Gastro

Question 1

prodrugs

Answer 1

Omiprosol reduce the action of clopidegral(at least 1 year )

Ticagrelor binds to an area on the P2Y12 receptor distinct from the ADP binding site. BRILINTA reversibly binds to the ADP P2Y12 receptor and prevents ADP from binding. This prevents the signal transduction and platelet activation that can lead to pathologic thrombus formation.

Question 2

peptic ulcer disease

Answer 2

duodinal ulcers&raquo_space;»gastric ulcers
risk facots - H. pylori (g -), NSAIDs
Behçet’s disease, Zollinger–Ellison syndrome, Crohn’s disease, and liver cirrhosis

H Pilori associations - gastric cancer, MALT limphoma , gastritis, gastric & Duodinal ulceration

Solingazollinesyn treatmenrt - high dose PPI
presentation - chronic, upper abdominal pain, nausea, and sometimes, bloating or belching, with pain potentially worsening or improving with food depending on the ulcer location

treatment - life style changes, H. Pilori - amoxicillin, clarithromycin, and metronidazole, PPIs, Antacids, Mucosal Protective Agents
Refractory cases: Use bismuth quadruple therapy (PPI + bismuth + tetracycline + metronidazole)

H pylori test - Urea Breath Test, CLO test, serum blood antibody test, stool antigen

Gastric ulcers: Repeat endoscopy at 6–8 weeks to confirm healing and exclude malignancy 37.
Duodenal ulcers: No routine follow-up endoscopy if symptoms resolve 7.
Annual review for patients on long-term PPIs to assess need for continued therapy

Question 3

Gilbert’s syndrome

Answer 3

common, which affects the liver’s ability to process bilirubin, leading to mild, chronic, and often asymptomatic, unconjugated hyperbilirubinemia. leading to occasional, mild jaundice (yellowing of the skin and eyes) caused by stress, fasting, commonly Asymptomatic

UGT1A1 gene has a variant that results in reduced activity of the bilirubin-UGT enzyme.
common autosomal recessive, raely autosomal dominant

Gilbert’s syndrome in combination with other prevailing conditions such as breast feeding, G-6-PD deficiency, thalassemia, spherocytosis, or cystic fibrosis may potentiate severe hyperbilirubinemia and/or cholelithiasis.

Question 4

Rotor Syndrome

Answer 4

autosomal recessive disorder caused by mutations in the SLCO1B1 and SLCO1B3 genes, which encode the organic anion transporting polypeptide (OATP) proteins, OATP1B1 and OATP1B3.

mild, intermittent jaundice, which may be an incidental finding, dark-colored urine and, rarely, abdominal pain or fatigue., Liver histology is normal,

elevated conjugated bilirubin levels, and characteristic findings on cholescintigraphy

Question 5

Dubin-Johnson syndrome (DJS)

Answer 5

a rare, benign, autosomal recessive liver disorder characterized by conjugated hyperbilirubinemia (increased levels of bilirubin in the blood) and a characteristic black liver due to pigment accumulation, without other liver damage

liver histology reveals a characteristic accumulation of dark, granular pigment, primarily in the centrilobular zone of hepatocytes, without other abnormalities.
pigment accumulation is most prominent in the centrilobular area. pigment appears as coarse, granular deposits within the hepatocyte cytoplasm. Hallmark

dark pigment helps differentiate DJS from Rotor syndrome

intermittent jaundice triggered by illness, pregnancy, or oral contraceptives. , Non-pruritic, Conjugated Hyperbilirubinemia, dark-colored urine. , Abdominal Pain, Fatigue, rarely - newborns with severe cholestasis and hepatomegaly.

Conjugated Hyperbilirubinemia- hallmark
Normal Liver Enzyme Levels
Total Bilirubin Levels
serum albumin, bolld, cholestorol, - normal
HIDA Scan, Liver Biopsy

Question 6

carcinoid tumor

Answer 6

collection of symptoms that can occur when a neuroendocrine tumor (NET), often a carcinoid tumor, releases hormones like serotonin into the bloodstream, leading to symptoms like flushing, diarrhea, and in some cases, heart problems, common in jejunum &ileum

Liver Metastasis:
Carcinoid syndrome is more likely to occur when a carcinoid tumor has spread to the liver, as the liver normally breaks down serotonin, and this breakdown is disrupted when the tumor is present in the liver.

testing bio chem- 24-hour urine 5-hydroxyindoleacetic acid (5-HIAA)- may false positive to some foods:, chromogranin A

pelegra

assoictations - Carcinoid Heart Disease: particularly affecting the fibrosis valves on the right side of the heart (tricuspid and pulmonic valves).

Triggers:
Certain foods, beverages (alcohol, caffeine), stress, and exercise

Question 7

gastrinoma

Answer 7

rare neuroendocrine tumor (NET) that produces excessive amounts of the hormone gastrin, leading to increased stomach acid production and potentially causing peptic ulcers and other symptoms, collectively known as Zollinger-Ellison syndrome (ZES).

Gastrinomas are typically well-differentiated neuroendocrine tumors (NETs)
NET markers like chromogranin A and synaptophysin
Ki67, a marker of cell proliferation, is used to assess the grade of the tumor

clinical - Peptic Ulcers, Diarrhea, Abdominal Pain, Abdominal Pain

Question 8

glucagonoma

Answer 8

rare pancreatic neuroendocrine tumor (NET) that produces excessive amounts of the hormone glucagon, leading to symptoms like a characteristic skin rash (necrolytic migratory erythema), diabetes, and weight loss, depression, DVT

Traid - Diabetes M, weightloss, NME

Fasting Glucagon Level: abnormally high levels of glucagon in the blood, > 500
CT scans and endoscopic ultrasounds to locate the tumor

associations - MEN1
Mutations in the glucagon receptor gene (GCGR)

Question 9

Refeeding syndrome

Answer 9

a potentially fatal condition, arises from rapid shifts in fluids and electrolytes when severely malnourished individuals are re-fed, often leading to electrolyte imbalances like hypophosphatemia, hypokalemia, and hypomagnesemia.

The main electrolyte imbalances, Potassium imbalances can lead to cardiac arrhythmias, QT prolongation weakness, fatigue, paralysis, and respiratory distress.

Question 10

ulcerative colitis

Answer 10

chronic inflammatory bowel disease (IBD) that causes inflammation and ulcers in the lining of the large intestine (colon and rectum), leading to symptoms like diarrhea, abdominal pain, and blood in the stool.

Symptoms:
Diarrhea, sometimes with blood or pus.
Abdominal pain and cramping.
Urgent need to have a bowel movement.
Weight loss.
Fever.
Fatigue.

smoking is protective

Immune System Dysregulation:
Overactive Immune Response:
In UC, the immune system mistakenly attacks the colon’s lining, leading to inflammation and ulceration.
T-cell Imbalance:
There’s evidence of an imbalance in T-cell subsets, particularly an overabundance of Th2 cells, which can contribute to the inflammatory response.
Cytokine Imbalance:
Cytokines, signaling molecules that regulate immune responses, are dysregulated in UC, with elevated levels of pro-inflammatory cytokines like TNF-alpha and IL-13.
Leukocyte Recruitment:
There is an upregulated release of the chemoattractant CXCL8 in ulcerative colitis so that leukocytes are recruited to the mucosa from systemic circulation.
3. Epithelial Barrier Defects:
Mucin and Tight Junction Defects:
The epithelial barrier, which protects the colon from harmful substances, is compromised in UC, potentially due to defects in mucin production and tight junctions.
Increased Antigens Uptake:
The compromised barrier allows increased uptake of luminal antigens, further fueling the inflammatory response.

Pouchitis — this may complicate 30% of colectomy cases, and presents with increased stool frequency, urgency, faecal incontinence, and nocturnal seepage.

Cytomegalovirus (CMV) colitis with UC - Severe UC, steroid-refractory disease

treatment - Antiviral therapy, such as ganciclovir

ulcerative colitis flare up management -
Aminosalicylates (5-ASAs): mesalazine, sulfasalazine, balsalazide, and olsalazine
Corticosteroids: corticosteroids like prednisone or budesonide
Immunosuppressants: infliximab
Anti-diarrheal medications:
Acetaminophen:
Colectomy - 8<stools, CRP>45,

Disease Classification and Assessment
Severity #Stool Frequency (per day)# Blood in Stool Systemic Features*# ESR/CRP#
Mild #<4 #Small amounts #None# Normal
Moderate# 4–6 #Moderate #None# Normal
Severe# ≥6 #Visible blood
≥1 of the following:
- Temp >37.8°C
- Pulse >90 bpm
- Hb <10 g/dL
- ESR >30 mm/hr or CRP >45 mg/L Elevated

Disease Extent
Proctitis: Inflammation limited to rectum
Left-sided colitis: Up to splenic flexure
Extensive/pancolitis: Beyond splenic flexure 48

Disease Severity
Severe UC is defined as:
≥6 bloody stools/day PLUS one or more of:
Temperature >37.8°C
Pulse >90 bpm
Haemoglobin <105g/L
CRP >45
Treatment Recommendations
Mild-to-Moderate UC
First-line therapy: - first presentation or inflammatory exacerbation
5-aminosalicylates (5-ASAs): First choice for mild-moderate UC-mesalazine and sulfasalazine -
Oral (Pentasa®/Octasa® 2-4.8g/day in divided doses)
Rectal (suppositories/enemas for distal disease)

Corticosteroids — monotherapy with a time-limited course of corticosteroids may be used for induction of remission if aminosalicylates are ineffective or not tolerated
Budesonide MMX (Cortiment®): Preferred steroid option due to lower systemic absorption (9mg once daily for 8 weeks)

Moderate-to-Severe UC
Advanced therapies (BSG 2025 advocates “top-down” approach)
Biologics: Anti-TNFs (infliximab, adalimumab, golimumab), vedolizumab, ustekinumab
Small molecules: JAK inhibitors (tofacitinib, filgotinib), S1P modulators (ozanimod, etrasimod)
Key changes in BSG 2025:
Earlier use of advanced therapies rather than step-up approach
More treatment options available with different mechanisms

Acute Severe UC (ASUC)
Management pathway
Hospital admission and IV steroids (methylprednisolone 60mg/day)
Daily monitoring (stool charts, bloods, abdominal exams)
Rescue therapy at day 3 if no response:
Infliximab (5mg/kg at 0, 2, 6 weeks)
Ciclosporin (IV 2mg/kg, monitor levels)
Ciclosporin — may be used for acute severe disease, especially if intravenous corticosteroids are not effective
Thiopurines — azathioprine or mercaptopurine may be considered to maintain remission in people using aminosalicylates who have required two or more courses of oral corticosteroids

Note: thiopurines may increase the risk of non-melanoma skin cancer

Early surgical consultation for non-responders

Surgical Management
Indications:
Medically refractory disease
Toxic megacolon
Dysplasia/cancer
Options:
Total colectomy with ileostomy
Ileal pouch-anal anastomosis (J-pouch)

Monitoring and Support
Key aspects:
Regular blood monitoring for patients on immunosuppressants
Bone protection for those on steroids (calcium/vitamin D ± bisphosphonates)
Thromboprophylaxis during hospital admissions

Question 11

duodenal ulcer

Answer 11

sore that develops in the lining of the duodenum, the first part of the small intestine, and is a type of peptic ulcer, along with gastric ulcers

often caused by Helicobacter pylori (H. pylori)

NSAIDs inhibit cyclooxygenase (COX) enzymes, which are responsible for producing prostaglandins
By inhibiting prostaglandin synthesis, NSAIDs reduce the production of protective mucus and bicarbonate, and impair mucosal blood flow, leading to increased susceptibility to acid and pepsin damage.

Question 12

small intestinal bacterial overgrowth

Answer 12

an excessive amount of bacteria in the small intestine, leading to various gastrointestinal symptoms and potentially malabsorption

breath test

diatary - high in FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols)

Epidemiology & Risk Factors
Prevalence
Estimated 2.5–22% in the general population.
Higher in older adults, IBS patients (30–85%), and those with motility disorders.

Key Risk Factors
Structural/Anatomical Abnormalities
Small bowel strictures, diverticula, surgical blind loops (e.g., post-Roux-en-Y).

Motility Disorders
Gastroparesis, scleroderma, diabetic neuropathy, chronic opioid use.
Hypochlorhydria
Chronic PPI use, atrophic gastritis, post-gastrectomy.
Immune Dysfunction
IgA deficiency, HIV, immunosuppressive therapy.
Other Conditions
Cirrhosis, pancreatitis, celiac disease, Crohn’s disease.

Pathophysiology
Bacterial Overgrowth: Normally, the small intestine has <10³ CFU/mL bacteria; in SIBO, levels exceed 10⁵–10⁸ CFU/mL (mostly colonic species like E. coli, Klebsiella, Enterococcus).
Mechanisms of Symptoms:
Fermentation of carbs → hydrogen (H₂) & methane (CH₄) gas → bloating, distension.
Bile salt deconjugation → fat malabsorption → steatorrhea.
Vitamin B12 deficiency (bacterial consumption) vs. folate excess (bacterial production).
Inflammation & leaky gut → systemic symptoms (fatigue, joint pain).

Clinical Features
Common Symptoms
Bloating, abdominal distension (most common).
Diarrhea (more in hydrogen-dominant SIBO).
Constipation (more in methane-dominant SIBO = “IMO” - Intestinal Methanogen Overgrowth).
Fatigue, weight loss, nutrient deficiencies (B12, iron, fat-soluble vitamins A/D/E/K).

Associated Conditions
IBS (especially IBS-D or IBS-C with bloating).
Fibromyalgia, rosacea, restless legs syndrome (iron/B12 deficiency).

Diagnosis
1. Gold Standard: Jejunal Aspirate & Culture
>10³ CFU/mL confirms SIBO (rarely done due to invasiveness).

2. Breath Testing (Most Common)
   Lactulose or glucose breath test: Measures H₂ & CH₄ at baseline and every 15–30 mins for 3 hours.

Positive if:
H₂ rise ≥20 ppm within 90 mins (lactulose) or 120 mins (glucose).
CH₄ ≥10 ppm at any time (indicates methane-dominant SIBO/IMO).

3. Clinical Diagnosis (Empirical Treatment Trial)
   Used when testing is unavailable; symptom improvement with antibiotics supports SIBO.
4. Exclusion of Mimics
   Celiac disease, pancreatic insufficiency, Crohn’s, lactose intolerance.

Treatment
1. Antibiotics (First-Line)
Drug Dose Duration Notes
Rifaximin 550 mg TID 10–14 days Best for H₂-SIBO (50–70% response)
Neomycin 500 mg BID 10–14 days For CH₄-dominant SIBO (often combined with rifaximin)
Metronidazole 250–500 mg TID 7–10 days Alternative for methane producers
Retreatment may be needed (30–50% relapse rate).

2. Prokinetics (For Motility Disorders)
   Prucalopride (1 mg/day), erythromycin (50–100 mg before bed).
3. Dietary Modifications
   Low-FODMAP diet (reduces fermentable carbs).
   Elemental diet (2–3 weeks) in refractory cases.
4. Adjunctive Therapies
   Probiotics (e.g., Lactobacillus casei, Bifidobacterium) – mixed evidence.
   Herbal antimicrobials (berberine, oregano oil, allicin for methane).

Question 13

IgG4-related disease

Answer 13

chronic, immune-mediated, fibroinflammatory condition that can affect multiple organs, often presenting with tumor-like masses and fibrosis, and is characterized by an abundance of IgG4-positive plasma cells in affected tissues.

Mimics Malignancy, IgG4-RD cause organ damage and complications.

Question 14

Tropical sprue

Answer 14

malabsorption syndrome, primarily affecting individuals in tropical regions, characterized by chronic diarrhea - steatorrhea, weight loss, and nutritional deficiencies due to damage to the small intestine’s lining, potentially caused by an infection.
Deficiencies in folate, vitamin B12

Antibiotics - tetracyclin & nutritional support

Question 15

haemolytic anaemia caused by drugs

Question 16

Zollinger-Ellison syndrome (ZES)

Answer 16

a rare condition caused by tumors (gastrinomas) in the pancreas or small intestine that produce excessive amounts of gastrin, leading to overproduction of stomach acid and peptic ulcers

Hypergastrinemia, Acid-Suppressing Medications,

because the excessive acid and the use of acid-suppressing medications (like proton pump inhibitors or PPIs) to manage ZES can disrupt the normal process of vitamin B12 absorption.

• MEN1

Question 17

Hereditary hemochromatosis

Answer 17

Caused by mutations in the HFE gene, leading to increased iron absorption and accumulation in organs

The HFE protein, encoded by the HFE gene, helps regulate iron levels in the body by sensing iron and influencing hepcidin production, a hormone that controls iron absorption.
Mutations in the HFE gene can disrupt this regulation, leading to increased iron absorption from the diet.
The most common HFE mutations associated with hemochromatosis are C282Y and H63D.

The condition can lead to various complications, including liver damage, diabetes, heart problems, and joint pain

While HFE is the most common cause of hereditary hemochromatosis, mutations in other genes, such as HJV, HAMP, TFR2, and SLC40A1, can also lead to the condition

Question 18

Ascites

Answer 18

transudate
Ascitic fluid with low protein levels (less than 30 g/L)
Cirrhosis, Heart Failure, Nephrotic Syndrome, Constrictive Pericarditis- Scarring or thickening of the pericardium,
Venous Obstruction - Budd-Chiari syndrome, where there’s a blockage of the hepatic veins, can also cause increased pressure in the portal system and lead to transudative ascites.

Exudative ascites
characterized by high protein levels in the ascitic fluid, is primarily caused by conditions that lead to inflammation and increased permeability of the peritoneal capillaries, or by the presence of malignant cells.
Causes - malignancy - varian, breast, colon, stomach, and pancreatic cancers, as well as other cancers that metastasize to the peritoneum, infection - tuberculous peritonitis, SBP, and other , pancreatitis, vasculitis and inflammatory processes.

associated conditions - Cirrhosis and Portal Hypertension, Heart Failure, Hypoalbuminemia

Question 19

Wilson’s disease

Answer 19

In autosomal recessive disorder, is caused by a genetic defect in the ATP7B gene, leading to impaired copper excretion and subsequent accumulation in the liver, brain, and other tissues, causing various organ damage and clinical manifestations.

liver disease (jaundice, fatigue, abdominal swelling), neurological issues (tremors, movement disorders, speech problems), and psychiatric symptoms (personality changes, depression). Kayser-Fleischer rings, a hallmark sign

Liver Disease:
Jaundice: Yellowing of the skin and whites of the eyes.
Fatigue: Persistent tiredness.
Abdominal swelling: Fluid buildup in the abdomen.
Loss of appetite: Reduced interest in eating.
Liver failure: In severe cases, leading to liver damage and potential failure.
Acute liver failure: A life-threatening condition requiring urgent transplantation, characterized by coagulopathy, jaundice, and hepatic encephalopathy

Neurological Issues:
Tremors: Involuntary shaking of the hands, arms, or legs.
Movement disorders: Including dystonia (muscle contractions) and chorea (uncontrolled, jerky movements).
Dysarthria: Difficulty with speech.
Dysphagia: Difficulty swallowing.
Slurred speech: Imprecise or unclear speech.
Drooling: Excessive saliva production.
Parkinsonism: Symptoms similar to those of Parkinson’s disease, like tremors and stiffness.
Seizures: Uncontrolled electrical activity in the brain.
Cognitive impairment: Problems with thinking, memory, and concentration.

Psychiatric Symptoms:
Personality changes: Uncharacteristic or unusual behavior.
Depression: Persistent sadness and loss of interest.
Mood swings: Rapid and extreme changes in emotions.
Anxiety: Excessive worry and nervousness.
Psychosis: Delusions or hallucinations (in rare cases).
Other Signs:
Kayser-Fleischer rings: Greenish-gold or brownish rings around the iris of the eye.
Abnormal eye movements: Restricted gaze or other eye movement problems.
Skeletal involvement: Weak, fragile bones (osteoporosis) and joint pain (arthritis).
Skin changes: Bluish discoloration of the fingernails (lunulae ceruleae).
Bone problems: Fractures, osteopenia, and premature osteoarthritis.
Renal problems: Kidney stones and kidney dysfunction.
Cardiac problems: Increased risk of atrial fibrillation and heart failure.
Hematologic problems: Anemia, low platelet counts, and low white blood cell counts.

Age onset - between the ages of 5 and 35

Low Serum Ceruloplasmin:
Ceruloplasmin is a protein that carries copper in the blood. In Wilson’s disease, ceruloplasmin levels are significantly lower, often below 10 mg/dL.
Low Serum Copper, total serum copper may be normal or slightly low, Elevated Urinary Copper, Elevated Hepatic Copper
Initial tests: Liver function tests, serum ceruloplasmin, 24-hour urinary copper, slit-lamp examination for Kayser-Fleischer rings
Advanced testing: Liver biopsy with quantitative copper measurement when diagnosis uncertain

Pharmacological Treatment
First-line Therapy
D-penicillamine:
Traditional first-line chelator in England
Dose: 20 mg/kg/day in divided doses (max 2g/day)
Side effects: Proteinuria, bone marrow suppression, lupus-like reactions
Neurological worsening occurs in 15-20% of patients

Trientine dihydrochloride:
Alternative first-line or for penicillamine intolerance
Dose: 20 mg/kg/day in divided doses
Better neurological tolerance than penicillamine

Maintenance Therapy
Zinc salts (acetate or sulfate):
Low-copper diet

Acute Liver Failure Management
Urgent referral to liver transplant center
Plasma exchange as bridge to transplantation
Albumin dialysis (MARS) in selected cases
Combination therapy: Chelators plus zinc may be attempted in mild cases

Question 20

Barrett’s esophagus

Answer 20

flat, pink lining of the esophagus is replaced by a red, thick lining due to chronic acid reflux, a condition known as gastroesophageal reflux disease (GERD)

Metaplasia
Cellular Change:
The damaged squamous cells are replaced by a different type of cell, columnar epithelium,
Intestinal Metaplasia:
This columnar epithelium may further develop goblet cells, a characteristic of the small intestine, a process known as intestinal metaplasia.
Protective Mechanism:
Metaplasia is believed to be a protective mechanism against the damaging effects of acid, as columnar epithelium is more resistant to acid exposure.

Dysplasia:
Metaplastic cells can sometimes develop abnormal changes (dysplasia), which may be low-grade or high-grade.
Adenocarcinoma:
High-grade dysplasia can progress to esophageal adenocarcinoma, a type of esophageal cancer.

Diagnostic Methods
Endoscopy with Biopsy:
Gold standard; salmon-colored mucosa ≥1 cm above the gastroesophageal junction (GEJ) with histologic confirmation of intestinal metaplasia
Prague classification (circumferential [C] and maximal [M] extent) and Paris classification (lesion morphology) are used for staging

Non-Endoscopic Tools:
Cytosponge: A swallowable capsule with a sponge that collects esophageal cells for TFF3 immunostaining; cost-effective for screening

General Approach
Lifestyle Modifications: Weight loss, smoking cessation, avoiding late-night meals, and reducing alcohol/caffeine intake
Acid Suppression: High-dose proton pump inhibitors (PPIs; e.g., omeprazole) to control reflux and reduce inflammation
Dysplasia-Specific Management
No Dysplasia:
Surveillance endoscopy every 3–5 years (shorter intervals for long-segment BE)

Low-Grade Dysplasia (LGD):
Repeat endoscopy in 6 months; if confirmed, consider radiofrequency ablation (RFA) or surveillance every 6–12 months
High-Grade Dysplasia (HGD) or Early EAC:
Endoscopic eradication therapy (EET): Combines endoscopic mucosal resection (EMR) for visible lesions and RFA/cryotherapy for flat dysplasia
Esophagectomy: Reserved for invasive cancer or failed EET

Emerging Therapies
Chemoprevention: Aspirin and statins are under investigation for reducing cancer risk
Molecular Risk Stratification: Tools like TissueCypher assess genetic markers to personalize surveillance/treatment plans

Question 21

Whipple disease

Answer 21

gram-positive bacteria, Tropheryma whippelii

mutation in the IRF4 gene, HLA-B27 gene

present as combination of gastrointestinal, musculoskeletal, and neurological symptoms.

Traid - weightloss, polyarthralgia, diahorrea

common symptoms include weight loss, diarrhea (often with steatorrhea), abdominal pain, and arthralgia, often described as migratory and affecting large joints. Other possible symptoms include fever, peripheral edema, and neurological deficits such as ataxia, cognitive changes, and eye movement problems. lung involvement

Arthralgia: Joint pain is a hallmark of Whipple’s diseas - large joints

iron deficiency, and folate or vitamin B12 deficiency. Neutrophilia - 1/3. Mild lymphocytopenia is common. Eosinophilia and thrombocytopenia rarely occur. Hypoalbuminemia is prevalent, whereas serum globulin levels are normal. The prothrombin time is prolonged.

when granulomatous inflammation is present, elevated ACE levels can be observed in the blood.

Ceftriaxone or Penicillin G two weeks, followed by the maintenance phase with Trimethoprim 160 mg- Sulfamethoxazole 800 mg twice daily for twelve months

Diagnostic criteria require positive results for PAS-positive foamy macrophages in the small bowel biopsy

histiocytes (macrophages) in the small intestine are typically infiltrated by PAS-positive material, a hallmark of the disease.

Question 22

Irritable Bowel Syndrome (IBS)

Answer 22

a common digestive disorder, causes abdominal pain, bloating, and changes in bowel habits, often including diarrhea, constipation, or both

Symptoms must have been present for at least six months

Full blood count.
Inflammatory markers such as erythrocyte sedimentation rate and C-reactive protein.
Coeliac serology.
Faecal calprotectin.
gluton free diet

Low FODMAP Diet- certain carbohydrates (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols

Detects antibodies against gluten, specifically IgA tissue transglutaminase (tTG), IgA anti-endomysial antibodies (EMA), and sometimes IgG antibodies.

Question 23

Hep B

Question 24

MALT lymphoma

Answer 24

a slow-growing type of non-Hodgkin lymphoma B cell.

Presence of dense diffuse infiltrate of marginal‐zone cells in lamina propria with prominent lymphoepithelial lesions

Infectious triggers:
H. pylori (gastric MALT)
Chlamydia psittaci (ocular adnexal and pulmonary MALT)
Campylobacter jejuni (small intestine)
Borrelia burgdorferi (cutaneous MALT)
Autoimmune associations:
Hashimoto’s thyroiditis (thyroid MALT)
Sjögren’s syndrome (salivary gland MALT)

Site Common Symptoms
Stomach #Indigestion, abdominal pain, nausea, loss of appetite
Lung #Persistent cough, breathlessness
Ocular #Red eye, photophobia, proptosis, visual disturbances
Skin #Nodules, papules
Salivary gland# Painless swelling
Thyroid Goiter, hypothyroidism symptoms
5% of patients experience systemic “B symptoms

Essential Investigations
Histopathology:
Biopsy of affected site (endoscopic for gastric, bronchoscopic for pulmonary, etc.)
Immunohistochemistry panel: CD20+, CD3-, CD5-, CD10-, BCL2+, CD21/CD23
Molecular studies for characteristic translocations
Infection testing:
H. pylori (histology, stool antigen, urea breath test, serology)
Hepatitis B/C, HIV serology
Site-specific infections (e.g., Chlamydia psittaci PCR for ocular cases)

Staging:
Complete blood count, LDH, β2-microglobulin
CT/PET-CT scan (42-100% sensitivity depending on stage)
Bone marrow biopsy (for advanced cases)
Endoscopic ultrasound (for gastric cases)
Gastric MALT Lymphoma
First-line for H. pylori-positive cases:
Triple therapy antibiotics (PPI + amoxicillin + clarithromycin/metronidazole)
Repeat testing at 4-8 weeks post-treatment
Follow-up endoscopy at 3-6 months

For treatment failures:
Second-line antibiotics if persistent H. pylori
Involved-site radiotherapy (ISRT; 24-30 Gy) for localized disease
Rituximab monotherapy or combination chemoimmunotherapy for disseminated disease
H. pylori-negative or t(11;18)-positive cases:
ISRT as preferred option
Rituximab ± chemotherapy alternatives

Non-Gastric MALT Lymphoma
Localized disease:
Radiotherapy (dose 24-30 Gy) for most cases
Surgery for specific sites (thyroid, breast, colon)
Antibiotics for infection-associated cases (e.g., ocular C. psittaci)
Advanced disease:
Observation for asymptomatic cases
Rituximab ± chemotherapy for symptomatic disease:
Bendamustine + rituximab (preferred)
R-CHOP/R-CVP alternatives
Lenalidomide + rituximab (category 2B)

Emerging Therapies
BTK inhibitors (acalabrutinib, zanubrutinib) for relapsed/refractory cases
Novel monoclonal antibodies (e.g., anti-CD19 therapies

For gastric MALT lymphoma, initial treatment often involves eradicating Helicobacter pylori infection with antibiotics and proton pump inhibitors.

Non-gastric MALT lymphoma may be treated with antibiotics for associated infections, radiotherapy, chemotherapy, or immunotherapy like rituximab

Question 25

Autoimmune hepatitis

Answer 25

a liver disease that happens when the body's immune system attacks the liver HLA Genes: Genetic predisposition is primarily linked to polymorphisms in human leukocyte antigen (HLA) alleles, especially those in the MHC class II HLA DRB1 region. DRB1 Alleles: In Caucasian European and North American populations, AIH-1 is associated with HLA-DRB10301, DRB10401, and DRB30101 alleles. In Brazil, the primary susceptibility allele for AIH-1 is DRB11301, with DRB1*0301 also playing a role. Antibodies: Type 1 AIH: Characterized by the presence of anti-smooth muscle antibodies (ASMA) and/or anti-nuclear antibodies (ANA). Type 2 AIH: Distinguished by anti-liver/kidney microsome (anti-LMK) type 1 antibodies and/or anti-liver cytosol (anti-LC) type 1 antibodies. ymptoms include fatigue, malaise, abdominal discomfort, joint pain, and jaundice. Laboratory Findings: Elevated Liver Enzymes: AST, ALT Increased IgG - Serum IgG . Autoantibodies: Presence of autoantibodies, ANAs, ASMs Other Autoantibodies: Tests for antibodies to liver-kidney microsome type 1 (anti-LKM-1), soluble liver antigen (anti-SLA), and liver cytosol type 1 (anti-LC1) may be helpful in atypical cases. Liver Biopsy: necessary to confirm the diagnosis and assess the severity of liver damage, showing interface hepatitis, Lymphoplasmacytic Infiltration and other characteristic features. Diagnostic Criteria: Diagnostic scoring system It's crucial to rule out other liver diseases, including viral hepatitis, drug-induced liver injury, and alcoholic liver disease.

Question 26

Primary sclerosing cholangitis (PSC)

Answer 26

PSC is a progressive liver disease characterized by inflammation and scarring (fibrosis) of the bile ducts, which transport bile from the liver to the small intestine. This inflammation and scarring can lead to narrowing (strictures) and obstruction of the bile ducts. Associated with IBD - 70-80% PANCA positive, Anti SMA, Anti ANA positive fatigue, itching, and jaundice. Some individuals may also experience abdominal pain, fever, and weight loss. may be asymptomatic fibrosis of the bile ducts, both inside bile duct infections, cirrhosis, and liver failure. cholangiocarcinoma, other liver cancers, General Diagnostic Approach PSC is diagnosed based on clinical presentation, biochemical markers, imaging findings, and exclusion of secondary causes. Key features include: Cholestatic liver biochemistry: Elevated alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT), especially in pediatric cases Typical cholangiographic findings: Multifocal strictures and dilatations in intra- and/or extrahepatic bile ducts Exclusion of secondary sclerosing cholangitis (e.g., IgG4-related disease, infections, ischemia) 2. Imaging Criteria First-line modality: Magnetic resonance cholangiopancreatography (MRCP) (non-invasive, high sensitivity/specificity: 86%/94%) Findings: Beaded appearance, pruning, or diverticulum-like outpouchings Endoscopic retrograde cholangiopancreatography (ERCP): Reserved for equivocal MRCP cases or therapeutic interventions 3. Subtypes and Special Populations A. Large Duct PSC Diagnosis: MRCP/ERC showing biliary strictures + elevated ALP/GGT Key exclusion: IgG4-related sclerosing cholangitis (test serum IgG4, biopsy if needed) B. Small Duct PSC Criteria: Normal cholangiography. Histologic findings: Fibrous cholangitis, onion-skin fibrosis Liver biopsy is mandatory for diagnosis

Question 27

obstetric cholestasis

Answer 27

a liver disorder that can develop during pregnancy, primarily characterized by intense itching without a skin rash intense itching, often worse at night and more noticeable on the palms of the hands and soles of the feet. Other possible symptoms include dark urine, pale stools, tenderness or pain on the right side of the abdomen, and jaundice (yellowing of the skin and eyes). - after 28 weeks Elevated bile acid levels, normal Urate, Fat sol vit malabsorption, INR prolong Treatment - monitoring fetal well-being, ursodeoxycholic acid (UDCA)

Question 28

Acute Fatty Liver of Pregnancy (AFLP)

Answer 28

rare but serious condition where excessive fat accumulates in the liver during pregnancy, leading to liver failure and potentially life-threatening complications for both mother and baby. nausea, vomiting, abdominal pain, and jaundice, along with other symptoms like fatigue, loss of appetite, and sometimes excessive thirst. In advanced cases, liver failure may manifest as coagulopathy, encephalopathy, or renal failure associated with Preclampsia elevated liver enzymes (AST, GGT and ALT), bilirubin, and ammonia, along with hypoglycemia, and coagulopathy. Other potential abnormalities include leukocytosis, renal impairment (elevated creatinine and blood urea nitrogen), and prolonged prothrombin time. Prompt delivery to improve maternal and fetal outcomes Fetal Fatty Acid Oxidation Defects: In some cases, AFLP is linked to defects in the fetus's ability to process fatty acids, particularly LCHAD deficiency. LCHAD Deficiency: This is an autosomal recessive disorder where both parents must be carriers of the mutation for their child to inherit it. Mitochondrial Dysfunction: The enzyme deficiency can lead to an accumulation of fatty acids in the liver, potentially causing damage and triggering AFLP in the mother. Maternal Liver Disease: Studies have shown that fetal LCHAD deficiency can increase the risk of maternal liver diseases, including AFLP.

Question 29

Acute Fatty Liver of Pregnancy (AFLP) and HELLP syndrome

Answer 29

AFLP is characterized by more severe liver dysfunction, including coagulopathy and hypoglycemia, while HELLP syndrome typically presents with hemolysis, elevated liver enzymes, and low platelet counts. HELLP syndrome is usually accompanied by hypertension AFLP may or not AFLP is often associated with renal dysfunction

Question 30

Ovarian carcinosarcoma

Answer 30

both carcinomatous (epithelial) and sarcomatous (mesenchymal) components Aggressive abdominal pain, bloating, early satiety (feeling full quickly), and gastrointestinal complaints. Many patients present with advanced-stage disease (FIGO Stage III and IV) and symptoms like abdominal pain, weakness, and weight loss.

Question 31

pyogenic liver abscess vs amebic liver abscess

Answer 31

Pyogenic abscesses can appear anywhere in the liver, but are more likely to be multiple and involve both lobes. Amebic abscesses are more frequently solitary and tend to be located in the right lobe.

Question 32

End-stage liver disease (ESLD)

Answer 32

ESLD is often the result of chronic liver diseases like hepatitis (B or C), alcohol-related liver disease, or fatty liver disease (MASH). managing itching can involve medications like colestyramine, rifampicin, or naltrexone

Question 33

Crohn's disease

Answer 33

chronic inflammatory bowel disease (IBD) that can affect any part of the digestive tract, but commonly affects the small intestine and the beginning of the large intestine diarrhea, abdominal pain, and cramping. Other common symptoms include fatigue, weight loss, and in some cases, blood in the stool. *** NESTS - No blood or mucus, Entire GI tract affected, Skip lesions, Terminal ileum most affected and Smoking*** NOD2 and IRGM mutations (IBD) characterized by inflammation that can affect any part of the gastrointestinal tract, from the mouth to the anus, but most commonly affects the small intestine and the beginning of the large intestine. The inflammation in Crohn's disease is transmural, characteristic features - cobblestone mucosa and deep ulcers. high CPR & ESR , Ferritin, vitamin B12, folate, and vitamin D, anemia Corticosteroids: to reduce inflammation in the digestive system and relieve symptoms. They are typically used for short periods to manage flares and then tapered off gradually.

Question 34

alcoholic hepatic steatosis

Answer 34

AST/ALT >2 is the earliest and most common stage of alcohol-related liver disease, characterized by the accumulation of fat in the liver cells, often reversible with abstinence from alcohol. steatosis appears as large lipid droplets (macrovesicular steatosis) within the liver cells, displacing the nucleus.

Question 35

Bile acid malabsorption (BAM)

Answer 35

occurs when the small intestine struggles to reabsorb bile acids, leading to excess bile acids in the colon, which can cause chronic watery diarrhea and other digestive issues. Causes of Bile Acid Malabsorption Crohn's disease, Ileal resection, Radiation enteritis, Cholecystectomy, Idiopathic bile acid malabsorption Diagnosis SeHCAT scan, Fecal bile acid analysis

Question 36

pancreatic pseudocyst

Answer 36

develop due to pancreatic duct injury, leading to leakage of pancreatic fluid and enzyme-rich secretions into the surrounding tissue. This fluid accumulation is encapsulated by fibrous tissue, creating a "pseudocyst" that lacks an epithelial lining. The process is often associated with acute or chronic pancreatitis, and can also occur after abdominal trauma. take 4 to 6 weeks to fully form include observation, drainage of the cyst, or surgical removal,

Question 37

Diverticulitis

Answer 37

a complication that can affect people with diverticulosis, small pockets on the inside of their colon lower abdominal pain, fever, and changes in bowel habits. The pain is often felt on the left side of the abdomen, may be sudden and severe, and can be exacerbated by eating. Other symptoms may include nausea, vomiting, and constipation or diarrhea Complete Blood Count (CBC): An elevated WBC count, especially with a "left shift" (an increase in immature WBCs), normal WBC count, particularly those who are elderly, immunocompromised, or have mild disease. Elevated CRP levels A definitive diagnosis of diverticulitis - contrast-enhanced CT scan of the abdomen and pelvis - A thickened colonic wall, especially if exceeding 4 mm in the large bowel, - Pericolic Fat Stranding - Paracolic Inflammation -

Question 38

Paracetamol overdose

Answer 38

pH< 7.3 OR all of three Prothrombin Time >100s, Creatinine >300 micromoles/L, grade 3 or 4 encephalopathy continued nausea and vomiting, abdominal pain, and a tender hepatic edge. Hepatic necrosis and synthetic dysfunction manifest as jaundice, coagulopathy, hypoglycemia, and hepatic encephalopathy, Acute kidney injury

Question 39

familial hypercholesterolemia

Answer 39

Elevated LDL cholesterol levels due to defects in the LDL receptor or other related genes. This impaired LDL clearance leads to a buildup of LDL in the bloodstream, increasing the risk of premature cardiovascular disease. autosomal dominant pattern, gene mutations - LDL receptor (LDLR), apolipoprotein B (APOB), or proprotein convertase subtilisin/kexin type 9 (PCSK9). Clinical Manifestations: Abdominal Pain and Bloating: Pelvic or abdominal pain, discomfort, or bloating are common symptoms. Gastrointestinal Issues: Early satiety, difficulty eating, and changes in bowel habits (like constipation) can occur. Urinary Changes: Urgent or frequent urination may be present. Other Potential Symptoms: Weight loss, fatigue, and back pain can also be associated with ovarian cancer, including OCS. Advanced Stage Symptoms: In more advanced stages, patients may experience weakness, abdominal distention, and gastrointestinal complaints

Question 40

LPL Deficiency:

Answer 40

autosomal recessive pattern - chrom 8p22. Familial lipoprotein lipase deficiency is a rare genetic disorder where the body lacks sufficient LPL, leading to a buildup of chylomicrons (fatty droplets) in the blood. Abdominal Pain: severe, colicky abdominal pain Pancreatitis: Recurrent episodes of pancreatitis leading to chronic pancreatitis and diabetes. Hepatomegaly and Splenomegaly failure to thrive in infants, lipemia retinalis (fat buildup in the retina), and eruptive xanthomas (fat deposits under the skin). Hypertriglyceridemia Pancreatitis Hepatomegaly and Splenomegaly Eruptive Xanthomas, Lipemia Retinalis Low-Fat Diet, Supplementation, RNA therapy (Volanesorsen) and monoclonal antibodies

Question 41

alpha 1 antitrypsin deficiency

Answer 41

deficiency in alpha-1 antitrypsin, leading to lung and liver damage, emphysema and COPD, cirrhosis. mutations in the SERPINA1 gene , AAT protein - autosomal codominant inherited disorder Diagnosis - low AAT levels, protein phenotyping, and potentially genetic testing. PiZZ genotype is a common form of AAT deficiency where individuals inherit two copies of the mutated gene. shortness of breath, wheezing, and chronic cough, often leading to emphysema and bronchiectasis. Liver issues Lung Manifestations: Shortness of breath, Wheezing, Chronic cough, Emphysema, Bronchiectasis, Neonatal cholestasis Cirrhosis, Liver fibrosis, Jaundice Swelling in the legs or abdomen Panniculitis Vascular disease: Increased risk of C-ANCA-positive vasculitis (granulomatosis with polyangiitis). Skin lesions: Some individuals may experience skin lesions or bumps.

Question 42

Hepatocellular carcinoma

Answer 42

Causes : Chronic viral hepatitis: HBV in Asia/Africa) and hepatitis C virus (HCV) (50-70% in Western countries) Cirrhosis: Present in 70-90% of HCC cases, regardless of etiology Metabolic dysfunction-associated steatotic liver disease (MASLD) Alcohol-related liver disease Aflatoxin exposure Other factors: Diabetes, obesity, smoking, and certain genetic conditions (hemochromatosis, alpha-1-antitrypsin deficiency) Symptoms Right upper quadrant pain or fullness Unexplained weight loss and anorexia Fatigue and weakness Jaundice , Abdominal distension from ascites Paraneoplastic syndromes (hypercalcemia, hypoglycemia, erythrocytosis) Imaging: Ultrasound (initial screening modality) Multiphasic CT or MRI showing characteristic arterial hyperenhancement with venous/delayed phase "washout" Contrast-enhanced ultrasound (CEUS) as an alternative Biomarkers: Alpha-fetoprotein (AFP) - elevated in 60-70% of cases but limited sensitivity/specificity Emerging markers (AFP-L3%, DCP) show promise but not yet standard Biopsy: Required when imaging is inconclusive or in non-cirrhotic patients Histology shows trabecular, pseudoacinar, compact, or sarcomatoid patterns Curative Options (BCLC 0-A) Liver transplantation: Gold standard for eligible patients within Milan criteria (single ≤5cm or 2-3 nodules ≤3cm) 5-year survival >75% with recurrence rates <15% Surgical resection: Preferred for solitary tumors in non-cirrhotic livers or Child-Pugh A cirrhosis with adequate future liver remnant Anatomic resections (segmentectomy, hemihepatectomy) preferred over wedge resections Ablative therapies: Radiofrequency ablation (RFA) - first-line for tumors <3cm not suitable for surgery Microwave ablation and ethanol injection alternatives Locoregional Therapies (BCLC B) Transarterial chemoembolization (TACE): Delivers chemotherapy + embolic agents to tumor vasculature Improves 2-year survival from 27% to 63% versus supportive care Radioembolization (TARE): Yttrium-90 microspheres provide targeted radiation Particularly useful for larger or multifocal tumors Stereotactic body radiation therapy (SBRT): Precise high-dose radiation for tumors unsuitable for ablation Systemic Therapies (BCLC C) First-line options: Atezolizumab + bevacizumab: PD-L1 inhibitor + VEGF inhibitor showing superior survival versus sorafenib (median OS 19.2 vs 13.4 months) Tremelimumab + durvalumab: CTLA-4 + PD-L1 inhibitors with median OS 16.4 months Lenvatinib: Multikinase inhibitor non-inferior to sorafenib (median OS 13.6 vs 12.3 months) Second-line options (after progression): Regorafenib, cabozantinib, ramucirumab (for AFP ≥400 ng/mL), nivolumab ± ipilimumab, pembrolizumab Palliative Care (BCLC D) Focuses on symptom management and quality of life

Question 43

Crigler-Najjar syndrome

Answer 43

Autosomal recessive inheritance UGT1A1 gene, which is responsible for producing the enzyme uridine diphosphate glucuronosyltransferase (UGT). This enzyme is crucial for converting bilirubin into a form that can be excreted from the body Type 1: Characterized by severe jaundice, high bilirubin levels, and a high risk of irreversible neurological damage (kernicterus). Type 2: Less severe, with lower bilirubin levels and a possibility of surviving into adulthood without neurological damage. type of unconjugated hyperbilirubinia

Question 44

Variceal bleeding

Answer 44

harmacological Therapy A. Vasoactive Drugs First-line: Terlipressin (2 mg IV bolus, then 1–2 mg q4–6h) – reduces portal pressure Contraindications: Severe coronary artery disease (use octreotide instead). Alternative: Octreotide (50 µg bolus, then 50 µg/hr infusion) if terlipressin unavailable B. Antibiotic Prophylaxis All cirrhotic patients with variceal bleeding should receive IV ceftriaxone (1 g/day) or oral ciprofloxacin (if no resistance) for 5–7 days to prevent bacterial infections. 3. Endoscopic Management A. Urgent Endoscopy (<12–24 hours) Gold standard: Esophagogastroduodenoscopy (EGD) confirms diagnosis and provides therapy. Therapies: Band ligation (EBL): First-line for esophageal varices Cyanoacrylate glue injection: For gastric varices B. Rescue Therapies if Endoscopy Fails Balloon tamponade (Sengstaken-Blakemore tube): Temporizes severe bleeding until definitive therapy (TIPS) Self-expanding metal stents: Alternative to balloon tamponade 4. Secondary Prevention & Long-Term Management A. Secondary Prophylaxis Combination therapy: Non-selective beta-blockers (NSBB): Propranolol or carvedilol (reduces rebleeding risk) Repeat EBL: Until variceal eradication B. Transjugular Intrahepatic Portosystemic Shunt (TIPS) Indications: Refractory bleeding despite endoscopic + pharmacologic therapy. High-risk patients (Child-Pugh B/C) Timing: Early TIPS (within 72 hrs) improves survival in high-risk cases sucess rate to band ligation - 90% Baloon tampnade - 80% mortality - 30% Transjugular Intrahepatic Portosystemic Shunt (TIPS): A common procedure that creates a shunt between the portal and hepatic veins. gastric Vareceal bleeding - Endoscopic Cyanoacrylate sclerotherapy

Question 45

risk factors for squamous cell carcinoma

Answer 45

Achalasia tylosis, Bloom syndrome, Fanconi anemia bisphosphonates HPV

Question 46

spontaneous bacterial peritonitis

Answer 46

occurs when bacteria from the gut migrate into the ascitic fluid (fluid in the abdominal cavity) due to weakened immune defenses and altered intestinal permeability in individuals with advanced liver disease E Coli

Question 47

Achalasia cardia

Answer 47

primarily diagnosed using a combination of esophageal manometry, endoscopy, and barium swallow. Difficulty Swallowing (Dysphagia), Chest Pain Heartburn, Weight Loss , Coughing, Food "Sticking" in the Esophagus Esophageal Manometry: assess the function of the esophagus and LES. Normal findings include: Impaired LES relaxation (IRP) of ≥ 10 mmHg. Lack of peristalsis in the lower esophagus.

Question 48

Coeliac disease

Answer 48

autoimmune disorder triggered by gluten, a protein found in wheat, barley, and rye. In individuals with celiac disease, the immune system mistakenly attacks the small intestine when gluten is ingested, leading to inflammation and damage to the villi Villous atrophy is a characteristic feature of coeliac disease, where the finger-like projections in the small intestine (villi) flatten or become damaged due to the body's immune response to gluten specific HLA genes (HLA-DQ2 or HLA-DQ8) Blood Tests (Serology): tTG-IgA, EMA-IgG, DGP-IgG, or tTG-IgG, Genetic Testing: HLA-DQ2 or HLA-DQ8 diarrhea, bloating, and abdominal pain, as well as extra-intestinal symptoms such as fatigue, weight loss, and skin rashes. Dermatitis Herpetiformis: An itchy, blistering rash that typically appears on the elbows, knees, buttocks, or scalp, Growth Failure in Children, Osteoporosis or Osteomalacia Associations - type 1 diabetes, autoimmune thyroid disease, Down syndrome, Turner syndrome, and certain cancers T cell lymphoma. Dermatitis Herpetiformis, arthritis, Addison's disease, and Crohn's disease, Autoimmune Thyroid Disease, autoimmune hepatitis, primary biliary cholangitis, microscopic colitis, and Sjogren's syndrome. resection of illiac & hemicolec- Gallestones,

Question 49

Ménétrier's disease

Answer 49

a rare, acquired condition characterized by massive overgrowth of the stomach's inner lining, causing giant folds and excessive mucus production Characteristics: Giant gastric folds, Foveolar hyperplasia Protein-losing gastropathy, Hypochlorhydria or achlorhydria Treatment: Addressing H. pylori infection: Targeting TGF-alpha:

Question 50

Gastric Antral Vascular Ectasia

Answer 50

"watermelon stomach" where the stomach lining develops red, vertical stripes that resemble a watermelon. These stripes are caused by the enlargement and bleeding of blood vessels in the stomach's antrum, the lower part near the pylorus. iron deficiency anemia, blood in the stool or vomit, and abdominal pain. Treatment options include endoscopic therapies like argon plasma coagulation (APC) and laser photoablation. GAVE is diagnosed through endoscopy, where a thin, flexible tube with a camera is inserted into the stomach to visualize the lining.

Question 51

Absolute contraindications for liver transplantation

Answer 51

Hepatocellular carcinoma (HCC), HIV/AIDS, alcohol abuse, relative - Lack of psychosocial support, smoking, BM 40

Question 52

Angiodysplasia

Answer 52

involves the development of small, fragile blood vessels in the gastrointestinal (GI) tract, often leading to bleeding End-stage renal disease, von Willebrand disease, aortic stenosis, and left ventricular assist devices. Diagnosis - endoscopic procedures like colonoscopy and upper endoscopy May resolve spontanously Endoscopic Therapies: Argon Plasma Coagulation (APC)

Question 53

percutaneous liver biopsy

Answer 53

Contraindications - Significant coagulopathy or thrombocytopenia (unless corrected), recent NSAID use, patient refusal of blood transfusions, and suspected hemangioma, vascular tumor, or echinococcal cyst

Question 54

fecal elastase

Answer 54

non-invasive method for detecting exocrine pancreatic insufficiency (EPI)

Question 55

omeprazole mechanism of action

Answer 55

a selective and irreversible proton pump inhibitor. It suppresses stomach acid secretion by specific inhibition of the H+/K+-ATPase system found at the secretory surface of gastric parietal cells

Question 56

villous adenoma

Answer 56

a type of benign growth in the colon and rectum, characterized by finger-like or leaf-like epithelial projections have a higher risk of malignant transformation compared to other adenomas, especially if they are larger than 2 cm. blood in the stool, diarrhea, or abdominal pain. Larger villous adenomas can cause more severe symptoms like rectal bleeding, changes in bowel habits, and even dehydration due to secretory diarrhea.

Question 57

Chronic pancreatitis

Answer 57

hronic pancreatitis is primarily caused by alcohol misuse and smoking, Other risk factors genetic conditions, autoimmune diseases, hyperlipidemia, and hypercalcemia. gallstones, Mutations in genes like PRSS1, SPINK1, CPA1, and CFTR can increase the risk of both acute and chronic pancreatitis. Elevated lipase and amylase levels are not specific for chronic pancreatitis Fecal elastase-1 is a useful indirect test of pancreatic exocrine function, particularly in cases of exocrine insufficiency. 72-Hour Fecal Fat - gold standard for assessing fat malabsorption. CT - initial modality for detecting severe chronic pancreatitis and identifying complications like pseudocysts

Question 58

DILI

Answer 58

Acute hepatocellular injury: severe inflammation with necrosis and apoptosis seen in isoniazid (INH), aspirin, and phenytoin Chronic hepatocellular injury: findings as above with fibrosis resembling other chronic liver disease seen in amoxicillin-clavulanate, valproic acid, amiodarone Acute cholestasis: bile plugging with hepatocellular cholestasis, commonly seen in anabolic steroid use, eastogen, asatha, clopro, haperidole, erythro Chronic cholestasis: bile stasis, portal inflammation, bile jury, bile plugs, and duct paucity seen in amoxicillin-clavulanate Steatosis: microvesicular often related to mitochondrial injury seen in tetracycline and valproic acid Zonal necrosis: usually in intrinsic DILI and associated with poor outcomes, seen in acetaminophen toxicity Granulomas: associated with milder injury and can result from many drugs or even talc exposure through the bloodstream Antibiotics (45.4%): amoxicillin-clavulanate (most common), sulfamethoxazole-trimethoprim, ciprofloxacin, isoniazid (INH) DD Liver diseases: viral hepatitis (A, B, C, E), cytomegalovirus (CMV), Epstein-Barr virus, ischemic hepatitis, autoimmune hepatitis, Hemochromatosis, Wilson disease, non-alcoholic fatty liver disease (NAFLD), alcoholic hepatitis, Gilbert syndrome Biliary disease: cholangitis, choledocholithiasis, primary biliary cirrhosis, primary sclerosing cholangitis Malignancy: hepatocellular cancer, lymphoma, pancreaticobiliary malignancy

Question 59

acute cholangitis

Answer 59

Clinical features: Charcot’s triad (fever, RUQ pain, jaundice), pruritus, pale stools, dark urine, nausea/vomiting; Reynold's pentad (Charcot’s triad + hypotension and confusion) Acute cholangitis: infection of the biliary tree due to biliary outflow obstruction and infection; life-threatening with 17-40% mortality; median age 50-60 years. Aetiology: usually caused by obstruction (e.g., gallstones, tumours) leading to infection (E. coli, Klebsiella, Enterococcus); biliary sludge provides an ideal growth medium for bacteria. Risk factors: gallstone disease, iatrogenic biliary injury, tumours, sclerosing cholangitis, biliary strictures, parasitic infections.

Question 60

Alcoholic complications

Question 61

Dieulafoy lesion

Answer 61

vascular abnormality in the gastrointestinal tract, specifically a dilated, tortuous submucosal artery that protrudes through the mucosa, causing bleeding large vessel's pressure or pulsation weakens the overlying mucosa, leading to erosion and bleeding.

Question 62

Non-alcoholic fatty liver disease (NAFLD)

Answer 62

Associated Conditions - Cirrhosis Obesity Type 2 Diabetes - metabolic sybndrome involves a complex interplay of factors, including insulin resistance, lipotoxicity (toxicity from fat accumulation), and inflammation, leading to a spectrum of liver damage ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and potentially cirrhosis. Insulin Resistance: NAFLD is strongly linked to insulin resistance, a hallmark of metabolic syndrome. Lipotoxicity: Excessive accumulation of fat in the liver (lipotoxicity) can damage liver cells (hepatocytes) and trigger inflammation. Adipokines: Hormones produced by fat cells (adipocytes) can influence inflammation and insulin sensitivity. Gut Microbiota: Changes in the gut's microbial community can impact liver health and NAFLD progression. Mitochondrial Dysfunction: Abnormalities in the mitochondria, the liver's powerhouses, can contribute to NAFLD progression. Genetic Predisposition: Certain genetic variations can increase susceptibility to NAFLD. Asymptomatic: Many individuals with NAFLD are asymptomatic, and diagnosis is often incidental. Symptomatic: Some individuals may experience fatigue, right upper quadrant pain, or discomfort. Obesity and Metabolic Syndrome: NAFLD is strongly associated with obesity, diabetes, and other features of the metabolic syndrome. Liver Function Tests: Abnormal liver function tests, specifically mildly elevated ALT (alanine transaminase), may be observed. Histological Findings: Steatosis: The accumulation of fat in liver cells (hepatocytes), which can be macrovesicular (large fat droplets) or microvesicular (small fat droplets). Inflammation: Inflammation in the liver, including lobular and portal inflammation, is a key feature of NASH. Ballooning Degeneration: Hepatocytes may show swelling and rarefaction of cytoplasm, a hallmark of NASH. Fibrosis: The development of scar tissue in the liver, which can range from mild to severe and progress to cirrhosis in advanced cases. Mallory-Denk Bodies: These are irregular, basophilic inclusions in the cytoplasm of hepatocytes, commonly seen in NASH. Other Findings: Apoptotic bodies, glycogenated nuclei, and megamitochondria may also be observed. Liver biopsy remains the gold standard for diagnosing NAFLD and differentiating between NAFL (simple steatosis) and NASH. Imaging for Steatosis: Ultrasound: First-line. Shows a "bright" echogenic liver. Transient Elastography (e.g., FibroScan®): Can quantify steatosis (CAP score) and, crucially, assess fibrosis Pharmacotherapy: Treat Comorbidities: Optimize control of T2DM, dyslipidemia, and hypertension. Vitamin E: An antioxidant that can be used in non-diabetic, biopsy-proven MASH patients. Pioglitazone: An insulin sensitizer that can be used in patients with and without T2DM with biopsy-proven MASH. (Monitor for weight gain, osteoporosis, heart failure). Newer Agents: GLP-1 Receptor Agonists (e.g., semaglutide) show very promising results for both weight loss and direct liver histology improvement. Obeticholic acid is approved in some regions for advanced MASH.

Question 63

Gastrin

Answer 63

It's a hormone that stimulates the release of stomach acid, promotes gastric mucosal growth, and influences gastric motility. Disruptions in gastrin levels and its signaling pathways can lead to conditions like peptic ulcers, hypergastrinemia, and certain types of gastric tumors. Acid Secretion: Gastrin, released by G cells in the stomach antrum, stimulates parietal cells to produce hydrochloric acid (HCl). Mucosal Growth: Gastrin promotes growth and differentiation of gastric epithelial cells, including parietal and other secretory cells. Gastric Motility: Gastrin influences gastric emptying and motility, though its exact role is still under investigation. Hypergastrinemia: Elevated levels of gastrin can occur in several conditions: Autoimmune atrophic gastritis: Damage to parietal cells leads to reduced acid secretion, triggering increased gastrin production by G cells to compensate. Helicobacter pylori infection: Chronic infection can cause inflammation and altered gastric physiology, leading to hypergastrinemia. Gastrinomas (Zollinger-Ellison Syndrome): Tumors in the pancreas or duodenum produce excessive gastrin, causing increased acid secretion and ulcers. Antisecretory medications: Long-term use of drugs like proton pump inhibitors can increase gastrin levels. Diagnosis of Zollinger-Ellison Syndrome: Measuring gastrin levels is a key part of diagnosing and monitoring gastrinomas. Monitoring Therapy: Assessing gastrin levels can help track the effectiveness of treatments for conditions like hypergastrinemia and peptic ulcers. Understanding Gastric Cancer: Research on gastrin and its role in gastric cancer development is ongoing

Question 64

crohn's disease vs ulcerative colitis

Answer 64

Crohn's disease can affect any part of the gastrointestinal tract from the mouth to the anus, with inflammation often appearing in a patchy, discontinuous pattern (skip lesions) and involving all layers of the bowel wall (transmural inflammation). Ulcerative colitis, on the other hand, primarily affects the colon and rectum, with continuous inflammation of the inner lining (mucosa) Ulcerative Colitis: Inflammation usually starts in the rectum and progresses proximally, often affecting the entire colon. The inner lining of the colon develops ulcers, leading to bleeding, edema, and electrolyte loss. Ulcerative colitis is a mucosal disease, meaning it primarily affects the inner lining of the colon. Crohn's Disease: Inflammation can occur anywhere in the GI tract, most commonly in the ileum and colon. Inflammation is often patchy, with alternating areas of healthy and inflamed tissue (skip lesions). Crohn's disease involves all layers of the bowel wall (transmural inflammation). It can lead to complications like fistulas, strictures, and abscesses, as well as extra-intestinal manifestations.

Question 65

coxib

Answer 65

Coxibs work by selectively inhibiting cyclooxygenase-2 (COX-2), an enzyme involved in inflammation and pain. This selective inhibition may reduce the risk of gastrointestinal side effects compared to traditional NSAIDs, which inhibit both COX-1 and COX-2. Coxibs are known to have a lower risk of gastrointestinal complications like ulcers and bleeding compared to traditional NSAIDs.

Question 66

Protein-losing enteropathy (PLE)

Answer 66

condition where excessive amounts of blood proteins leak into the digestive tract, leading to low serum protein levels causing edema, ascites, and malnutrition Hypoproteinemia, Edema, Ascites, Pleural and pericardial effusions, Diarrhea, Malnutrition. Fatigue, weight loss, and increased susceptibility to infections. Crohn's disease, celiac disease, Whipple's disease, intestinal infections, Congestive heart failure, cirrhosis, lupus, sarcoidosis, and other conditions that can increase pressure in the central venous system or obstruct mesenteric lymphatics. Intestinal lymphangiectasia, which is characterized by dilated lymphatic vessels in the intestines, can lead to fluid leakage. Other conditions: Tuberculosis, retroperitoneal fibrosis, intestinal endometriosis, lymphoma, and Whipple's disease can also contribute to PLE.

Question 67

Immune reconstitution inflammatory syndrome (IRIS)

Answer 67

a paradoxical worsening of existing infections or the development of new infections in HIV patients after starting antiretroviral therapy (ART) Whipple's disease, IRIS is characterized by a paradoxical worsening of symptoms, like fever and joint pain, after initial improvement with antibiotic treatment.

Question 68

Pancreatic adenocarcinoma

Answer 68

the most common type of pancreatic cancer, accounting for about 90% Jaundice (yellowing of the skin and eyes), weight loss, abdominal pain, and changes in stool. aggressive nature, poor prognosis, and often subtle symptoms Clustered ducts with irregular jagged contours (diameter: 0.5 mm - 1 cm) Desmoplastic and myxoid stroma, intraluminal neutrophils and granular debris. Focal microcystic appearance due to marked ectasia of infiltrating neoplastic glands, particularly near duodenal muscularis propria

Question 69

pharyngeal pouch

Answer 69

known as Zenker's diverticulum, is a sac-like outpouching of the pharynx (the part of the throat behind the mouth) that occurs at the top of the esophagus difficulty swallowing (dysphagia), regurgitation of food, and halitosis (bad breath), Gurgling

Question 70

Amoebiasis

Question 71

Melanosis Coli

Answer 71

As these laxative supplements pass through the colon, they become active and cause cell death and apoptosis in the lining of the colon, eventually causing dark pigmentation of the colon. Senna glycoside (senna) is the main causative laxative Anthraquinones laxatives work in 3 ways: It stimulates the active transport of chloride into the gut, which in turn causes an osmotic gradient and pulls water into the gut lumen. It inhibits Na-K adenosine triphosphate (ATP)ase on the enterocytes, which further inhibits the reabsorption of water, sodium, and potassium, ultimately excreting it into the feces. It stimulates local prostaglandins, which stimulate peristalsis and decrease transit time through the bowel.

Question 72

Giardiasis

Answer 72

In intestinal infection caused by the microscopic parasite Giardia duodenalis, leading to symptoms like diarrhea, bloating, and gas Giardiasis is typically diagnosed through a stool sample examination, which can detect the Giardia parasite - confirmed by the finding of trophozoites and cysts on microscopy Treatment: metronidazole, tinidazole, or nitazoxanide Lactose Intolerance: Many people develop lactose intolerance after a giardiasis infection, which can persist even after the initial infection clear Reactive Arthritis and Irritable Bowel Syndrome: In some cases, long-term symptoms like reactive arthritis or irritable bowel syndrome Chronic Fatigue: Some individuals experience chronic fatigue as a post-infectious symptom. Extra-intestinal Manifestations: Rarely, giardiasis can cause complications outside the digestive tract, such as allergic reactions, eye problems, or even potential links to cancer.

Question 73

Hepatitis C and Chronic Kidney Disease

Answer 73

Hepatitis, particularly Hepatitis B and C, is associated with an increased risk of developing chronic kidney disease (CKD). Hepatitis C, in particular, is linked to faster progression of CKD and higher mortality rates, especially in kidney transplant patients. Hepatitis B can also lead to kidney damage and CKD through various mechanisms, including inflammation and toxin buildup.

Question 74

Hep

Question 75

Intestinal lymphangiectasia

Answer 75

a rare digestive disorder where the lymph vessels in the small intestine become abnormally enlarged and blocked, leading to protein and fat malabsorption. This condition, also known as Waldmann's disease, causes lymph fluid to leak from these swollen vessels into the intestines instead of being absorbed into the bloodstream Primary/Congenital - CCBE1 and FAT4, which can cause Hennekam syndrome. Other disorders like Noonan syndrome can also be associated with intestinal lymphangiectasia. Secondary: tuberculosis or HIV. Inflammatory conditions: Like amyloidosis. Malignancies: Including lymphoma and Mechanical obstruction

Question 76

Gamma-Glutamyl Transferase (GGT) levels

Answer 76

elevated: Liver damage: Hepatitis, cirrhosis, alcohol use disorder, fatty liver disease, and certain medications can cause GGT levels to rise. Bile duct issues: Biliary obstruction or cholestasis (blocked bile ducts) can also lead to elevated GGT. Other causes: Pancreatitis, heart failure, and certain medications can also elevate GGT.

Question 77

Hep D

Question 78

lactose intolerance

Question 79

Risk factors for Gallstones

Question 80

Melioidosis

Answer 80

serious bacterial infection caused by Burkholderia pseudomallei Southeast Asia and northern Australia Can range from mild localized infections to severe, life-threatening sepsis, with symptoms like fever, cough, pneumonia, abscesses, and septic shock. Risk Factors: Individuals with underlying conditions like diabetes, chronic kidney disease, and immunosuppression Culture: Culturing B. pseudomallei from blood, urine, sputum, or other samples is considered the gold standard.

Question 81

Primary biliary cholangitis (PBC)/ Primary Biliary Cirrhosis

Answer 81

fatigue and itchy skin to more advanced symptoms like jaundice, ascites, and edema Fatigue: A common initial symptom, often extreme. Pruritus (Itchy Skin): Another early symptom, which can be severe and persistent. Bone and Joint Aches: Some individuals experience these pains. Abdominal Discomfort: Pain or discomfort in the upper right abdomen, where the liver is located. Dry Eyes and Mouth: Can be a symptom of Sjögren's syndrome, often associated with PBC. Mechanism: Anti-mitochondrial antibodies (AMA) target the E2 subunit of pyruvate dehydrogenase complex (PDC-E2) on biliary epithelial cells. CD4+ and CD8+ T-cell infiltration → Bile duct destruction. Cytokine release (TNF-α, IL-12, IFN-γ) promotes fibrosis. Genetics: HLA-DRB1*08, IL12A, POU2AF1. AMA (anti-mitochondrial Ab) >95% sensitivity (anti-PDC-E2 most specific). Liver Biopsy (Not always needed if AMA+) Florid duct lesions (lymphocytic destruction of bile ducts). Granulomas (non-caseating, in 40% DD Primary Sclerosing Cholangitis (PSC) (AMA-negative, bile duct strictures on MRCP). Autoimmune Hepatitis (AIH) (ALT dominant, anti-smooth muscle Ab). Drug-induced cholestasis (e.g., anabolic steroids).

Question 82

Pernicious Anemia

Answer 82

Pernicious anemia (PA) is a megaloblastic anemia caused by vitamin B12 deficiency due to autoimmune destruction of gastric parietal cells, leading to intrinsic factor (IF) deficiency and impaired B12 absorption. . Autoimmune Mechanism Anti-parietal cell antibodies (APCA): Target H⁺/K⁺ ATPase pumps → Chronic atrophic gastritis. Anti-intrinsic factor antibodies (AIFA): Type 1 (blocking): Prevent B12 binding to IF. Type 2 (binding): Prevent IF-B12 complex absorption in the ileum. B. Consequences of B12 Deficiency Impaired DNA synthesis → Megaloblastic anemia (large, fragile RBCs). Neurological damage (demyelination) → Peripheral neuropathy, subacute combined degeneration of the spinal cord. 2. Clinical Features A. Hematologic Anemia symptoms: Fatigue, pallor, weakness. Megaloblastic changes: Macrocytic RBCs (MCV >100 fL), hypersegmented neutrophils (≥5 lobes). B. Neurologic Peripheral neuropathy: Numbness, paresthesia (hands/feet). Subacute combined degeneration: Ataxia, loss of proprioception/vibration sense (posterior/lateral spinal cord). Cognitive changes: Memory loss, depression (mimicking dementia). C. Gastrointestinal Atrophic glossitis (smooth, beefy-red tongue). Dyspepsia (due to chronic gastritis). A. Laboratory Findings Test Findings CBC Macrocytic anemia (↑MCV), ↓Hb, ↓RBCs. Peripheral smear Hypersegmented neutrophils, oval macrocytes. Serum B12 <200 pg/mL (deficient). Methylmalonic acid (MMA) ↑↑ (more sensitive than B12). Homocysteine ↑↑ (elevated in B12/folate deficiency). Anti-IF antibodies Highly specific for PA (positive in ~50-70%). Anti-parietal cell antibodies Less specific (also in autoimmune gastritis). C. Endoscopy & Biopsy Atrophic gastritis with parietal cell loss (chlorhydria). Enterochromaffin-like (ECL) cell hyperplasia (due to chronic hypergastrinemia). 4. Management A. Vitamin B12 Replacement Intramuscular (IM) B12 (Cyanocobalamin): Loading dose: 1000 mcg IM daily × 1 week, then weekly × 1 month. Maintenance: 1000 mcg IM monthly for life. High-dose oral B12 (if no neurologic symptoms): 1000–2000 mcg/day (1% absorbed passively without IF) Differential Diagnosis Condition Key Differentiator Folate deficiency = Normal MMA, no neurologic symptoms. Myelodysplastic syndrome (MDS) = Dysplastic RBCs, normal B12/MMA. Chronic atrophic gastritis (non-autoimmune) = No anti-IF antibodies.

Question 83

Heparin-Induced Thrombocytopenia (HIT)

Answer 83

Definition and Types of HIT HIT is an immune-mediated adverse reaction to heparin, characterized by thrombocytopenia and a paradoxical increase in thrombosis risk Type I (Non-immune HIT): Mild, transient platelet drop (rarely <100 × 10⁹/L) within 48–72 hours of heparin exposure. Benign, resolves spontaneously; no thrombosis risk Type II (Immune-mediated HIT): IgG antibodies target platelet factor 4 (PF4)-heparin complexes, causing platelet activation, thrombocytopenia, and thrombosis Onset typically 5–14 days after heparin initiation (or sooner with recent exposure) 2. Pathophysiology Heparin binds to PF4, forming immunogenic complexes that trigger IgG antibody production Antibodies bind to platelet FcγIIa receptors, causing: Platelet activation → thrombocytopenia (consumption/clearance). Release of procoagulant microparticles → thrombin generation and thrombosis Additional mechanisms: Endothelial/monocyte activation → tissue factor expression. Neutrophil extracellular traps (NETs) → further prothrombotic state 3. Clinical Features Thrombocytopenia: Platelet drop >50% from baseline (nadir often 20–100 × 10⁹/L) Thrombosis (venous > arterial): Deep vein thrombosis (DVT), pulmonary embolism (PE), stroke, limb ischemia Other manifestations: Skin necrosis at injection sites. Acute systemic reactions (fever, chills, tachycardia) post-IV heparin bolus B. Laboratory Testing Immunoassays: ELISA for anti-PF4/heparin antibodies (high sensitivity but low specificity) Functional Assays: Serotonin release assay (SRA) (gold standard). Platelet activation tests (e.g., heparin-induced platelet aggregation) 5. Management A. Immediate Actions Stop all heparin (including flushes/LMWH) Avoid platelet transfusions (may worsen thrombosis) Initiate alternative anticoagulation: Direct thrombin inhibitors (DTIs): Argatroban (liver metabolism), bivalirudin (renal adjustment) Factor Xa inhibitors: Fondaparinux (off-label), DOACs (e.g., rivaroxaban/apixaban) Delay warfarin until platelets recover (>150 × 10⁹/L) to avoid warfarin-induced skin necrosis B. Adjunctive Therapies IV immunoglobulin (IVIG): For refractory/severe HIT Plasma exchange: In life-threatening cases (e.g., HIT with thrombosis) C. Duration of Therapy Isolated HIT: Anticoagulate for 4 weeks (thrombosis risk persists). HIT with thrombosis: 3 months of anticoagulation 6. Prognosis and Complications Mortality: Up to 20–30% if untreated Thrombotic risk: 30–50% of HIT patients develop thrombosis Long-term: Avoid heparin re-exposure (lifelong contraindication)

Question 84

Hepatorenal Syndrome (HRS)

Answer 84

Hepatorenal syndrome (HRS) is a life-threatening complication of advanced liver disease, characterized by functional renal failure in the absence of intrinsic kidney pathology. It occurs due to severe circulatory dysfunction in cirrhosis, leading to renal vasoconstriction and reduced glomerular filtration rate (GFR). 1. Type 1 HRS (Acute, Rapidly Progressive) Definition: Doubling of serum creatinine to >2.5 mg/dL (221 µmol/L) in <2 weeks. Oliguria (<500 mL urine/day). Prognosis: Median survival: 1–2 weeks without treatment. Most fatal complication of cirrhosis. 2. Type 2 HRS (Chronic, Slowly Progressive) Definition: Moderate, stable renal impairment (Cr 1.5–2.5 mg/dL [133–221 µmol/L]). Often associated with refractory ascites. Prognosis: Median survival: 3–6 months without treatment. Pathophysiology HRS develops due to systemic and splanchnic vasodilation in cirrhosis, leading to: Reduced effective arterial blood volume → Activation of renin-angiotensin-aldosterone system (RAAS) and sympathetic nervous system. Severe renal vasoconstriction → Decreased GFR and renal failure. Portal hypertension → Splanchnic arterial vasodilation (NO-mediated) worsens renal hypoperfusion. Key Triggers: Spontaneous bacterial peritonitis (SBP) (~30% of cases). Large-volume paracentesis without albumin. GI bleeding, dehydration, or nephrotoxic drugs (NSAIDs, contrast agents). Diagnostic Criteria (ICD-11 & EASL Guidelines) Major Criteria (All Must Be Present) Cirrhosis with ascites. Serum creatinine >1.5 mg/dL (133 µmol/L). No improvement in creatinine after 2 days of diuretic withdrawal & volume expansion (albumin 1 g/kg/day). Absence of shock, nephrotoxins, or structural kidney disease (proteinuria <500 mg/day, no hematuria, normal renal US). Supportive Findings Low urine sodium (<10 mEq/L). Low fractional excretion of sodium (FENa <1%). No significant proteinuria or hematuria. Exclusion of Other Causes (e.g., ATN, glomerulonephritis, drug-induced nephropathy). Management & Treatment 1. First-Line Therapy: Vasoconstrictors + Albumin Terlipressin (Preferred) Dose: 1–2 mg IV every 4–6h (or continuous infusion). Response: ~40–50% reversal of HRS. Contraindications: Severe cardiovascular disease, bowel ischemia. Noradrenaline (Alternative) Dose: 0.5–3 mg/h IV. Similar efficacy but requires ICU monitoring. Albumin (20–40 g/day) to maintain volume expansion. 2. Second-Line: Transjugular Intrahepatic Portosystemic Shunt (TIPS) May improve renal function in Type 2 HRS but not Type 1. Contraindicated in severe hepatic failure (MELD >18–20). 3. Definitive Treatment: Liver Transplantation Only curative option. Simultaneous liver-kidney transplant (SLK) considered if prolonged renal failure. 4. Renal Replacement Therapy (RRT) Bridge to transplant in selected cases. No survival benefit in non-transplant candidates. 5. Prevention Albumin (1.5 g/kg) for SBP reduces HRS risk. Avoid NSAIDs, aminoglycosides, excessive diuresis. Prognosis Type Untreated Survival Treatment Response Type 1 HRS 1–2 weeks 40–50% reversal with terlipressin Type 2 HRS 3–6 months May improve with TIPS Mortality: 90% at 3 months if untreated. Liver transplant improves survival to >60% at 5 years. Key Guidelines Summary EASL (2023): Terlipressin + albumin is first-line; avoid RRT unless bridging to transplant. AASLD (2021): Noradrenaline is an alternative if terlipressin unavailable. ICD-11: Defines HRS as functional AKI in cirrhosis without structural damage.

Question 85

Upper GI Bleeding Management

Answer 85

Endoscopic Management A. Non-Variceal Bleeding (e.g., Peptic Ulcers) First-line therapy: Mechanical methods (e.g., clips) or thermal coagulation combined with adrenaline injection Avoid adrenaline monotherapy (ineffective for long-term hemostasis) Refractory bleeding: Offer interventional radiology (e.g., embolization) or surgery if radiology is unavailable B. Variceal Bleeding Antibiotics: Prophylactic IV ceftriaxone or oral ciprofloxacin for 5–7 days Endoscopic therapy: Band ligation for esophageal varices Cyanoacrylate glue for gastric varices Rescue options: TIPS (Transjugular Intrahepatic Portosystemic Shunt) if bleeding persists post-ligation Balloon tamponade (e.g., Sengstaken-Blakemore tube) as a temporary measure 4. Pharmacological Therapy Proton pump inhibitors (PPIs): High-dose IV (e.g., omeprazole 80mg bolus + 8mg/hr infusion) for non-variceal bleeding Vasoactive drugs: Terlipressin (first-line for variceal bleeding) or octreotide if contraindicated 5. Post-Endoscopy Care & Follow-Up Low-risk patients: Discharge with GP follow-up within 5 days; consider outpatient endoscopy if symptoms recur High-risk patients: Monitor for rebleeding (e.g., repeat Hb, clinical assessment) Medication review: Continue low-dose aspirin for cardiovascular protection if hemostasis is achieved Avoid NSAIDs; use PPIs if antiplatelet/anticoagulant therapy is essential