Gastroenterology Flashcards

Question

Definition of Primary Biliary Cholangitis

Answer 1

Chronic disease of the small intrahepatic bile ducts that is characterised by excessive bile duct damage. Fibrosis develops as a consequence and toxic bile acids eventually lead to cirrhosis.

Answer 2

35/100,000 with peak age 55-65 years. Patients in their 20s can also present more aggressive forms, less likely to respond to treatment. More prevalent in European and western countries

Answer 3

Coeliac Disease Scleroderma Other autoimmune diseases

Answer 4

Main: Female sex Age between 45-65 Others: Family history Smoking UTI

Answer 5

Damage to and progressive destruction of biliary epithelial cells lining small intrahepatic ducts. This can lead to bile duct loss causing cholestasis and bile acid retention, which can lead to fibrosis or eventually cirrhosis.

Answer 6

Key Presentations Personal history of autoimmune disease or history of hypercholesterolaemia Signs Hepatomegaly Symptoms Dry eyes and mouth fatigue itch sleep disturbance Postural dizziness Possible jaundice and ascites Finger clubbing / cholesterol deposits Xanthelasma

Answer 7

1st Line LFT - ALT, AST, ALP and Gamma-GT all elevated Serum Albumin - decreased AMA and ANA - present Abdominal ultrasound scan and magnetic resonance cholangiopancreatography - excludes obstructive lesion with visible bile ducts. Gold Standard Blood test AMA positive Others Liver biopsy - bile duct lesions Prothrombin time - prolonged Serum immunoglobulin - elevated IgM and IgG Transient elastography - decreased liver elasticity.

Answer 8

Cholestatic liver biochemistry (elevated LFT) Compatible serological tests (AMA and or PBC specific ANA) Compatible liver histology

Answer 9

Early stage: Bile acid analogue - ursodeoxycholic acid If have significant inflammatory component then immunomodulatory therapy With cholestatic pruritus - antipruritic therapy With fatigue - lifestyle modification For end stage liver disease - Liver transplantation.

Answer 10

Hypercholesterolaemia Osteoporosis Portal hypertension secondary to cirrhosis Hepatoma

Answer 11

Slow progression X2 risk of mortality with or without a liver disease Impaired quality of life with side effects.

Answer 12

Obstructive bile duct lesion - much more prominent pain and bacterial cholangitis much more likely Small-duct primary sclerosing cholangitis - Associated with IBD and more common in younger males. PSC marker present. Drug induced cholestasis - Antibody not associated and history of relevant drug exposure Cholestasis of pregnancy Infiltrative malignancy within the liver - liver biopsy.

Answer 13

Acute gallbladder inflammation. Complete cystic duct obstruction which leads to inflammation of the gallbladder wall. In 5% cases, bile stasis can block the cystic duct, causing acalculous cholecystitis.

Answer 14

Occurs in 10% of symptomatic patients. 3x more common in women than men up to the age of 50 years.

Answer 15

Gallstones Starvation, TPN, narcotic analgesics immobility EBV

Answer 16

Main: Cholelithiasis Total parenteral nutrition (TPN) Diabetes Medications Others: Physical inactivity, Low fibre, Trauma, Infections

Answer 17

Fixed obstruction or passage of gallstones into the gallbladder neck or cystic duct can cause acute inflammation of the gallbladder wall. The impacted gallstone causes bile to be trapped in the gallbladder, which causes irritation and increases pressure. This stimulates prostaglandin synthesis which mediates an inflammatory response and can result in secondary bacterial infection if untreated. It may resolve spontaneously 5-7 days after onset.

Answer 18

Key Presentations Pain and tenderness in RUQ or epigastric area which can radiate to back Fever Palpable mass Signs Murphy's sign, Pyrexia Symptoms Nausea, Malaise, Anorexia, vomiting

Answer 19

1st Line FBC - elevated WCC CRP, Bilirubin, AST, ALT and Gamma-GT elevated Serum lipase / amylase elevated Abdo USS - distended and thickened gallbladder >3mm. With pericholecystic fluid CT or MRI - irregular thickening of gallbladder wall, increased density of fatty tissue and gas in gallbladder wall or lumen. Gold Standard Ultrasonography - Ultrasound - murphy's sign. Others MRCP EUS

Answer 20

Analgesia, fluid resuscitation and antibiotics Laparoscopic cholecystectomy

Answer 21

Suppurative cholecystitis Bile duct injury due to surgery Gallstone ileus Cholecystoenteric fistulas

Answer 22

If gallbladder perforates, mortality is 30%. Untreated acute acalculous cholecystitis is associated with up to 50% mortality.

Answer 23

Cholangitis - Has jaundice whereas cholecystitis doesn't Chronic cholecystitis - persistent Peptic ulcer disease - normal LFT GORD - more heartburn and acid reflux than right pain. Pancreatitis - amylase and lipase elevated more.

Answer 24

Disorder of the exocrine pancreas and is associated with acinar cell injury with local and systemic inflammatory responses.

Answer 25

56/100,000 a year and is one of the most common GI diseases leading to hospital admission. Approx 50% caused by gallstones and 25% by alcohol. More common in women >60 yo and more common in with patients with microlithiasis.

Answer 26

Gallstones Ethanol Trauma Steroids Mumps Autoimmune diseases Scorpion Hypercalcaemia ERCP Drugs GET SMASHED

Answer 27

Main: Middle aged women and young-middle aged men Hypertriglyceridemia Causative drugs Trauma ERCP Others: Hypercalcaemia Coxsackievirus Pancreatic cancer

Answer 28

Abnormal intracellular calcium accumulation causes an increase in calcium transients. This causes premature activation of zymogens leading to enzyme activation which destruct acinar cells, leading to an inflammatory response. Ethanol-induced pancreatitis as ethanol has direct toxic result on acinar cell, causing inflammation and enzyme destruction.

Answer 29

Key Presentations Mid-epigastric or LUQ pain that radiates to the back. Sudden onset and constant and severe and is worse with movement. Tripoding relieves pain Signs Diminished bowel sounds if ileus has developed. Hypotension, oliguria, hyperhidrosis, Past medical history / risk factors. Grey turner / cullens sign Symptoms Nausea, Vomiting, Anorexia,

Answer 30

1st Line Serum Lipase and Amylase - >3 times normal (3-5 upper limit in diabetes) FBC - WBC count >12x10 9 or <4 x 10 9. Elevated haematocrit >44% (pancreatic necrosis) CRP >200mg/L = Pancreatic necrosis Elevated urea and creatinine LFT - high ALT >3 times limit signals gallstones as cause. Gold Standard Blood serum lipase and amylase Others Abdo ultrasound - confirms presence of gallstones

Answer 31

Mild acute - no organ failure or local or systemic complications Moderate acute - presence of transient organ failure (resolves in 48 hours) and or local complications or exacerbation of comorbidity Severe - persistent organ failure >48 hours and local complications common. Peripancreatic fluid collections, pancreatic and peripancreatic necrosis, pseudocysts and walled off necrosis. Radiological classification: Balthazar A Normal B Focal or diffuse gland enlargement with small intra-pancreatic fluid collection C Peripancreatic inflammatory changes and <30% gland necrosis D Any of above plus single extra-pancreatic fluid and 30-50% necrosis E Extensive extra-pancreatic fluid, pancreatic abscess and >50% gland necrosis.

Answer 32

Early-goal fluid resuscitation with crystalloid fluid plus analgesia Establish oral feeding as soon as patient can tolerate it. Gallstone - arrange emergency endoscopic retrograde cholangiopancreatography ERCP within 24 hours Alcohol related - alcohol abstinence programme Do not request CECT in first 3-4 days as it cannot detect necrosis that early Consider supplemental oxygen, antiemetic, IV antibiotics (if infection is confirmed) and nutritional support with severity assessment

Answer 33

Acute renal failure Pancreatic abscess Chronic pancreatitis Sepsis ARDS Pancreatic effusion

Answer 34

80% recovery in 3-5 days. 25-30% in severe pancreatitis mortality.

Answer 35

Peptic ulcer disease - Normal or low lipase / amylase. Intestinal obstruction - normal lipase and amylase Cholangitis - normal lipase and amylase Cholecystitis - normal or slightly elevated lipase and amylase with RUQ pain and thickened gallbladder wall on USS.

Answer 36

Recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures - resulting in scarring and loss of function.

Answer 37

Hereditary - age 10-14 years Juvenile idiopathic chronic pancreatitis - 19-23 years Alcoholic acute pancreatitis - 36-44 years and senile at 56-62 years. More prevalent in men over the age of 45 years.

Answer 38

TIGAR-O Toxins - alcohol, smoking, CKD, Hypercalcaemia/lipidaemia Idiopathic Genetic Autoimmune Recurrent and severe acute pancreatitis Obstruction

Answer 39

Main: Smoking High fat / protein diet Genetic predisposition Coeliac Others: Psoriasis Tropical geography Coxsackievirus.

Answer 40

Persistent cytokine secretion, pancreatic stellate cells secrete collagen stimulating fibrosis and chronic pancreatitis.

Answer 41

Key Presentations Presence of risk factors, Abdominal pain in LUQ and epigastric region and Steatorrhoea Signs Weight loss and malnutrition Symptoms Nausea, vomiting, Dyspnoea

Answer 42

1st Line CT / MRI - pancreatic calcifications, focal or diffuse enlargement of pancreas and or vascular complications Gold Standard CT/MRI Others EUS - only used if diagnosis is still in question which will show ductal and parenchymal abnormalities s-MRCP - abnormal exocrine function

Answer 43

Acute pain - smoking and alcohol cessation Persistent pain - Alcohol and smoking cessation, analgesia, PPI and pancreatic enzymes. Dietary modifications

Answer 44

Pancreatic exocrine insufficiency Diabetes mellitus Pancreatic calcifications Opioid addiction Pancreatic duct obstruction

Answer 45

Generally pain decreases or disappears overtime. 10 year survival is 20-30% lower than general population Most common cause of death is pancreatic carcinoma.

Answer 46

Pancreatic cancer - CT/MRI may show mass or lesion Mesenteric ischaemia Biliary colic Peptic ulcer disease Acute pancreatitis Intestinal obstruction

Answer 47

Alcoholic liver disease has 3 stages of liver damage: Steatosis, Alcoholic hepatitis and alcoholic liver cirrhosis.

Answer 48

3 millions deaths annually worldwide. Approx 40-80g/day in men and 20-40g/day in women for 10-12 years. There is approximately 14g in one shot of alcohol. 14.2 million people >18 years have alcohol use disorder and of these 9 million were men.

Answer 49

Chronic alcohol use and alcoholism.

Answer 50

Main: Obesity Smoking - hepatocellular carcinoma Others: HCV Female

Answer 51

Alcohol is metabolised by alcohol dehydrogenase and cytochrome P450 2E1. Alcohol dehydrogenase converts alcohol to acetaldehyde which is then converted to acetate by acetaldehyde dehydrogenase. This process converts NAD to NADH, which in excess inhibits gluconeogenesis and increases fatty acid oxidation. When there is not enough acetaldehyde dehydrogenase, it binds to cellular proteins and produces acetaldehyde adducts which stimulate an immune response, causing inflammation and necrosis by neutrophils. Cytochrome P450 2E1, increases production of free radicals through oxidation of NADPH to NADP. This creates more ROS. Improper metabolism of these ROS can stimulate hypoxia inducible factor 1 alpha - which increases TNF, and further intensifies immune response that leads to tissue injury. Alcohol also damages intestinal mucosa, leading to endotoxemia, ending in hepatic inflammation.

Answer 52

Key Presentations Asymptomatic RU abdominal discomfort with acute alcoholic hepatitis Signs Hepatomegaly, Ascites, malnutrition, (Splenomegaly, jaundice, palmar erythema, asterixis) Symptoms Weight changes, anorexia, fatigue

Answer 53

1st Line Serum AST and ALT - men >30 units/l women >19 and ratio of AST/ALT >2. Can be decreased with excessive necrosis Serum ALP and gamma GT - normal or elevated Serum bilirubin - elevated Serum albumin - low FBC - anaemia, leukocytosis, thrombocytopenia, high MCV U+E - high urea, low electrolytes. Hepatic ultrasound Gold Standard LFT’s Others Viral hepatitis serology which will indicate absence of antigens. CT abdo Liver biopsy

Answer 54

Alcohol abstinence and alcohol withdrawal management Consider: Weight reduction and smoking cessation Nutritional supplementation Immunisation - HAV and HBV Liver Transplant - only if alcohol abstinent for >3 months Corticosteroids - hepatic encephalopathy

Answer 55

Hepatic encephalopathy - buildup of harmful toxins - ammonia. Portal hypertension - slowing of intrahepatic blood flow causing a backup of blood in portal vein GI bleeding Renal failure / hepatorenal syndrome - altered renal blood flow in response to altered blood flow in liver Sepsis - bacterial infections high with cirrhosis

Answer 56

Alcoholic fatty liver returns to normal with alcohol abstinence. 5 year survival of those with cirrhosis if they stop drinking is 90% compared with 70% if they continue. Glasgow alcoholic hepatitis score with a higher score indicating a worse prognosis.

Answer 57

Viral hepatitis - presence of antibodies Cholecystitis - presence of gallstones and positive murphy's sign. Acute liver failure Wilson’s disease - increased urinary copper

Answer 58

NAFLD is the presence of hepatic steatosis without secondary causes of hepatic fat e.g. alcohol. Occurs when intrahepatic fat is >= 5% of liver weight. NAFLD - presence of hepatic steatosis without evidence of hepatocellular injury in the form of hepatocyte ballooning NASH - Non-alcoholic steatohepatitis - hepatic steatosis and ballooning, with or without fibrosis. This can lead to liver failure.

Answer 59

>25% worldwide. Median age is 53 years but can occur at any age.

Answer 60

HCV Wilson's disease Starvation Parenteral nutrition Medications Acute fatty liver of pregnancy Metabolic disorders

Answer 61

Main: Obesity - truncal / central Insulin resistance or diabetes Dyslipidaemia Metabolic syndrome Rapid weight loss Medications Total parenteral nutrition Others: HCV Wilsons Lipodystrophy

Answer 62

Insulin resistance leading to accumulation of excessive triglyceride axxumulation in the liver and development of steatosis. Once developed, additional injury or oxidative injury can cause the necro-inflammatory component seen in steatohepatitis. Antioxidant deficiency, hepatic iron, fat derived hormones (leptin and resistin) and intestinal bacteria have been linked to NASH development from NAFLD.

Answer 63

Key Presentations Presence of risk factors, absence of significant alcohol abuse, mild abnormality in LFT and truncal obesity Signs Hepatosplenomegaly Symptoms Fatigue, Malaise, RUQ abdominal discomfort

Answer 64

1st Line LFT - AST, ALT, ALP, GGT, Bilirubin normal or slightly elevated FBC - Anaemia and thrombocytopenia in cirrhosis and PHTN Metabolic panel - abnormal and hyponatremia Lipid panel - elevated total cholesterol, LDL, TGLY and low HDL. Gold Standard Liver Biopsy Others INR prothrombin - normal or elevated. Serum albumin - normal or decreased. Viral hepatitis - antibody negative Liver ultrasound - abnormal echotexture. Elastography - liver stiffness Abdo MRI - increased liver fat content Fasting insulin - elevated.

Answer 65

Weight loss with healthy diet and exercise Pioglitazone - improves liver histological scores but be aware of side effects of potential weight gain Vitamin E Weight loss pharmacotherapy - Orlistat prevents absorption of fats Gastric bypass - BMI >40 or >35 with at least one other obesity related comorbidity considered for bariatric surgery.

Answer 66

Ascites Variceal Haemorrhage Hepatocellular carcinoma Cirrhosis → liver failure Death - advanced stage 3 or 4 fibrosis

Answer 67

NASH associated with increased mortality over 14 years, usually as a result of CVD or other comorbidity rather than liver causes. Recurrent NAFLD is 20-100% after liver transplantation. Mortality increases as the fibrosis stage increases.

Answer 68

ALD - AST/ALT ratio >2 Cryptogenic cirrhosis Autoimmune hepatitis - antibody tests and hyperglobulinemia Viral hepatitis - presence of antibodies Haemochromatosis - elevated ferritin and iron saturation Primary biliary cholangitis - significant elevation in ALP, GGT and IgM Wilsons - elevated urinary copper and elevated hepatic copper.

Answer 69

Pathological end stage of any chronic liver disease, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules

Answer 70

In Europe, cirrhosis related to either Viral infection or alcohol abuse were the main indications of a liver transplant. 1.5 billion people worldwide have chronic liver disease.

Answer 71

NAFLD ALD Viral hepatitis Any chronic liver disease Cryptogenic - idiopathic

Answer 72

Main: Alcohol misuse IV drug misuse Unprotected intercourse Obesity Country of birth - HBV and HCV. Others: Blood transfusions Tattoos

Answer 73

Hepatic fibrosis occurs from hepatic stellate cells and leads to an accumulation of collagen I and III in hepatic parenchyma. With activation, stellate cells become contractile leading to increased portal resistance during liver fibrosis and cirrhosis. This leads to portal hypertension, development of ascites and gastro-oesophageal varices. Compensated cirrhosis - Cirrhosis investigations present but liver synthetic function is preserved and generally no complications Decompensated cirrhosis - Cirrhosis investigations present and liver synthetic function is decreased and development of complications such as PHTN, Variceal bleeding, hepatic encephalopathy and jaundice.

Answer 74

Key Presentations Ascites and abdominal distension Jaundice and pruritus Haematemesis (blood in vomit) and Melaena (black stool) Signs Palmar erythema, Spider naevi, leukonychia, hepatosplenomegaly, distension and collateral circulation, hepatic fetor, Peripheral oedema - salt retention. Symptoms Fatigue, weakness, weight loss,

Answer 75

1st Line LFTs - AST/ALT >=1 - cirrhosis. GGT elevated Serum albumin and sodium - reduced Serum potassium and prothrombin time - elevated Platelet count - reduced Depending upon aetiology - viral hepatitis antibodies may be positive. Gold Standard Liver Biopsy Others Abdo CT/MRI - liver surface nodularity with reduced liver size. USS or EUS /\ Liver elastography

Answer 76

Treatment of underlying chronic liver disease Monitoring - USS, CT, EUS, MRI Supportive and palliative care Sodium restriction and diuretic therapy for ascites / oedema Liver transplantation

Answer 77

Ascites Gastro-oesophageal varices Malnutrition and Sarcopenia Hepatocellular carcinoma Bleeding and thrombosis Hepatorenal syndrome.

Answer 78

10 year survival with compensated cirrhosis is 90% with decompensated 50% Mean survival time for decomp is 2 years 4 stages of cirrhosis: No varices or ascites - 1% mortality per year Varices with no bleeding, no ascites - 4% With ascites with or without varices and no bleeding - 20% GI bleeding due to PHTN with or without ascites - 57%

Answer 79

Budd-Chiari syndrome - Doppler ultrasound and CT - absence of hepatic vein filling Portal vein thrombosis - MRI normal hepatic venous pressure but doppler and abdo CT show portal vein filling defect Constrictive pericarditis Idiopathic portal hypertension - Liver biopsy shows no evidence of cirrhosis

Answer 80

PHTN - Portal hypertension is characterised by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver. Blood backs up in nearby veins in the oesophagus and stomach, causing varices.

Answer 81

Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of blood.

Answer 82

Vomiting fresh blood. This occurs as a result of bleeding occurring in any part of the upper gastrointestinal tract.

Answer 83

Brain dysfunction caused by advanced liver insufficiency and or portosystemic shunt.

Answer 84

30-40% of patients with cirrhosis develop HE within their illness. HE occurs in 55% of patients with a TIPS procedure within 2 years.

Answer 85

High ammonia levels GI bleeding Hypokalaemia Metabolic encephalopathy Brain atrophy Brain oedema

Answer 86

Cirrhosis Acute hepatic failure Portacaval shunt Hypovolaemia, GI bleeding Excessive protein intake Hypokalemia or hyponatremia Hypoxia and metabolic alkalosis.

Answer 87

Impaired LFT leads to impaired ammonia clearance, which can alter cerebral concentration of amino acids and affect neurotransmitter synthesis and electrical activity. It can also lead to increased intracellular astrocyte osmolarity, inducing astrocyte swelling and can lead to raised ICP. Patients with decompensated cirrhosis have altered intestinal microbiome and can lead to an overgrowth in potentially pathogenic bacteria, leading to pro-inflammatory cytokines such as IL1 and TNF. Systemic inflammation activates microglia in the brain producing neuroinflammation.

Answer 88

Key Presentations Altered mental status, confusion, mood and motor disturbances Signs Ataxia, bradykinesia, hypokinesia, slow monotonous speech, coma, hyper-reflexia and nystagmus. Palmar erythema, jaundice, hepatomegaly, ascites Symptoms Euphoria, depression, insomnia or hypersomnia,

Answer 89

1st Line LFT - abnormal Serum electrolytes - normal or hyponatremia / kalcemia FBC - normal or leukocytosis or thrombocytosis Blood ammonia - Raised CT scan - absence of other causes and presence of oedema Gold Standard Psychometric Hepatic Encephalopathy Score PHES. Others EEG - decrease in brain wave frequency and amplitude.

Answer 90

Supportive care, reversal of precipitating factors and investigation of alternative causes Lactulose - helps draw water from body into colon and soften stool. It also decreases intestinal production and absorption of ammonia. Rifaximin - all those with symptoms persisting after lactulose or those contraindicated to lactulose. Branches chain amino acids Consider transplant or shunt.

Answer 91

Death Falls Neurological deficits Re-admission

Answer 92

42% 1 year survival and 23% 3 year survival. When patient is at grade 4 (coma), mortality is at 80%.

Answer 93

Brain tumours - MRI Subdural haematoma - CT shows haemorrhage Acute stroke - CT shows haemorrhage or infarct Meningitis - Lumbar puncture shows cloudy CSF.

Answer 94

RNA virus with a faecal oral route of transmission. Most infections in adults and older children are symptomatic. Average incubation is 28 days. Not associated with chronic liver disease. 70% develop jaundice.

Answer 95

In developed countries, outbreaks are associated with contaminated food and water. High prevalence in Africa, Asia and Latin america. Mainly occur in early childhood. Vaccination to prevent this.

Answer 96

Close contact with an infected person Contaminated food and or water

Answer 97

Main: Living in or travelling to endemic region Close personal contact with infected person Homosexual men Homelessness and illegal drug use. Known foodborne outbreak Others: Occupational exposure - healthcare

Answer 98

Virus transported to intestinal epithelium then through mesenteric veins to liver. Virus enters hepatocytes and replicates, is then excreted in bile and blood from infected hepatocytes. Liver injury is when cytotoxic T cells lyse the infected hepatocytes. Viral particles are then excreted in stools.

Answer 99

Key Presentations Travel Fever Malaise Nausea and vomiting Jaundice RUQ pain Signs Hepatomegaly, clay coloured stools, Dark urine Symptoms Fatigue, Headache and pruritus

Answer 100

1st Line LFT - ALT and AST, bilirubin elevated U+E - elevated blood urea and serum creatinine Prothrombin - slightly prolonged of 11-26 seconds Gold Standard IgM anti-hepatitis A test - positive - active infection IgG anti-hepatitis A test - may be positive - will show recovery or recent infection Others Hepatitis A RNA detection - used if others inconclusive.

Answer 101

If known exposure <2weeks then immunisation if not already. If confirmed Hep A - rest and recovery with supportive care. If acute liver failure - liver transplant VERY RARE

Answer 102

Acalculous cholecystitis Pancreatitis

Answer 103

85% full recovery within 3 months. <1% patients have a fulminant course of illness and refer to liver transplant. 1 year expectancy with liver transplant for acute HAV is 69%.

Answer 104

Other viral hepatitis - detected through serology of viral antibodies. EBV - negative serology for all types of hepatitis and EBV IgG and IgM positive Coxsackievirus - atypical lymphocytes but no viral hep serology Autoimmune hepatitis - serum gamma-globulin more than 2x normal and sometimes have ANA antibodies. Alcohol hepatitis - AST/ALT ratio of at least 2. FBC show anaemia, leukocytosis and or thrombocytopenia.

Answer 105

DNA virus transmitted by percutaneous and permucosal routes. Can be prevented with immunisation

Answer 106

Most common liver infection globally. People from endemic areas (africa and asia) at increased risk. 350-400 million of the world population has chronic hepatitis B

Answer 107

Infected needles Unprotected sex Unsanitary conditions Childbirth

Answer 108

Main: Perinatal exposure to infant born with HBV positive mother High risk sexual behaviours IV drug use Born in highly endemic region Family history Others: Occupational workers Infected with HIV Possible haemodialysis

Answer 109

HBsAg - outer surface of virus (surface antigen) HBcAg - Core of the virus (core antigen) Viral DNA + E antigen (HBeAg) shows active replication and infection. Causes an immune response and removal of HBV infected cells via CD8+ T lymphocytes. At onset of virus, HBsAg and Viral DNA with HBeAg will be present. HBsAg for >6months indicates chronic infection

Answer 110

Key Presentations Presence of risk factors and asymptomatic. Signs VERY RARE - Liver common symptoms and signs

Answer 111

1st Line LFT - elevated AST, ALT and ALP with bilirubin. Decreased albumin FBC - microcytic anaemia and or thrombocytopenia U+E - hyponatremia and high urea Gold Standard Serum hepatitis B surface antigen or e antigen - Positive (in active onset or chronic) Serum hepatitis B antibody to both surface and core antigen - positive in IgG and IgM Others Test for coinfections

Answer 112

Supportive care - 95% of immunocompetent will achieve antibodies Antiviral therapy (entecavir) or liver transplant in those with acute liver failure In pregnant women give tenofovir disoproxil

Answer 113

Fulminant hepatic failure Cirrhosis Hepatocellular carcinoma Hep B associated glomerulonephritis.

Answer 114

20% will develop chronic HBV. Children under 6 at increased risk as 50% to chronic HBV and % increases with decreasing age.

Answer 115

Other viral hepatitis EBV - no viral antibodies HSV - HSV IgM and HSV PCR positive Acute alcoholic hepatitis - Negative for viral hepatitis Autoimmune hepatitis - serum gamma-globulin more than 2x normal and sometimes have ANA antibodies.

Answer 116

Percutaneous exposure to infected blood. Inflammation of the liver caused by hepatitis C virus. Chronic infection causes liver inflammation and fibrosis - leading to development of cirrhosis, liver failure or liver cancer over 20-50 years.

Answer 117

58 million people have hep C. European and eastern mediterranean regions have the highest prevalence rate. Genotype 1 is most prevalent worldwide.

Answer 118

Blood transmission Injections Sexual activity - homogenous Haemodialysis and Perinatally

Answer 119

Main: Unsafe medical practices IV or intranasal drug use Blood transfusions Heavy alcohol use HIV Others: Haemodialysis Healthcare workers Multiple sex partners Tattoos or body piercings.

Answer 120

Persistent infection appears due to weak CD4+ and CD8+ T cell responses during acute infection which fail to control viral replication. Liver damage is driven from local immune responses which triggers fibrogenesis.

Answer 121

Key Presentations Presence of risk factors Asymptomatic Signs RARELY - Liver condition symptoms.

Answer 122

1st Line Hep C antibody-enzyme immunoassay - Positive indicates current or past infection Serum aminotransferases - elevated. Gold Standard Hepatitis C RNA polymerase chain reaction - Indicates presence of active infection Others Liver biopsy - inflammation or fibrosis Test for co-infection - Hep B

Answer 123

Antiviral therapy e.g. glecaprevir Treatment of cirrhosis or acute liver failure accordingly.

Answer 124

Cirrhosis Hepatocellular carcinoma Rheumatological conditions Treatment related HBV reactivation

Answer 125

Europe - 5 year 91% survival and 10 year 79% with compensated cirrhosis 5 years 50% with decompensated survival .

Answer 126

Chronic hep B Alcoholic liver disease Steatohepatitis - USS shows fatty liver and Hep C antibody test negative Haemochromatosis - iron is abnormal

Answer 127

Chronic inflammatory disease of the liver of unknown aetiology.

Answer 128

Female adults and children more commonly affected than males AIH type 1 more common in women affecting age 10-60 Type 2 affects children.

Answer 129

Main: Genetic predisposition Female Others: Other viral hepatitis EBV Drugs or herbal agents

Answer 130

Alteration in T-cell function and or B cell function. Type 1 - ANA and smooth muscle antibody (SMA) positive Type 2 - Anti-liver kidney microsomal-1 or anti liver cytosol specific positive.

Answer 131

Key Presentations Fatigue / Malaise/ anorexia and abdominal discomfort. Signs Hepatomegaly / Jaundice Symptoms Pruritus, nausea, fever, spider angioma, arthralgia.

Answer 132

1st Line LFT - raised AST, ALP, Gamma GT and ALT and bilirubin Serum globulin - increased Serum albumin - decreased Prothrombin time - Increased Gold Standard Liver biopsy - periportal lesion or interface hepatitis. Others ANA and SMA test - elevated in type 1 Anti LC1 - positive in type 2

Answer 133

Acute severe - High dose corticosteroids - methylprednisolone sodium succinate or prednisolone. AIH and primary biliary cirrhosis - Corticosteroid plus immunosuppressant and ursodeoxycholic acid.

Answer 134

Osteoporosis, Truncal obesity, DM or hypertension - due to corticosteroid therapy Hepatocellular carcinoma Infections - due to immunosuppressant Liver failure.

Answer 135

Untreated 5 year survival 50% and 10 year 10%. 10 year survival with treated 90% 20 year with cirrhosis is 40% or 80% without.

Answer 136

Primary biliary cirrhosis - ALP and Gamma glutamyl transferase raised more. AMA and ANA present. Liver biopsy shows bile duct lesion or periductal fibrosis. Chronic Hepatitis - Presence of other viral hepatitis antibodies Alpha 1 antitrypsin deficiency - low serum level Wilsons - Serum copper decreased with excessive urinary copper excretion.

Answer 137

Escherichia coli gram negative rod shaped bacterium that colonises the gastrointestinal tract. Ecoli becomes pathogenic by acquiring virulence factors or genetic mutations. Infection of pathogenic strains through ingestion of contaminated food or water.

Answer 138

Older people, infants and people who are immunocompromised are more susceptible to infection and secondary complications. Can also be associated with UTI and pneumonia.

Answer 139

80% from enterohemorrhagic Ecoli (EHEC) infection 70% from enterotoxigenic E coli (ETEC) infection 30% from other types. Norovirus Rotovirus - most common cause

Answer 140

Main: Ingestion of contaminated food Travel Poor hygiene Infantile or advanced age Others: Immunocompromised state Contact with infected animals

Answer 141

Escherichia coli is a gram negative rod shaped bacteria that propels itself via flagella. Diarrhoea is caused by a combination of intestinal inflammation, loss of absorptive surface and increased mucosal permeability and ion secretion.

Answer 142

Key Presentations History of travel, contact with contaminated food or contact with infected people. Diarrhoea - bloody or watery. Signs Volume depletion - dry mucous, reduced skin turgor and tachycardia or hypotension Symptoms Abdominal pain, fever, nausea, anorexia and lethargy.

Answer 143

1st Line Stool cultures - positive for pathogenic E coli FBC - elevated leukocyte count, low haemoglobin and or platelets Renal function and electrolytes - raised urea and creatinine, Hypokalaemia Gold Standard / Others Blood cultures - positive for e coli Abdominal x ray - bowel wall thickening Abdo CT - mural thickening of colon.

Answer 144

Haemolytic uraemic syndrome Bacteraemia IBS

Answer 145

Most are asymptomatic and self limiting with average recovery 2-5 days. Foodborne enterohemorrhagic E Coli - Fatality of up to 2% in industrialised countries with higher rates of older people and children. Enterotoxigenic E coli - fatality of 0.1% in industrialised countries.

Answer 146

Viral gastroenteritis - shorter duration of 24-48 hours and no stool bacteria. Alternative gastroenteritis / travellers diarrhoea - stool cultures will identify alternative pathogen e.g. salmonella, shigella Amoebiasis - stool sample will show entamoeba Crohns - more chronic history, slower onset and prolonged diarrhoea and weight loss.

Answer 147

Rehydration and supportive therapy - preferably glucose containing as glucose promotes absorption of sodium and water in intestinal lumen Bismuth subsalicylate - reduce diarrhoea. Antibiotic for moderate to severe cases - ciprofloxacin or rifamycin

Answer 148

A group of autosomal recessive disorders of iron metabolism.

Answer 149

HFE related occurs primarily in norther european descent. 1 in 10 white people heterozygous for C282Y. Clinical disease more common in men. Typically age 30-50

Answer 150

Mutations in the HFE gene - C282Y and H63D Alcoholism Dysmetabolic syndrome

Answer 151

Middle age Male sex White ancestry Family history Supplemental iron

Answer 152

C282Y - hepatic hepcidin gene expression is low and macrophages continually release iron from erythrophagocytosis. Leads to an elevation in serum iron and transferrin saturation. Clinical manifestations are said to be caused by direct result of pro-oxidant effects iron has on organs - e.g. the liver where excess iron causes fibrosis.

Answer 153

Type 1: Hereditary HFE Autosomal recessive mutation of HFE gene on chromosome 6 1A = mutation in C282Y. 1B = C282Y and H63D. 1C = HFE S65C Type 2: Juvenile A = mutation of the hemojuvelin gene 1p21 B = Hepcidin gene 19q13 Type 3: Transferrin receptor 2 Mutation in 7q22. Type 4: Ferroportin SLC40A1 gene 2q32.

Answer 154

Key Presentations Mainly asymptomatic Calcium pyrophosphate crystal deposition, with pseudogout and chronic arthropathy - 2nd and 3rd metacarpophalangeal joints and proximal interphalangeal joints. Signs Hepatomegaly, Hypogonadism, Diabetes Symptoms Fatigue, weakness, lethargy.

Answer 155

1st Line Serum transferrin saturation >45% Serum ferritin >674 picomoles in men and >449 in women Gold Standard HFE mutation analysis. Others HFE mutation analysis - C282Y homozygosity or C282Y/H63D heterozygosity etc. Liver biopsy - raised iron content LFT - aminotransferases above normal Fasting blood sugar - raised ECG and Echo - Dilated Cardiomyopathy and T wave flattening Hormones - lowered

Answer 156

Stage 0 = C282Y homo with normal transferrin and ferritin with no clinical symptoms. Stage 1 = C282Y homo and increased transferrin and normal ferritin with no symptoms. Stage 2 = C282Y homo with both increased transferrin and serum ferritin but no symptoms Stage 3 = C282Y homo both increased transferrin and ferritin with mild clinical symptoms affect life Stage 4 = Same as stage 3 but with clinical symptoms manifesting organ damage.

Answer 157

Stage 0 = Patients monitored every 3 years with history, examination and BT Stage 1 = Patients monitored once yearly. Stage 2/3/4 = Phlebotomy every 1-4 weeks or 2-3 times yearly depending on stage by removing 7mL/kg blood per session to get levels in check. Avoid Alcohol, Vit C and iron supplements.

Answer 158

Cirrhosis Diabetes Mellitus Chronic congestive heart failure - fluid overload and arrhythmias. HCC - hepatocellular carcinoma. Hypogonadism Bone loss

Answer 159

Mean survival was 21 years and most will establish iron-overload related disease. 11% increase risk of dying from cancer.

Answer 160

Iron overload from chronic transfusion or anaemias - no HFE mutations Hep B and Hep C - Positive hep serology without homozygous HFE mutations Excessive iron supplementation - absence of homozygosity for HFE mutations.

Answer 161

Autosomal recessive disease of copper accumulation and toxicity caused by a defect in the ATP7B causing a defect in the enzyme metal P type ATPase involved in the excretion of copper within hepatocytes.

Answer 162

Between 1 in every 30,000-50,000 people. All sexes and ethnic groups were affected equally. Appears around age 10-40.

Answer 163

Genetic mutation in ATP7B gene

Answer 164

History of hepatitis Family history ATP7B gene mutation

Answer 165

ATP7B loads copper onto apoceruloplasmin to make ceruloplasmin and transports excess copper into bile. Loss of ATP7B function leads to lack of copper incorporation and it cannot be transported into bile and excreted into faeces. Copper accumulation exceeds liver capacity and is excreted into blood and accumulates in the tissues. High levels of copper cause toxicity by oxidant damage which results in cell injury, inflammation and death.

Answer 166

H1 = Acute hepatic - acutely occurring jaundice, either due to hepatitis like illness or coombs negative haemolytic disease. May progress to liver failure H2 = Chronic hepatic - any type of chronic liver disease with or without symptoms and may lead to or present as decompensated cirrhosis. N1 = associated with symptomatic liver disease N2 = not associated with Nx = presence or absence of liver disease not investigated.

Answer 167

Key Presentations Presence of kayser-fleischer rings Signs Acute liver failure, Tremor, Dysarthia, Dystonia, incoordination, poor handwriting Symptoms Behavioural abnormalities, depression, personality change

Answer 168

1st Line LFT - elevated AST and ALT and bilirubin with low albumin. INR - prolonged 24 hour urinary copper - >100mg Slit-lamp exam - KF rings of gold-brown pigment representing copper deposition in the membrane of descemet of the cornea. Serum ceruloplasmin - <200mg/L Gold Standard 24 hour urinary copper - >100mg (>40 is suggestive) Others FBC - anaemia or low WBC/platelet count Liver biopsy - liver copper >250mg/g Non-ceruloplasmin bound copper concentrations (NCC) - elevated DNA testing for ATP7B mutations

Answer 169

Liver transplantation in hepatic failure In mild hepatic failure - Oral chelation therapy plus zinc and dietary restriction of copper. Zinc inhibits intestinal absorption of copper. Penicillamine - oral chelator that promotes renal excretion of copper.

Answer 170

Liver failure

Answer 171

Normally if treatment started early, patients have a normal quality of life or in mild cases liver damage can recover.

Answer 172

Hepatitis - hep antibody positive Alpha 1 antitrypsin deficiency - Enzyme is deficient Autoimmune hepatitis - positive AMA and ANA antibody Steatohepatitis - fatty liver and inflammation on biopsy

Answer 173

Autosomal codominant genetic disorder from allele mutations in the SERPINA1 gene at the protease inhibitor (PI) locus.

Answer 174

Mean age that smokers with AAT deficiency present is 32-41 years. Liver involvement present in neonates and is the second most common cause of liver transplantation in children.

Answer 175

Family history of AAT deficiency Male Smoker aged 32-41

Answer 176

PI allele mutations in the rSERPINA1 gene that cause ineffective activity of specific protease inhibitor AAT, which is responsible for neutralising neutrophil elastase and preventing inflammatory tissue damage in the lungs. Variants of the enzyme may also polymerise and accumulate in the liver, causing hepatic failure.

Answer 177

Key Presentations Productive cough Dyspnoea on exertion Current cigarette smoker Signs Hepatomegaly, Ascites, Chest hyperinflation Symptoms Wheezing

Answer 178

1st Line Plasma AAT level <20 micromol/L Pulmonary function testing - signif reduce in FEV1, FVC, FEV1/FVC, increased TLC Cxr - large lung volume and basilar predominant emphysema Chest CT - panacinar emphysema and or bronchiectasis LFT - elevated AST, ALT, ALP and bilirubin Gold Standard Plasma AAT level <20 micromol/L Isoelectric focusing - AAT varients Others Genotyping - AAT alleles Gene sequencing - SERPINA1 mutation Exercise testing with ABG - reduced PaO2 and elevated A-a gradient

Answer 179

Smoking cessation, Pollution avoidance, Hepatitis vaccination With pulmonary manifestations - Standard COPD treatment and AAT augmentation therapy Hepatic - Standard liver disease treatment and alcohol avoidance

Answer 180

HCC Necrotising panniculitis

Answer 181

No cure but many have normal lifespans. Between 50-72% deaths are caused by respiratory failure Liver fibrosis occurs in 20-36% of asymptomatic adults with PI*ZZ AAT deficiency. ⅓ patients with advanced age and a homozygous phenotype will due to complications with PHTN and primary liver cancer.

Answer 182

COPD - long period of smoking and advanced age Asthma - clinically indistinguishable, reversibility of obstruction is partial in AAT deficient emphysema but fully in asthma Bronchiectasis - marked dilation of airways on CT Viral hepatitis - viral serology markers ALD - Altered Gamma GT, AST and ALT

Answer 183

Hepatocellular carcinoma (hepatoma) is a primary cancer arising from hepatocytes in a predominantly cirrhotic liver.

Answer 184

6th most common cause of cancer worldwide and 2nd leading cause of cancer related death. 44% cases of HCC worldwide are from chronic HBV. Mean age of diagnosis - 46 in africa, up to 60 in US and Europe.

Answer 185

Cirrhosis HBV HCV Diabetes Mellitus

Answer 186

Cirrhosis Heavy alcohol consumption Viral hepatitis Diabetes Family history Obesity Cigarette smoking AAT deficiency Oral contraceptives Haemochromatosis

Answer 187

Chronic HBV and HCV with metabolic conditions may lead to ROS from oxidative stress, that cause damage to DNA resulting in mutation of P53 gene. HBV is a direct carcinogen and may cause methylation of the p16 gene which is known to cause hepatocellular carcinogenesis causing HCC.

Answer 188

Key Presentations All key symptoms of liver damage e.g. Ascites, Jaundice, RUQ pain, Hepatic encephalopathy Signs Weight loss, Splenomegaly, Palmar erythema, spider naevi, Oedema Symptoms Early satiety, Fatigue, Diarrhoea

Answer 189

1st Line FBC - anaemia and or thrombocytopenia U+E - high urea and hyponatremia LFT - Elevated ALT, AST, ALP, bilirubin and low albumin INR - prolonged AFP - elevated USS - poorly defined margins and coarse, irregular internal echos Gold Standard Liver biopsy - poorly differentiated hepatocytes with large multinucleated giant cells having central necrosis

Answer 190

Stage 0 / A or very early - consider resection, thermal ablation or transplant Stage B - TACE or TARE or percutaneous ablation Stage C - atezolizumab and bevacizumab Stage D - Hospice care

Answer 191

Biliary obstruction Cachexia Hypoglycaemia Hepatic failure

Answer 192

5 year survival is 20% in general or 0-10% if symptomatic Non cirrhotic patients treated with surgical resection is 42% at 5 years Those with a transplant - 75% 4 year survival rate Stage D - 50% survival at <3 months

Answer 193

Cholangiocarcinoma - INR and transaminases mildly elevated or normal. Hepatic adenoma - Doppler shows venous pattern instead of arterial hypervascularization of HCC Haemangioma of liver - normal LFT and alpha fetoprotein

Answer 194

Pathological collection of fluid in the peritoneal cavity.

Answer 195

Portal hypertension Cirrhosis Chronic liver disease Congestive heart failure Hypoalbuminemia Fulminant hepatitis

Answer 196

Key Presentations Abdominal distension and tenderness. Signs Fluid on physical exam with shifting dullness Symptoms Early satiety, SOB,

Answer 197

1st Line USS, CT or MRI

Answer 198

Abdominal paracentesis

Answer 199

Spontaneous bacterial peritonitis

Answer 200

If SBP 10-28% mortality rate.

Answer 201

HCV ALD Congestive heart failure

Answer 202

Primary pancreatic ductal adenocarcinoma. Goes from pre-invasive pancreatic intraepithelial neoplastic lesions to invasive ductal adenocarcinoma.

Answer 203

Cigarette smoking Hereditary pancreatitis Family history

Answer 204

Smoking Family history pancreatic cancer Family history of other hereditary cancers

Answer 205

Most common at age 65-75 years and generally presents late. Median age was 70 and median age of death was 72.

Answer 206

65% in the head, 15% body and 10% tail of pancreas. Progression from normal epithelium to invasive carcinoma follows a linear progression. Early genetic alterations include telomere shortening and mutations in the KRAS2 oncogene followed by inactivation of the p16 tumour suppressor gene.

Answer 207

Key Presentations Jaundice, Non specific upper abdominal pain, weight loss and anorexia and back pain. Signs Hepatomegaly Symptoms Nausea, vomiting, early satiety, Polyuria, thirst, Steatorrhoea,

Answer 208

1st Line Pancreatic CT - mass in pancreas Abdo USS - pancreatic mass, dilated bile ducts or liver metastases LFT - bilirubin, ALP and Gamma GT raised in obstructive jaundice. Gold Standard Biopsy - EUS. Others PT - prolonged FBC - low platelets and anaemia in GI bleeds Cancer antigen - elevated

Answer 209

Stage I or II = Surgical resection with pancreatic enzyme replacement, followed by adjuvant chemotherapy Stage III or IV = Endoscopic stent insertion or palliative surgery with chemotherapy and pain management and pancreatic enzyme replacement

Answer 210

Surgical complications of pancreatic leaks or fistula, and early delayed gastric emptying Cholangitis DVT and pulmonary embolism

Answer 211

Average 5 year survival is 10.8% with a mean survival of 4.6 months. Stage I and II 10% of patients- 5 year survival is 20% with average of 15-18 months 50-55% patients present with metastatic disease with a survival of 3-6 months.

Answer 212

Chronic pancreatitis - histological features not present Bile duct stones - ERCP will rule out stricture (seen in pancreatic cancer) and confirm presence of bile duct stones Cholangiocarcinoma - CT/MRI show absence of pancreatic mass and thickening of bile duct

Answer 213

Protrusion of a viscous out of a containing cavity.

Answer 214

Inguinal - more common in men Femoral - more common in women More than 20 million hernias repaired every year around the world

Answer 215

A combination of pressure and an opening or weakness of muscle or fascia

Answer 216

Main: Male Older Chronic coughing - smokers Obesity Others: Pregnancy Family history

Answer 217

Contents of the abdominal cavity have herniated through the abdominal wall. Umbilicus, Inguinal canal, femoral region and at previous sites of surgery (incisional). Hiatus hernia, stomach passes up into chest cavity through diaphragm. Bowel that passes into a hernia can become stuck and ischaemic, called a strangulated hernia and is an emergency. Inguinal - Indirect - through deep inguinal ring and direct come into inguinal canal through defect in posterior wall of the canal. Femoral – irreducible and strangulated. Go down femoral canal and are usually found below and lateral to inguinal ligament. Umbilical - Omentum or bowel can herniate through them Epigastric - pass through linea alba above umbilicus Inscisional - appear along lines of previous incision during surgery

Answer 218

Key Presentations pain, swelling or fullness at the site of occurrence that can change with position or Valsalva. Most common asymptomatic and appear as a bulge when cough or strain.

Answer 219

1st Line Physical exam or Abdo CT, MRI or USS to confirm presence.

Answer 220

Reducing the hernia if possible Repair - mesh technique and surgery. Patients are advised to lose weight and stop smoking before op. Patients can return to work after 2 weeks or 4 weeks for geriatric.

Answer 221

Constipation Strangulation Intestinal obstruction

Answer 222

1% chance that any given hernia can become strangulated.

Answer 223

Diastasis recti, Abscess, Muscle strain Soft tissue malignancy

Answer 224

Excessive ingestion of paracetamol leading to toxic effects.

Answer 225

In UK, paracetamol is the most common drug taken in overdose, with 48% of poisoning hospital admissions.

Answer 226

>150mg/kg can cause serious effects and >12g is potentially fatal. Acute - <75mg / kg is unlikely to cause toxicity unless staggered. If a patient has ingested more or is in need of an urgent psychiatric assessment hospital admission is warranted. Staggered - excessive ingestion over period longer than an hour. >150mg/kg in any 24 hour period.

Answer 227

History of self harm History of frequent or repeated use of medications for pain relief Iatrogenic paracetamol poisoning following IV administration

Answer 228

Paracetamol is primarily metabolised in the liver. This occurs via conjugation with the addition of glucuronide to form a water soluble metabolite that can be excreted in the urine. When there is excess paracetamol, such as with overdose, conjugation become saturated and paracetamol is converted into the metabolite N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI has a short half-life and is usually conjugated by the addition of glutathione, which is then renally excreted. When glutathione stores are depleted, excess NAPQI binds to hepatocellular proteins and results in oxidative damage, mitochondrial dysfunction and ultimately hepatocellular injury.

Answer 229

Key Presentations Asymptomatic and mild GI symptoms. History and abdo pain. Signs scars - previous evidence of self harm, bruising, jaundice, tachycardia or coma Symptoms nausea and vomiting, anorexia, malaise, altered mental status

Answer 230

Date, Time, Period since ingestion and Amount Weight Pregnancy Current suicidal risk

Answer 231

1st Line LFT - raised ALT INR and prothrombin - raised and prolonged BG - <3.3mmol/L Creatinine - acutely elevated FBC - leukocytosis, anaemia or thrombocytopenia Gold Standard Serum paracetamol conc >700mg/L Others Urinalysis - haematuria or proteinuria Urine drug screen - positive

Answer 232

N-acetylcysteine for 21 hour regimen. Done over 3 infusions between 1 and 16 hours. After bloods are retaken to see any hepatic impairment. However, be aware of anaphylactoid reactions which occur in 30% of patients. Acute ingestion and <8 hours - Activated charcoal, look for abnormal bloods and treatment not normally required if asymptomatic. 4 hours post ingestion do paracetamol levels and blood and assess nomogram for if NAC is required. Treatment can be stopped when INR <1.31 and ALT within normal or raised range but not more than 2x limit.

Answer 233

DILI ALF - acute liver failure

Answer 234

If treated it has a 0.1% mortality

Answer 235

DILI or alternative toxicity Hepatitis Wilson disease