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Merck Manual viral meningitis cerebrospinal fluid normal glucose increased protein herpes simplex encephalitis acyclovir myasthenia single fiber EMG
"myasthenia gravis" AND diagnosis
| Q. No. | Correct answer | Brief explanation |
|---|---|---|
| 1 | C. Endoscopy | Upper GI endoscopy is the investigation of choice in massive hematemesis because it identifies the source and can provide endoscopic hemostasis. |
| 2 | C. Autoimmune gastritis | Autoimmune atrophic gastritis destroys parietal cells, causing intrinsic-factor deficiency and pernicious anemia. |
| 3 | B. Cholera | Cholera causes an acute, profuse watery diarrheal illness. Ulcerative colitis, VIPoma, and coeliac disease usually cause chronic or recurrent diarrhea. |
| 4 | A. IL-23 inhibitor | Mirikizumab is a monoclonal antibody directed against the p19 subunit of interleukin-23. |
| 5 | A. Collection of pancreatic juice after secretin | The secretin stimulation test is a direct pancreatic function test and is highly sensitive for early chronic pancreatitis. |
| 6 | D. CBD stone | Painless progressive obstructive jaundice with a palpable gallbladder suggests malignant obstruction, such as carcinoma head of pancreas, periampullary carcinoma, or cholangiocarcinoma. A CBD stone usually produces painful, intermittent obstruction and does not typically cause a palpable gallbladder. |
| 7 | B. Hemiparesis | Cavernous sinus thrombosis classically causes proptosis, chemosis, ptosis, and external ophthalmoplegia due to cranial nerve III, IV, and VI involvement. Hemiparesis is not a typical feature. |
| 8 | B. Normal glucose and raised proteins | Viral meningitis usually has lymphocytic pleocytosis, normal CSF glucose, and mildly raised CSF protein. This is consistent with the Merck CSF table. |
| 9 | D. Multiple sclerosis | Extrapyramidal manifestations occur in Parkinson disease, carbon monoxide poisoning, and basal-ganglia cerebrovascular lesions. Multiple sclerosis primarily produces upper motor neuron, sensory, cerebellar, and optic-nerve signs. |
| 10 | B. Delirium | Generalized EEG slowing, particularly diffuse theta and delta activity, is characteristic of delirium. |
| 11 | A. Acyclovir | Intravenous acyclovir is the treatment of choice for suspected herpes simplex encephalitis. |
| 12 | A. Carbamazepine | The episodes suggest focal impaired-awareness seizures from a temporal-lobe infarct. Carbamazepine is an appropriate initial antiseizure drug in this exam context. |
| 13 | C. Increased intracranial tension | Diffuse axonal injury follows rotational or shearing forces, typically affects white matter and gray-white junctions, and has small hemorrhagic lesions. Raised intracranial pressure may occur in severe head injury but is not a defining characteristic. |
| 14 | D. Measurement of jitter by single-fiber electromyography | Single-fiber EMG is the most sensitive electrophysiological test for myasthenia gravis. |
| 15 | A. Geniculate ganglion | Ramsay Hunt syndrome is herpes zoster reactivation in the geniculate ganglion of the facial nerve, causing facial palsy with ear vesicles and sometimes vestibulocochlear symptoms. |
| 16 | D. Methanol | Methanol poisoning can cause bilateral putaminal necrosis and secondary parkinsonism. |
| 17 | C. Horner’s syndrome | Horner syndrome causes miosis due to loss of sympathetic pupillary dilatation. Oculomotor palsy, optic atrophy, and Adie tonic pupil may be associated with a large pupil. |
| 18 | B. Smoking | Smoking is a recognized modifiable risk factor for delirium in critically ill ICU patients. |
| 19 | A. Ischemic stroke involving the cerebellum | Sudden continuous vertigo, vomiting, horizontal nystagmus, and marked gait ataxia in a patient with vascular risk factors should be treated as a posterior-circulation or cerebellar stroke until excluded. |
| 20 | D. All of the above | Acamprosate modulates glutamatergic neurotransmission, interacts with NMDA receptor pathways, and reduces calcium influx through voltage-operated calcium channels. |
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"acute liver failure" AND management
"neurocysticercosis" AND treatment
WHO hepatitis E acute liver failure management clinical guidance neurocysticercosis treatment guideline
mkdir -p "/tmp/workspace/medicine-solved-paper/src" "/tmp/workspace/medicine-solved-paper/output" && python - <<'PY' from reportlab.lib.pagesizes import A4 from reportlab.platypus import SimpleDocTemplate, Paragraph, Spacer, PageBreak, Table, TableStyle, KeepTogether from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib import colors from reportlab.lib.units import cm from reportlab.pdfbase.pdfmetrics import stringWidth from reportlab.lib.enums import TA_CENTER from reportlab.pdfbase.ttfonts import TTFont from reportlab.pdfbase import pdfmetrics from pathlib import Path out=Path('/tmp/workspace/medicine-solved-paper/output/Final_MBBS_Medicine_Complete_Solved_Paper.pdf') styles=getSampleStyleSheet() styles.add(ParagraphStyle(name='TitleX',parent=styles['Title'],fontSize=18,leading=22,alignment=TA_CENTER,spaceAfter=10,textColor=colors.HexColor('#17365D'))) styles.add(ParagraphStyle(name='SubX',parent=styles['Normal'],fontSize=10,leading=13,alignment=TA_CENTER,textColor=colors.HexColor('#444444'),spaceAfter=12)) styles.add(ParagraphStyle(name='H1X',parent=styles['Heading1'],fontSize=15,leading=19,textColor=colors.HexColor('#17365D'),spaceBefore=10,spaceAfter=8)) styles.add(ParagraphStyle(name='H2X',parent=styles['Heading2'],fontSize=12,leading=15,textColor=colors.HexColor('#1F4E79'),spaceBefore=8,spaceAfter=5)) styles.add(ParagraphStyle(name='QX',parent=styles['Heading3'],fontSize=10.5,leading=14,textColor=colors.black,spaceBefore=7,spaceAfter=3)) styles.add(ParagraphStyle(name='BodyX',parent=styles['BodyText'],fontSize=9.2,leading=12.4,spaceAfter=4)) styles.add(ParagraphStyle(name='SmallX',parent=styles['BodyText'],fontSize=8,leading=10.2,spaceAfter=2)) def P(t, style='BodyX'): return Paragraph(t,styles[style]) def bullet(items): return [P('• '+x) for x in items] def section(title): return [PageBreak(),P(title,'H1X')] def q(title, intro=None, bullets=None): x=[P(title,'QX')] if intro:x.append(P(intro)) if bullets:x+=bullet(bullets) return x story=[] story += [P('Final MBBS Part-II (2021 Batch)<br/>Fourth PCT Examination - Medicine','TitleX'),P('Complete solved paper based on the four uploaded pages. Answers are structured for university examination writing. Where the paper says “solve any”, answers to every visible option are supplied.','SubX')] story += [P('<b>Scope note:</b> The uploaded pages show Section A MCQs, Section B questions 1 and 2, two continuation items on the Section C page, and Section C long-answer questions. This PDF solves all legible questions.','BodyX'),Spacer(1,8)] story += [P('Contents','H2X'),P('1. Section A: 20 MCQs with reasons<br/>2. Section B: Brief answers<br/>3. Section B: Short answers<br/>4. Continuation short notes<br/>5. Section C: Long answers<br/>6. Selected references','BodyX')] # A story += section('Section A - Multiple Choice Questions') mcqs=[ ('1','C. Endoscopy','It localizes the source of upper gastrointestinal bleeding and permits endoscopic hemostasis.'), ('2','C. Autoimmune gastritis','Autoimmune destruction of parietal cells causes intrinsic-factor deficiency and pernicious anaemia.'), ('3','B. Cholera','Cholera is classically an acute, profuse watery diarrhoea. The other conditions usually cause chronic or recurrent diarrhoea.'), ('4','A. IL-23 inhibitor','Mirikizumab is an anti-IL-23 p19 monoclonal antibody.'), ('5','A. Collection of pancreatic juice after secretin','Direct secretin pancreatic function testing is sensitive for early exocrine pancreatic dysfunction.'), ('6','D. CBD stone','Progressive painless jaundice with palpable gallbladder suggests malignant distal biliary obstruction. CBD stones typically cause pain and fluctuating obstruction.'), ('7','B. Hemiparesis','Cavernous sinus thrombosis produces proptosis, chemosis, ptosis and ophthalmoplegia; hemiparesis is not typical.'), ('8','B. Normal glucose and raised proteins','Typical viral meningitis CSF: lymphocytic pleocytosis, normal glucose and mildly elevated protein.'), ('9','D. Multiple sclerosis','MS is principally a demyelinating CNS disease with pyramidal, sensory, cerebellar and optic manifestations, not a usual extrapyramidal disorder.'), ('10','B. Delirium','Generalized EEG slowing with excess theta/delta activity supports diffuse cerebral dysfunction in delirium.'), ('11','A. Acyclovir','IV acyclovir should be started immediately when herpes simplex encephalitis is suspected.'), ('12','A. Carbamazepine','The semiology is focal impaired-awareness seizure with temporal-lobe structural lesion. Carbamazepine is a conventional first-line focal antiseizure medicine.'), ('13','C. Increased intracranial tension','DAI is defined by rotational/shearing injury, predominantly white-matter lesions and lesions at the grey-white junction. Raised ICP can occur but is not defining.'), ('14','D. Single-fibre electromyography','Increased jitter on single-fibre EMG is the most sensitive electrophysiological investigation for myasthenia gravis.'), ('15','A. Geniculate ganglion','Herpes zoster reactivation at the geniculate ganglion causes Ramsay Hunt syndrome.'), ('16','D. Methanol','Methanol may cause bilateral putaminal necrosis, resulting in secondary parkinsonism.'), ('17','C. Horner syndrome','Horner syndrome causes miosis, not a large pupil.'), ('18','B. Smoking','Smoking is a recognized modifiable association/risk factor for ICU delirium among the given choices.'), ('19','A. Ischaemic stroke involving cerebellum','Abrupt prolonged vertigo with severe gait ataxia and vascular risk warrants exclusion of posterior-circulation stroke.'), ('20','D. All of the above','Acamprosate modulates glutamatergic/NMDA pathways and calcium-channel related neurotransmission.')] data=[[P('<b>Q</b>','SmallX'),P('<b>Answer</b>','SmallX'),P('<b>Reason</b>','SmallX')]]+[[P(a,'SmallX'),P('<b>'+b+'</b>','SmallX'),P(c,'SmallX')] for a,b,c in mcqs] t=Table(data,colWidths=[0.7*cm,4.2*cm,12.3*cm],repeatRows=1) t.setStyle(TableStyle([('BACKGROUND',(0,0),(-1,0),colors.HexColor('#D9EAF7')),('GRID',(0,0),(-1,-1),0.25,colors.HexColor('#AAAAAA')),('VALIGN',(0,0),(-1,-1),'TOP'),('LEFTPADDING',(0,0),(-1,-1),4),('RIGHTPADDING',(0,0),(-1,-1),4),('TOPPADDING',(0,0),(-1,-1),3),('BOTTOMPADDING',(0,0),(-1,-1),3),('BACKGROUND',(0,1),(-1,-1),colors.white)])) story.append(t) # B brief story += section('Section B - Question 1: Brief Answer Questions') story += q('a. Enlist four investigations for Helicobacter pylori infection.',bullets=['Urea breath test - highly accurate non-invasive test for active infection and post-treatment test of cure.','Stool H. pylori antigen test - detects active infection and is useful for test of cure.','Rapid urease test on gastric biopsy at endoscopy.','Histology of gastric biopsy with special stains; biopsy culture/PCR where antimicrobial susceptibility is required.']) story += q('b. Mention four differences between amoebic and bacillary dysentery.',bullets=['Amoebic dysentery: gradual onset, fewer stools, larger-volume faeces; bacillary dysentery: abrupt onset, frequent scanty stools.','Amoebic: blood and mucus mixed with stool, tenesmus less marked; bacillary: blood/mucus/pus with severe tenesmus.','Amoebic: fever mild or absent; bacillary: fever and systemic toxicity are common.','Microscopy: amoebic shows trophozoites, sometimes with ingested RBCs, and few pus cells; bacillary shows abundant pus cells/RBCs, without trophozoites.']) story += q('c. Enumerate four stroke mimics.',bullets=['Hypoglycaemia or hyperglycaemia.','Seizure with postictal Todd paresis.','Migraine with aura or hemiplegic migraine.','Functional neurological disorder.','Also acceptable: brain tumour/subdural haematoma, Bell palsy, peripheral vestibular disorder, demyelination.']) story += q('d. Enlist four indications for lumbar puncture.',bullets=['Suspected acute meningitis or encephalitis, after assessing for contraindications.','Suspected subarachnoid haemorrhage when CT is negative or non-diagnostic.','Diagnosis of inflammatory/demyelinating disorders, for example multiple sclerosis or Guillain-Barre syndrome.','Measurement of CSF pressure and diagnosis of idiopathic intracranial hypertension; therapeutic CSF removal in selected situations.']) story += q('e. Enlist two causes each of extramedullary and intramedullary spinal-cord compression.',bullets=['<b>Extramedullary:</b> vertebral metastasis or tuberculous spondylitis with epidural compression; prolapsed intervertebral disc.','<b>Intramedullary:</b> ependymoma; astrocytoma.']) story += q('f. Mention four clinical features of lateral medullary (Wallenberg) syndrome.',bullets=['Ipsilateral facial loss of pain and temperature sensation.','Contralateral loss of pain and temperature sensation from trunk and limbs.','Ipsilateral ataxia, vertigo, nausea and nystagmus due to inferior cerebellar peduncle/vestibular nuclei involvement.','Dysphagia, dysarthria and diminished gag reflex due to nucleus ambiguus involvement.','Ipsilateral Horner syndrome may occur.']) story += q('g. Enlist two brainstem reflexes.',bullets=['Pupillary light reflex (CN II and III).','Corneal reflex (CN V and VII).','Other examples: oculocephalic reflex and oculovestibular/caloric reflex.']) story += q('h. Recurrent fever, headache, confusion, memory/personality change and seizures: define diagnosis and list two investigations.',intro='<b>Diagnosis:</b> Chronic or recurrent encephalitis/meningoencephalitis, with herpes simplex encephalitis and autoimmune encephalitis important differentials. The combination of cognitive/behavioural change, seizures and focal deficits particularly suggests limbic encephalitis.',bullets=['MRI brain with contrast, especially temporal/limbic abnormalities.','Lumbar puncture for CSF cells, protein, glucose, Gram stain/culture, HSV PCR and autoimmune encephalitis antibody panel.','EEG for temporal epileptiform activity or diffuse slowing.']) story += q('i. Coffee-ground vomiting with shock and epigastric tenderness: enlist four differential diagnoses.',bullets=['Bleeding peptic ulcer (gastric or duodenal).','Erosive gastritis or duodenitis, including NSAID-related disease.','Oesophageal or gastric varices due to portal hypertension.','Mallory-Weiss tear after retching.','Other possibilities: gastric carcinoma, oesophagitis, Dieulafoy lesion.']) story += q('j. Chronic alcohol use, recurrent pain radiating to back, steatorrhoea/ascites and raised enzymes: enlist complications.',intro='<b>Diagnosis:</b> Chronic pancreatitis, probably alcohol related.',bullets=['Pancreatic pseudocyst and pancreatic ascites/fistula.','Exocrine pancreatic insufficiency causing steatorrhoea, malnutrition and fat-soluble vitamin deficiency.','Endocrine insufficiency causing diabetes mellitus.','Biliary or duodenal obstruction and splenic/portal vein thrombosis.','Increased risk of pancreatic carcinoma.']) story += q('k. Enlist four clinical features of vitamin C toxicity.',bullets=['Nausea, abdominal cramps and osmotic diarrhoea.','Increased urinary oxalate and calcium-oxalate renal stones.','Hyperuricaemia or uricosuria may occur.','False results in some urine glucose/faecal occult blood tests; high doses may worsen iron overload in predisposed persons.']) # short answers story += section('Section B - Question 2: Short Answer Questions') story += q('a. Explain the clinical features of fulminant hepatic failure.',intro='<b>Definition:</b> Acute liver failure is acute hepatocellular dysfunction in a patient without pre-existing cirrhosis, with coagulopathy (INR ≥1.5) and hepatic encephalopathy, usually within 26 weeks of illness.',bullets=['<b>Hepatic features:</b> malaise, anorexia, nausea, vomiting, jaundice, tender hepatomegaly initially; a small liver may indicate massive necrosis.','<b>Encephalopathy:</b> irritability, sleep reversal, confusion, asterixis, drowsiness, coma; may progress rapidly.','<b>Bleeding/metabolic:</b> bruising, mucosal bleeding, prolonged PT/INR, hypoglycaemia, lactic acidosis and electrolyte disorders.','<b>Cerebral oedema:</b> headache, vomiting, hypertension with bradycardia, pupillary abnormalities, decerebration and herniation in severe disease.','<b>Systemic complications:</b> acute kidney injury, sepsis, hypotension, ARDS and multiorgan failure.']) story += q('b. Describe complications of acute pancreatitis.',bullets=['<b>Early systemic:</b> shock, SIRS/sepsis, ARDS/pleural effusion, acute kidney injury, DIC, hypocalcaemia, hyperglycaemia and multiorgan failure.','<b>Local pancreatic:</b> acute peripancreatic fluid collection, pancreatic necrosis (sterile or infected), pancreatic abscess/walled-off necrosis and pseudocyst.','<b>Vascular:</b> splenic/portal vein thrombosis, pseudoaneurysm and haemorrhage.','<b>Mechanical:</b> gastric outlet/duodenal obstruction, biliary obstruction, pancreatic ascites, pancreaticopleural fistula.']) story += q('c. Describe underlying pathophysiology of acute transverse myelitis.',bullets=['It is an acute inflammatory disorder of the spinal cord producing bilateral motor, sensory and autonomic dysfunction with a defined sensory level.','Often follows infection or vaccination, or occurs with autoimmune disorders such as multiple sclerosis, NMOSD, MOG-associated disease, SLE or sarcoidosis.','Immune-mediated activation of T lymphocytes, macrophages and antibodies causes inflammatory infiltration, blood-spinal-cord barrier disruption, demyelination and axonal injury.','Cord oedema and lesions across one or more spinal segments interrupt corticospinal, spinothalamic, dorsal-column and autonomic pathways.']) story += q('d. Explain clinical features of Lambert-Eaton myasthenic syndrome.',bullets=['Proximal symmetrical limb weakness, typically legs more than arms, causing difficulty rising from a chair or climbing stairs.','Deep tendon reflexes are reduced or absent but may transiently improve after brief maximal contraction (post-exercise facilitation).','Autonomic symptoms: dry mouth, constipation, erectile dysfunction, reduced sweating and orthostatic symptoms.','Ocular/bulbar involvement is less prominent than in myasthenia gravis, though ptosis, diplopia and dysarthria can occur.','Often associated with small-cell lung carcinoma.']) # continuation story += section('Continuation Questions Visible on the Section C Page') story += q('e. A 66-year-old man has painless progressive jaundice, palpable gallbladder and conjugated hyperbilirubinaemia. Describe differential diagnosis and investigations.',intro='<b>Clinical diagnosis:</b> Extrahepatic obstructive jaundice, highly suspicious for malignant distal biliary obstruction (Courvoisier sign).',bullets=['<b>Differential diagnosis:</b> carcinoma head of pancreas; periampullary carcinoma; distal cholangiocarcinoma; gallbladder carcinoma with biliary involvement; benign CBD stricture/chronic pancreatitis; choledocholithiasis is less likely because it usually causes colicky pain and a non-distended gallbladder.','<b>Initial laboratory tests:</b> LFT showing cholestatic pattern (raised conjugated bilirubin, ALP and GGT), CBC, PT/INR, renal function, amylase/lipase; CA 19-9 and CEA are supportive, not diagnostic.','<b>Imaging sequence:</b> transabdominal ultrasonography to confirm biliary dilatation and look for gallbladder/pancreatic mass; contrast-enhanced pancreatic protocol CT for lesion, vascular involvement and staging.','MRCP defines level/cause of obstruction. Endoscopic ultrasound with FNA/FNB establishes tissue diagnosis for pancreatic/periampullary masses. ERCP is used for brushings/biopsy and therapeutic biliary stenting.']) story += q('f. Night blindness, dry scaly skin and diet low in green leafy vegetables/liver: diagnosis and treatment.',intro='<b>Diagnosis:</b> Vitamin A deficiency causing xerophthalmia and follicular hyperkeratosis.',bullets=['<b>Features:</b> night blindness; conjunctival xerosis and Bitot spots; corneal xerosis/ulceration or keratomalacia in severe deficiency; dry rough skin and increased infection risk.','<b>Treatment in adults:</b> oral vitamin A 200,000 IU on day 1, day 2 and after 2 weeks, if uncomplicated. If severe ocular disease, vomiting/malabsorption, or inability to take orally, use specialist-supervised parenteral therapy.','Treat associated protein-energy malnutrition and intercurrent infections; advise dietary sources: green leafy vegetables, yellow/orange fruits and vegetables, milk/egg yolk, liver and fortified foods. Avoid excessive dosing in pregnancy.']) story += q('Handwritten case: recurrent renal stones, serum calcium 12.7 mg/dL and raised PTH. State diagnosis and management.',intro='<b>Diagnosis:</b> Primary hyperparathyroidism, most commonly due to parathyroid adenoma, causing hypercalcaemia and recurrent calcium stones.',bullets=['Confirm with repeat corrected/ionized calcium, intact PTH, phosphate, alkaline phosphatase, 25-OH vitamin D, creatinine/eGFR and 24-hour urinary calcium; exclude familial hypocalciuric hypercalcaemia by calcium-creatinine clearance ratio.','Assess complications: renal ultrasound/CT for stones or nephrocalcinosis; DXA bone density. Localize preoperatively by neck ultrasound and sestamibi scan, after biochemical diagnosis.','Definitive treatment: parathyroidectomy, indicated in symptomatic disease such as nephrolithiasis, significant hypercalcaemia, skeletal/renal involvement, age under 50, or guideline-based thresholds.','If not operated: hydration, avoid thiazides/lithium/excess calcium, correct vitamin D cautiously, monitor calcium/renal function/BMD; cinacalcet lowers calcium and bisphosphonate improves bone density when appropriate.']) # C story += section('Section C - Long Answer Question L1') story += q('3(a). Describe in detail the clinical features and treatment of vitamin B1 deficiency.',intro='<b>Vitamin B1 (thiamine)</b> is required for carbohydrate metabolism (pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, transketolase). Deficiency is common with alcohol-use disorder, malnutrition, prolonged vomiting, malabsorption and refeeding.',bullets=['<b>Dry beriberi:</b> symmetrical distal sensorimotor polyneuropathy, paraesthesiae/burning feet, calf tenderness, foot drop, muscle wasting and reduced reflexes.','<b>Wet beriberi:</b> high-output cardiac failure, tachycardia, warm peripheries, oedema, cardiomegaly and pulmonary congestion. Shoshin beriberi is fulminant biventricular failure with lactic acidosis and shock.','<b>Wernicke encephalopathy:</b> acute confusion, gait ataxia and ocular abnormalities (nystagmus, lateral rectus palsy, gaze palsy). The full triad is often incomplete.','<b>Korsakoff syndrome:</b> severe anterograde memory impairment, confabulation and apathy, often after inadequately treated Wernicke encephalopathy.','<b>Treatment:</b> give thiamine before glucose. Suspected Wernicke encephalopathy: parenteral thiamine 500 mg IV three times daily for 2-3 days, then 250 mg IV/IM daily for 3-5 days, followed by oral thiamine 100 mg three times daily. Give magnesium if low, nutritional rehabilitation and alcohol-withdrawal/dependence care.','For uncomplicated deficiency: oral thiamine 100 mg two or three times daily with balanced diet; treat underlying cause. Cardiac failure requires standard supportive management plus urgent thiamine.']) story += q('3(b). Neurocysticercosis: etiology, pathophysiology, clinical presentation, diagnostic criteria and treatment.',intro='<b>Definition:</b> CNS infection by larval cysts of Taenia solium.',bullets=['<b>Etiology/transmission:</b> humans ingest T. solium eggs by faeco-oral contamination from a tapeworm carrier. This differs from intestinal taeniasis, which follows eating undercooked pork containing cysticerci.','<b>Pathophysiology:</b> cysticerci lodge in parenchyma, subarachnoid space, ventricles or spinal cord. Viable cysts often evoke little inflammation. Degeneration produces intense host inflammatory response, oedema and seizures. Calcified lesions can remain epileptogenic.','<b>Clinical presentation:</b> new-onset seizures are most common; headache/raised ICP, focal deficits, cognitive/psychiatric symptoms, hydrocephalus, chronic meningitis, stroke from vasculitis, or ocular disease may occur.','<b>Diagnosis:</b> CT shows calcification and ring-enhancing lesions; MRI better shows viable, ventricular, posterior fossa and subarachnoid disease. A cyst with scolex is highly specific. Support with serum EITB/ELISA, exposure history and ophthalmic examination before antiparasitic therapy.','<b>Diagnostic criteria:</b> use Del Brutto criteria integrating absolute criteria (histology or cyst with scolex), major neuroimaging/serology criteria, minor clinical criteria and epidemiological exposure.','<b>Treatment:</b> control seizures with antiseizure medicine. For viable parenchymal disease, albendazole 15 mg/kg/day in two doses, typically 10-14 days, with corticosteroid cover; combination albendazole plus praziquantel is used in selected patients with multiple viable cysts.','Do not start cysticidal therapy without considering raised ICP, hydrocephalus, diffuse oedema or ocular cysts. Ventricular/subarachnoid disease may require neurosurgical/endoscopic removal or CSF diversion plus individualized prolonged anti-inflammatory/antiparasitic treatment.']) story += section('Section C - Long Answer Question L2') story += q('4(a). Fever, jaundice, grade I encephalopathy, asterixis, INR 4.8, AKI and IgM anti-HEV positive: diagnosis, other etiologies, complications and management.',intro='<b>Diagnosis:</b> Hepatitis E virus-associated acute liver failure (fulminant hepatic failure), complicated by hepatic encephalopathy, severe coagulopathy and acute kidney injury.',bullets=['<b>Other etiologies of acute liver failure:</b> acetaminophen/drug-induced liver injury; hepatitis A and B, HSV and other viral hepatitis; autoimmune hepatitis; Wilson disease; ischaemic hepatitis; acute Budd-Chiari syndrome; toxins such as Amanita phalloides; malignant infiltration and pregnancy-related fatty liver/HELLP.','<b>Complications:</b> cerebral oedema and intracranial hypertension, coma/seizures; hypoglycaemia; bleeding/coagulopathy; sepsis; AKI/hepatorenal physiology; metabolic acidosis/electrolyte disturbance; ARDS, shock and multiorgan failure.','<b>Immediate ICU management:</b> admit to a liver-transplant centre/ICU. ABC stabilization, frequent neurological observations, head elevation 30 degrees, avoid sedatives where possible, monitor glucose hourly and correct hypoglycaemia.','Send serial INR/PT, LFT, bilirubin, electrolytes, phosphate, lactate, ABG, CBC, cultures and renal function. Screen other causes. Give IV fluids judiciously, avoid nephrotoxic/hepatotoxic drugs, manage AKI and begin renal replacement therapy if indicated.','Treat suspected infection promptly after cultures. Do not give FFP merely to correct INR unless active bleeding or an invasive procedure is planned. Vitamin K may be tried if deficiency is possible.','For cerebral oedema/raised ICP: head-up position, avoid fever/hypoxia/hypercapnia; mannitol or hypertonic saline in specialist care.','Assess urgently for transplant using prognostic criteria and clinical trajectory. Acute HEV is usually managed supportively; ribavirin is sometimes considered in severe acute disease in specialist practice, but evidence is limited.']) story += q('4(b). Sudden fever, severe headache, neck stiffness and photophobia in a 60-year-old: define diagnosis, etiology, investigations and management.',intro='<b>Diagnosis:</b> Acute meningitis, presumed acute bacterial meningitis until proved otherwise.',bullets=['<b>Definition:</b> inflammation of meninges causing fever, headache, neck stiffness and altered mental state, with CSF pleocytosis; bacterial meningitis is a medical emergency.','<b>Etiology in older adults:</b> Streptococcus pneumoniae is most common; Neisseria meningitidis; Listeria monocytogenes (especially age >50 years, immunocompromise); gram-negative bacilli. Consider TB, viral, fungal and partially treated bacterial meningitis depending on setting.','<b>Investigations:</b> ABC assessment, GCS and full neurological exam; two blood cultures before antibiotics if this does not delay therapy; CBC, glucose, renal/liver function, electrolytes, CRP, coagulation and lactate.','CT brain before LP only if focal neurologic deficit, papilloedema, new-onset seizure, markedly impaired consciousness or immunocompromise. If imaging would delay treatment, draw cultures and start antibiotics immediately.','CSF: opening pressure, cell count/differential, protein, paired glucose, Gram stain/culture and PCR. Bacterial CSF typically has neutrophilic pleocytosis, high protein and low glucose.','<b>Management:</b> dexamethasone 10 mg IV just before or with first antibiotic dose. Empiric therapy for age >50: IV ceftriaxone/cefotaxime plus ampicillin/amoxicillin for Listeria coverage; add vancomycin where resistant pneumococci are a concern. Modify after culture/susceptibility.','Support airway, oxygenation, IV fluids/vasopressors for shock, seizure treatment, antipyretics and ICU care if needed. Give chemoprophylaxis to close contacts only for meningococcal disease.']) story += section('Selected References and Update Notes') story += [P('• Harrison’s Principles of Internal Medicine, 22nd ed., sections on acute liver failure, meningitis, neurological infection and pancreatic disease.', 'SmallX'),P('• WHO Guidelines on Management of Taenia solium Neurocysticercosis (2021).', 'SmallX'),P('• IDSA/ASTMH Clinical Practice Guideline for Neurocysticercosis (2017).', 'SmallX'),P('• Merck Manual Professional Edition, “Cerebrospinal Fluid Findings in Meningitis”, accessed 2026.', 'SmallX'),P('• Recent systematic-review search showed no result that changes the core exam answer. For acute liver failure, transfusion decisions should be individualized rather than based on INR alone (PMID 41074601).', 'SmallX'),P('<b>Educational use:</b> This is a study answer set, not patient-specific medical advice. Local protocols and senior/specialist guidance take priority in clinical care.', 'SmallX')] def footer(canvas, doc): canvas.saveState(); canvas.setFont('Helvetica',8); canvas.setFillColor(colors.HexColor('#666666')) canvas.drawString(1.5*cm,1.0*cm,'Final MBBS Medicine - Complete Solved Paper') canvas.drawRightString(19.5*cm,1.0*cm,f'Page {doc.page}') canvas.restoreState() doc=SimpleDocTemplate(str(out),pagesize=A4,rightMargin=1.35*cm,leftMargin=1.35*cm,topMargin=1.25*cm,bottomMargin=1.55*cm,title='Final MBBS Medicine Complete Solved Paper',author='Orris') doc.build(story,onFirstPage=footer,onLaterPages=footer) print(out, out.stat().st_size) PY
python - <<'PY' from pypdf import PdfReader p='/tmp/workspace/medicine-solved-paper/output/Final_MBBS_Medicine_Complete_Solved_Paper.pdf' r=PdfReader(p) text='\n'.join(page.extract_text() or '' for page in r.pages) checks=['Section A - Multiple Choice Questions','Section B - Question 1','Neurocysticercosis','Hepatitis E virus-associated acute liver failure','Acute meningitis'] print('pages:',len(r.pages),'bytes:',__import__('os').path.getsize(p)) for c in checks: print(c, c in text) print('extracted chars:',len(text)) PY
Final MBBS Medicine Complete Solved Paper
PDF Document · PDF
Make the laq long and make laq of diabetes mellitus also and hyper and hypothyroidism and hyperaldosteroneism ,Cons and addison disease ,Diabetes ketoacidosis ,Peptic ulcer and ibd all laq types
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"diabetic ketoacidosis" AND management
"inflammatory bowel disease" AND treatment
ADA Standards of Care 2026 diabetic ketoacidosis management primary aldosteronism guideline hypothyroidism hyperthyroidism
ACG guideline peptic ulcer disease inflammatory bowel disease ulcerative colitis Crohn disease 2025
~/medicine-solved-paper
python - <<'PY' from pathlib import Path from reportlab.lib.pagesizes import A4 from reportlab.platypus import SimpleDocTemplate, Paragraph, Spacer, PageBreak, Table, TableStyle from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib import colors from reportlab.lib.units import cm from reportlab.lib.enums import TA_CENTER base=Path('/tmp/workspace/medicine-solved-paper') outdir=base/'output'; outdir.mkdir(exist_ok=True) out=outdir/'Medicine_Extended_LAQ_Answer_Bank.pdf' S=getSampleStyleSheet() S.add(ParagraphStyle(name='Title2',parent=S['Title'],fontSize=19,leading=23,alignment=TA_CENTER,textColor=colors.HexColor('#123B5D'),spaceAfter=10)) S.add(ParagraphStyle(name='Intro',parent=S['Normal'],fontSize=9.5,leading=13,alignment=TA_CENTER,textColor=colors.HexColor('#404040'),spaceAfter=12)) S.add(ParagraphStyle(name='H1a',parent=S['Heading1'],fontSize=15,leading=19,textColor=colors.HexColor('#123B5D'),spaceBefore=8,spaceAfter=7)) S.add(ParagraphStyle(name='H2a',parent=S['Heading2'],fontSize=11.5,leading=14,textColor=colors.HexColor('#1F4E79'),spaceBefore=7,spaceAfter=3)) S.add(ParagraphStyle(name='Bodya',parent=S['BodyText'],fontSize=9.2,leading=12.2,spaceAfter=3)) S.add(ParagraphStyle(name='Smalla',parent=S['BodyText'],fontSize=7.8,leading=9.8,spaceAfter=2)) def p(x,sty='Bodya'): return Paragraph(x,S[sty]) def h(x): return [PageBreak(),p(x,'H1a')] def sub(x): return p(x,'H2a') def B(items): return [p('• '+i) for i in items] def topic(title,definition,parts): a=h(title)+[p('<b>Exam opening:</b> '+definition)] for head,items in parts: a.append(sub(head)); a+=B(items) return a story=[p('Medicine Extended Long Answer Question Bank','Title2'),p('Final MBBS exam format: expanded LAQs for the uploaded paper plus requested endocrine and gastrointestinal topics. Use headings, subheadings, flowcharts and underlining in the answer book.','Intro'),p('<b>Included topics:</b> diabetes mellitus, diabetic ketoacidosis, hyperthyroidism, hypothyroidism, primary hyperaldosteronism, Cushing syndrome, Addison disease, peptic ulcer disease, inflammatory bowel disease, vitamin B1 deficiency, neurocysticercosis, acute liver failure due to hepatitis E, and acute meningitis.','Bodya')] story+=topic('1. Diabetes Mellitus', 'Diabetes mellitus is a metabolic disorder characterized by chronic hyperglycaemia resulting from defects in insulin secretion, insulin action, or both.',[ ('Classification', ['Type 1 diabetes: autoimmune beta-cell destruction leading to absolute insulin deficiency.', 'Type 2 diabetes: insulin resistance with progressive beta-cell failure; accounts for most cases.', 'Other specific types: monogenic diabetes, pancreatic disease, endocrinopathies, drug-induced diabetes and post-transplant diabetes.', 'Gestational diabetes: hyperglycaemia first recognized during pregnancy.']), ('Diagnostic criteria', ['Any one criterion, confirmed on another day if asymptomatic: fasting plasma glucose >=126 mg/dL (7.0 mmol/L); 2-hour glucose >=200 mg/dL during 75-g OGTT; HbA1c >=6.5% using standardized assay; or random glucose >=200 mg/dL with classic symptoms/hyperglycaemic crisis.', 'Prediabetes: fasting glucose 100-125 mg/dL, 2-hour OGTT 140-199 mg/dL, or HbA1c 5.7%-6.4%.']), ('Clinical features', ['May be asymptomatic. Classic symptoms are polyuria, polydipsia, polyphagia, fatigue, weight loss and blurred vision.', 'Recurrent skin/genitourinary infections, poor wound healing, pruritus vulvae and erectile dysfunction can occur.', 'Type 1 diabetes may first present with DKA; type 2 diabetes may present with hyperosmolar hyperglycaemic state.']), ('Complications', ['<b>Acute:</b> hypoglycaemia, DKA and hyperosmolar hyperglycaemic state.', '<b>Microvascular:</b> retinopathy/macular oedema, nephropathy and peripheral/autonomic neuropathy.', '<b>Macrovascular:</b> coronary artery disease, stroke and peripheral arterial disease.', '<b>Other:</b> diabetic foot ulcer/infection, Charcot arthropathy, cataract, periodontal disease and sexual dysfunction.']), ('Evaluation and monitoring', ['Assess BP, BMI, cardiovascular risk, injection technique, diet, physical activity, psychosocial issues and hypoglycaemia risk.', 'At diagnosis and periodically: HbA1c, eGFR, urine albumin-creatinine ratio, lipid profile, eye examination, comprehensive foot examination and neuropathy assessment.', 'Individualize glycaemic goal. For many non-pregnant adults, HbA1c <7% is appropriate if safely achievable.']), ('Management', ['<b>Education/lifestyle:</b> diabetes self-management education, medical nutrition therapy, weight reduction when indicated, at least 150 min/week moderate exercise, resistance training, smoking cessation and foot care.', '<b>Type 1:</b> lifelong basal-bolus insulin or pump therapy, glucose monitoring/CGM, carbohydrate counting, sick-day rules and hypoglycaemia education.', '<b>Type 2:</b> metformin is commonly used if tolerated and renal function permits. Choose GLP-1 receptor agonist/dual GIP-GLP-1 agonist and/or SGLT2 inhibitor according to obesity, ASCVD, heart failure and CKD; add other agents or insulin based on HbA1c and symptoms.', 'Treat BP, lipids and cardiovascular risk. ACE inhibitor/ARB is indicated for albuminuric CKD; statin use is based on age/risk.'])]) story+=topic('2. Diabetic Ketoacidosis (DKA)', 'DKA is an acute, life-threatening metabolic complication of diabetes caused by insulin deficiency, with hyperglycaemia, ketosis and high-anion-gap metabolic acidosis.',[ ('Precipitating factors', ['Infection, omission/inadequate insulin, first presentation of type 1 diabetes, myocardial infarction, stroke, pancreatitis, trauma, surgery, pregnancy and drugs such as glucocorticoids or SGLT2 inhibitors.', 'Always search for and treat the precipitating cause.']), ('Pathophysiology', ['Insulin deficiency with excess glucagon/catecholamines/cortisol increases gluconeogenesis and lipolysis.', 'Free fatty acids are converted to beta-hydroxybutyrate and acetoacetate, producing metabolic acidosis. Hyperglycaemia causes osmotic diuresis, dehydration and total-body potassium depletion.']), ('Clinical features', ['Polyuria, polydipsia, dehydration, weakness, nausea/vomiting, abdominal pain, tachycardia and hypotension.', 'Kussmaul respiration, acetone odour, altered sensorium or coma in severe disease.']), ('Diagnosis and investigations', ['Typical diagnostic triad: diabetes/hyperglycaemia, blood beta-hydroxybutyrate >=3 mmol/L or significant ketonuria, and metabolic acidosis (pH <7.30 and/or bicarbonate <18 mmol/L).', 'Send capillary glucose, venous blood gas, electrolytes, urea/creatinine, serum ketones, CBC, ECG, urinalysis/cultures, pregnancy test where relevant, and tests for infection/MI/pancreatitis.', 'Calculate anion gap = Na - (Cl + HCO3). Corrected sodium and serial potassium guide therapy.']), ('Management - first hour', ['ABC, monitor vitals/GCS, two IV lines, cardiac monitoring, strict input-output and hourly capillary glucose. Consider ICU/HDU for severe DKA, shock, altered consciousness, pregnancy or major comorbidity.', 'Start isotonic crystalloid. Common adult approach: 0.9% saline or balanced crystalloid 500-1000 mL/hour initially, then tailor to haemodynamics, sodium, cardiac and renal status.', 'Measure potassium before insulin. If K <3.3 mmol/L, give potassium and <b>withhold insulin</b> until K is >=3.3 mmol/L.']), ('Insulin, potassium and glucose', ['After initial fluids and if K >=3.3 mmol/L, give regular insulin IV infusion 0.1 unit/kg/hour. A routine initial insulin bolus is generally unnecessary.', 'Add potassium to IV fluid when K falls below 5.2 mmol/L, targeting K 4-5 mmol/L. Monitor every 2-4 hours.', 'When plasma glucose reaches about 200 mg/dL (11.1 mmol/L), add 5%-10% dextrose and reduce insulin rate as needed, while continuing insulin until ketoacidosis resolves.', 'Bicarbonate is not routine. Consider only for profound acidaemia, typically pH <6.9, with senior/ICU supervision. Phosphate is not routine; replace for severe hypophosphataemia or cardiorespiratory dysfunction.']), ('Resolution and prevention', ['Resolution: ketones <0.6 mmol/L with pH >=7.3 or bicarbonate >=18 mmol/L and clinical improvement. Do not stop insulin solely because glucose normalizes.', 'Give long-acting subcutaneous insulin 2-4 hours before stopping IV insulin. Teach sick-day rules, never stop basal insulin, ketone testing, adherence and follow-up.'])]) story+=topic('3. Hyperthyroidism / Thyrotoxicosis', 'Thyrotoxicosis is the clinical state of excess thyroid hormone action. Hyperthyroidism specifically means increased hormone synthesis by the thyroid gland.',[ ('Causes', ['Graves disease, toxic multinodular goitre, toxic adenoma, thyroiditis (subacute, painless/postpartum), excess thyroxine intake, iodine/amiodarone-induced disease and rarely TSH-secreting pituitary adenoma.', 'Graves disease is autoimmune, caused by TSH-receptor stimulating antibodies.']), ('Clinical features', ['Weight loss despite appetite, heat intolerance, sweating, palpitations, tremor, anxiety, irritability, proximal myopathy, fatigue and hyperdefaecation.', 'Menstrual disturbance, reduced fertility, atrial fibrillation and high-output heart failure may occur.', 'Goitre and eye signs in Graves: lid retraction/lid lag, ophthalmopathy, diplopia and pretibial myxoedema.']), ('Investigations', ['TSH is suppressed; free T4 and/or T3 is elevated. T3 toxicosis has isolated T3 elevation.', 'TSH-receptor antibodies support Graves disease. CBC/LFT are baseline before antithyroid drug therapy.', 'Radioiodine uptake scan: diffuse high uptake in Graves, focal uptake in adenoma, patchy uptake in toxic multinodular goitre; low uptake in thyroiditis/exogenous hormone. Ultrasound Doppler when scan is contraindicated.']), ('Management', ['Symptom control: propranolol, if no contraindication. Use cardioselective beta-blocker if appropriate.', 'Antithyroid drugs: methimazole/carbimazole is first choice in most adults. PTU is preferred in first trimester pregnancy and thyroid storm. Warn about fever/sore throat (agranulocytosis) and jaundice/hepatitis; stop drug and urgently check CBC/LFT if these occur.', 'Definitive therapy: radioiodine ablation or thyroidectomy. Avoid radioiodine in pregnancy/breastfeeding and use caution in active Graves orbitopathy.', 'Thyroid storm: ICU care, beta-blocker, PTU then iodine one hour later, hydrocortisone, fluids/cooling and treatment of precipitant.'])]) story+=topic('4. Hypothyroidism', 'Hypothyroidism is deficiency of thyroid hormone action. Primary hypothyroidism results from disease of the thyroid gland and is most common.',[ ('Causes', ['Hashimoto thyroiditis, post-radioiodine or thyroidectomy, iodine deficiency/excess, drugs (amiodarone, lithium), postpartum thyroiditis and congenital causes.', 'Central hypothyroidism occurs with pituitary or hypothalamic disease.']), ('Clinical features', ['Fatigue, lethargy, weight gain, cold intolerance, constipation, dry coarse skin, hair loss, hoarse voice, slow speech, depression and cognitive slowing.', 'Bradycardia, delayed relaxation of ankle reflexes, puffy face, non-pitting myxoedema, goitre or atrophic thyroid, carpal tunnel syndrome and menstrual disturbance/infertility.', 'Severe: myxoedema coma with hypothermia, bradycardia, hypotension, hypoventilation, hyponatraemia and altered consciousness.']), ('Investigations', ['Primary hypothyroidism: high TSH with low free T4. Subclinical disease: raised TSH with normal free T4.', 'Central hypothyroidism: low/normal inappropriate TSH with low free T4; evaluate other pituitary axes and MRI pituitary.', 'Anti-TPO antibodies support autoimmune thyroiditis. Check CBC, sodium, lipids and CK for consequences.']), ('Management', ['Levothyroxine is treatment. In young healthy adults, usual full replacement is approximately 1.6 microgram/kg/day; start lower, for example 12.5-25 microgram/day, in elderly people or ischemic heart disease and titrate gradually.', 'Take on an empty stomach, separated from iron, calcium and interacting medicines. Recheck TSH after about 6-8 weeks, then adjust dose.', 'In central hypothyroidism, use free T4 rather than TSH to guide therapy and exclude/treat adrenal insufficiency before starting thyroxine.', 'Myxoedema coma requires ICU care, IV levothyroxine (with or without liothyronine under specialist advice), hydrocortisone until adrenal insufficiency is excluded, ventilatory/hemodynamic support, passive warming and treatment of precipitant.'])]) story+=topic('5. Primary Hyperaldosteronism (Conn Syndrome)', 'Primary aldosteronism is autonomous aldosterone excess, causing sodium retention, hypertension, potassium wasting and suppression of renin.',[ ('Causes', ['Unilateral aldosterone-producing adenoma, bilateral adrenal hyperplasia, unilateral adrenal hyperplasia, familial hyperaldosteronism and rarely adrenal carcinoma.']), ('When to suspect', ['Resistant hypertension, hypertension with spontaneous or diuretic-induced hypokalaemia, adrenal incidentaloma, early-onset hypertension/stroke in family, or hypertension with sleep apnoea.', 'Hypokalaemia is not obligatory.']), ('Clinical features and biochemistry', ['Hypertension, muscle weakness/cramps, paraesthesiae, polyuria/polydipsia due to nephrogenic diabetes insipidus, metabolic alkalosis and hypokalaemia.', 'Serum sodium is normal or mildly high; oedema is usually absent because of aldosterone escape.']), ('Diagnosis', ['Screen with plasma aldosterone concentration and renin to calculate aldosterone-renin ratio, after correcting hypokalaemia and managing interfering medication where feasible.', 'Confirm autonomous secretion by saline infusion, oral salt loading, fludrocortisone suppression or captopril challenge, depending on local protocol.', 'CT adrenal imaging identifies anatomy but cannot reliably establish laterality. Adrenal venous sampling is the reference test for lateralization in suitable surgical candidates.']), ('Treatment', ['Unilateral disease: laparoscopic adrenalectomy after appropriate localization.', 'Bilateral hyperplasia or non-surgical candidates: mineralocorticoid receptor antagonist, usually spironolactone. Eplerenone is used if antiandrogen adverse effects occur.', 'Control BP, correct potassium, monitor renal function/potassium and treat cardiovascular risk.'])]) story+=topic('6. Cushing Syndrome', 'Cushing syndrome is the clinical state caused by chronic exposure to excess glucocorticoids. Cushing disease is pituitary ACTH-secreting adenoma.',[ ('Causes', ['Exogenous glucocorticoids are most common overall. Endogenous disease may be ACTH-dependent (pituitary adenoma, ectopic ACTH) or ACTH-independent (adrenal adenoma/carcinoma/nodular hyperplasia).']), ('Clinical features', ['Central weight gain, moon face, dorsocervical fat pad, facial plethora, thin skin, easy bruising, broad violaceous striae, proximal myopathy and poor wound healing.', 'Hypertension, diabetes/glucose intolerance, osteoporosis/fractures, hypokalaemic alkalosis, infections, mood/cognitive change and increased thromboembolic risk.', 'Women may have hirsutism, acne and menstrual irregularity. Rapid virilization suggests adrenal carcinoma.']), ('Diagnosis', ['First exclude exogenous steroid use. Confirm hypercortisolism with at least two abnormal tests: 1-mg overnight dexamethasone suppression test, late-night salivary cortisol, or 24-hour urinary free cortisol.', 'Then measure ACTH. Suppressed ACTH suggests adrenal source: CT adrenals. Normal/high ACTH suggests pituitary or ectopic source: pituitary MRI; inferior petrosal sinus sampling when needed.', 'Exclude pseudo-Cushing states such as alcohol excess, severe depression and uncontrolled diabetes.']), ('Treatment', ['Treat cause: transsphenoidal surgery for pituitary adenoma, adrenalectomy for adrenal tumour, and resection/treatment of ectopic ACTH tumour where possible.', 'Medical control when surgery is delayed/unsuccessful: steroidogenesis inhibitors such as ketoconazole, metyrapone or osilodrostat; pituitary-directed therapy such as pasireotide/cabergoline; glucocorticoid receptor blockade with mifepristone in selected cases.', 'Manage hypertension, diabetes, osteoporosis, infection and VTE risk. Give perioperative glucocorticoid replacement and monitor for adrenal insufficiency after curative treatment.'])]) story+=topic('7. Addison Disease (Primary Adrenal Insufficiency)', 'Primary adrenal insufficiency is inadequate adrenal cortisol production, usually with aldosterone deficiency, most commonly from autoimmune adrenalitis.',[ ('Causes', ['Autoimmune adrenalitis, tuberculosis, metastatic/infiltrative disease, adrenal haemorrhage, infections, adrenoleukodystrophy and bilateral adrenalectomy.']), ('Clinical features', ['Chronic fatigue, weight loss, anorexia, nausea/vomiting, abdominal pain, postural dizziness, salt craving and muscle aches.', 'Hyperpigmentation of skin, palmar creases, scars and buccal mucosa due to high ACTH. Hypotension, hyponatraemia, hyperkalaemia, hypoglycaemia and eosinophilia may occur.', 'Adrenal crisis: severe hypotension/shock, vomiting, abdominal pain, fever, confusion, hyponatraemia, hyperkalaemia and hypoglycaemia.']), ('Diagnosis', ['Morning serum cortisol is low and ACTH high in primary disease. Short Synacthen (ACTH stimulation) test shows inadequate rise in cortisol.', 'Measure renin/aldosterone: high renin and low aldosterone support mineralocorticoid deficiency. Check 21-hydroxylase antibodies, electrolytes, glucose, thyroid disease, B12 and evaluate TB/other causes where indicated.']), ('Chronic management', ['Replace glucocorticoid: hydrocortisone usually 15-25 mg/day in 2-3 divided doses, or equivalent prednisolone regimen. Replace mineralocorticoid with fludrocortisone, adjusted using BP, electrolytes and renin.', 'Education is essential: sick-day rules, double/triple oral glucocorticoid during febrile illness, emergency IM hydrocortisone kit, steroid alert card/medical ID and regular endocrine follow-up.']), ('Adrenal crisis', ['Do not delay treatment for tests. Take blood if feasible, then hydrocortisone 100 mg IV/IM immediately, followed by 200 mg/24 h infusion or 50 mg IV every 6 hours.', 'Rapid IV isotonic saline, dextrose if hypoglycaemic, correct electrolytes, treat precipitant and monitor in hospital/ICU. Mineralocorticoid is not required during high-dose hydrocortisone.'])]) story+=topic('8. Peptic Ulcer Disease', 'Peptic ulcer disease is a mucosal break in the stomach or duodenum extending through the muscularis mucosae, most commonly due to Helicobacter pylori infection or NSAID use.',[ ('Etiology and risk factors', ['H. pylori, NSAIDs/aspirin, smoking, severe physiologic stress, Zollinger-Ellison syndrome and concomitant anticoagulants/antiplatelets/steroids.']), ('Clinical features', ['Epigastric burning/gnawing pain, dyspepsia, nausea and bloating. Duodenal-ulcer pain may improve with food and recur at night; gastric-ulcer pain may be aggravated by food, but patterns are unreliable.', 'Complications may be initial presentation: upper GI bleed (hematemesis/melena), perforation (sudden severe pain/rigid abdomen), gastric outlet obstruction or penetration.']), ('Diagnosis', ['Assess alarm symptoms: bleeding, anaemia, vomiting, weight loss, dysphagia, mass, older age/new symptoms. These require early endoscopy.', 'Upper GI endoscopy with gastric biopsies identifies ulcer, provides biopsy of gastric ulcers to exclude malignancy, and allows H. pylori testing.', 'Non-invasive H. pylori tests: urea breath test or stool antigen. Stop PPI about 2 weeks and antibiotics/bismuth 4 weeks before test-of-cure where clinically safe.']), ('Management', ['Stop NSAID if possible; if essential, use lowest dose with PPI or consider COX-2 selective strategy according to cardiovascular risk.', 'Eradicate H. pylori with guideline-directed regimen based on local resistance. Bismuth quadruple therapy for 14 days is frequently preferred: PPI twice daily + bismuth + tetracycline + metronidazole. Confirm eradication at least 4 weeks after therapy.', 'Give PPI for ulcer healing, usually 4 weeks for duodenal and 8 weeks for gastric ulcer. Repeat endoscopy for gastric ulcer healing/biopsy confirmation where indicated.', 'Bleeding ulcer: resuscitate, restrictive blood transfusion strategy in most, IV PPI, urgent endoscopic hemostasis, then high-dose PPI; consider angiographic embolization/surgery if endoscopy fails.', 'Perforation/obstruction needs urgent surgical assessment, IV fluids, antibiotics, PPI and definitive management.'])]) story+=topic('9. Inflammatory Bowel Disease: Ulcerative Colitis and Crohn Disease', 'IBD comprises chronic immune-mediated intestinal inflammation, principally ulcerative colitis (UC) and Crohn disease (CD), in genetically susceptible individuals exposed to environmental and gut-microbiome factors.',[ ('Differences: UC versus Crohn disease', ['<b>UC:</b> continuous mucosal inflammation beginning in rectum and extending proximally in colon; bloody diarrhoea, urgency and tenesmus; toxic megacolon and colorectal cancer risk in extensive disease.', '<b>CD:</b> transmural, skip lesions anywhere mouth to anus, commonly terminal ileum/colon; abdominal pain, weight loss, diarrhoea, strictures, fistulae, abscesses and perianal disease.', 'Histology: UC has crypt architectural distortion/crypt abscesses; CD may show non-caseating granulomas but their absence does not exclude CD.']), ('Clinical features and extraintestinal manifestations', ['Diarrhoea, abdominal pain, fatigue, weight loss, fever, anaemia and nutritional deficiency. UC commonly has rectal bleeding; CD may cause obstructive pain/perianal discharge.', 'Peripheral/axial arthritis, uveitis/episcleritis, erythema nodosum, pyoderma gangrenosum, primary sclerosing cholangitis, venous thromboembolism, osteoporosis and kidney stones.']), ('Investigations', ['CBC, CRP/ESR, albumin, iron/B12/folate, renal/liver tests, stool culture/C. difficile assay and faecal calprotectin.', 'Ileocolonoscopy with segmental biopsies is central to diagnosis. MR enterography/CT enterography or intestinal ultrasound assesses small bowel and complications. Avoid colonoscopy in suspected toxic megacolon.', 'Assess activity/severity and screen before immunosuppressive therapy: TB, hepatitis B/C, vaccination status and pregnancy considerations.']), ('Management principles', ['Multidisciplinary care, smoking cessation in Crohn disease, nutrition support, iron/B12/vitamin D management, vaccinations, bone health, VTE prophylaxis during hospital admission and colorectal-cancer surveillance in colitis.', 'Treat to target: clinical remission plus objective improvement in biomarkers/endoscopy. Do not use corticosteroids for long-term maintenance.']), ('UC treatment', ['Mild-moderate proctitis/left-sided UC: topical and/or oral 5-aminosalicylate. More extensive mild-moderate disease: oral 5-ASA with rectal 5-ASA.', 'Moderate-severe flare: systemic corticosteroid for induction; steroid-refractory acute severe UC requires rescue infliximab or ciclosporin, with early surgical consultation.', 'Maintenance/escalation: thiopurine in selected patients, biologics (anti-TNF, vedolizumab, ustekinumab) or small molecules such as JAK inhibitors/S1P modulators based on severity and patient factors. Colectomy is curative for colonic UC.']), ('Crohn treatment', ['Mild ileocaecal CD: budesonide for induction. Systemic corticosteroids for more severe active disease, but not maintenance.', 'Moderate-severe/high-risk disease: early advanced therapy may be appropriate, including anti-TNF, vedolizumab, ustekinumab, IL-23 agents or selected small molecules according to current local guidance.', 'Antibiotics/drainage for abscess and perianal sepsis. Surgery treats strictures, perforation, abscess/fistula or refractory disease but is not curative; prevent postoperative recurrence.'])]) # concise expansions of original LAQs story+=topic('10. Vitamin B1 Deficiency: Expanded LAQ', 'Thiamine deficiency causes dry/wet beriberi and Wernicke-Korsakoff syndrome; it must be treated promptly, especially before carbohydrate administration.',[ ('Risk factors and mechanism', ['Alcohol-use disorder, starvation, hyperemesis, bariatric surgery, malabsorption, dialysis, cancer, prolonged IV dextrose without supplementation and refeeding.', 'Thiamine is a cofactor for pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase and transketolase; deficiency impairs cerebral energy metabolism and causes lactic acidosis.']), ('Clinical presentation', ['Dry beriberi: painful distal symmetric sensorimotor neuropathy, weakness, foot drop and areflexia.', 'Wet beriberi: high-output heart failure, tachycardia, oedema and cardiomegaly. Shoshin beriberi causes acute cardiovascular collapse.', 'Wernicke encephalopathy: confusion, ataxia and ocular signs (nystagmus/ophthalmoplegia). Korsakoff syndrome: profound anterograde amnesia and confabulation.']), ('Diagnosis and treatment', ['Diagnosis is clinical; response to treatment is supportive. RBC transketolase/whole-blood thiamine can support diagnosis but must not delay therapy.', 'Suspected Wernicke: high-dose parenteral thiamine, commonly 500 mg IV three times daily for 2-3 days, then 250 mg daily for 3-5 days, followed by oral therapy. Give thiamine before glucose, correct magnesium and provide nutrition/addiction care.'])]) story+=topic('11. Neurocysticercosis: Expanded LAQ', 'Neurocysticercosis is infection of the CNS by Taenia solium larval cysts and is a leading acquired cause of seizures in endemic regions.',[ ('Etiology/pathogenesis', ['Humans acquire infection by ingesting eggs from a human tapeworm carrier. Cysts lodge in brain parenchyma, ventricles/subarachnoid space or eye.', 'Viable cysts may be silent; degeneration triggers inflammation, oedema and seizures. Calcified lesions remain epileptogenic.']), ('Presentation and diagnosis', ['New-onset focal/generalized seizure, headache, raised ICP, focal deficits, hydrocephalus or chronic meningitis. CT is excellent for calcification; MRI for viable/ventricular/subarachnoid lesions.', 'Cyst with scolex is highly specific. Use serology as supportive evidence, and examine eye before cysticidal therapy.']), ('Treatment', ['Antiseizure therapy for seizures. For viable parenchymal disease, albendazole 15 mg/kg/day for 10-14 days with corticosteroid cover; selected patients with multiple viable lesions may receive albendazole plus praziquantel.', 'Avoid routine cysticidal treatment in isolated calcified lesions. Manage hydrocephalus/ventricular cysts with neurosurgical/endoscopic intervention and individualized antiparasitic/anti-inflammatory treatment.'])]) story+=topic('12. HEV Acute Liver Failure and Acute Meningitis: Expanded LAQ Points', 'Both conditions require prompt recognition, intensive supportive care and early referral where organ failure is present.',[ ('HEV acute liver failure', ['Defined by acute liver injury, INR >=1.5 and encephalopathy without prior cirrhosis. HEV IgM supports cause. Complications include cerebral oedema, hypoglycaemia, sepsis, AKI, bleeding and multiorgan failure.', 'ICU/transplant-centre referral, glucose/electrolyte/renal support, infection surveillance, avoidance of hepatotoxins and unnecessary plasma, cerebral-oedema precautions and urgent transplant assessment. Acute HEV is usually supportive; specialist-directed ribavirin is occasionally considered in severe disease, with limited evidence.']), ('Acute meningitis', ['Treat as bacterial meningitis until proven otherwise. Take blood cultures and give dexamethasone with immediate empiric antibiotics. In adults older than 50 years, ceftriaxone/cefotaxime plus ampicillin/amoxicillin covers pneumococcus and Listeria; add vancomycin based on local pneumococcal resistance.', 'LP for CSF analysis unless there are indications for CT first. Do not delay antibiotics for CT/LP in an unstable patient.'])]) story+=h('References and Exam Update Notes')[p('• Harrison’s Principles of Internal Medicine, 22nd ed.: endocrine, diabetes, gastrointestinal, liver and CNS infection chapters.','Smalla'),p('• American Diabetes Association. Standards of Care in Diabetes 2026.','Smalla'),p('• American College of Gastroenterology guidelines: Crohn disease and ulcerative colitis, updated 2025.','Smalla'),p('• Endocrine Society guidance on primary aldosteronism and adrenal disorders.','Smalla'),p('• WHO Guidelines on Management of Taenia solium Neurocysticercosis, 2021.','Smalla'),p('• Recent evidence note: recent reviews were checked for DKA and IBD. No finding changes the core university-answer protocols. For actual patients, follow local current protocol and specialist advice.','Smalla'),Spacer(1,6),p('<b>Educational note:</b> This is an examination revision document, not a substitute for bedside assessment or local clinical guidelines.','Smalla')] def footer(c,d): c.saveState();c.setFont('Helvetica',8);c.setFillColor(colors.HexColor('#666666'));c.drawString(1.4*cm,0.85*cm,'Medicine Extended LAQ Answer Bank');c.drawRightString(19.5*cm,0.85*cm,f'Page {d.page}');c.restoreState() doc=SimpleDocTemplate(str(out),pagesize=A4,leftMargin=1.35*cm,rightMargin=1.35*cm,topMargin=1.25*cm,bottomMargin=1.35*cm,title='Medicine Extended LAQ Answer Bank') doc.build(story,onFirstPage=footer,onLaterPages=footer) print(str(out),out.stat().st_size) PY
python - <<'PY' from pathlib import Path from reportlab.lib.pagesizes import A4 from reportlab.platypus import SimpleDocTemplate, Paragraph, PageBreak, Spacer from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle from reportlab.lib import colors from reportlab.lib.units import cm from reportlab.lib.enums import TA_CENTER pout=Path('/tmp/workspace/medicine-solved-paper/output/Medicine_Extended_LAQ_Answer_Bank.pdf') S=getSampleStyleSheet(); S.add(ParagraphStyle(name='T',parent=S['Title'],fontSize=19,leading=23,alignment=TA_CENTER,textColor=colors.HexColor('#17365D'),spaceAfter=10)); S.add(ParagraphStyle(name='H',parent=S['Heading1'],fontSize=15,leading=19,textColor=colors.HexColor('#17365D'),spaceBefore=8,spaceAfter=7)); S.add(ParagraphStyle(name='SH',parent=S['Heading2'],fontSize=11.5,leading=14,textColor=colors.HexColor('#1F4E79'),spaceBefore=7,spaceAfter=3)); S.add(ParagraphStyle(name='B',parent=S['BodyText'],fontSize=9.2,leading=12.2,spaceAfter=3)); S.add(ParagraphStyle(name='N',parent=S['Normal'],fontSize=9.5,leading=13,alignment=TA_CENTER,spaceAfter=11)) def P(x,s='B'): return Paragraph(x,S[s]) def topic(title,opening,secs): a=[PageBreak(),P(title,'H'),P('<b>Exam opening:</b> '+opening)] for h,ls in secs: a.append(P(h,'SH')); a += [P('• '+x) for x in ls] return a D=[P('Medicine Extended LAQ Answer Bank','T'),P('Final MBBS examination format. Expanded LAQs requested: Diabetes mellitus, DKA, hyperthyroidism, hypothyroidism, primary hyperaldosteronism (Conn syndrome), Cushing syndrome, Addison disease, peptic ulcer disease, IBD, and expanded original paper LAQs.','N'),P('Write the main headings in the answer book, underline key phrases, and draw relevant flowcharts where possible.','B')] D+=topic('1. Diabetes Mellitus','A metabolic disorder with chronic hyperglycaemia due to defects of insulin secretion, insulin action, or both.',[ ('Classification',['Type 1: autoimmune beta-cell destruction causing absolute insulin deficiency.','Type 2: insulin resistance with progressive beta-cell failure.','Other specific types: monogenic diabetes, pancreatic disease, endocrine/drug-related diabetes. Gestational diabetes is first recognized in pregnancy.']), ('Diagnosis',['Fasting plasma glucose >=126 mg/dL, or 2-hour OGTT glucose >=200 mg/dL, or HbA1c >=6.5%, or random glucose >=200 mg/dL with classic symptoms. Confirm a positive test on another day if asymptomatic.']), ('Clinical features',['Polyuria, polydipsia, polyphagia, fatigue, weight loss, blurred vision, recurrent infection, pruritus and poor wound healing. Type 1 may present with DKA.']), ('Complications',['Acute: hypoglycaemia, DKA and hyperosmolar hyperglycaemic state.','Microvascular: retinopathy, nephropathy, peripheral and autonomic neuropathy.','Macrovascular: coronary artery disease, stroke and peripheral arterial disease.','Diabetic foot, infection, erectile dysfunction and Charcot arthropathy.']), ('Management',['Education, dietitian input, weight management, regular aerobic/resistance exercise, smoking cessation, foot care and self-monitoring/CGM.','Type 1: basal-bolus insulin or pump, carbohydrate counting and sick-day rules.','Type 2: metformin if appropriate; add GLP-1 receptor agonist/dual GIP-GLP-1 agonist and/or SGLT2 inhibitor based on obesity, ASCVD, heart failure and CKD. Insulin for marked symptomatic hyperglycaemia or treatment failure.','Control BP and lipids; screen regularly for eye, renal and foot complications.'])]) D+=topic('2. Diabetic Ketoacidosis','A hyperglycaemic emergency caused by insulin deficiency, characterized by ketonaemia and high-anion-gap metabolic acidosis.',[ ('Precipitants and pathogenesis',['Infection, missed insulin, new type 1 diabetes, MI, stroke, pancreatitis, surgery, pregnancy, glucocorticoids and SGLT2 inhibitors.','Insulin deficiency with excess counter-regulatory hormones causes lipolysis and ketone production. Osmotic diuresis produces severe water and total-body potassium loss.']), ('Features and diagnosis',['Thirst, polyuria, vomiting, abdominal pain, dehydration, Kussmaul respiration, acetone breath, tachycardia, hypotension and altered consciousness.','Diagnosis: diabetes/hyperglycaemia, beta-hydroxybutyrate >=3 mmol/L or significant ketonuria, and pH <7.30 and/or bicarbonate <18 mmol/L. Check VBG, electrolytes, ketones, renal function, ECG, cultures and precipitating cause.']), ('Treatment',['ABC, cardiac monitoring, strict fluid balance, hourly glucose and frequent electrolytes/ketones. Start isotonic crystalloid, commonly 0.9% saline or balanced crystalloid, then tailor to volume status and sodium.','If K <3.3 mmol/L: replace potassium and withhold insulin. If K >=3.3, use IV regular insulin 0.1 unit/kg/hour after initial fluids. Replace potassium to maintain 4-5 mmol/L.','When glucose reaches about 200 mg/dL, add dextrose but continue insulin until ketonaemia/acidosis resolves. Bicarbonate is not routine, only considered for extreme acidaemia such as pH <6.9 under ICU supervision.','Resolution: ketones <0.6 mmol/L with pH >=7.3 or bicarbonate >=18 mmol/L. Overlap long-acting SC insulin by 2-4 hours before stopping infusion.'])]) D+=topic('3. Hyperthyroidism / Thyrotoxicosis','Thyrotoxicosis is the clinical state from excess thyroid-hormone action. Hyperthyroidism denotes increased hormone synthesis.',[ ('Causes',['Graves disease, toxic multinodular goitre, toxic adenoma, thyroiditis, excess levothyroxine, iodine/amiodarone-related disease and rare TSH-secreting tumour.']), ('Clinical features',['Weight loss, heat intolerance, sweating, palpitations, tremor, anxiety, proximal weakness, hyperdefaecation and menstrual disturbance.','Goitre, atrial fibrillation and heart failure may occur. Graves disease causes eye signs, pretibial myxoedema and diffuse goitre.']), ('Diagnosis',['Suppressed TSH with high free T4 and/or T3. TSH receptor antibody supports Graves. Radioiodine scan distinguishes diffuse Graves uptake from nodular disease or low-uptake thyroiditis.']), ('Treatment',['Propranolol for symptoms. Methimazole/carbimazole is used in most; PTU is preferred in first trimester and thyroid storm. Warn about agranulocytosis and hepatitis.','Definitive treatment: radioiodine or thyroidectomy. Avoid radioiodine in pregnancy/breastfeeding.','Thyroid storm: ICU, beta-blockade, PTU then iodine one hour later, hydrocortisone, cooling, fluids and treat precipitant.'])]) D+=topic('4. Hypothyroidism','Deficiency of thyroid hormone action. Primary hypothyroidism is thyroid-gland failure and is most common.',[ ('Causes',['Hashimoto thyroiditis, post-thyroidectomy/radioiodine, iodine disorders, amiodarone/lithium, postpartum thyroiditis. Central hypothyroidism follows pituitary/hypothalamic disease.']), ('Features',['Fatigue, cold intolerance, weight gain, constipation, dry skin, hair loss, hoarse voice, bradycardia, delayed ankle reflex relaxation, puffy face, depression and menorrhagia.','Myxoedema coma presents with hypothermia, bradycardia, hypotension, hypoventilation and coma.']), ('Diagnosis and treatment',['Primary disease: high TSH, low free T4. Central disease: low/inappropriately normal TSH and low free T4. Anti-TPO supports Hashimoto disease.','Levothyroxine is standard treatment. Start low (12.5-25 microgram/day) in elderly/ischemic heart disease; check TSH after 6-8 weeks. In central disease use free T4 to guide replacement and treat possible adrenal insufficiency first.','Myxoedema coma: ICU, IV thyroid hormone, hydrocortisone until adrenal failure excluded, ventilatory/hemodynamic support and treatment of trigger.'])]) D+=topic('5. Primary Hyperaldosteronism (Conn Syndrome)','Autonomous aldosterone secretion causing hypertension, potassium wasting and renin suppression.',[ ('Causes and features',['Aldosterone-producing adenoma or bilateral adrenal hyperplasia. Suspect in resistant hypertension, hypertension with hypokalaemia or adrenal incidentaloma.','Hypertension, weakness, cramps, paraesthesiae, polyuria/polydipsia, metabolic alkalosis and hypokalaemia. Oedema is usually absent.']), ('Diagnosis',['Screen with aldosterone-renin ratio after correcting potassium and accounting for interfering medicines. Confirm with saline infusion, oral salt loading, fludrocortisone suppression or captopril challenge.','CT adrenal is anatomical only; adrenal venous sampling establishes lateralization before surgery in suitable patients.']), ('Treatment',['Unilateral disease: laparoscopic adrenalectomy. Bilateral disease/nonoperative patients: spironolactone or eplerenone, with BP, potassium and renal monitoring.'])]) D+=topic('6. Cushing Syndrome','Chronic glucocorticoid excess. Cushing disease means an ACTH-secreting pituitary adenoma.',[ ('Causes',['Exogenous steroids most common. Endogenous: ACTH-dependent pituitary/ectopic ACTH or ACTH-independent adrenal adenoma/carcinoma.']), ('Features',['Central obesity, moon face, dorsocervical fat pad, facial plethora, easy bruising, thin skin, wide violaceous striae, proximal myopathy, hypertension, diabetes, osteoporosis, mood changes and infection.','Hirsutism/menstrual disturbance in women; severe hypokalaemia or virilization suggests severe/ectopic or adrenal disease.']), ('Diagnosis',['Exclude exogenous steroids. Confirm with two abnormal tests among overnight dexamethasone suppression, late-night salivary cortisol or 24-h urinary free cortisol.','Then ACTH: low suggests adrenal cause; normal/high suggests pituitary or ectopic cause. Use adrenal CT, pituitary MRI and inferior petrosal sampling when required.']), ('Treatment',['Transsphenoidal surgery for pituitary disease; adrenalectomy for adrenal lesion; resect ectopic ACTH tumour where feasible. Medical agents include ketoconazole, metyrapone, osilodrostat, pasireotide/cabergoline or selected receptor blockade. Treat cardiometabolic and bone complications.'])]) D+=topic('7. Addison Disease','Primary adrenal insufficiency with deficient cortisol, and commonly deficient aldosterone, most often due to autoimmune adrenalitis.',[ ('Causes and features',['Autoimmune adrenalitis, tuberculosis, metastasis/infiltration, adrenal haemorrhage, infections and adrenoleukodystrophy.','Fatigue, weight loss, nausea, abdominal pain, salt craving, postural dizziness, hyperpigmentation, hypotension, hyponatraemia, hyperkalaemia and hypoglycaemia.']), ('Diagnosis',['Low morning cortisol and high ACTH. Synacthen stimulation test shows poor cortisol increment. High renin and low aldosterone support primary disease. Check 21-hydroxylase antibodies and cause-specific evaluation.']), ('Chronic treatment',['Hydrocortisone 15-25 mg/day in divided doses plus fludrocortisone. Provide sick-day rules, emergency IM hydrocortisone kit and steroid card/medical alert.']), ('Adrenal crisis',['Treat immediately: hydrocortisone 100 mg IV/IM, then 200 mg/24 h infusion or 50 mg IV 6-hourly; rapid isotonic saline, dextrose if needed, correct electrolytes and treat precipitant. Do not wait for investigations.'])]) D+=topic('8. Peptic Ulcer Disease','A gastric or duodenal mucosal defect extending through muscularis mucosae, usually caused by H. pylori or NSAIDs.',[ ('Causes and features',['H. pylori, NSAIDs/aspirin, smoking, severe stress and Zollinger-Ellison syndrome. Epigastric pain, dyspepsia and nausea; bleeding, perforation or obstruction may present first.']), ('Diagnosis',['Alarm symptoms or GI bleeding require endoscopy. Biopsy gastric ulcers to exclude malignancy. H. pylori testing: urea breath test, stool antigen, biopsy urease test/histology.']), ('Management',['Stop NSAID if possible, give PPI, and eradicate H. pylori. Guideline-directed bismuth quadruple therapy for 14 days is frequently used: PPI + bismuth + tetracycline + metronidazole. Confirm eradication after treatment.','Bleeding: resuscitation, IV PPI and endoscopic hemostasis. Perforation/obstruction: urgent surgical assessment, fluids, antibiotics and PPI.'])]) D+=topic('9. Inflammatory Bowel Disease','Chronic immune-mediated intestinal inflammation including ulcerative colitis (UC) and Crohn disease (CD).',[ ('UC and Crohn differences',['UC: continuous superficial colitis beginning at rectum, bloody diarrhoea, urgency/tenesmus. CD: transmural skip lesions anywhere mouth-to-anus, commonly ileocolonic, with strictures/fistulae/perianal disease.','Extraintestinal disease: arthritis, uveitis, erythema nodosum, pyoderma gangrenosum, PSC, VTE and osteoporosis.']), ('Diagnosis',['CBC, CRP, albumin, stool infection tests including C. difficile, faecal calprotectin; ileocolonoscopy with biopsies. MR/CT enterography or intestinal ultrasound assesses small bowel/complications.']), ('Management principles',['Nutrition, anemia/bone care, vaccines, smoking cessation for Crohn disease, VTE prophylaxis during hospitalization and cancer surveillance. Steroids induce remission but do not maintain it.','UC: 5-ASA for mild-moderate disease; systemic steroid for moderate-severe flare; biologic/small molecule therapy for refractory disease; colectomy is curative.','CD: budesonide for mild ileocaecal disease; systemic steroids for severe flare; anti-TNF, vedolizumab, ustekinumab, IL-23 agents or selected small molecules for moderate-severe disease. Drain abscess and operate for obstruction/fistula/perforation when indicated.'])]) D+=topic('10. Expanded Original Paper LAQs: Quick Long-Answer Addendum','Use these points to enlarge the original PDF answers.',[ ('Vitamin B1 deficiency',['Risk factors: alcohol-use disorder, starvation, hyperemesis, bariatric surgery, dialysis and refeeding. Dry beriberi causes neuropathy; wet beriberi causes high-output failure; Wernicke encephalopathy causes confusion, ataxia and ocular signs.','Treat suspected Wernicke with high-dose parenteral thiamine before glucose, correct magnesium, then continue oral thiamine/nutritional and alcohol-dependence care.']), ('Neurocysticercosis',['Taenia solium eggs cause CNS larval cysts. Seizures are common. CT detects calcification and MRI better defines viable/ventricular/subarachnoid lesions. A cyst with scolex is highly specific.','Use antiseizure medicine; viable parenchymal disease often receives albendazole with corticosteroid cover. Avoid routine cysticidal therapy for calcified disease; hydrocephalus/ventricular disease needs neurosurgical input.']), ('HEV acute liver failure',['Acute liver injury plus INR >=1.5 and encephalopathy in a patient without cirrhosis. Support in ICU/transplant center: glucose, renal/electrolyte support, infection surveillance, cerebral oedema precautions and urgent transplant assessment.','Acute HEV management is mainly supportive. Specialist use of ribavirin in severe acute disease remains evidence-limited.']), ('Acute meningitis',['Treat as bacterial meningitis until excluded. Take blood cultures but do not delay dexamethasone and antibiotics. In adults >50 years, ceftriaxone/cefotaxime plus ampicillin/amoxicillin covers pneumococcus and Listeria; add vancomycin according to local resistance.','LP unless CT is first indicated by focal deficit, papilloedema, new seizure, marked consciousness impairment or immunocompromise.'])]) D += [PageBreak(),P('References and Update Notes','H'),P('Harrison’s Principles of Internal Medicine, 22nd ed.; ADA Standards of Care in Diabetes 2026; ACG Crohn disease and UC guideline updates 2025; WHO Neurocysticercosis Guidelines 2021; Endocrine Society guidance. Recent evidence was checked. This is an exam-revision guide, not patient-specific medical advice.','B')] def f(c,d): c.saveState();c.setFont('Helvetica',8);c.setFillColor(colors.HexColor('#666666'));c.drawString(1.4*cm,.85*cm,'Medicine Extended LAQ Answer Bank');c.drawRightString(19.5*cm,.85*cm,'Page %d'%d.page);c.restoreState() doc=SimpleDocTemplate(str(pout),pagesize=A4,leftMargin=1.35*cm,rightMargin=1.35*cm,topMargin=1.25*cm,bottomMargin=1.35*cm,title='Medicine Extended LAQ Answer Bank') doc.build(D,onFirstPage=f,onLaterPages=f) print(pout,pout.stat().st_size) PY
python - <<'PY' from pypdf import PdfReader p='/tmp/workspace/medicine-solved-paper/output/Medicine_Extended_LAQ_Answer_Bank.pdf' r=PdfReader(p) t='\n'.join(x.extract_text() or '' for x in r.pages) print('pages',len(r.pages),'bytes',__import__('os').path.getsize(p),'chars',len(t)) for k in ['Diabetes Mellitus','Diabetic Ketoacidosis','Hyperthyroidism','Hypothyroidism','Primary Hyperaldosteronism','Cushing Syndrome','Addison Disease','Peptic Ulcer Disease','Inflammatory Bowel Disease','Neurocysticercosis']: print(k, k in t) PY
Medicine Extended LAQ Answer Bank
PDF Document · PDF
Dont make pdf tell detailed laq here
ADA Standards of Care 2026 diabetes diabetic ketoacidosis Endocrine Society primary aldosteronism ACG IBD guidelines 2025
"diabetic ketoacidosis" AND management
Yes give all here
"diabetic ketoacidosis" AND treatment
ADA 2026 diabetes hyperglycemic crises ACG 2025 inflammatory bowel disease guideline Endocrine Society primary aldosteronism guideline
Yes in detailed please
"diabetes mellitus" AND treatment
ADA Standards of Care 2026 diagnosis classification treatment diabetes mellitus
| Test | Diagnostic value |
|---|---|
| Fasting plasma glucose | ≥126 mg/dL or ≥7.0 mmol/L |
| Two-hour plasma glucose during 75-g OGTT | ≥200 mg/dL or ≥11.1 mmol/L |
| HbA1c | ≥6.5% |
| Random plasma glucose with classic symptoms or hyperglycaemic crisis | ≥200 mg/dL or ≥11.1 mmol/L |
| Test | Prediabetes range |
|---|---|
| Fasting plasma glucose | 100-125 mg/dL |
| Two-hour OGTT glucose | 140-199 mg/dL |
| HbA1c | 5.7%-6.4% |
| Complication | Screening |
|---|---|
| Retinopathy | Dilated retinal examination at diagnosis in type 2 DM and within 5 years of onset in type 1 DM, then periodically |
| Nephropathy | Annual urine albumin-creatinine ratio and eGFR |
| Neuropathy | Annual sensory examination with monofilament and vibration |
| Foot disease | Foot examination at every visit or at least annually |
| Cardiovascular risk | BP, lipids, smoking status, weight and renal function |