MRCP - 1 Jan 2010

[wellwisher.]

1. A patient on methotrexate for rheumatoid arthritis. CT abdomen- widespread lymphadenopathy..diagnosis?
TB
Lymphoma
angio immunoblastic lymphadenopathy?

CREST syndrome..bibasal crackles, CXR- lower zone shadowing.
Diagnosis?
?Left ventricular failure
cant remember other options

cell organelle breaking down peptides..
? peroxisome?proteasome

Patient on a usual combination of cardiac medication presenting late onset with facial swelling? angioodema 2 to ramipril??

A mother unable to speak at all following her son yelling at her or being rude to her or somethin..
1. akinetic mutism
2Psychogenic aphonia <<<? ANS

Most common cause of death in some with CKD who has been on dialysis for 5 yrs
1 hyperkalemia
2 Cardiac disease
3
4
5

Contraindications to liver biospy.
1. Platelet range
2. Hb
3 clotting range
4
5 USg finding..Intra heptic duct dilatation<< ?ans

Most common bug isolated from sputum of someone having bronchectasis.
1Haemophilus influenzae
2Pseudomonas spp
3klebsiella
4
5

Single most diagnostic finding for diabetes type 1
1ketonuria
2glycosuria
3
4
5

Young man dies suddenly while playing football, cause of death..
1. long qt interval
2 hocm
3
4
5

patient while a parietal lobe cerebral infraction having difficult reading whats cause..
1hemiaponia
2agraphia
3
4
5

Patient had been investigated for caner last year all test negative this year convienced has some sort of cardiac pain
or somethin
1Malingering
2
3
4
5somatoform disorder

angiodema on cardiac mediacations- aspirin
mother unable to apeak- akinetic mutism

facial swelling was a bit late onset so i thought maybe ace inhibitors
mother unable to speak i thought psychogenic aphonia which occur in females under stress due to family pressures

Akinetic mutism is a medical term describing patients who tend neither to speak (mutism) nor move (akinesia). It is the result of severe frontal lobe injury in which the pattern of inhibitory control is one of increasing passivity and gradually decreasing speech and motion.

Commonest organism causing meningitis in a patient with a closed head injury
1S pneumoniae meningitis
2Neisseria meningitides
3
4
5

Patient has had a drug eluting stent inserted 6 months ago and is on plavix for 6 months, is due for elective hernia surgery
what r the op tions.
1. delay operation for 6 months
2. stop plavix
3. stop plavix, continue with heparin and aspirin

[subha.]

1. patient of rheumatoid arthritis with LAP -- due to rheumatoid arthritis (extra-articular feature)
2. CREST with lower zone shadowing -- I think this was pulmonary edema
3. orgenelle breaking down peptides is perioxysome.
4. cardiac medications --- edema due to I think it was aspirin.
5. mother unable to Speak -- psychogenic
6. CKD patient cause of death -- Cardiac disease (ischemic)
7. liver biopsy contra-indications -- biliary dilatations on USG
8. bronchiactesis most common organism -- H flue
9. Type I diabetes -- Ketonuria (3+) as other occure to type 2 to some extent.
10. young football player suddenly dies due to HOCM
11. pariental lobe infarct with difficulty in reading, is hemianopia as agraphia is inability to write/form images.
12. women with cancer suspecion and now with chest pain is hypochnodism

[wellwisher.]

1.size of RNA using DNA ?pcr or northen
2.there is lyme disease in exam?
3.loss of ankel reflex with weakness of knee?sciatic nerve
4.loss of abduction of thumb?median nerve
5.inferior infarction with heart block? rt coronary
6.anaphlaxisis measure by? mast tryptase
7.contact dermatitis ?delayed hypersenstivity
8.poly peptid degradation? perostosome but i do peroxisome
9.bloody diahrea?camplyobacter
10.kapose?HHV8
11.one egyption with picture of meningitis and lymphoccyte in csf?polio
12.skin rash at hand with nodule at penis?syphalis
13.high lft with tender liver?IG A
14.OBESITY AND HIGH LFT ?NASH
15.ANTIPARITEAL CELL ANTIBODY ? FUNDS OR BODY
16.16.2 QAUESTION one high IG A,one high IG G... didnt remember
17.JAK 2?POLYCYTHEMIA....the same
18.teardrop?mylofibrosis.....the same
19.ALL adverse prognosis? phladiphia.....the same
20.one female 79 years with one lymph node ,lymphocytosis?immunophenotyping.....the same
21.low iron ?bone marrow most specific......didnt remember
22.anemia high HBA2 and basophlic stabling?lead poisoning
23.most common finding in early blood transfusion reaction?HBemia....didnt remember
24.CML ttt?imitinap
26.pt with ITP FRIST ttt?predisolon....the same
27.pt with petechia and low plt normal pt .renal function?ITP....the same
28.PT WITH lymph adnopathy and atypical lymph?IMN....the same
29.NEONATAL LUPUS?ANTI RO.....I got wrong
30.anti ccp normal rf? rhumatoid....the same
31.rhumatoid activation?methotreaxat....the same
32.multi pn and HTN AND KIDENY AFFECTION? PAN....the same
33.SYSTEMIC SCLEROSIS AND DYSPNEA?PROGREESIVE FIBROSIS....not sure
34.ANKLOSING X RAY?CALCIFICATION OF VERTEBRAL JOINT.....Sclerosis
35.ASTHMA, STRIDOR ?FLOW CURVE...the same
36.GULLIAN BS ?FORCED VITAL CAPACITY....the same
37.HIGH KCO?PULMONARY HEMORRHAGE....the same
38.LOW FEV1/FVC?EMPHYSEMA....the same
39.HYPER VENTILATION?LOW H IN BLOOD....Not sure( I went for HCO3)
40.CUSHING?METABOLIC ALKALOSIS....the same
41.CANCER LUNG CONFUSION?HYPERCALCEMIA....didnt remember
42.PLURAL EFFUSION NOT ASPIRATE?THORACOSCOBY.....CT(?)
43.MESOTHELIOMA?TARC OF MALIGNANCY ON ASPIRATION....the same
44.ALLERGIC PULMONARY ASPERGILLOSIS?PREDINSOLON....the same
45.pulmonary hyper tension?echo.....the same
46.hocm?thickness of wall>3cm....the same
47.during exercise arrested not responding to CPR ?arrythmogenic cardiomypathy.....didnt remember
48.x ray in pulmonary empolism? normal...I got wrong
49.pulmonary embolism in COPD?ct angio....the same
50.ECG IN pricartitis?wid ST elevation....I got wrong
51.ECG IN hypokalemia?u wave.....the same
52.mi after surgry?PCI....the same
53.LOSS OF PULSE ON RT HAND AND HORNER?AORTIC DISSECTION....the same
54.INFECTIVE ENDOCARDITIS IN PROTHETIC AND STREPT VIRDAN?PEN+GEN......vanco+rifam(?)
55.VAVE REPLACEMENT AND ANEMIA HIGH BILIRUBIN?HEMOLYSIS...the same
56.FRIST DRUG IN TYPE 2 DM ?METFORMIN....the same
57.MI+DM ?INSULIN....the same
58.GLUCOSURIA ,NORMAL BLOOD GLUCOSE HIGH BLOOD PRESSURE?CUSHING....didnt remember
59.SKIN HYPOPIGMENTATION+THYROTOXICOSIS?VITILIGO...
60.LOW FREE T4 NORMAL TSH IN PT TAKING DRUH?ADEQUTE BUT I THINK IT IS WRONG.....Adequate
61.OLD FEMAL HIGH CALICUM PLUS LOW PHOS?HYPERPARA....the same
62.LOW CALCIUM,PHOS.?DONT REMEMBER CHOICE......didnt remember
63.HYPOGLYCEMIA? INSULIN C PEPTIT.....the same
64.OLD AGE FATIGE BLURING OF VISION?WALDENSTORM.....didnt remember
65.MULITIPELE MYLOMA....the same
66.ACROMEGALY?GTT......OGTT+GH
67.HYPERKALEMIA+HYPOTENSION?SHORT SYNCHT......the same
68.HYPOADRENALISM,HYPOTHYROID HIGH LH FSH?OVERIAN FALIURE.....the same
69.AMENORHEA +HIGH LH ,TESTOSTERON?PCO....the same
70.TESTICULAR FEMINAZATION?FEMALE PICTURE+EXTERNAL FEMAL GENITALIA....the same
71.MUSLIM AND ON METFORMIN?1000MG AFTER BREKFAST AND 500 AT FAJER.....didnt see this one
72.CYSTIC FIBROSIS?2/3 CARRIER.....1/2(might wrong)
73.19 YEAR WITH NEPHROTIC?MINIMAL CHANGE....the same
74.DRT ACIDOSIS?NEPHROCALCINOSIS....the same
75.HIGH PTH IN CKD?LOW CALCIUM......didnt remember
76.RENAL TRANSPLANT WITH DIARRHEA?CMV.....the same
77.PCKD BLOOD GROUP O HIS FATHER45 YEAR BLOOD GROUP A NOT ACCEPT?STILL CHANCE TO BE PCKD
78.DICLOPHENAC?AIN....the same
79.AMYLODOSIS IN KID?B2 MICROGLO.... the same
80CAUSE OF DEATH IN ESRD?IHD....I got wrong with (DC)
81.PT WITH CKD WHAT IS ONE ACCURATE?ANEMIA
82.PT RECURRENT UTI HTN .STROKE,SHRINK KIDENY?RASTENOSIS
83.ERYTHROPITIN ?LOW IMMUNOGINIC
84.ABDOMINAL PAIN +RASH+JOINT? HCPURPURA
85.CYSTIC FIBROSIS +DIARRHEA?FECAL ELASTASE
86.RECTUM AND BIOPSY GRANULOMA? CROHNS
87.ACTION OF TERPELISERN?SPLANCHANIC VC
88.HEMOOCHROMATOSIS SCREEN?TRANSFERRITIN SATURATION
89.CHOREA AND HIGH LIVER ENZYME?WLISON
90.DRE EYE ITCHING?PRIARRY BILIARRY
91.OLD AGE WITH ANEMIA?GASTROSCOPY
92.CONTRANDICATION TO LIVER BIOBSY?INTRAHEPATIC DILATATION
93.VAGINAL DISCHARGE SCANTY?METRONIDAZOL
94.PNUMOCYSTIC?COTRIMEXAZOL
95.RING ENHANCEMENT?TOXOPLASMOSIS
96.AFTER APPENDICTOMY BLOOD CULTURE TAKEN? CRP ITIS WRONG
97.DRUG ABUSER AND CHEST INFECTION?VANCOMYCIN
[snip].TYPE 1 DM +HIGH CHOLESTROL NO FAMILY HISTROY?NO NEED TTT
99.FEMALE ON OCP WITH LOW K.CA.DENTAL EROSION?EARLY PREGNANCY DUO TO HIGH ALKALINE PHOSPHATASE
100.PARENTAL NUTRION?HYPO PHOS
101.CEREBRAL HEMORRHGE PIN POINT PUPILE?PON
102.PARIETAL LOBE?AGRAPHIA---------- (IT IS WRONG)
103.T.B ISOLATION?SPUTUM CULTURE
104.PNUMOTHORAX? OBSERVE
105.NEUTROPENIA .8?OBSERVE
106.PAIN AT LATERAL OF HIP?BRUSITIS
107ENTECAPRON?TNF ANTAGONIST
108.OPTIC ATROPH+ATAXIA? M SCLEROSIS
109.CLUSTER HEADECHE
110AMYLOD LATERAL SCLEROSIS
111.ANTERIOR CORD SYNDROME
112.ACOUSTIC NEUROMA?EARLY LOSS OF CORNEAL REFLEX
113.TRIGEMINAL NEURALGIA PROPHLAXISIS?CARBEMAZEPIN----WRONG I THINK TRI ANTIDEPRESSENT
114.BELLS PALSY?HYPERASTHSISAE
115.ADI PUPILE
116.PARKINSON?ASYMMETRICAL
117.EPLIPSY AND SUB ANGEL FIBROMA?TUBEROUS SCLEROSIS
118.DILATED FIXED PUPIL?3RD CRANIAL NERVE

119.CANCER ?HYPOCHONDRISM
120.MULITIPLE FUNCTIONAL SYMPTOMES AFTER MOTHER DIED?SOMATOFORM
121.TAKING DRUG AFTER LIFT GIRL FRIEND?PARANOID SCHIZOPHRENIA
122.MOTHER DONT SPEAK AFTER STRUGGLE WITH SON?PSYCHOGENIC APHASIA
123.BEFORE SLEEP OR DURING AWAK NOTABLE TO MOVE?SLEEP PARALYSIS
124.LESION IN LEFT HAND IN PSYCHIC PT?SELF HARM
125.SEEING SOMETHING IN BED IN ALCOHOLIC?ALCOHOLIC WITHDRAWAL
126.WRINKES TTT?THIAMIN
127.STUDENT FEEL HIS TEATCHER----------?SCHIZOPHRENIA
128CHOLESTEROL EMBOLISM?ESINOPHILIA
129ATRIAL MYXOMA?LT ATRIUM
130.PREGNANA VSD WORET?PULMONARY HTN
131.AF +DIGOXIN+WARFARIN SINCE 3 WEEK+LV DYSFUNCTION NOT CONTROL RAT ?BISPROLOL
132.ATOPIC ECZEMA+PUSTULE IN FACE AND TRUNK?ORAL AMOXACILLIN
133.HEREPES THEN SKIN LESSION?ERETHYMA MULITIFORMIS
134.TENDE PAPULE IN SHIN ?RESOLOVED SPONTENOUSE
135.OLD AGE FEMALE WITH BULOUS?[bleep] PIMPHYGOID
136.MALIGNANT MELLANOMA PROGNOSIS?THICKNESS
137.DISCOID LUPUS TTT?CHOLOROQUIN
138BUTERFLY RASH IN FACE CROSE NOSE ,WHAT IS IN BLOOD?ESINOPHILIA-------------I THINK IT IS WRONG
139.LESSION IN FACE ERYTHEMA AND IN SCALP+SCALING?TTT BY METRONIDAZOL---------------I THINK ALSO WRONG
140.UNILATERAL EXOPHOTHALMOSE +ANTIPEROXIDASE?GRAVESE
141.DKA?KETONURIA
142.142.SMALL SAMPLE ?SED
143.AGE HIGHT SEX AND BLOOD PREESURE? REGRRESION
144.IN CANCER PROSTATE ?ODD RATIO
145.+PREDICTIVE ?50%
146.SENSTIVITY
147.COCAIN ?CHEST PAIN
148.PLAVIX AN SURGRY ?ONE WEEK
149.CARBAMAZEPIN AND NEED TO INCRESE DOSE ?AUTOINDUCTION
150.ICRASR EFFECT OF DRUG? CLARITHROMYCIN
151.ANTI HTN IN PREGNANCY ?METHYL DOPA
152.PROTONRIA ?USE RAMIPRIL
153. ANT HTN AND EDEMA IN MOUTH ?RAMIPRIL
154. LITHUM TOXICITY ?RAMIPRIL
155.LL OEDEMA IN HTN ?NIFEDIPIN
156.THIAZID ?EARLY DCT
157.PROPRANOLOL AND BRADYCARDIA BP 85/55 AND NO RESPONSE TO ATROPIN ?IV GLUCAGON
158.PT WITH BIPOLAR DISORDER AND POLYURIA?DRUG INDUCED DI
159ALOPECIA ?NA VALOPRATE
160.TTT OF ALZAHIMER ?DONAZEPIL
161.CICLOSPORING ?NEPHROTOXICITY
162.PT WITH PN SHOULD STOPE ? VINCRISTIN
163.SIADH ?FLUOXTIN
164.PARAMOLE OVER DOSE RISK IN ?ANOREXIA NERVOSA
165.PT TTT AFTER DRUG OVER DOSE HAVE BLURRING OF VISSION?METHYL ALCOHOL
166.PINPOINT PUPILE ?DIHYDROCODIAN
167.FLUDAAPIN AND CAPI -----------?LOW DISTRIBUTION

[qquin.]

1. A 55yr old man C/O=fatigue was found to have hypochromic microcytic anaemia with raised HbA2 of 3.8%(2-3%) and eosinophilic stippling=beta thal trait.
2. Drug that causes lithium toxicity= ACEI
3. Bloody diarrhea from Egypt=shigella.
4. Adequate thyroid control with normal TSH and T3 but low T4.
5. Thyroid nodule with euthyroidism investigation= radionucleotide scan,FNAC?
6. Methotrexate as the drug of choice in rheumatoid.
7. Guy with cystic fibrosis what are the odds of his sister being a carrier=1:2.
8. Uncontrolled AF with digoxin, what to add = bisoprolol.
9. Guy with CLL with plt's 17 and thigh bruise, what to do= observe, give plt's?
10. Pancreatitis in preg woman cause= gall stones?.
11. Protein degradation in the cell= proteasome
12. Hair loss= valproate.
13. CML drug of choice= imatinib
14. Mitochondrial inheritance=optic atrophy.
15. Bradycardia, hypotention, RR=8 = dihydrocodeine.
16. Erythema artifacta.
17. RNA= northern blot
18. Guy from surgical ward with appendicectomy develops MI, is on aspirin and clopidogrel, what to add= PCI.
19. Diarrhea with rectal biopsy with inflammation throughout the lamina propria with lymphocyte proliferation and granulomas= crohns.
20. Which supports idiopathic Parkinson= asymmetrical dyskinesia.
21. 22yr male with diabetes, BMI 22, sugar 38, urine 3sug and 3acetone, which supports type 1= ketoneuria, age?.
22. 55 diabetic, obese, normal renal funct. 1st chice drug= metformin.
23. Pt with MI has high blood sugar of 12, which is the optimal Rx= i.v.insulin.
24. Patient with pneumocystis jiv… pneumonia, which drug to give=cotrimoxazole
25. Antibiotic for alpha haemolytic streptococci in IE?
26. 19 male with nephrotic syndrome, which is the commonest GN= membranous, minimal change?
27. 25 male dies suddenly in football match, what is the commonest cause= HOCM.
28. Which is ass with risk of sudden death in HOCM= vent septum 3.3cm, systolic anterior motin of the mitral valve, left atrial press of 30mmHg, mitral regurgitation.
29. Best way to screen relatives of a guy with haemochromatosis= serum iron, serum ferritin, transferring sat, TIBC
30. Diagnosis of CLL= BM, genetic
31. Commonest cause of death in dialysis pts= cardiomyopathy, ischaemic HD, sepsis, hyperkalaemia.
32. Renal transplant for guy with PKD from his 40yr brother, donor is A+ and recipient is O+ but the doc says no, why= acute rejection, unethical, cadaveric transplant would be better, transplanted kidney would develop PKD.
33. Guy who drinks 50 units alcohol develops gait unsteadiness and ataxia, has past hx of optic neuritis last yr which lasted 3 wks. Diagnosis= MS, wernik's-korsakof.
34. Woman who develops hypoglycaemia esp in the morning every day and takes sugar, what to do during the next attak= RBS, sulphonylurea screen, insulin and c-peptide.
35. Hereditary angioedema is caused by= C1INH deficiency.
36. Pt with Burkitt's lymphoma, what to do before starting chemo= treat hyperuricaemia.
37. HH8 is associated with which disease= Kaposi sarcoma, nasopharyngeal carcinoma, hodgkin's lymphoma, burkitt's lymphoma.
38. Thiazide diuretics action site= distal part of the DCT, proximal part of the DCT, ascending loop, descending loop, collecting duct.
39. 24yr man returns from holiday with swollen painful knee and ankle joints and a rash on both soles, what is the diagnosis= gonococcal arthritis, reactive arthritis, psoriatic arthritis.
40. Woman is disobeyed by her son and suddenly she cant speak= akinetic mutism, psycogenic aphonia.
41. 24 female presents with abd pain and diarrhea, has past hx of chest pain, hemiplegia, eye pain with no identified cause but did not respond to reassurance= somatoform, facticious, hypochondriasis, malingering.
42. A patient with the JAK2 mutation= polycythemia rubra vera.
43. Non alcoholic FLD
44. Pt with ITP and plts 9 and bruising, initial management= plt transfusion, prednisolone, hydroxyurea.
45. Carbamazepine, started with 200mg then needed 400mg= autoinduction.
46. Panadol poisoning, which is ass with increased risk of hepatotoxicity= anorexia nervosa, alcohol.
47. Investigation for diagnosis of pul HT= CT, echo,….
48. Pt with previous MI and drug iluting stents presents with hemiplegia= thromboembolism.
49. Peripheral neuropathy is a SE of which drug= vincristine.
50. Pt with complete androgen insensitivity, which phenotype= female with cliteromegaly, female with female external genitalia, male with…..
51. Pt on statin, which drug induces myopathy= cipro, claril.
52. The commonest site for myxoma in the heart= left atrium.
53. Pt with on chronic dialysis develops amyloidosis, which type= amyloid B.
54. Methaemoglobinaemia 35% wat rx= methyelene blue, hyperbaric O2.
55. Confirm anaphylaxis= serum IgE.
56. Rx of Alzheimer's which drug= Domepizol.
57. Pt with signs of motor neurone disease= ALS.
58. The action of octreotide in hepatorenal syndrome= constriction of the splanchnic complex.
59. Solitary ring enhancing lesion on CT brain of HIV pt= toxoplasmosis.
60. Investigation of a woman with signs of post comm. Art aneurysm= brain angiography.
61. Inferior MI= rt coronary artery.
62. Pt with pleural effusion on x-ray but dry tap on aspiration, which investigation= chest US, CT chest, lateral x-ray.
63. Capecitabine vs fluorouracil= low bioavalability, oral,….
64. The commonest type of lung cancer= small cell, non-small cell.
65. Mother cant talk after fight with her son= akinetic mutism, psychotic aphonia.
66. Old lady with hip pain and lateral tenderness but movements are normal without pain= osteoarthritis.
67. Plasma GH measurement with OGTT to diagnose acromegally.
68. Man from india with jaundice picture= Hep A.
69. Anti-RO Ab's associated with= heart block.
70. Commonest SE of cyclosporine= nephrotoxicity.
71. FEV1/FVC low + increased lung compliance= Emphysema.
72. Hypokalaemia, what else is found on ECG= U wave.
73. Cholesterol embolisation what else is found= eosinophilia.
74. Hypertension in pregnancy= methyldopa, atenolol,….
75. Beta blocker toxicity with no response to atropine= glucagon.
76. Pt took cocaine, what else is expected= ischaemic chest pain.
77. Prophylaxis for trigeminal neuralgia= carbamazepine.
78. Malignant melanoma= thickness.
79. Glandular fever with atypical lymphocytes.
80. Guillain Barre, monitor resp funct= VC
81. Stridor, investigate= flow volume loop
82. Pt with polyarthritis and anti CCP= RA
83. Refeeding syndrome= hypophosphataemia.
84. Sarcoidosis most likely outcome= resolves.
85. COPD with suspected PE, which investigation= CTP.
86. ALL poor prognosis= Philadelphia chromosome.
87. Young girl with teeth erosion and normal BMI= bulimia nervosa.
88. Pneumothorax less than 1cm= discharge and advise follow-up.
89. Latex allergy= delayed HS.
90. Hyker= lyme disease.
91. Raised PTH,Ca and low phosphate= primary hyperparath.
92. Sleep paralysis.
93. Dry eyes with anti-RO= sjogren's syndrome.
94. Reduced kidney size bilaterally= renal artery stenosis.
95. Dry eyes + itching PBC.
96. Cluster headaches.

[qquin.]

1. A 55yr old man C/O=fatigue was found to have hypochromic microcytic anaemia with raised HbA2 of 3.8%(2-3%) and eosinophilic stippling=beta thal trait. Beta thalassemias are due to mutations in the HBB gene on chromosome 11, also inherited in an autosomal-recessive fashion. The severity of the disease depends on the nature of the mutation. Mutations are characterized as (βo or β thalassemia major) if they prevent any formation of β chains (which is the most severe form of beta Thalassemia); they are characterized as (β+ or β thalassemia intermedia) if they allow some β chain formation to occur. In either case there is a relative excess of α chains, but these do not form tetramers: rather, they bind to the red blood cell membranes, producing membrane damage, and at high concentrations they form toxic aggregates. Hemoglobin A2 is composed of two alpha and two delta chains. The level of Hb A2 increases gradually through the first year of life at which time adult levels are reached. Elevated levels (3.5 -7.0%) of Hb A2 are seen with beta thalassemia trait. Several abnormal hemoglobins including Hb S, E, C and O may cause spurious elevation. To avoid misinterpretation, hemoglobin electrophoresis should be run on all samples. Hb A2 may be increased with megaloblastic anemia and decreased with iron deficiency anemia.

2. Drug that causes lithium toxicity= ACEI Lithium has been in use since the 1870s. Lithium was initially used to treat depression, gout, and neutropenia, and for cluster headache prophylaxis, but it fell out of favor because of its side effects. In the 1940s, the US Food and Drug Administration (FDA) banned the use of lithium because of fatalities but lifted the ban in 1970. Presently, lithium is commonly used as maintenance treatment of bipolar disorder. Lithium poisoning occurs frequently, since it is used in a population at high risk for overdose. Furthermore, lithium has a relatively narrow therapeutic index that predisposes patients on chronic lithium maintenance treatment to poisoning with relatively minor changes in medications or health status.

3. Bloody diarrhea from Egypt=shigella. Shigella is a genus of Gram-negative, non-spore forming rod-shaped bacteria closely related to Escherichia coli and Salmonella. The causative agent of human shigellosis, Shigella cause disease in primates, but not in other mammals. It is only naturally found in humans and apes. During infection, it typically causes dysentery.

4. Adequate thyroid control with normal TSH and T3 but low T4.

5. Thyroid nodule with euthyroidism investigation= radionucleotide scan,FNAC? Solitary thyroid nodule is a common clinical entity encountered by the otorhinolaryngologist and physcians. The optimum diagnostic strategy for the euthyroid patient with a soilitary thyroid nodule is still a matter of debate. The goal of diagnostic workup now is to select those patients for surgery who have a high likelihood of harbouring malignancy in the solitary thyroid nodule. The present study was undertaken to evaluate the utility of FANC in the preoperative diagnosis of solitary thyroid nodule and to evaluate the efficacy of FNAC, VSG and RNS in differentiating between benign and malignant nodules.

6. Methotrexate as the drug of choice in rheumatoid. There are three general classes of drugs commonly used in the treatment of rheumatoid arthritis: non-steroidal anti-inflammatory agents (NSAIDs), corticosteroids, and disease modifying anti-rheumatic drugs (DMARDs). NSAIDs and corticosteroids have a short onset of action while DMARDs can take several weeks or months to demonstrate a clinical effect. DMARDs include methotrexate, sulfasalazine, leflunomide (Arava), etanercept (Enbrel), infliximab (Remicade), adalimumab (Humira), abatacept (Orencia), rituximab (Rituxan), anakinra (Kineret), antimalarials, gold salts, d-penicillamine, cyclosporin A, cyclophosphamide and azathioprine (Imuran). Because cartilage damage and bony erosions frequently occur within the first two years of disease, rheumatologists now move more aggressively to a DMARD agent early in the course of disease, usually as soon as a diagnosis is confirmed.

7. Guy with cystic fibrosis what are the odds of his sister being a carrier=1:2. Mutations in the CFTR gene cause cystic fibrosis.
The CFTR gene provides instructions for making a channel that transports negatively charged particles called chloride ions into and out of cells. The flow of chloride ions helps control the movement of water in tissues, which is necessary for the production of thin, freely flowing mucus.
Mutations in the CFTR gene disrupt the function of the chloride channels, preventing them from regulating the flow of chloride ions and water across cell membranes. As a result, cells that line the passageways of the lungs, pancreas, and other organs produce mucus that is unusually thick and sticky. This mucus clogs the airways and glands, causing the characteristic signs and symptoms of cystic fibrosis.

8. Uncontrolled AF with digoxin, what to add = bisoprolol. A 58-year-old man presented to the emergency department with sudden onset rapid palpitations and significant presyncope while walking on the flat. The previous day he had undergone DC cardioversion for atrial fibrillation (AF) which had been initially successful. However, 6 h after cardioversion he was aware of intermittently raised but regular heart rates. On arrival at the emergency department (ED) he was well with no haemodynamic compromise. The ECG showed an atrial tachycardia instead of AF. Medications consisted of propafenone 300 mg twice daily, bisoprolol 5 mg at night and warfain. Bisoprolol was increased to 5 mg twice daily and he was discharged with a plan for outpatient ablation. He collapsed in the hospital car park with rapid palpations, chest tightness and vagal symptoms.

9. Guy with CLL with plt's 17 and thigh bruise, what to do= observe, give plt's? B-cell chronic lymphocytic leukemia (B-CLL), also known as chronic lymphoid leukemia (CLL), is the most common type of leukemia. Leukemias are abnormal and malignant neoplastic proliferations ("cancers") of the white blood cells (leukocytes). CLL involves a particular subtype of white blood cells, which is a lymphocyte called a B cell. B cells originate in the bone marrow, develop in the lymph nodes, and normally fight infection. In CLL, the DNA of a B cell is damaged, so that it can't fight infection by producing antibodies. Additionally, they grow out of control and accumulate in the bone marrow and blood, where they crowd out healthy blood cells.

10. Pancreatitis in preg woman cause= gall stones?. The incidence of pancreatitis ranges from 1 in 1,066 live births to 1 in 3,333 pregnancies. The most common predisposing cause of pancreatic symptoms during pregnancy is cholelithiasis (i.e., gallstones that block the pancreatic duct). A second common scenario noted in pregnancy is hypertriglyceride-induced pancreatitis. This results from the increased estrogen effect of pregnancy and the familial tendency for some women toward high triglyceride levels. Drugs, specifically tetracycline and thiazides (not commonly used in pregnancy), as well as increased alcohol consumption, can also cause pancreatitis. Recently, pancreatitis has been linked to more than 800 mutations of the cystic fibrosis transmembrane conductance regular gene. Pancreatitis can be seen throughout pregnancy and when noted, is most likely to be secondary to cholelithiasis.

[aftaab]

11. Protein degradation in the cell= proteasome Serine proteases include the digestive enzymes trypsin, chymotrypsin, and elastase. Different serine proteases differ in substrate specificity. For example, chymotrypsin prefers an aromatic side chain on the residue whose carbonyl carbon is part of the peptide bond to be cleaved (R-group colored blue below). Trypsin prefers a positively charged Lys or Arg residue at this position. It has been suggested that degradation of polyubiquitylated proteins is coupled to dissociation of 26S proteasomes. In contrast, using several independent types of experiments, we find that mammalian proteasomes can degrade polyubiquitylated proteins without disassembling. Thus, immobilized, 35S-labeled 26S proteasomes degraded polyubiquitylated Sic1 and c-IAP1 without releasing any subunits. In addition, it is predicted that if 26S proteasomes dissociate into 20S proteasomes and regulatory complexes during a degradation cycle, the reassembly rate would be limiting at low proteasome concentrations.

12. Hair loss= valproate. Up to 12% of patients taking sodium valproate experience hair loss. Once other causes for the patient's hair loss have been ruled out, options for changing the medication (since there are so many other antiepileptics available now) can be discussed with the neurologist. If the neurologist maintains that the patient must stay on the drug, there are some controversial data to suggest that supplementation with selenium may counteract the alopecia seen in patients on sodium valproate. As long as you work with the patient's neurologist, you may be able to find a common ground with selenium supplementation and continue the antiepileptic drug. Unfortunately, there are no published recommendations that I know of for selenium supplementation dosages

13. CML drug of choice= imatinib Approximately 10,000 new cases of chronic myeloid leukemia (CML) occur in the United States and Europe annually. The principal cause of CML has been identified as a constitutively active tyrosine kinase encoded by the Bcr-Abl fusion gene, the product of the t(9;22) Philadelphia translocation. Until now, standard therapy for CML has been interferon-alfa combined with cytarabine. Imatinib mesylate (imatinib, STI571, Gleevec, Novartis) is a novel signal transduction inhibitor that targets the Bcr-Abl protein, potentially preventing the growth and production of CML cells. On May 10, 2001, imatinib was approved by the US Food and Drug Administration (FDA) for the treatment of patients with Philadelphia chromosome-positive CML in blast crisis, accelerated phase, or chronic phase after failure of interferon-alfa therapy. Imatinib is currently approved for this indication in more than 65 countries worldwide, including the European Union (EU), Switzerland, Australia , and Japan.

14. Mitochondrial inheritance=optic atrophy. Some of the estimated 20,000 genes in the human genome are located in small compartments in the cell called the mitochondria, rather than on chromosomes in the cell’s nucleus. Some cells contain many hundreds of mitochondria
• The genes found within the mitochondria contain the information that codes for the production of many of the important enzymes that drive the biochemical reactions to produce the body’s source of energy: a chemical called ATP (adenosine triphosphate). The cells in the body, especially in organs such as the brain, heart, muscle, kidneys and liver, cannot function normally unless they are receiving a constant supply of energy
• Faulty mitochondrial genes can result in absence of these enzymes, or enzymes that are impaired and do not work properly.
This leads to a reduction in the supply of ATP, and may result in problems with the body’s functions
• The pattern of inheritance of conditions due to faulty mitochondrial genes is often called maternal inheritance. This is because a child inherits the great majority of their mitochondria from their mother through the egg
• Usually a mother will have a mixture of mitochondria containing the working gene copy and others containing the faulty gene.
For a condition to develop, the number of mitochondria with the faulty gene must be above a critical level (the threshold)
• The cells of different tissues and organs can have varying amounts of mitochondria with a faulty gene, and the number of cells with the faulty mitochondria in each tissue or organ may vary

15. Bradycardia, hypotention, RR=8 = dihydrocodeine. Approved indication for dihydrocodeine is the management of moderate to moderately severe pain as well as coughing and shortness of breath. As is the case with other drugs in this group, the antitussive dose tends to be less than the analgesic dose, and dihydrocodeine is a powerful cough suppressant like all other members of the immediate codeine family (see below) and their cousins hydrocodone, oxycodone and ethylmorphine (a.k.a. dionine and codethyline), whole opium preparations, and the strong opioid hydromorphone.
For use against pain, dihydrocodeine is usually formulated as tablets or capsules containing a quarter grain (15 or 16 mg) or a half grain (30 or 32 mg) with or without other active ingredients such as aspirin, paracetamol (acetaminophen), ibuprofen, or others. The usual dose is one tablet taken every 4–6 hours when necessary.

16. Erythema artifacta. People with dermatitis artefacta usually have an underlying psychological problem. It can be caused by stress and drugs (particularly methamphetamine or "crank"). Abuse and Munchausen's Syndrome by Proxy are other causes of what may seem to be self-infliction of injuries, at first glance. Types of Dermatitis Artefacta Single Episode: If the dermatitis artefacta is a single episode that was triggered by a particularly difficult situation (such as job loss or divorce), about 70% will stop injuring themself once the triggering situation is resolved. Multiple Episodes: However for about 30%, dermatitis artefacta is ongoing and recurrent, as part of a long history of psychological problems. Drugs: People on drugs, particularly street drugs such methamphetamine, which is known as "crank", sometimes think they see and/or feel bugs on their body. They pick at the "bugs" trying to remove them, creating open wounds and scabs. Methamphetamine: Crank Bug Bites. A phenomenon sometimes seen in methamphetamine users is referred to as "crank bug bites." Patients claim to see and/or feel bugs on their body and attempt to remove them or pick at them until they create open wounds and scabs.

17. RNA= northern blot Northern blots are not used very often for diagnostic purposes; they are used mainly in research. The techniques are fairly sophisticated and other methods yield acceptable results (such as Southern blots or PCR). However, a description of Northern blots is included here in the interest of completeness and the probability that you will run across the term in some of the papers you may read.
A northern blot is very similar to a Southern blot except that it is RNA rather than DNA which is extracted, run on a gel and transferred to a filter membrane. There are 3 types of RNA: tRNA (transfer RNA - active in assembly of polypeptide chains), rRNA (ribosomal RNA - part of the structure of ribosomes) and mRNA (messenger RNA - the product of DNA transcription and used for translation of a gene into a protein). It is mRNA which is isolated and hybridized in northern blots.

18. Guy from surgical ward with appendicectomy develops MI, is on aspirin and clopidogrel, what to add= PCI. Dr. Steinhubl and Dr. Topol, authors of CREDO,1 disagree with my analysis of long-term clopidogrel therapy after percutaneous coronary intervention (PCI) in the PCI–CURE and CREDO trials.2 However, their arguments seem biased and misleading.
The CURE trial3 showed a minor absolute reduction of 1.1% (p=0.009) in the composite of death, myocardial infarction or stroke from one month to the end of follow-up (mean nine months) in patients receiving clopidogrel in addition to aspirin, compared with aspirin alone. However, the number of ischaemic events was nearly identical in the clopidogrel and placebo groups after the first three months.4 In fact, among patients given 101–199 mg aspirin per day in CURE, clopidogrel did not contribute to any further reduction in ischaemic events.5 If 1000 patients in CURE received clopidogrel instead of placebo for nine months, 15 myocardial infarctions would be avoided (12 of which during the first three months) at the price of an extra 10 major and 27 minor bleedings. No life would be saved, no stroke prevented, and the costs of clopidogrel to accomplish this would be around 500000 EUR. This is clearly an injudicious way to utilize healthcare resources.

19. Diarrhea with rectal biopsy with inflammation throughout the lamina propria with lymphocyte proliferation and granulomas= crohns. nflammatory bowel diseases (ulcerative colitis and Crohn's disease) are chronic long-lasting inflammatory diseases with yet unknown etiology. Recent advancement revealed that both diseases are associated with genetic predisposition and environmental factors such as luminal microorganisms and antigens. Crohn's disease is associated with histopathologic features such as granuloma formation and longitudinal ulceration. In this article we describe the role of granuloma in the immunopathogenesis of Crohn's disease. Granuloma of Crohn's disease may play crucial roles as antigen-presenting cites to memory type T cells, which leads to activation and proliferation of T cells. Antigens presented at granuloma may be closely related to the disease.

20. Which supports idiopathic Parkinson= asymmetrical dyskinesia. Fifty four patients with idiopathic Parkinson's disease receiving levodopa therapy were studied. Thirty three of these patients displayed peak-dose dyskinesia. Neither the duration of Parkinson's disease nor the duration of levodopa therapy discriminated between patients with and patients without peak-dose dyskinesia. Consequently, these criteria could not determine whether the first appearance of peak-dose dyskinesia depends on the duration of Parkinson's disease--a factor that is related to the severity of the disease--or on the duration of levodopa therapy. A subgroup of nineteen patients with unilateral or unequivocally asymmetrical peak-dose dyskinesia was examined 12 hours after withdrawal of levodopa.

21. 22yr male with diabetes, BMI 22, sugar 38, urine 3sug and 3acetone, which supports type 1= ketoneuria, age?. Secondary consequences of the primary metabolic derangements in diabetic ketoacidosis include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones and glucose. Patients are often profoundly dehydrated and have a significantly depleted potassium level (as high as 5 mEq per kg of body weight). A normal or even elevated serum potassium concentration may be seen due to the extracellular shift of potassium in acidotic conditions, and this very poorly reflects the patient's total potassium stores. The serum potassium concentration can drop precipitously once insulin treatment is started, so great care must be taken to repeatedly monitor serum levels. Urinary loss of ketoanions with brisk diuresis and intact renal function may also lead to a component of hyperchloremic metabolicacidosis.

22. 55 diabetic, obese, normal renal funct. 1st chice drug= metformin. Metformin (INN) (pronounced /mɛtˈfɔrmɪn/; originally sold as Glucophage) is an oral anti-diabetic drug. It is the first-line drug of choice for the treatment of type 2 diabetes, particularly in overweight and obese people and those with normal kidney function. Evidence is also mounting for its efficacy in gestational diabetes, although safety concerns still preclude its widespread use in this setting. It is also used in the treatment of polycystic ovary syndrome and has been investigated for other diseases where insulin resistance may be an important factor.

23. Pt with MI has high blood sugar of 12, which is the optimal Rx = i.v.insulin. Glucose is the major carbohydrate used as fuel in our body to supply energy. It can easily be measured because some circulates in our blood stream, and can be easily checked with finger sticks. Average blood sugar levels are 100 mg/dl (70-120 mg/dl) or 5 mmol/L. The risk of developing Diabetes is increased when FASTING blood sugars stay consistently > 125mg/dl or 7 mmol/L. The risk of developing a Hypoglycemic Coma occurs when blood sugars are consistently < 45 mg/dl or 2.5 mmol/L. Under normal circumstances glucose is the preferred fuel of brain cells, and also muscle cells in early exercise. Improved blood-glucose control decreases the progression of diabetic microvascular disease, but the effect on macrovascular complications is unknown. There is concern that sulphonylureas may increase cardiovascular mortality in patients with type 2 diabetes and that high insulin concentrations may enhance atheroma formation. We compared the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial.

24. Patient with pneumocystis jiv… pneumonia, which drug to give=cotrimoxazole The causative organism of PCP is distributed worldwide and Pneumocystis pneumonia has been described in all continents except Antarctica. It was originally described as a rare cause of pneumonia in neonates. It is commonly believed to be a commensal organism (dependent upon its human host for survival). The possibility of person-to-person transmission has recently gained credence, with supporting evidence coming from many different genotyping studies of Pneumocystis jirovecii isolates from human lung tissue. For example, in one outbreak of 12 cases among transplant patients in Leiden, it was suggested as likely, but not proven, that human-to-human spread may have occurred. Greater than 75% of children are seropositive by the age of 4, which suggest a high background exposure to the organism.

25. Antibiotic for alpha haemolytic streptococci in IE? Penicillin is the preferred medication. Oral penicillin must be taken for 10-days. Patients need to take the entire amount of antibiotic prescribed and not discontinue taking the medication when they feel better. Stopping the antibiotic early can lead to a return of the strep infection. Occasionally, a single injection of long-acting penicillin (Bicillin) is given instead of 10 days of oral treatment.
About 10% of the time, penicillin is not effective against the strep bacteria. When this happens a doctor may prescribe other antibiotics such as amoxicillin (Amoxil, Pentamox, Sumox, Trimox), clindamycin (Cleocin), or a cephalosporin (Keflex, Durocef, Ceclor). Erythromycin (Eryzole, Pediazole, Ilosone), another inexpensive antibiotic, is given to people who are allergic to penicillin. Scarlet fever is treated with the same antibiotics as strep throat.
Alpha-hemolytic Streptococcus
1. Streptococcus Pneumoniae (Pneumococcus)
2. Viridans streptococcus (bacterial endocarditis)

26. 19 male with nephrotic syndrome, which is the commonest GN= membranous, minimal change? It is postulated that MCD is a disorder of T cells, which release a cytokine that injures the glomerular epithelial foot processes. This, in turn, leads to a decreased synthesis of polyanions. The polyanions constitute the normal charge barrier to the filtration of macromolecules, such as albumin. When the polyanions are damaged, leakage of albumin follows. The identity of this circulating permeability factor is uncertain, although it is postulated that it may be hemopexin.
Some of the cytokines that have been studied in MCD are interleukin-12 (IL-12) and interleukin-4 (IL-4). IL-12 levels have been found to be elevated in peripheral blood monocytes during the active phase and normalized during remission. Interleukin-18 (IL-1 can synergize with IL-12 to selectively increase the production of vascular permeability factor from T cells. In addition, levels of IL-4 and CD23 (a receptor for immunoglobulin E [IgE]1 ) have been found to be elevated in peripheral blood lymphocytes.

27. 25 male dies suddenly in football match, what is the commonest cause= HOCM. Mitral valve changes: The narrowing of the left ventricular outflow tract disrupts the proper function of the mitral valve, resulting in outflow obstruction and increased pressure in the left ventricle.
The obstruction is the result of the mitral valve striking the septum. When this occurs, the mitral valve frequently leaks, causing the blood to go back into the left atrium.
Stiffness in the left ventricle occurs as a result of cellular changes that occur in the heart muscle when it thickens. The left ventricle is unable to relax normally and fill with blood. Since there is less blood at the end of filling, there is less oxygen-rich blood pumped to the organs and muscles. The stiffness in the left ventricle causes pressure to increase inside the heart and may lead to the symptoms described below.

28. Which is ass with risk of sudden death in HOCM= vent septum 3.3cm, systolic anterior motin of the mitral valve, left atrial press of 30mmHg, mitral regurgitation. It has been proposed, based on genotype–phenotype correlations, that disease causing mutations in genes encoding sarcomeric proteins could also be unfavourable (or favourable) primary determinants of sudden death.7 While such a molecular based treatment strategy is attractive,7 caution is warranted in translating the “good gene/bad gene” hypothesis to the practical clinical management of HCM patients.8 Available epidemiologic–genetic data are based on relatively small numbers of genotyped families; each of the 10 known disease causing HCM mutant genes (and approximately 200 individual mutations) occur infrequently in the general population of this genetically heterogeneous disease. Furthermore, genotyping involves complex, time consuming, and expensive laboratory techniques which are presently confined to only a select few research oriented laboratories.

29. Best way to screen relatives of a guy with haemochromatosis= serum iron, serum ferritin, transferring sat, TIBC Primary haemochromatosis is an inherited disease.
It is thought to be mainly caused by a mutation of a gene called HFE, which probably allows excess iron to be absorbed from the diet. This mutation is known as C282Y and to develop haemochromatosis you usually need two genes (one from each parent) to be C282Y. However, not everyone with the mutation may develop the disease and it may occur if only one C282Y gene is present.
Confusingly another mutation labelled H63D elsewhere on the HFE gene may occur alone or with C282Y and also influence iron levels.

30. Diagnosis of CLL= BM, genetic B-cell chronic lymphocytic leukemia (CLL) is the most common leukemia in adults. The morphologic features and immunophenotype of CLL cells are well characterized. A unique, recurring genetic alteration has not been identified in CLL, but chromosomal aberrations occurring in CLL have been linked to prognosis.1-3 For example, deletions of chromosomes 17p and 11q are associated with an adverse clinical outcome, with overall survival of 3 years and 6 to 7 years, respectively. Patients with isolated 13q deletions have a favorable clinical course and best overall survival, 11 years. The clinical course of patients with CLL with trisomy 12q is intermediate between the groups with inferior and favorable outcomes. Early genetic studies of CLL using conventional chromosome banding analysis detected chromosomal aberrations in 40% to 60% of cases.4,5 However, only dividing cells are evaluated by chromosome banding techniques. Because it has been difficult to stimulate CLL cells to divide, novel stimulation techniques have been reported to improve the detection of chromosomal aberrations, particularly translocations, in CLL lymphocytes.