnostic.* Pneumonia, hyponatremia and diarrhea are almost classic for Legionella.* Under most physiologic conditions, sodium, urea, and glucose generate the osmotic pressure of blood. Plasma osmolality is calculated according to the following expression: Posm = 2Na+ + Glu + BUN (all in mmol/L), or, using conventional laboratory values in which glucose and BUN are expressed in milligrams per deciliter: Posm = 2Na+ + Glu/18 + BUN/2.8. The calculated and determined osmolality should agree within 10-15 mmol/kg H20. When the measured osmolality exceeds the calculated osmolality by >15-20 mmol/kg H20, one of two circumstances prevails. Either the serum sodium is spuriously low, as with hyperlipidemia or hyperproteinemia (pseudohyponatremia), or osmolytes other than sodium salts, glucose, or urea have accumulated in plasma.

Medicine

Fluid & Electrolyte

88224960-32ab-424f-8817-82cb0d84b1fd

Mauriac's syndrome is characterized by all except

Diabetes

Obesity

Dwarfism

Cardiomegaly

multi

Ans. is 'd' i.e., Cardiomegaly Mauriac Sydrome Children with poorly controlled type I diabetes may develop Mauriac syndrome. It is characterized by : - Growth attenuation Delayed pubey Hepatomegaly Abnormal glycogen storage and steatosis Cushingoid features Rare in modern era of insuling therapy but is occasionlly repoed.

Medicine

86275511-77fc-43c3-a868-423d1cde049a

The diabetes control and complication trial (DCCT) provided definitive proof that reduction In chronic hyperglycemia helps to improve -

Microvascular complications of type 1 DM

Microvascular complications of type 1 DM

Microvascular complications of type 2 DM

Macro vascular complications of type 2 DM

single

The Diabetes Control and Complications Trial (DCCT) found definitive proof that a reduction in chronic hyperglycemia can prevent many of the complications of type 1 diabetes mellitus (DM). This multicenter randomized trial enrolled over 1400 patients with type 1 DM to either intensive or conventional diabetes management and prospectively evaluated the development of retinopathy, nephropathy, and neuropathy. The intensive group received multiple administrations of insulin daily along with education and psychological counseling. The intensive group achieved a mean hemoglobin A1C of 7.3% versus 9.1% in the conventional group. Improvement in glycemic control resulted in a 47% reduction in retinopathy, a 54% reduction in nephropathy, and a 60% reduction in neuropathy. There was a nonsignificant trend toward improvement in macrovascular complications. The results of the DCCT showed that individuals in the intensive group would attain up to 7 more years of intact vision and up to 5 more years free from lower limb amputation. Later, the United Kingdom Prospective Diabetes Study (UKPDS) studied over 5000 individuals with type 2 DM. Individuals receiving intensive glycemic control had a reduction in microvascular events but no significant change in macrovascular complications. These two trials were pivotal in showing a benefit of glycemic control in reducing microvascular complications in patients with type 1 and type 2 DM, respectively. Another result from the UKPDS was that strict blood pressure control resulted in an improvement in macrovascular complications Ref - pubmed.com

Medicine

Endocrinology

2c528ae4-9e61-4789-8d93-3c139d02998b

Alopecia areata is not associated with which of the folllowing condition?

Exclamation sign

Atopy

Pitting nails

Geographical tongue

single

Alopecia areata may be associated with atopy, downs syndrome, vitiligo, pernicious anemia, myxedema , diabetes or hypeension in the family. Sho,1-2 mm fractured hairs can frequently be seen at the active margins of alopecia areata. These hairs are described as exclamation mark hairs because these characteristic hairs fracture at their distal end and taper proximally to a pencil point giving them appearance of an exclamation mark . nail pitting is a common finding in alopecia areata . Ref Harrison20th edition pg 1236

Dental

Anatomy of skin

46686ff7-1daf-4389-8788-f82db1916eb0

Cardiomyopathy is/are due to deficinency of:

Selenium

Phosphorus

Boron

Zinc

single

Ans.: A (Selenium) ' Selenium deficiency causes Keshan disease(endemic cardiomyopathy)"Shinde 7th/594Possible causes of cardiomyopathy include; www.may- odinic.com/heaith/cardiomyopa thy/DS00519/DSECTION# Long-term high blood pressure# Defects in heart valve# Heart tissue damage from a previous heart attack# Chronic rapid heart rate# Metabolic disorders, such as thyroid disease or diabetes# Nutritional defdencies of essential vitamins or minerals, such as thiamin (vitamin B-l), selenium, calcium and magnesium# Pregnancy# Excessive use of alcohol over many years# Abuse of cocaine or antidepressant medications, such as tricyclic antidepressantsUse of some chemotherapy drugs to treat cancerSome viral infections, which may injure the heart and trigger cardiomyopathyIron buildup in your heart muscle (hemochromatosis)Genetic conditionsReversible cardiomyopathy due to carnitine deficiency from renal tubular wasting.Table (Harrison 18th/595): Deficiencies of MetalsElementDeficiencyBoronNo biologic function determinedCalciumReduced bone mass, osteoporosisCopperAnemia,, growth retardation, defective keratinization and pigmentation of hair, hypothermia, degenerative changes in aortic elastin, osteopenia, mental deteriorationChromiumimpaired glucose toleranceFluoride| Dental cariesIodineThyroid enlargement, |T4, cretinismIronMuscle abnormalities, koilonychia, pica, anemia, 4work performance, impaired cognitive development, premature labor, Tperinatal maternal mortalityManganeseImpaired growth and skeletal development, reproduction, lipid and carbohydrate metabolism; upper body rashMolybdenumSevere neurologic abnormalitiesSeleniumCardiomyopathy, heart failure, striated muscle degenerationPhosphorusRickets (osteomalacia), proximal muscle weakness, rhabdomyolvsis, paresthesia, ataxia, seizure, confusion, heart failure, hemolysis, acidosisZincGrowth retardation, !taste and smell, alopecia, dermatitis, diarrhea, immune dysfunction, failure to thrive, gonadal atrophy, congenital malformations

Biochemistry

Nutrition & Digestion

84005893-dc82-4db3-bbb5-1cb3b0728506

The parents of a 2-year-old boy with hyposadias (urethra opens on the ventral aspect of the penis) visit a genetic counselor to discuss the chances that a similar birth defect will occur in their future offspring. This birth defect shows which of the following patterns of inheritance?

Autosomal recessive

Autosomal dominant

Multifactorial

X-linked dominant

single

The inheritance of a number of birth defects is multifactorial. Most normal human traits are inherited neither as dominant nor as recessive mendelian attributes, but rather in a more complex manner. For example, multifactorial inheritance determines intelligence, height, skin color, body habitus, and even emotional disposition. Similarly, most of the common chronic disorders of adults represent multifactorial genetic diseases and are well known to "run in families." Such maladies include diabetes, atherosclerosis, and many forms of cancer and arthritis, and hypertension. The inheritance of a number of birth defects is also multifactorial (e.g., cleft lip and palate, pyloric stenosis, hypospadias, and congenital heart disease). The concept of multifactorial inheritance is based on the notion that multiple genes interact with various environmental factors to produce disease in an individual patient. Such inheritance leads to familial aggregation that does not obey simple mendelian rules (see choices A, B, D, and E). As a consequence, the inheritance of polygenic diseases is studied by the methods of population genetics, rather than by the analysis of individual family pedigrees.Diagnosis: Hypospadias, multifactorial inheritance

Pathology

Genetics

93c6d428-1715-4e72-9938-95e966efb2ff

Which of the following tests are used to screen for gestational diabetes in a 22 year old primigravida?

Oral glucose tolerance test

Fasting blood sugar

Glycocyalted hemoglobin measurement

Random glucose challenge

multi

Glucose challenge test (GCT) is commonly used in screening for gestational diabetes. No special preparation is needed for this test. Fifty grams of oral glucose is given between 24-28 weeks of gestation irrespective of the time or the meal and blood glucose is determined 1 hour later. A plasma value of 140 mg/dl is considered significant to perform the confirmatory diagnostic test. Ref: Essential of Obstetrics By Arulkumaran, 2004, Page 149 ; Dutta, 6th ed, Page 285

Gynaecology & Obstetrics

0694bf16-506e-4ff8-9d70-4957cc848008

Atherosclerosis is due to

HDL receptor defect

Apo protein E deficiency

Decreased LDL activity

Decreased lipoprotein lipase

single

Atherosclerosis is a slowly progressive disease of large to medium-sized muscular aeries and large elastic aeries characterised by elevated focal intimal fibrofattyPlaques. Principal larger vessels affected are the abdominal aoa, descending thoracic aoa, internal carotid aeries and medium to smaller sized vessels affected are popliteal aeries, coronary aeries, and circle of Willis in brain. The atheroma may be preceded by fatty streaks that are intimal collection of lipid-laden macrophages and smooth muscle cells, occurring in persons as young as one year of age.The disease typically manifests in later life as the vessel lumen is compromised, predisposing to thrombosis and the underlying media is thinned, predisposing to aneurysm formation. It is the number one killer disease, 50 per cent of all deaths in the USA are attributed to atherosclerosis and half of theseare due to acute myocardial infarctions. The remainder include cerebrovascular accidents ("stroke"), aneurysm rupture, mesenteric occlusion and gangrene of theextremities. Etiological Factors Major risk factors in CHD have been discussed earlier. Risk of developing atherosclerosis increases with age, a positive family history, cigarette smoking, diabetes mellitus, hypeension, and hypercholesterolemia. The risk is correlated with elevated LDL and inversely related to the HDL level. Hereditary defects, e.g. familial hypercholesterolemia involving the LDL receptor or the LDL apoproteins cause elevated LDL, hypercholesterolemia andaccelerated atherosclerosis. Lesser influences on the risk of atherosclerosis include sedentary, or high-stress lifestyle, obesity and oral contraceptives.Ref: M.N. Chatterjee - Textbook of Biochemistry, 8th edition, page no: 454 - 456

Biochemistry

Metabolism of lipid

f196ff59-2196-4fd8-bc54-b48aa0acd09b

A 50 years old man was recently diagnosed to be having coronary artery disease. There was no added risk factors except for a LDL value of 150-165mgs/dl. The single drug most appropriate for initial therapy is

Gemfibrozil

Nicotinic acid

Bile acid binding resins

Statins (Any)

multi

Answer: d) Statins (any)DYSLIPIDEM1AType of disorderLipo Proteins increasedLipids elevatedRisk of CADtreatmentTri GlyceridesCholesterolICM+++NormalNoNoneIIaLDLNormal+++++StatinsIIbVLDL and LDL+++++++Statins, fibrates, nicotinic acidIIIIDLand CM++++++FibratesIVVLDL++Normal++Fibrates, nicotinic acidVVLDL and CM++NormalNoNone* TG is elevated in all except type lla; Cholesterol is elevated only in type II (lla, lib) and type III.* Type II is treated with statins and III and IV with fibrates.* I and V do not increase the risk of atherosclerosis and require no treatment. DesirableBorderline to highHighTotal cholesterol<200200-239>240LDL cholesterol<130130-159>160HDL cholesterol >60Men>40 Women>50 Triglycerides<150150-199>200CAUSES OF:HypercholesterolemiaHypertriglyceridemia* Hypothyroidism* Early nephrosis* Resolving lipemia* Immunoglobulin- lipoprotein complex disorders* Anorexia nervosa* Cholestasis* Hypopituitarism* Corticosteroid excess* Diabetes mellitus* Alcohol ingestion* Severe nephrosis* Immunoglobulin- lipoprotein complex disorders* Lipodystrophy* Isotretinoin* Protease inhibitors* Estrogens* Uremia* Corticosteroid excess* Myxedema* Glycogen storage disease* Hypopituitarism* AcromegalyANTI - PYSLIPIDEMIC DRUGS* HMG-CoA reductase inhibitors (Statins): Lovastatin, Simvastatin, Pravastatin, Atorvastatin, Rosuvastatin, Pitavastatin* Bile acid sequestrants(Resins): Cholestyramine, Colestipol* Lipoprotein lipase activators (PPARa activators, Fibrates): Clofibrate, Gemfibrozil, Bezafibrate, Fenofibrate.* Lipolysis and triglyceride synthesis inhibitor: Nicotinic acid* Sterol absorption inhibitor: Ezetimibe.* First line drugs - statins, bile acid binding resins and intestinal cholesterol absorption inhibitors.* Second line drug include fibrates and niacin.STATINS: (HMG CoA reductase inhibitor)* Most powerful LDL lowering agents, also lower TG, IDL and VLDL and increases HDL slightly.* No effect on lipoprotein (a).* Have pleotropic effects (antioxidant, anti-inflammatory and anti-proliferative properties).* In response to the reduced free cholesterol content within hepatocytes, synthesis of LDL receptors is increased and their degradation is reduced.* The greater number of LDL receptors on the surface of hepatocytes increases removal of LDL from the blood* Most potent statin is rosuvastatin > atorvastatin >fluvastatin and lovastatin(least potent)* Activity of HMG CoA reductase is maximum at night, so these drugs are administered at night.* Rosuvastatin (ti/2 =14 hours) -long acting drug,* Pravastatin: decreases plasma fibrinogen levels.* Lovastatin and simvastatin are administered as prodrugs.* All drugs except Pravastatin are metabolized extensively by hepatic microsomal enzymes.* Statins have pleiotropic effects (effects unrelated, or indirectly related, to their effect on plasma LDL)o Improved endothelial functiono Reduced vascular inflammationo Reduced platelet aggregabilityo Increased neovascularisation of ischaemic tissueo Increased circulating endothelial progenitor cellso Stabilisation of atherosclerotic plaqueo Antithrombotic actionso Enhanced fibrinolysiso Inhibition of germ cell migration during developmento Immune suppressiono Protection against sepsis.* Major adverse effect - myopathy (high when combined with fibrates or niacin) & hepatotoxicity* These drugs are the first line drugs for type lla, type lib and secondary hyperlipoproteinemia.BILE ACID BINDING RESINS* Bind to bile acids in the intestinal lumen - decrease its reabsorption - depletion of cholesterol pool of liver* Bile acids inhibit TG production in the liver and their deficiency results in elevation of TGs.* Bile acid binding resins are used only for type lla disorder (TGs are normal in this condition). Drugs in this group include cholestyramine, colestipol and colesevelam (better compliance).FIBRATES* Inhibits lipoprotein lipase by activating a nuclear receptor, PPARa (peroxisome proliferators activated receptor alpha).* Major effect of the fibrates is to reduce TG (contained in VLDL) and to increase HDL.* Clofibrate - malignancies, post cholecystectomy complications & did not prevent Ml (banned now).* Gemfibrozil, fenofibrate and bezafibrate are currently available.* Fenofibrate is a prodrug with longest half life. It has maximum LDL cholesterol lowering action.* Risk of myopathy is lower & also reduce plasma fibrinogen level.* DOC in hypertriglyceridemia (type III and IV) and can be used with other drugs in type Mb (fenofibrate, as it has maximum LDL reducing action).* DOC for treating type III hyperlipoproteinemia as well as subjects with severe hypertriglyceridemia (triglycerides >1000 mg/dL) who are at risk for pancreatitis.* Fenofibrate is uricosuric -can be used in hyperuricemia.* Fenofibrate: risk of elevation of creatinine.* Gl distress and elevation of aminotransferases are important adverse effects of fibric acid derivatives.* Risk of myopathy is increased if used with statins (except bezafibrate).NICOTINIC ACID (Niacin, (vitamin B3))* Decreases LDL, VLDL and triglycerides along with increase in HDL cholesterol.* Acts by inhibiting lipolysis in the adipose tissue.* Among all hypolipidemic drugs, niacin has maximum HDL increasing property.* Niacin is the only lipid-lowering drug that reduces Lp(a) levels significantly, by "40%;* It is useful for type lib, III and IV disorders.* Adverse effects: cutaneous flushing, pruritis, Gl toxicity and hyperuricemia. Niacin can also lead to hepatotoxicity which is manifested by fall in both LDL as well HDL cholesterol.INTESTINAL CHOLESTEROL ABSORPTION INHIBITOR* Ezetimibe acts by inhibiting the absorption of cholesterol by the intestine by blocking uptake via the Neimann-Pick C-like 1 protein.* Can be used alone or combined with statins for type lla and lib hyperlipoproteinemia.MISCELLANEOUS DRUGS* Probucol inhibits oxidation of LDL and cause reduction in levels of both HDL and LDL cholesterol.* Gugulipid causes modest decrease in LDL & slight increase in HDL. Diarrhea is the adverse effect.* Saroglitazar: dual PPAR- and PPAR-agonist. Novel therapeutic agent for diabetic dyslipidemia. Decreases serum triglycerides, HbAlC & increases HDL cholesterol. Dosage: 4mg OD* a-tocopherol acetate (vitamin E) has no effect on lipid levels but is a powerful antioxidant.* Niacin is the best agent available for increasing HDL (increments of 30-40%); it also |, triglycerides by 35-45% (as effectively as fibrates & statins) and |, LDL levels by 20-30%* Changes in plasma lipoprotein levels, particularly increases in high-density lipoprotein (HDL), have been associated with the protective effects of ethanol.* Factors associated with elevation of plasma FFA followed by increased output of triacylglycerol and cholesterol into the circulation in VLDL include emotional stress and coffee drinking.* Red wine increases HDL, because of its content of antioxidants.* Regular exercise lowers plasma LDL but raises HDL.NEWER DRUGS* Avasimibe is an inhibitor of enzyme ACAT-1 (acetyl coenzyme A: cholesterol acetyl transferase -1) which forms cholesterol ester from cholesterol.* Torcetrapib, Anacetrapib: increases HDL by inhibiting cholesterol ester triglyceride transport protein.ALCOHOL* Regular alcohol consumption inhibits hepatic oxidation of free fatty acids, thus promoting hepatic TG synthesis and VLDL secretion.* Regular alcohol use also raises plasma levels of HDL-C and should be considered in patients with the unusual combination of elevated TGs and elevated HDL-C.DrugEffect on LDLEffect on TriglyceridesEffect on HDLStatins||||||||Fibrates||||||||Niacin|||||||||Bile acid Winding resins|||Minimal/ slight increase|Cholesterol Absorption In tilts It ors|Minimal EffectMinimal Effect

Pharmacology

Hypolipidemic

b3e71cfc-3dce-4058-bdf0-3699eef53091

Which of the following types of pancreatitis has the best prognosis

Alcoholic pancreatitis

Gall stone pancreatitis

Post operative pancreatitis

Idiopathic pancreatitis

multi

.Ranson's prognostic criteria On admission:--* Old age >55 years * Blood sugar >200 mg% * TC >16,000/mm3 * Serum LDH > 350 IU/L * Serum SGOT > 250 IU/L In 48 hrs: * Base deficit > 4 mEq/L * Serum calcium < 8 mEq/L * Haematocrit : altered by 10% * Aerial O2 (PO2) < 60 mm Hg * Extravascular space fluid loss: > 6 * Blood urea (BUN) altered > 5 mg% of the normal Total score is 11 Scores up to 5 -- better prognosis 5-7 -- equivocal--but dangerous >7 -- is highly dangerous Glasgow criteria-* Age > 55 years * PO2 < 8 KPa * Total count >15000 cells/mm3 * Serum calcium < 2 mmoles/L * Blood urea > 16 mmol/L * Blood glucose > 10 mmols/L (200 mg%, no H/O diabetes) * SGPT > 200 IU/L * LDH > 600 U/L * Serum albumin < 3.2 gm/dl Note: * Decrease serum calcium level is worst prognostic indicator of pancreatitis. * These scoring systems differ for non gall stone pancreatitis and gall stone pancreatitis. * Other scoring systems which are often used are APACHE II (Acute Physiology And Chronic Health Evaluation II) and SAP (simplified acute physiology) scoring systems. Twelve variables are used to assess in APACHE II scoring. ref:SRB&;S manual of surgery,ed 3,pg no 620

Surgery

G.I.T

a819d1ee-14d4-4562-a5df-e90f5b4020f1

A patient presents with melaena normal renal function, hypeension and mononeuritis multiplex. The most probable diagnosis is:

Classical polyaeritis nodosa

Microscopic polyangiitis

Henoch-Schonlein purpura

Buerger's disease

multi

Answer is A (Classic PAN) : Amongst the options provided, mononeuritis multiplex is a feature of classical PAN and microscopic polyangitis. Presence of hypeension (infrequent in microscopic polyangitis) and normal renal function (infrequent in microscopic polyangitis) leads us to a diagnosis of classical polyaeritis nodosa. Renal involvement in classic PAN Pathology in kidney is that of aeritis without glomeruionephritis (involves small & medium sized muscular aeries) Renal impairment is uncommon-- Hypeension is frequent Renal involvement is mainly in the form of Renovascular hypeension . Renal involvement in microscopic polyangitis Pathology in kidney is that of glomerulonephritis Rapid renal impairment is characteristic-- API 7th/1183 Hypeension is infrequent-API 7th/1183 Causes of mononeuritis multiplex : Common causes Uncommon causes Classic polaeritis nodosa Mixed cryoglobulinemia Microscopic polyangitis Sjogren syndrome RA Wegner's granulomatosis SLE Progressive systemic sclerosis Mixed connective tissue disease Churg-strauss allergic granulomatosis Hypersensitivity angitis Leprosy Amyloidosis Diabetes

Medicine

c208136e-f01f-4dfd-9666-d6dfeadfd8c5

Ebstein anomaly is known teratogenic effect due to this drug:

Clozapine

Phenytoin

Lithium

Lamotrogine

single

(Ref: Katzung, 14th ed. pg. 527)* Lithium is DOC in manic disorder.* DOC for prophylaxis of mania: Lithium* DOC for acute attack of mania: Sedative + Atypical antipsychotics* DOC for mania in pregnancy: Atypical antipsychotics* Side effect of lithium (Mn: LITTH)# L: LEUCOCYTOSIS# I: Insipidus diabetes# T: Tremors (MC side effect- Coarse tremor)# T: Teratogenic (Ebstein anomaly)# H: HypothyroidismTherapeutic Plasma concentration of Lithium* Acute mania: 0.8-1.4mEq/L* Prophylaxis: 0.5-0.8mEq/L* Toxic plasma cone level:>2mEq/L

Pharmacology

C.N.S

f96ed7ff-a25e-4357-9306-6b77f1bf1f68

Criteria for a pancreas donor include:

No history of diabetes

No liver donation

No replaced hepatic aery vessels arising from the superior mesenteric aery (SMA)

No previous splenectomy

single

- Combined liver-pancreas procurement should be routine, even if the right hepatic aery arises from the superior mesenteric aery. - In this situation, since the transplanted liver is the life-saving organ, the proximal superior mesenteric aery should remain with the liver and the distal superior mesenteric aery supplying the head of the pancreas can be reconstructed on a Y-graft of iliac aery with the splenic aery. - Successful pancreas transplantation can be performed using donors who have previously undergone splenectomy; however, there should be no significant pancreatitis and no history of diabetes in the donor.

Surgery

Transplantation

b137d458-4957-4d0b-92ef-d242a3a820da

All are true about Exenatide except -

Decreases glucagon secretion

It is GLP 1 analogue

Used in type 1 DM

Given subcutaneously

multi

Ans. is 'c' i.e., Used in type I diabetes mellitus Exenatide is a synthetic glucagon-like peptide -1 (GLP-l) analogue. o It acts similar to GLP-1 --> Enhancement of postprandial insulin release, suppression of glucagon release and appetite as well as slowing of gastric emptying. o It is given by subcutaneous route & used in type 2 DM

Pharmacology

d4d3c56d-5b55-49bf-845b-4128ff053407

True regarding level of sugar in hyperosmolar non ketotic hyperglycemia is: September 2005

No change

Mild elevation

Moderate elevation

Severely elevated

multi

Ans. D: Severely elevated Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) is being diagnosed with increasing frequency in obese children with type 2 diabetes mellitus (T2 DM). The syndrome is characterized by severe hyperglycemia, a marked increase in serum osmolality and dehydration without accumulation of beta-hydroxybutyric or acetoacetic ketoacids. Significant ketogenesis is restrained by the ability of the pancreas to secrete small amount of insulin. Prolonged phase of osmotic diuresis leads to severe depletion of body water, which exceeds that of sodium, resulting in hypeonic dehydration. These children, usually obese adolescents with T2 DM, present with signs of severe dehydration and depressed mental status but continue to have increased rather than decreased urine output and are at increased risk of developing rhabdomyolysis and malignant hypehermia.

Medicine

404aed9d-7bb7-4437-aa22-432f9fd368cf

Cutaneous sign of diabetes mellitus are all except

Necrobiosis lipoidica

Carotinosis

Shin spots (granuloma annulare)

Angiokeratomas

multi

Ans: d (Angiokeratomas)Ref: IADVL, 3rd ed. vol. 2 pg. 1369- 1371Angiokeratoma corporis diffusum is a manifestation of Fabry's disease. All others are dermatological manifestations of diabetes mellitus.Skin manifestations of diabetis mellitus: Diabetic dermopathy Pigmented pretibial papules Shin spots Necrobiosis lipoidicaClear cell syringoma Diabetic bullae Xanthoma rubeosis

Skin

Miscellaneous

dcff52be-fb5b-4119-9e1e-12ed61aa183a

Indications of prophylactic cholecystectomy are all except

Diabetes

Hemoglobinopathy

Gallstone size >3 cm

Porcelain GB

multi

Diabetes Mellitus Patients with diabetes may have a higher incidence of gallstones from the indirect effects of the metabolic syndrome, obesity, and a family history of gallstones No data show worse evolution of asymptomatic cholelithiasis in diabetes, and prophylactic cholecystectomy in asymptomatic gallstones carriers with diabetes is not recommended Ref: Blumga 5th edition Pgno : 486

Anatomy

G.I.T

d043103e-7fb1-4308-bf51-749be1cdab13

True about Type 1 diabetes mellitus

Decreased hepatic Glucose output

Increase glucose uptake

Increased lipolysis

Decreased protein catabolism

multi

* Patients may become hyperglycemic in poorly controlled type 1 diabetes mellitus . The reason being - due to lack of insulin to stimulate uptake and utilization of glucose and also because in the absence of insulin which antagonize the actions of glucagon, there is increase in gluconeogenesis from amino acids in liver. * Lack of insulin (which antagonize the actions of glucagon) results in increased lipolysis in adipose tissue , and the resultant NEFAs become substrates for ketogenesis in the liver. There is defect in the utilization of ketone bodies in muscle because of lack of oxaloacetate . * In uncontrolled diabetes, ketosis is severe enough to cause pronounced acidosis (ketoacidosis). * Coma results from both the acidosis and also the considerably increased osmolality of extracellular fluid (mainly as a result of the hyperglycemia, and diuresis resulting from the excretion of glucose and ketone bodies in the urine). Ref:- Harper 30/e; pg num:- 149

Biochemistry

Metabolism of carbohydrate

7c49853e-b89a-4f3c-8191-83ae435071fb

X-linked muscular dystrophy is?

Myotonic dystrophy

Spinal muscular atrophy

Neurogenic muscular atrophy

Duchene muscular dystrophy

single

Ans. is 'd' i.e., Duchenne's muscular atrophy X-linked Recessive disordersMusculoskeletalHematologicalImmuneMetabolicNervous* Duchene muscular dystrophy* Chronic granulomatous disease* Hemophilia A & B* G-6-PD deficiency* Agamma - globulinemia* Wiskott - Aldrich synd.* Diabetes insipidus* Lesch Nyhan syndrome* Fragile - X- syndrome* Colour blindnessX-linked dominant disorders* Vitamim D resistant (X-linked hypophosphatemic) Rickets.* Familial hypophosphatemia.* Incontinentia pigmenti.

Pathology

Genetics

a2cba597-3313-4eb2-a461-1dfca7333cc7

All of the following can cause DIC during pregnancy except:

Diabetes mellitus

Amniotic fluid embolism

Intrauterine death

Abruptio placentae.

multi

Ans. is a, i.e. Diabetes mellitusDIC is a pathological condition associated with inappropriate activation of coagulation and fibrinolytic system. It is a secondary phenomenon resulting from an underlying disease state.Obstetric conditions associated with DIC:More commonLess common* Intrauterine fetal death* Chorioamnionitis* Amniotic fluid embolism* Pyelonephritis in pregnancy* Pre eclampsia- Eclampsia* H. mole* HELLP syndrome* Instillation of intraamniotic hypertonic saline* Placenta Abruption* Feto maternal bleed* Septic Abortion* Incompatible blood transfusion* Viremia -HIV, varicella, CMV hepatitis. COGDT p 997Pathogenesis:

Gynaecology & Obstetrics

Antepartum Haemorrhage

61569796-c7f7-4681-a4d7-e8657633db3b

All of the following are causes of acalculous cholecystitis except

Bile duct stricture

Schitosoma

Prolonged TPN

Major operations

multi

Causes of Acalculous cholecystitis Common causes Elderly and critically ill patients after trauma Burns Longterm TPN Major operations(Abdominal aneurysm repair and cardiopulmonary bypass) Diabetes mellitus Uncommon causes Vasculitis Obstructing GB adenocarcinoma GB torsion Parasitic infestation Unusual bacterial infection - Leptospira, streptococcus, salmonella , Vibrio cholera Ref: Harrison's 19th edition Pgno : 2081

Anatomy

G.I.T

3afea785-3cae-40c0-b566-52f38010c446

The complication of diabetes which cannot be prevented by strict control of blood sugar is -

Amyotrophy

Nerve conductivity

Macular edema

Microalbuminuria

single

Ans. is 'c' i.e., Macular edema o The DCCT demonstrated that improvement of glvcemia controly Reduced nonproliferative and proliferative retinopathy (47% reduction).y Microalbuminuria (39% reduction).y Clinical nephropathy (54% reduction).y Neuropathy (60% reduction).y Improved glycemic control also slowed the progression of early diabetic complication.y There vras a nonsignificant trend in reduction of macrovascular events during the trial.o The UKPDS demonstrated that each percentage point reduction in AIC was associated with a 35% reduction in microvascular complications.

Medicine

Diabites & Inappropriate Antidiuretic Hormone

638da813-7930-423d-8edf-5d99478f4aff

A 70-year-old man with a history of diabetes presents with severe pain in his right ear. The patient was diagnosed with external otitis. Further tests suggested that the patient suffered bone and nerve damage. Clinical laboratory analysis showed that the isolated microorganism produced a distinct blue pigment as well as an ADP-ribosylation toxin. What is the most likely causative agent?

Staphylococcus epidermidis

Staphylococcus aureus

Pseudomonas aeruginosa

Enterococcus faecalis

single

External otitis or swimmer's ear is an inflammation of the outer ear and the ear canal. In the virulent form of the disease-malignant external otitis, which occurs in people with diabetes, damage to the cranial nerves and bone may occur. External otitis is caused by either bacterial or fungal pathogens. Bacterial pathogens include Pseudomonas aeruginosa, Staphylococcus aureus, Staphylococcus epidermidis, and Enterococcus faecalis. Fungal pathogens include Candida albicans and Aspergillus spp. The majority of bacterial external otitis is caused by P. aeruginosa. P. aeruginosa produces pyocyanin, which is a blue pigment that catalyzes the production of superoxide and hydrogen peroxide. Pyocyanin also stimulates the release of IL-8 (CXCL8 in humans). P. aeruginosa also produces exotoxin A, which ADP-ribosylates EF-2 in the eukaryotic cell leading to the cessation of protein synthesis and cell death. Neither pyocyanin nor exotoxin A is produced by the other pathogens listed (S. aureus, S. epidermidis, E. faecalis, and C. albicans).

Microbiology

Bacteria

dcec74e5-ffd7-49e2-b935-45d850b235d6

Which of the following condition is not true about Hemochromatosis?

Hypogonadism

Ahropathy

Diabetes mellitus

Desferrioxamine is treatment of choice

multi

Phlebotomy is the treatment of choice of hemochromatosis. Chelating agent desferrioxamine is indicated when anemia or hypoproteinemia is severe enough to preclude phlebotomy. Hemochromatosis is a common inherited disorder of iron metabolism in which dysregulation of intestinal iron absorption results in deposition of excessive amounts of iron in parenchymal cells resulting in tissue damage and organ dysfunction. Liver is the first organ to be affected and hepatomegaly is seen in more than 95% of patients. Diabetes mellitus occur in 65% of patients with advanced disease. Ahropathy is seen in 20-25% of symptomatic patients. Second and third metacarpophalangeal joints are the first joints to be involved. Manifestations of hypogonadism includes loss of libido, impotence, amenorrhea, testicular atrophy and gynecomastia. Most common cardiac manifestation is congestive hea failure.

Medicine

dd418072-cc4b-4cbf-9612-6c013781d955

Pramlintide is ?

Synthetic amylin analogue

Inhibitor of DPP 4

GLP 1 analogue

PPAR gamma

single

Ans. is 'a' i.e., Synthetic amylin analogue NEWER ANTIDIABETIC DRUGS Exenatide Exenatide is a synthetic glucagon-like peptide - 1 (GLP-1) analogue. GLP-1 is an impoant incretin that is released from gut in response to oral glucose. But GLP-1 can not be used clinically as it is degraded rapidly by enzyme dipeptidly peptidase - (DPP-4). Exenatide is resistant to DPP-4. It acts similar to GLP-1 - Enhancement of postprandial insulin release, suppression of glucagon release and appetite as well as slowing of gastric emptying. It is given by subcutaneous route & used in type 2 DM Nausea is most impoant side effect. Sitagliptin This is orally active inhibitor of DPP-4. It prevents degradation of endogenous GLP-1 and other incretins, potentiating their action, resulting in limitation of postprandial hyperglycemia. It is used in type 2 DM. Other DPP-4 inhibitor is vildagliptin Pramlintide This is a synthetic amylin analogue (Amylin is a polypeptide produced by pancreatic (3-cells which reduces glucagon secretion from a-cells and delays gastric emptying). Pramlintide attenuates postprandial hyperglycemia and exes a centrally mediate anorectic action. o It is given by subcutaneous route and is used in both Type 1 and Type 2 DM. Glucomannan This is powdered extract from tuber of konjar. It is promoted as a dietary adjunct for diabetes. It swells in stomach by absorbing water and is claimed to reduce appetite, blood sugar, serum lipids and relieve constipation. Bromocriptine Recently bromocriptine has been approved by FDA, as an adjunct to diet and exercise to improve glycemic control in type 2 DM. It has been found that dopamine alter insulin resistance by acting on hypothalmus and bromocriptine blocks O2 receptors.

Pharmacology

f9f1fa00-f4e6-4a9f-9c67-98f6cfef96ad

A 28-year-old woman with diabetes presents with lesions on her leg. They are not painful, and have a central depression and raised irregular margin. Which of the following is the most likely diagnosis?

eruptive xanthomas

necrobiosis lipoidica diabeticorum

gangrene

staphylococcal infection

single

(b) Source: (Kasper, p. 2169)This lesion is more frequent in females and may antedate other clinical signs and symptoms of diabetes. The plaques are round, firm, and reddish-brown to yellow in color. They most commonly involve the legs but can also involve the hands, arms, abdomen, and head.

Medicine

Endocrinology

0f86537a-a64f-4d10-a49e-60b77abeaeb3

True about Post traumatic fat embolism syndrome is A/E

Bradycardia occur

Systemic hypoxia may occur

Fracture mobility is a risk factor

Associated diabetes pose a risk

multi

D i.e. Associated diabetes pose a risk. Fat Embolism Syndrome A syndrome caused by an inflammatory response to embolized fat globules Symptoms usually occur 1-3 days after a traumatic injury and are predominantly pulmonary (shoness of breath, hypoxemia), neurological (agitation, delirium, or coma), dermatological (petechial rash), and haematological (anaemia, low platelets). Epidemiologyincidence 3-4% with isolated long bone trauma 10-15% with polytrauma Pathophysiologyfat and marrow elements are embolized into the bloodstream during acute long bone fractures intramedullary instrumentation intramedullary nailing hip & knee ahroplasty pathophysiologytwo theories regarding the causes of fat embolism includemechanical theory embolism is caused by droplets of bone marrow fat released into venous system metabolic theory stress from trauma causes changes in chylomicrons which result in formation of fat emboli Diagnosis CriteriaMajor (1) hypoxemia (PaO2 < 60) CNS depression (changes in mental status) petechial rash pulmonary edema Minor (4) tachycardia pyrexia retinal emboli fat in urine or sputum thrombocytopenia decreased HCT Additional PCO2 > 55 pH < 7.3 RR > 35 dyspnea anxiety TreatmentNonoperative mechanical ventilation with high levels of PEEP (positive end expiratory pressure) indications acute fat emboli syndrome Preventionearly fracture stabilization indications early fracture stabilization (within 24 hours) of long bone fracture is most impoant factor in prevention of FES techniques to reduce the risk of fat emboli overreaming of the femoral canal during a TKA use of reamers with decreased shaft width reduces the risk during femoral reaming for intramedullary fixation use of external fixation for definitive fixation of long bone fractures in medically unstable patients decreases the risk

Surgery

e1ea8dcc-206e-4e9e-9a8f-8e453a6b27ff

An elderly male accompanied by his son.The son tells his father has fever, cough, shoness of breath since 2 weeks. The patient is a known case of chronic bronchitis and diabetes. Travel history to Wuhan City, China is present. What is the symmetry of the causative virus?

Naked helical symmetry

complex symmetry

Enveloped helical symmetry

Icosahedral symmetry

single

The patient is suffering from coronavirus disease 2019. The symmetry of the causative virus is enveloped helical symmetry. Coronaviridae is a family of which have the following propeies: Unsegmented genome of positive-sense, single-stranded RNA viruses. They are enveloped viruses. They exhibit helical symmetry. Coronavirus is the causative agent of severe acute respiratory syndrome (SARS-CoV). Viruses with Helical Symmetry: Mnemonic: ABC FOR PARAmedics Arenavirus Bunyavirus Coronavirus Filovirus Ohomyxovirus Rhabdovirus Paramyxovirus Reference: Ananthanarayan and Paniker&;s Textbook of Microbiology Tenth edition

Microbiology

Virology

50f415e5-550c-403b-9173-77d734723012

Which of the following does not cause Polyuria?

Interstitial nephritis

Hypokalemia

A.D.H insufficiency

Rhabdomyolysis

single

Rhabdomyolysis leads to myoglobinuria which leads to blockage of tubules and thereby reduction of urine output. Interstitial nephritis is characterized by tubular damage leading to polyuria. Hypokalemic nephropathy in choice B and ADH insufficiency (diabetes insipidus) in choice C leads to Polyuria.

Medicine

Nephrotic and Nephritic syndrome

dc5e4fb4-834c-4460-9237-6dc7165e4bc4

Monogenic transmission of diabetes mellitus occurs in:

Insulin Dependent Diabetes Mellitus (IDDM)

Non-insulin Dependent Diabetes Mellitus (NIDDM)

Latent Autoimmune Diabetes in Adults (LADA)

Maturity Onset Diabetes of the Young (MODY)

single

d. Maturity Onset Diabetes of the Young (MODY)(Ref: Nelson's 20/e p 2760-2780, Ghai 8/e p 541-548)MODY refers to forms of diabetes are associated with monogenic defects in pancreatic b-cell function.

Pediatrics

Endocrinology

5ee69c94-23d1-4c09-95cb-cd003d6c1915

Not a fungal infection is:

Mycoses fungoides

Tinea nigra Palmaris

White Piedra

Black Piedra

single

Ans: A (Mycoses fungoides) Ref: Rook's Dermatology, 8th ed.Explanation:Mycosis Fungoides/Sezary SyndromeMycosis fungoides and Sezary syndrome are different manifestations of a tumor of CD4+ helper T cellsClinically, the cutaneous lesions of mycosis fungoides typically progress through three somewhat distinct stages, an inflammatory premycotic phase, a plaque phase, and a tumor phaseHistologically, the epidermis and upper dermis are infiltrated by neoplastic T cells, which often have a cerebriform appearance due to marked infolding of the nuclear membrane.Sezary syndrome is a variant in which skin involvement is manifested as a generalized exfoliative erythroderma.In contrast to mycosis fungoides, the skin lesions rarely proceed to tumefaction, and there is an associated leukemia of "Sezary" cells with characteristic cerebriform nuclei.The tumor cells express the adhesion molecule CLA and the chemokine receptors CCR4 and CCR10Transformation to aggressive T-cell lymphoma occurs occasionally as a terminal event.FUNGAL INFECTIONSNatural defence against fungiFatty acid content of the skinpH of the skin, mucosal surfaces and body fluidsEpidermal turnoverNormal floraPredisposing factorsTropical climate, Manual labour populationLow socioeconomic status. Profuse sweatingFriction with clothes, synthetic innerwearMalnourishment, Immunosuppressed patientsHIV, Congenital Immunodeficiencies, patients on corticosteroids, immunosuppressive drugs. DiabetesFungal Infections: ClassificationSuperficial cutaneous:Surface infections eg. P.versicolor, Dermato- phytosis. Candidiasis, T.nigra, PiedraSubcutaneous:Mycetoma, Chromoblastomycosis, SporotrichosisSystemic (opportunistic infection)Histoplasmosis, CandidiasisOf these categories, Demiatophvtosis, P.versicolor, Candidiasis are common in daily practicePityriasis versicolorEtiologic agent: Malassezia furfurClinical Features:Multiple, discrete, discoloured, macules.Fawn, brown, grey or hypopigmentedPinhead sized to large sheets of discolourationSeborrheic areas, upper half of body: trunk, arms, neck, abdomen.Scratch sign positiveWood's Lamp examination: Yellow fluoro-scenceKOH preparation: Spaghetti and meatball appearanceCoarse mycelium, fragmented to short filaments 2-5 micron wide and up to 2-5 micron long, together with spherical, thick-walled yeasts 2-8 micron in diameter, arranged in grape like fashion.TreatmentTopical:Ketoconazole. Clotrimazole. Miconazole, Bifonazole, Oxiconazole, Butenafine.Terbinafine. Selenium sulfide. Sodium thiosulphateOral:Fluconamg 4(X)mg single doseKetoconazole 2(X)mg OD x I4daysGriseofulvin is NOT effective.Hypopigmentation will take weeks to fadeScaling will disappear soonPityrosporum folliculitisEtiology: Malassezia furfurAge group: Teenagers or young adult malesClinical features: Itchy papules and pustules, scattered on the shoulders and back.Treatment: Oral Itraconazole, Ketaconazole, Fluconazole or topical Ketoconazole shampoo.Tinea nigra palmarisEtiology: Exophiala werneckiiClinical features: Asymptomatic superficial infection of palms; deeply pigmented, brown or black macular, non-scaly patches, resembling a silver nitrate stain.Treatment: Topical Econazole. Ketoconazole. Benzoic acid compound, Thiabendazole 2% in 90% DMSO or 10% Thiabendazole suspension.Black piedraEtiology: Piedraia hortaeClinical features: Hard, dark, multiple superficial nodules: firmly adherent black, gritty, hard nodules on hairs of scalp, beard, moustache or pubic area, hair may fracture easily.Treatment:Shaving or cutting the hair.Terbinafine, Benzoic acid compound ointment, 1:2000 solution of mercury perchlorideWhite piedraEtiology: Trichosporon beigeliiClinical features:Soft, white, grey or brown superficial nodules on hairs of the beard, moustache, pubic areas. Hair shaft weakened and breaks.Treatment: Shaving or cutting the hair. Responses to topical antifungals, azoles and allvamines have been reported but are unpredictable.DermatophytosisMycology:Three genera:Microsporum, Trichophyton, EpidermophytonThrive on dead, keratinized tissue - within the stratum comeum of the epidermis, within and around the fully keratinized hair shaft, and in the nail plate and keratinized nail bed.Tinea capitisEndothrix and EctothrixMost common - trichophyton violaceumVarieties:Non inflammatoryGray patchBlack dotSeborrheic dermatitisInflammatoryFavusKerion. agminate folliculitisNon inflammatory Tinea capitis:Black dot/Grey patchBreakage of hair gives rise to 'black dots*Patchy alopecia, often circular, numerous broken-off hairs, dull greyWood's lamp examination: green fluorescence (occasional non-flu ore scent cases)Tinea capitis: Kerion, agminate folliculitisInflammatory varietyMicrosporum,Trichophyton verrucosum. Trichophyton mentagrophytesPainful, inflammatory boggy swelling with purulent discharge.Hairs may be matted, easily pluckableLymphadenopathyCo-infection with bacteria is commonMay heal with scarring alopeciaTinea capitis: FavusInflammatory varietyKashmirTrichophyton schonleiniiYellowish, cup-shaped crusts develop around a hair with the hair projecting centrally.Extensive patchy hair loss with cicatricial alopeciaTinea facieiErythematous scaly patches on the faceAnnular or circinate lesions and indurationItching, burning and exacerbation after sun exposureSeen often in immunocompromised adultsTinea barbaeRingworm of the beard and moustache areasInvasion of coarse hairsDisease of the adult maleHighly inflammatory, pustular folliculitisHairs of the beard or moustache are surrounded by inflammatory' papulopustules, usually with oozing or crusting, easily pluckablePersist several monthsTinea corporisLesions of the trunk and limbs, excluding ringworm of the specialized sites such as the scalp, feet and groins etc.The fungus enters the stratum corneum and spreads centrifugally. Central clearing results once the fungi are eliminated.A second wave of centrifugal spread from the original site may occur with the formation of concentric erythematous inflammatory rings.Classical lesion:Annular patch or plaque with erythematous papulovesicles and scaling at the periphery with central clearing resembling the effects of ring worm.Polycyclic appearance in advanced infection due to incomplete fusion of multiple lesionsSites: waist, under breasts, abdomen, thighs etc.Tinea crurisItchingErythematous plaques, curved with well demarcated margins extending from the groin down the thighs.Scaling is variable, and occasionally may mask the inflammatory changes.Vesiculation is rareTinea mannumTwo varieties:Non inflammatory: Dry, scaly, mildly itchyInflammatory: Vesicular, itchy Tinea pedisWearing of shoes and the resultant macerationAdult males commonest, children rarelyPeeling, maceration and fissuring affecting the lateral toe clefts, and sometimes spreading to involve the undersurface of the toes.Varieties:Interdigital typePapulosquammous ('moccasin foot')Vesiculo-bullousTinea UnguiumDirty, dull, dry, pitted, ridged, split, discoloured, thick, uneven, nails with subungual hyperkeratosis Different types described depending on the site of nail involvement and its depth.Distal and lateral onychomycosesProximal subungual onychomycosesWhite superficial onychomycosesTotal dystrophic onychomycosesTreatment: RingwormTopical: Bifonazole. Ketoconazole Oxiconazole, Clotrimazole, Miconazole, Butenafine, Terbinafine.Vehicle: Lotions, creams, powders, gels are available.CANDIDIASISCausative organism:Candida albicans, Candida tropicalis, Candida pseudotropicalisSites of affection:Mucous membraneSkinNailsCandidiasis : MucosalOral thrush:Creamy, curd-like, white pseudomembrane, on ery thematous baseSites:Immunocompetent patient: cheeks, gums or the palate.Immunocompromised patients: affection of tongue with extension to pharynx or oesophagus; ulcerative lesions may occur.Angular cheilitis (angular stomatitis / perleche): Soreness at the angles of the mouthVulvovaginitis (vulvovaginal thrush): Itching and soreness with a thick, creamy white dischargeBalanoposthitis:Tiny papules on the glans penis after intercourse, evolve as white pustules or vesicles and rupture.Radial fissures on glans penis in diabetics. Vulvovaginitis in conjugal partnerCandidiasis - FlexuralIntertrigo: (Flexural candidiasis)Erythema and maceration in the folds; axilla, groins and webspaces.Napkin rash:Pustules, with an irregular border and satellite lesionsCandidiasis: FlailChronic Paronychia:Swelling of the nail fold with pain and discharge of pus.Chronic, recurrent.Superadded bacteria! infectionOnychomycosis:Destruction of nail plate.Treatment of candidiasisTreat predisposing factors like poor hygiene, diabetes, AIDS, conjugal infectionTopical:Clotrimazole, Miconazole, Ketoconazole. Ciclopirox olamineOral:Ketoconazole 200mg, Itraconazole 100-200mg and Fluconazole 150mg

Skin

Cutaneous Manifestations of Microvascular Occlusion Syndromes

6e0e399d-5e3d-4f98-9740-4bc8c330e280

Commonest cause of cataract

Hereditary

DM

Trauma

Age related

single

D i.e. Age related Radiation cataract is caused by exposure to almost all types of radiation energy such as infrared or heat (in glass-blowers or glass-workers, and iron-workers), irradiation caused by X-rays, gamma-rays or neutrons (in workers in atomic energy plant, survivors of atomic bomb and in patients inadequately protected during treatment for malignant conditions near eye) and sunlight (especially the ultraviolet A and UV-B components). Microwave radiation has shown to cause cataract in animals. But MRI has no radiation exposure. - Cataract may be caused by chloroquine, coicosteroids, copper metabolism error (Wilson's disease), Calcium decrease (hypocalcemia or hypoparathyroidism or parathyroid tetany), galactosemia, hypo glycemia and diabetes mellitusQ. (Mn- CG=Cataract G) Cataract is the most common cause of blindness in India Q. Senile cataract or age related cataract is the commonest type of acquired cataract Q affecting equally persons of either sex usually above the age of 50 years. Overall incidence of acquired cataract is more than congenital.

Ophthalmology

0ac4ba5d-a465-474d-9390-f737a6985e03

Facial nerve palsy can be caused by -

Cholesteatoma

Multiple sclerosis

Mastoidectomy

All of the above

multi

Ans. is 'd' i.e., Ail of the above Causes of facial paralysis1. Central :-Brain abscess, pontine glioma, Polio, multiple sclerosis2. Intracranial part (cerebellopontine angle) :- Acoustic neuroma, meningioma, congenital cholesteatoma, metastatic carcinoma, meningitis3. Intratemporal part:-Idiopathic :- Bell's palsy, Melkersson's syndromeInfections:- ASOM, CSOM, Herpes zoster oticus, malignant otitis externaTrauma:- Surgical (mastoidectomy, stapedectomy), accidental (fractures of temporal bone)Neoplasms :- Malignancies of external and middle ear, glomus jugular, facial nerve neuroma, metastasis (from breast, lung etc).4. Extracranial part :- Malignancies or surgery or injury to parotid gland5. Systemic diseases :- Diabetes, hypothyroidism, uremia, PAN, Sarcoidosis (Heerfordt's syndrome), leprosy, leukaemia, demyelinating disease

ENT

Facial Nerve And Its Disorders

1c3ab0ae-6ef9-4dad-b40f-25ff49e4e1c3

All reduce lactation except - a) Maternal anxiety b) Retracted nipple c) Dehydration d) Diabetes e) Antibiotics

abc

abd

cde

ace

multi

Medicine

ae99c0de-0afd-424b-ab63-6996aaca70cc

A 75-year-old man with a history of myocardial infarction 2 years ago, peripheral vascular disease with symptoms of claudication after walking half a block, hypeension, and diabetes presents with a large ventral hernia. He wishes to have the hernia repaired. Which of the following is the most appropriate next step in his preoperative workup?

He should undergo an electrocardiogram (ECG).

He should undergo an exercise stress test.

He should undergo coronary aery bypass prior to operative repair of his ventral hernia

He should undergo a persantine thallium stress test and echocardiography.

multi

The patient should undergo persantine thallium stress testing followed by echocardiography to assess his need for coronary angiogram with possible need for angioplasty, stenting, or surgical revascularization prior to repair of his hernia. Although exercise stress testing is an appropriate method for evaluating a patient's cardiac function preoperatively, this patient's functional status is limited by his peripheral vascular disease and therefore a pharmacologic stress test would be the preferred method of cardiac evaluation. An ECG should be performed in this patient with a history of cardiovascular disease, hypeension, and diabetes, but a normal ECG would not preclude fuher workup. While myocardial infarction (MI) within 6 months of surgery is considered to increase a patient's risk for a cardiac complication after surgery using Goldman's criteria, a remote history of MI is not prohibitive for surgery in and of itself.

Anaesthesia

Preoperative assessment and monitoring in anaesthesia

894609c1-46cf-4987-9fbf-d12bd75b2122

Patients with diabetes frequently report changing visual acuities when their glucose levels are chronically high. Which of the following could explain the fluctuating acuity with high blood glucose levels?

Increased sorbitol in the lens

Decreased fructose in the lens

Increased oxidative phosphorylation in the lens

Macular degeneration

multi

Fluctuating levels of sugars and sugar alcohols in the lens can cause fluctuating visual acuity. With high blood glucose, there would be increased levels of sorbitol in the lens. The lens does not contain mitochondria and cannot use the TCA cycle/electron transport chain to generate energy. Galactitol causes the same problems as sorbitol, but galactitol is derived from galactose, whereas sorbitol is produced from glucose. The patient has high glucose levels, so galactitol would not be expected to accumulate in the lens. Macular degeneration affects the retina, but in this case, it is the lens that is the affected tissue. Reducing fructose levels in the lens would reduce sorbitol levels, which would ease the visual acuity problem, not make it occur.

Biochemistry

Carbohydrates

315ab04d-95e5-4f94-83fd-48266b7ed082

All the following statement about clozapine are true except -

It is used in schizophrenia

May precipitate seizure

May cause agranulocytosis

Extrapyramidal side effects are seen

multi

Clozapine It blocks D4, 5-HT, and α-adrenergic receptors. Despite of anticholinergic property, it causes hypersalivation. It also blocks H1-histaminic receptors. The important side effects are agranulocytosis & myocarditis. It can induce seizures even in nonepileptics. It causes weight gain and precipitation of diabetes. It does not produce extrapyramidal side effects.

Psychiatry

596275d2-892d-4b34-8ad2-0a611d279f36

Endemicity of a disease means:

Occurs clearly in excess of normal expectancy

Is constantly present in a population

Exhibits seasonal pattern

Is prevalent among animals

single

Endemic Is the constant presence of a disease agent in a defined geographical area ; refers to 'usual or expected frequency' of a disease in a population. For instance, common cold is endemic because somebody always has one. Endemic diseases in India are : Measles, mumps, rubella, chicken pox, peussis, TB, HIV, Cancers, diabetes, hypeension etc. Epidemics can arise from uncontrolled endemics also.

Social & Preventive Medicine

Time Distribution, Epidemics

26a8ae0c-ec74-4613-80a8-e64bae766023

All are absolute contraindication of OCP except:

Pregnancy

Thromboembolic disorder

Hepatic failure

Endometriosis

multi

Ans. D. EndometriosisOCP are contraindicated in pregnancy, hepatic renal failure, thromboembolic disorder, breast CA, hypertension, diabetes. But in case of endometriosis, it regulates the irregular bleeding which is non-contraceptive use of OCP.

Pharmacology

Endocrinology

5585da3c-5132-4b3d-89f5-cd27c8172713

A 67-year-old man with an 18-year history of type 2 diabetes mellitus presents for a routine physical examination. His temperature is 36.9 C (98.5 F), his blood pressure is 158/98 mm Hg and his pulse is 82/minute and regular. On examination, the physician notes a non tender, pulsatile, mass in the mid-abdomen. A plain abdominal x-ray film with the patient in the lateral position reveals spotty calcification of a markedly dilated abdominal aoic walI. Following surgery, the patient is placed on a low-fat diet to reduce the risk of continued progression of his atherosclerotic disease. A bile acid sequestrant is added to interrupt enterohepatic circulation of bile acids. Which of the following agents was MOST likely prescribed?

Atorvastatin

Cholestyramine

Clofibrate

Gemfibrozil

single

Cholestyramine and colestipol are bile acid sequestrants that bind bile acids in the intestine, thereby interrupting enterohepatic circulation of bile acids. This has an indirect effect to enhance LDL clearance and lower lipids in the blood. Atorvastatin and lovastatin are lipid-lowering drugs that competitively inhibit HMG-CoA reductase, an early step in cholesterol biosynthesis. Clofibrate and gemfibrozil are fibric acid derivatives that may increase the activity of lipoprotein lipase. Ref: Bersot T.P. (2011). Chapter 31. Drug Therapy for Hypercholesterolemia and Dyslipidemia. In L.L. Brunton, B.A. Chabner, B.C. Knollmann (Eds), Goodman & Gilman's The Pharmacological Basis of Therapeutics, 12e.

Pharmacology

e3292ae9-466e-4837-912e-64e6fe0a32c1

Gallstone are associated with which Neuro Endocrine Tumour :-

Insulinoma

VIPoma

Somastostatinoma

Glucagonoma

multi

Somatostatinoma syndrome is a triad of diabetes mellitus, diarrhea and gallstones, but also includes weight loss and hypochlorhydria.

Surgery

Gallbladder

096bead7-9d30-4410-ad72-4f96eb774844

In which of the following condition is OCP contraindicated ?

Hea disease

Thromboembolism

Breast cancer

All of the above

multi

ABSOLUTE CONTRAINDICATIONS OF OCP: *Known or suspected breast cancer *Severe hyperiglyceridemia/hypercholestrolemia *Undiagnosed vaginal bleeding *Thrombophlebitis/thromboembolism , cerebral and cardiac disorders *Pregnancy *Hypeension (moderate to severe) *Impaired liver RELATIVE CONTRAINDICATIONS OF OCP: *Migraine with aura *Diabetes mellitus/gestational diabetes *Hypeension *Smoking *Uterine lieomyoma *Elective surgery *Seizure disorder *Sickle cell disease *Gall bladder disease *SLE *Mitral valve prolapse *Hyperlipidemia *Hepatic disease

Gynaecology & Obstetrics

18809fc3-640b-47c5-a7cf-09978e3f8159

Diabetes mellitus is associated with all except -

Pendred syndrome

Down's syndrome

Turner's syndrome

Klinefelters syndrome

multi

Ref -researchgate.net

Medicine

Endocrinology

0a306fee-da1d-434b-a4b1-73244e826f09

A 28-year-old woman with type 1 diabetes presents to the clinic for evaluation of skin lesions on her leg. They are not painful or itchy and have developed gradually over time. There is no history of previous trauma to the site either.On physical examination the skin changes have a central depression and raised irregular margin. The surrounding area is not red, tender, or indurated. They are shown in Figure below. Which of the following is the most likely diagnosis?

eruptive xanthomas

necrobiosis lipoidica diabeticorum

gangrene

staphylococcal infection

multi

Necrobiosis lipoidica diabeticorum is more frequent in females and may antedate other clinical signs and symptoms of diabetes. The plaques are round, firm, and reddish-brown to yellow in color. They most commonly involve the legs but can also involve the hands, arms, abdomen, and head. This in not a staphylococcal skin infection since it is not tender, indurated or warm to touch, and erythema nodosum is characterized by round, tender elevated lesions usually on the anterior shin.

Medicine

Endocrinology

ac215f3c-a456-4a2d-82d0-37bd7b97c313

The triad of cirrhosis, hemochromatosis and diabetes are referred to as

Silver diabetes

Diabetes mellitus

Diabetes insipidus

Bronze diabetes

single

Medicine

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A patient is having random plasma glucose levels of 110 mg/ dl and 113 mg/ dl on two separate occasions. What you will advise him: March 2012

Declare him as having Diabetes mellitus

Proceed for oral glucose tolerance test

Declare patient as normal

Check for Glycosylated hemoglobin and if it is raised, declare him as having DM

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Ans: C i.e. Declare patient as normal Diagnosis of DM Random plasma glucose levels of more than 200 mg/dl along with symptoms suggesting diabetes, confirms the diagnosis Random plasma glucose ranging between 140-198 mg/dl is an indication to perform oral glucose tolerance test The use of HbA1c for diagnosing diabetes is unceain. HbAlc is used to monitor glycemic control. The recommended target HbA1c is 7% or less, to minimise the risk of vascular complications So analyzing the options given, RBS values of 110 mg/dl and 113 mg/dl falls in normal range

Medicine