Hepatobiliary Flashcards

Question

What are the first line investigations of CLD

Answer 1

1st line LFTs: bilirubin, PT/INR, serum AST + ALT, NH3, GGT all raised. Serum albumin and glucose decreased. FBC: anaemia, thrombocytopenia, leukopenia. U&E (urea and creatinine raised, deranged electrolytes)

Answer 2

Abdominal ultrasound, ascites tap

Answer 3

Budd Chiari, portal vein thrombosis, constrictive pericarditis

Answer 4

1st line – prevent progression, lifestyle monitoring (less alcohol, reduce BMI), liver transplant (MELD score – model for end-stage liver disease. Assesses severity and transplant likelihood). Manage complications: hepatic encephalopathy, ascites, etc.

Answer 5

- **Hepatocellular Carcinoma -** - Six monthly surveillance with ultrasound +/- AFP (tumour marker) as patients with cirrhosis are at high risk of HCC

Answer 6

- **Hepatic encephalopathy** - **Ascites** - **Gastrointestinal bleeding** (i.e. variceal bleed) - **Bacterial infections** (i.e. SBP) - **Acute kidney injury** - **Hepatorenal syndrome** - **Hepatopulmonary syndrome** - **Hepatocellular carcinoma** - **Acute-on-chronic liver failure**

Answer 7

2 years without transplant

Answer 8

- Red blood cells are broken down, releasing haemoglobin. - Haemoglobin is broken down into haem and globin, with haem being further broken down into unconjugated bilirubin and iron. Globin and iron from haem is recycled for erythropoiesis.

Answer 9

- Unconjugated bilirubin is a **breakdown product of haem** from senescent red blood cells - Unconjugated bilirubin is **not water-soluble** and requires **conjugation** for excretion in bile

Answer 10

- **UGT (UDP-glucuronosyltransferase)** in the liver converts unconjugated bilirubin into conjugated bilirubin, making it water-soluble - Conjugation involves the addition of glucuronic acid to bilirubin - Conjugated bilirubin is secreted into the bile canaliculi and **stored in the gallbladder** as a component of bile

Answer 11

- When it is released into the intestinal tract, conjugated bilirubin is broken down into **urobilinogen** and then **stercobilin** by bacteria - Stercobilin is excreted in **faeces**, giving it a brown colour - Some urobilinogen is reabsorbed and is either directed back into making bile (enterohepatic circulation) or transported to the kidney and excreted in the **urine**, giving it a yellow colour

Answer 12

Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.

Answer 13

- Gallstones affect up to 20% of the population. - F>M - Prevalence increases with age, before levelling off in the sixth - seventh decade of life. - More common in caucasians, Native American's and Hispanics. - The vast majority of people with gallstones will remain asymptomatic (80%).

Answer 14

Bile is secreted by hepatocytes into the biliary circulation. It is stored in the gallbladder. Bile is composed of bile acids (or salts), phospholipid, bilirubin, cholesterol and water. Imbalance in composition and stasis leads to stone formation.

Answer 15

5 Fs: Fat, Fertile, Forty, Female, Fair Family history, rapid weight loss, diabetes and medications

Answer 16

Gallstones: biliary colic severe colicky RUQ pain, comes and goes (>30 minutes), worse after eating a fatty meal. Nausea and vomiting.

Answer 17

Gallstones: abdominal USS (1. Identify stones, 2. Gallbladder wall thickness – inflammation, 3. Duct dilation)

Answer 18

Gallstones: raised ALP, normal FBC and CRP, raised bilirubin if gallstone is blocking bile duct

Answer 19

Pancreatitis, peptic ulcer disease, gallbladder cancer

Answer 20

Gallstones: NSAIDs/analgesia. Elective cholecystectomy (surgical removal of gallbladder) Bile duct clearance if gallstones in bile ducts (ERCP).

Answer 21

Gallstones > cholecystitis > cholangitis. Sepsis

Answer 22

The majority of patients with gallstones will be asymptomatic. 1-4% of patients develop gallstone-related complications, the most common being biliary colic. 10-20% of those who have had an attack of biliary colic will go on to develop a more serious complication, such as acute cholecystitis.

Answer 23

Biliary colic refers to a pain in the RUQ/epigastrium caused by gallstones. Though termed a 'colic' the pain is normally constant lasting from 30 minutes to 6 hours.

Answer 24

- It is the most common symptomatic manifestation of cholelithiasis (gallstones) affecting around 10-20% of patients. - Prevalence increases with age - F>M - More common in caucasians, Native American's and Hispanics.

Answer 25

Risk factors for gallstones: 5 Fs: Fat, Fertile, Forty, Female, Fair

Answer 26

The pain occurs when a stone impacts against the cystic duct during contraction of the gallbladder with increased pressures in the gallbladder itself.

Answer 27

- Nausea and vomiting - Right upper quadrant pain - Epigastric pain - Pain may radiate to right shoulder or interscapular region Episodes typically last 30 minutes - 6 hours. Often worse after ingestion of fatty foods. Note: there are no signs on abdominal examination. Murphy's sign negative.

Answer 28

Abdominal ultrasound - can identify gallstones as well as looking for dilation of the CBD and presence of stones in CBD. LFTs - may show derangement of LFTs - indicative of stones within the biliary system (which can be asymptomatic). It is essential to identify patients with CBD stones prior to any cholecystectomy.

Answer 29

- Cholecystitis - Ascending cholangitis - Common bile duct stone - Gastritis - Peptic ulcer disease - IBS - Carcinoma on right side of colon - Renal colic - Pancreatitis

Answer 30

NSAIDs/analgesia. Elective cholecystectomy (surgical removal of gallbladder) Bile duct clearance if gallstones in bile ducts (ERCP).

Answer 31

- **Obstructive jaundice:** due to ****a stone that obstructs the common bile duct; presents with jaundice, pale stools and dark urine - **Cholecystitis:** inflammation of the gallbladder results in **fever**, r**ight** **upper** **quadrant** **pain** (usually > 6 hours) and positive **Murphy’s sign** - **Ascending cholangitis:** infection of the biliary tree results in ‘Charcot’s triad’ (**right** **upper** **quadrant** **pain**, **fever** and **jaundice)** - **Acute pancreatitis:** gallstones are the most common cause - **Gallbladder empyema** - **Gallstone ileus:** a rare form of small bowel obstruction due to impaction of a gallstone within the lumen of the small intestine via a cholecysto-duodenal fistula - **Gallbladder cancer**: gallstones are thought to increase the risk by up to 5-fold

Answer 32

Acute cholecystitis refers to inflammation of the gallbladder most commonly occurring due to impacted gallstones (calculous cholecystitis) Relatively rarely acute cholecystitis occurs in the absence of gallstones (acalculous cholecystitis).

Answer 33

Acute cholecystitis occurs in 10% of patients with symptomatic gallstones

Answer 34

5 Fs: Fat, Fertile, Forty, Female, Fair

Answer 35

Cholecystitis: gallstones block the cystic duct, preventing the gallbladder from draining. Bile builds up and distends the gallbladder which can reduce vascular supply and leads to inflammation.

Answer 36

Cholecystitis: RUQ pain, may radiate to right shoulder, fever, fatigue, RUQ tenderness. Murphy’s sign: press on GB and inhale, patient will wince in pain and stop inspiration. Nausea and vomiting.

Answer 37

Cholecystitis: abdominal USS (gallstones, thick gallbladder walls from inflammation, fluid around gallbladder)

Answer 38

Cholecystitis: positive murphy’s sign, FBC: raised WCC and CRP, LFTs may be elevated (ALP, bilirubin, AST and ALT)

Answer 39

- Pancreatitis - Peptic ulcer disease - Cholangitis - Appendicitis - Basal pneumonia

Answer 40

Cholecystitis: IV fluids, antibiotics, analgesia. Cholecystectomy surgery within 72 hours of symptoms. ERCP if gallstones in bile ducts.

Answer 41

- **Gallbladder empyema:** acute inflammation results in the gallbladder filling with pus and can lead to perforation - **Gallstone ileus:** when a gallstone passes from the biliary tract into the intestine via a fistula resulting in small bowel obstruction - **Acute cholangitis:** infection of the biliary tree commonly caused by gallstones which move into the common bile duct - **Obstructive jaundice:** if stone moves to CBD - **Procedure-related**: bile duct injury

Answer 42

Prompt medical management with intravenous antibiotics and identification of sepsis alongside an early laparoscopic cholecystectomy is associated with a very good prognosis. In patients with biliary colic without cholecystitis, early laparoscopic cholecystectomy reduces the risk of future episodes and the risk of cholecystitis. Gallbladder perforation has a mortality of over 30%, whilst untreated acute acalculous cholecystitis has a mortality of up to 50%

Answer 43

Murphy's sign is indicative of cholecystitis. As the patient breathes out, place your hand below the right costal margin. As the patient breathes in an inflamed gallbladder moves inferiorly, the patient catches their breath. To be considered positive, it should be absent on the left side.

Answer 44

Chronic inflammation of the gallbladder +/- colic

Answer 45

- Repeated lodging and dislodging of gallstone in CBD, causing inflammation and fibrosis of the gallbladder - In some cases, there may not be lodging and dislodging of gallstones. Instead, gallstones within the gallbladder can cause irritation to the gallbladder and causes damage this way. - Overtime, this leads to inflammation, fibrosis and maybe even calcification. This is known as porcelain gallbladder. This makes the gallbladder visible on x-ray

Answer 46

- Flatulent dyspepsia - Abdominal discomfort - RUQ pain (esp after meal) - Distension - Nausea - Fat intolerance (fat stimulates cholecystokinin release and gallbladder contraction)

Answer 47

- **Ultrasound** - to image stone and assess CBD diameter - **MRCP** - used to find CBD stones - **X-ray -** may show porcelain gallbladder

Answer 48

- If symptoms persist post-treatment, consider: - Hiatus hernia - IBS - Peptic ulcer - Chronic pancreatitis - Tumour

Answer 49

- Cholecystectomy - ERCP + sphincterectomy prior to surgery

Answer 50

Increased risk of gallbladder cancer

Answer 51

Acute ascending cholangitis refers to infection of the biliary tree characteristically resulting in pain, jaundice and fevers.

Answer 52

- Acute cholangitis is relatively uncommon and presents as a complication of gallstones in about 1% of patients. - Age > 50 years - Affects men and women equally - There appears to be greater incidence in caucasians, hispanics and Native Americans - following the distribution of gallstones. - It occurs following ERCP in around 0.5 - 3%. - Recurrent pyogenic cholangitis is seen in southeast Asian populations.

Answer 53

- Choledocholithiasis - Benign stricture - Malignant stricture

Answer 54

- **Gallstones:** the most common predisposing factor - **Stricture of the biliary tree:** benign or malignant - **Post-procedure injury** of the bile ducts e.g. post-ERCP

Answer 55

Ascending cholangitis: infection and inflammation of the bile ducts due to prolonged bile duct blockage from gallstones, or bacterial infection from ERCP procedure (E. coli, klebsiella, enterococcus). Bile isn’t ‘flushing out’ the ducts so bacteria migrate from GI tract and cause biliary tree infection. Bile is prevented from entering the GI tract causing jaundice

Answer 56

Ascending cholangitis: Charcot’s triad: RUQ pain, fever, jaundice. Patient may have sepsis.

Answer 57

Cholangitis: ERCP endoscopic retrograde cholangio-pancreatography (direct observation of bile duct and stones)

Answer 58

Cholangitis: FBC: raised WCC and CRP, leucocytosis. LFTs: raised ALP, aminotransferases, and bilirubin. Blood cultures. Abdominal USS: bile duct dilation and gallstones

Answer 59

- Acute cholecystitis - Peptic ulcer disease - Pancreatitis - Hepatic abscess - Appendicitis - Biliary colic

Answer 60

Cholangitis: IV antibiotics (cefuroxime and metronidazole), fluids, blood cultures (sepsis risk). ERCP (bile duct clearance) then cholecystectomy.

Answer 61

- **Biliary sepsis:** the commonest complication and typically presents with Reynolds’ pentad - **Acute pancreatitis:** CBD stones can obstruct the pancreatic duct - **Hepatic abscess** - **Risks of ERCP**: duodenal perforation, pancreatitis, biliary sepsis, intra-abdominal bleeding

Answer 62

The majority of patients recover quickly with effective resuscitation, initiation of antibiotics and adequate biliary drainage. The prognosis is worse if decompression is delayed or emergency surgical drainage is required (rather than non-surgical). Factors that predict a poor prognosis include high fever, hyperbilirubinaemia, hypoalbuminaemia, and older age.

Answer 63

Autoimmune disease where T cells attack cells of small bile ducts in the liver causing inflammation. Leads to cholestasis and subsequent leakage of bile into the circulation

Answer 64

- Rare disease with a **prevalence of < 0.05%** - **Middle-aged:** peak incidence between 45 and 60 years old - **Female gender**: ten times more common in females

Answer 65

Unknown. Genetic predisposition and environmental factors

Answer 66

Female, age 45-60, smoking, other autoimmune disease, rheumatoid diseases, past pregnancy, chronic UTI

Answer 67

Immune system attacks small intralobular bile ducts in the liver which obstructs bile outflow causing cholestasis. Bile acids, bilirubin and cholesterol build up in the blood as they aren’t being excreted in bile. Bile acids cause itching, bilirubin cause jaundice and cholesterol causes deposits in the skin (xanthelasma) and blood vessels. The back-pressure of the bile obstruction and overall disease process leads to fibrosis, cirrhosis, and liver failure.

Answer 68

Pruritis, fatigue, Jaundice, xanthelasma

Answer 69

Signs: Pale stools, signs of cirrhosis (hepatomegaly, ascites, spider naevi) Symptoms: Abdominal pain, joint pain

Answer 70

Anti-microbial antibodies (AMA) present

Answer 71

LFTs: raised bilirubin, alkaline phosphatase, aminotransferases, GGT. Decreased albumin. Abdominal USS (excludes extrahepatic cholestasis)

Answer 72

Liver biopsy (bile duct lesions and granuloma formation)

Answer 73

Primary sclerosis cholangitis (AMA would not be found), obstructive bile duct lesion, cholestasis (pregnancy, drug-induced)

Answer 74

1st line – Ursodeoxycholic acid (bile acid analogue reduces intestinal absorption of cholesterol and dampens the inflammatory response). Cholestyramine (bile acid analogue) for pruritis. Liver transplant if severe

Answer 75

Regular LFT; ultrasound +/- AFP if cirrhotic (with chronic liver diseases, such as hepatitis and cirrhosis, AFP may be chronically elevated).

Answer 76

Liver cirrhosis, portal hypertension, steatorrhea, osteoporosis, hypercholesterolaemia, malabsorption

Answer 77

Portal hypertension, advanced histological stage, and failure to respond to ursodeoxycholic acid are poor prognostic factors. Median survival is approximately 9 years, however, in patients diagnosed at an asymptomatic stage, survival is twice as high compared to those diagnosed at a symptomatic stage.

Answer 78

Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts, resulting in strictured ‘beaded’ appearance of bile ducts.

Answer 79

Male, heavily associated with IBD especially ulcerative colitis, less common than PBC, more common in northern europe and NA. Mean diagnosis is 40

Answer 80

Male sex, aged 40-50, inflammatory bowel disease (UC and Crohn’s), family history

Answer 81

Inflammation of intrahepatic and extrahepatic bile ducts leads to fibrosis and stricturing. This obstructs bile flow causing cholestasis. The biliary strictures lead to build up of bile acids and bilirubin in the blood causing pruritis and jaundice. Ongoing strictures eventually leads to fibrosis, cirrhosis, and liver failure.

Answer 82

Pruritis, fatigue, Charcot’s triad: RUQ abdominal pain, fever, jaundice, hepatomegaly, IBD signs and symptoms

Answer 83

MRCP (magnetic resonance cholangiopancreatography) – bile duct strictures or lesions

Answer 84

1st line LFTs: raised bilirubin, ALP, AST and ALT, GGT. Decreased albumin. Serology: no antimicrobial antibodies (AMA), maybe pANCA antibodies

Answer 85

Primary biliary cholangitis/cirrhosis, secondary sclerosing cholangitis, hepatitis

Answer 86

1st line – symptomatic treatment. Ursdeoxycholic acid doesn’t work. Cholestyramine for pruritis (bile acid analogue). Consider liver transplant. Encourage a health lifestyle

Answer 87

Portal hypertension, cirrhosis, cholangiocarcinoma, colorectal cancer, hepatic encephalopathy

Answer 88

The average survival of patients newly diagnosed with PSC is 9.3 to 18 years. Despite the rare nature of this disease, PSC is the 5th leading indication for liver transplantation in the USA. For those who receive a liver transplantation, the 5-year survival rate is approximately 85%.

Answer 89

Sudden and rapid onset inflammation of the pancreas

Answer 90

- In the UK there are an estimated 30 per 100,000 cases each year and the incidence is increasing globally - The overall mortality rate in the UK is reported as around 5%, rising to 25% for patients with severe disease. - In the UK, around 50% of cases are caused by gallstones, 25% by alcohol, and 25% by other factors. - Increases with advancing age - Afro-Caribbean ethnicity: risk is 2-3 fold higher in black populations than white - Sex: alcohol-related pancreatitis is more common in males, whilst gallstone-related pancreatitis is more common in females - Gallstone pancreatitis is more common in white women >60 years of age, especially among patients with microlithiasis.

Answer 91

I GET SMASHED: Idiopathic, Gallstones, Ethanol (alcohol), Trauma, Steroids, Mumps, Autoimmune, Scorpion sting, Hyperlipidaemia, ERCP, Drugs (diuretics)

Answer 92

Middle-age woman, young/middle-age man, gallstones (MC women), alcohol (MC men), ERCP, diet, obesity, T2DM, family history

Answer 93

Gallstones block flow of bile and pancreatic juices into the duodenum. Reflux of bile into pancreatic duct and prevention of pancreatic juice containing enzymes from being secreted results in inflammation. Cascade of zymogen/enzyme activation which triggers the recruitment of inflammatory cells and the release of inflammatory mediators. Alcohol is directly toxic to pancreatic cells causing inflammation. Autoimmune: pancreas releases exocrine enzymes which auto digest the pancreas.

Answer 94

Severe epigastric pain radiating to the back, vomiting, abdominal tenderness, hypocalcaemia

Answer 95

Signs: Jaundice, tachycardia, Chvostek sign, grey turner (flank bruising) and Cullen sign (periumbilical bruising), signs of hypovolemia and pleural effusion Symptoms: Dyspnoea, fever, nausea and vomiting

Answer 96

Serum lipase raised (3 times the upper limit level)

Answer 97

Serum amylase raised (3 times the upper limit level), FBC: leucocytosis with left shift (increase in immature:mature WBCs), raised haematocrit, raised CRP. Raised urea, low calcium. Imaging: chest x-ray, abdominal USS (gallstones), CT scan (inflammation, necrosis, effusions) Diagnosis needs 2 of 3: acute abdominal pain, elevated pancreatic enzymes (amylase/lipase), abnormal imaging

Answer 98

Glasgow score (severity of pancreatitis): Pao2 low, Age >55, Neutrophils raised, Calcium low, uRea raised, Enzymes raised, Albumin low, Sugar raised (PANCREAS)

Answer 99

Abdominal aortic aneurysm, peptic ulcer disease, cholangitis, oesophageal spasm

Answer 100

1st line – ABCDE, IV fluids, analgesia, nil by mouth, oxygen, antibiotics, electrolyte replacement. ERCP for gallstones, treat complications

Answer 101

Renal failure, ARDS, sepsis, pancreatic abscess, pseudocysts, pancreatic necrosis

Answer 102

25% of acute pancreatitis cases are severe and associated with complications. Severe cases often require critical care input, and are associated with prolonged hospital stay and an increased mortality rate (25%), compared to the overall mortality rate (5%).

Answer 103

A severe subtype of acute pancreatitis - Necrosis presents within the **first 24-48 hours** resulting in the death of portions of the pancreas - It should be suspected in those who continue to have **abdominal pain, nausea and fever** despite supportive management of acute pancreatitis - The **key diagnostic factor** is non-enhancing low attenuating pancreatic tissue on **CT imaging**, which signifies necrosis - Some hospitals perform **fine-needle aspiration** to determine if necrotic tissue is infected, but false negatives are possible - **Walled-off necrosis** (WON) occurs after 4 weeks, at which point percutaneous drainage or open necrosectomy may be indicated; **early** necrosectomy has a **high mortality rate** - Despite the above, the presence of sepsis and multi-organ dysfunction may warrant **early surgery** - It carries a **poor prognosis** and has a high risk of becoming infected

Answer 104

Chronic pancreatitis refers to inflammation of the pancreas. Unlike acute pancreatitis, chronic pancreatitis is irreversible. It is characterised by structural changes e.g. fibrosis, calcification and atrophy which leads to a decline in function of the pancreas.

Answer 105

- Alcohol is the primary risk factor accounting for 80% of cases, whilst 20% of cases have an unknown cause - The age at presentation varies with aetiology. Hereditary pancreatitis has a peak age at 10 to 14 years, juvenile idiopathic chronic pancreatitis at 19 to 23 years, alcoholic chronic pancreatitis at 36 to 44 years, and senile idiopathic chronic pancreatitis at 56 to 62 years. - M>F - Worldwide prevalence is around 4-5%

Answer 106

Alcohol consumption, progression from acute pancreatitis, trauma, chronic kidney disease, cystic fibrosis

Answer 107

- Alcohol excess - Smoking - Family history - Ductal obstruction e.g. gallstones, tumours, structural abnormalities - Genetic - cystic fibrosis and haemochromatosis

Answer 108

Repeated bouts of acute pancreatitis can progress to chronic pancreatitis. With each bout of acute pancreatitis, there is ductal dilatation and damage to pancreatic tissue. Fibrotic tissue forms causing narrowing of ducts leading to stenosis.

Answer 109

Severe pain in epigastric region which can radiate to back, steatorrhea, jaundice, loss of exocrine function (no pancreatic enzymes secreted in GI tract, especially lipase), loss of endocrine function (lack of insulin causing diabetes),

Answer 110

Weight loss, nausea and vomiting

Answer 111

X-ray/CT/MRI scan shows calcification of pancreas and dilated ducts

Answer 112

1st line Faecal-elastase 1 (low), faecal fat (high), pancreatic function tests (decreased function), ERCP for visualisation of ducts, bloods (low/no amylase and lipase)

Answer 113

Pancreatic cancer, acute pancreatitis, abdominal aorta aneurysm, peptide ulcer disease

Answer 114

1st line – control pain (analgesia, NSAIDs) and risk factors (less alcohol, less smoking, obesity) Replace pancreatic enzymes in deficiency (lipase), nutritional supplements. Insulin for diabetes. ECRP with stenting. Surgery to drain bile ducts

Answer 115

Patients are recommended to be seen yearly for non-invasive testing, to include laboratory blood work and perhaps stool tests to monitor for specific complications, including: - Cholestasis and biliary obstruction (LFTs) - Malnutrition - Baseline bone densitometry in high-risk patients - Steatorrhoea (qualitative faecal fat) - Diabetes (glucose).

Answer 116

Pancreatic exocrine insufficiency, diabetes mellitus, pancreatic calcification, steatorrhea, pancreatic pseudocysts, pancreatic cancer, malabsorption, gastric varices, metabolic bone disease

Answer 117

Almost all patients will develop exocrine insufficiency, and up to 75% will develop endocrine insufficiency. Survival is dependent upon the underlying cause, with a life expectancy of 55-72% in chronic pancreatitis due to alcohol excess.

Answer 118

Effects of long-term alcohol consumption on the liver. Fatty liver > alcoholic hepatitis > liver cirrhosis

Answer 119

- The prevalence of alcohol-use disorders among men and women in the European region was 14.8% and 3.5%, respectively, in 2016. In the UK, it is estimated that 24% to 28% of adults drink in a hazardous or harmful way. - M>F prevalence - Main cause of liver disease and failure

Answer 120

Chronic heavy alcohol consumption

Answer 121

Progression of alcoholic liver disease. 1. Fatty liver (steatosis): drinking leads to build up of fat in the liver. Treatment: stop drinking alcohol. 2. Alcoholic hepatitis: long term alcohol drinking causes inflammation in liver sites. Damaged intermediate fibres = bundles of Mallory bodies. Treatment: permanent alcohol abstinence. 3. Cirrhosis: liver is made up of scar tissue instead of healthy liver tissue. Irreversible.

Answer 122

Early stages (asymptomatic). Later: abdominal pain, hepatomegaly, jaundice, spider naevi (cluster of minute blood vessels under skin), alcohol dependency

Answer 123

Signs: Palmar erythema, dupuytren’s contracture (fingers bend towards palm of hand), ascites, hepatic encephalopathy, caput medusae (enlarged superficial epigastric veins), bruising, asterixis (flapping tremor), gynecomastia Symptoms: Abdominal pain, fatigue, weight loss, confusion, fever, N+V

Answer 124

Liver biopsy: steatosis, inflammation, Mallory bodies

Answer 125

LFTS: Gamma-glutamyl transferase (raised), AST and ALT (transaminases - raised), AST:ALT (ratio>2), ALP (alkaline phosphatase - raised), bilirubin (raised), albumin (low), FBC: anaemia, thrombocytosis, high MCV

Answer 126

Ultrasound, CT, alcohol dependence (CAGE and AUDIT)

Answer 127

Hepatitis A B C, acute liver failure

Answer 128

1st line - Completely stopping alcohol consumption. Give chlordiazepoxide for delirium tremens – alcohol withdrawal (tremors, agitation, ataxia, disorientation) Also: weight loss, stop smoking, corticosteroids for alcoholic hepatitis (prednisolone), liver transplant if severe (must abstain from alcohol for 3 months first)

Answer 129

Wernicke-Korsakoff syndrome (thiamine deficiency), hepatic encephalopathy, renal failure, hepatocellular carcinoma, portal hypertension

Answer 130

Good if you stop alcohol

Answer 131

Chronic liver disease with evidence of hepatic steatosis (fat build up) which is not a secondary cause of alcohol consumption. Stages: non-alcoholic steatosis, non-alcoholic steatohepatitis, fibrosis, cirrhosis

Answer 132

- Commonest liver disorder in industrialised western countries - Affects around 3/4's of all obese individuals - Individuals with metabolic syndrome

Answer 133

Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia

Answer 134

Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia. Drugs (NSAIDs, amiodarone)

Answer 135

Stages of NAFLD: 1. Non-alcoholic steatosis (fat build up in hepatocytes) 2. Non-alcoholic steatohepatitis (steatosis and inflammation) 3. Fibrosis 4. Cirrhosis Insulin resistance plays a role. Overtime, insulin receptors are less responsive to insulin so liver increases fat storage and decreases fatty acid oxidation. This means there is less secretion of fatty acids into the blood stream. There is also increased synthesis and uptake of free fatty acids from the blood (known as steatosis). This ultimately damages lipid membrane, leading to mitochondrial dysfunction and cell death. This generates inflammation. Inflammation + steatosis = steatohepatitis. Damage also attracts neutrophils to the liver. Chronic steatoheptitis can trigger stellate cells to lay down fibrotic tissue (fibrosis). The architecture then changes to the point where disease is now classed as cirrhosis

Answer 136

Asymptomatic. Very severe = liver failure signs: Hepatomegaly, jaundice, ascites, pain in upper right quadrant. Absence of chronic alcohol consumption

Answer 137

Fatigue, malaise, nausea, vomiting

Answer 138

Liver biopsy (steatosis, inflammation, fibrosis)

Answer 139

Deranged LFTs: increased PT/INR, low albumin, increased bilirubin, increased AST and ALT, increased GGT FBC: anaemia, thrombocytopenia. Lipid profile (raised LDL, cholesterol, triglyceride) Liver ultrasound (fatty infiltrates)

Answer 140

Assess risk of fibrosis with fibrosis score

Answer 141

Alcoholic liver disease, hepatitis BC, Wilson’s disease

Answer 142

1st line – treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL). Medication: pioglitazone, vitamin E, statins, ACEi. End stage (cirrhosis irreversible): liver transplant

Answer 143

Ascites, variceal haemorrhage, portal hypertension, hepatocellular carcinoma, hepatic encephalopathy

Answer 144

The overall prognosis in patients with steatosis (fatty liver without evidence of active inflammation) is considered to be good and a majority of patients will remain stable throughout their lifetime. The same cannot be said of non-alcoholic steatohepatitis (NASH), which is considered the progressive form of NAFLD. Patients who have NASH progress to cirrhosis 9% to 20% of the time. Up to one third of these patients will die from complications from liver failure or require liver transplantation. Recurrent NAFLD following liver transplantation is now a well-recognised phenomenon. The incidence of the development of post-liver transplantation steatosis ranges anywhere from 25% to 100%, and the incidence of NASH ranges from a low of 10% to as high as 37.5%. Hepatic steatosis affects up to 80% of patients with chronic hepatitis C infection. Concurrent fatty liver disease with hepatitis C includes increased disease progression, elevated risk of primary liver cancer, and a decreased response to antiviral therapy.

Answer 145

Result chronic inflammation and damage to liver cells. When the liver cells are damaged, they are replaced with scar tissue (fibrosis) and nodules of scar tissue within the liver (regenerative nodules)

Answer 146

- Liver disease is the third biggest cause of premature mortality in the UK with 62,000 working life years lost. - In Europe, cirrhosis related to either viral infection (21% with 13% of HCV infection and 7% of hepatitis B virus infection), or alcohol abuse (19%) are the main indications of liver transplant.

Answer 147

Most common: Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C Rarer: haemochromatosis, Wilson’s disease, alpha 1 trypsin deficiency

Answer 148

Alcohol misuse, IV drug use, unprotected sex, obesity

Answer 149

Fibrosis of liver leads to irreversible chronic scarring and damage – cirrhosis. “End-stage liver damage”. Injured liver cells form regenerative nodules with fibrotic tissue in between. Regenerative nodules make the liver bumpier compared to a normal liver.

Answer 150

Hepatomegaly, jaundice, ascites, regenerative nodules, splenomegaly, hepatic encephalopathy (asterixis), palmar erythema, spider naevi, xanthelasma (yellow growths on eyelids), caput medusae, hepatic fetor

Answer 151

Signs: Gynecomastia, haemoptysis, melaena (black stools due to GI bleeding), bruising, peripheral oedema, altered mental state, bleeding Symptoms: Abdominal pain, nausea, vomiting, confusion, pruritis, bleeding

Answer 152

Liver biopsy (distortion of liver parenchyma – regenerative nodules)Hat

Answer 153

LFTs: bilirubin, PT/INR, serum AST + ALT, NH3, GGT all raised. Serum albumin and glucose decreased. FBC: anaemia, thrombocytopenia, leukopenia. U&E (urea and creatinine raised, deranged electrolytes)

Answer 154

Abdominal ultrasound (nodules, hepatomegaly). Child-Pugh score: severity and prognosis of cirrhosis. Involves - bilirubin, albumin, INR, ascites, encephalopathy. MELD score: model for end-stage liver disease. Gives 3 month mortality estimate and liver transplant advice

Answer 155

Budd Chiari, portal vein thrombosis, constrictive pericarditis

Answer 156

1st line – treatment of underlying cause (stop alcohol, antivirals for hepatitis C). Lifestyle modification (alcohol, low LDL, low salt). Treat complications 2nd – liver transplantation

Answer 157

Development of hepatocellular carcinoma, spontaneous bacterial pericarditis, oesophageal varices ruptures, Hepatic encephalopathy (lactulose), hepato-renal syndrome, ascites (diuretics), bleeding (vitamin K)

Answer 158

2 years without transplant

Answer 159

Complication of cirrhosis. Increased blood pressure in hepatic portal venous system. (portal vein, splenic vein, mesenteric vein)

Answer 160

Pre-hepatic: portal vein obstruction (thrombus) Intrahepatic: cirrhosis, sarcoidosis, schistosomiasis, myeloproliferative disease, congenital hepatic fibrosis Post-hepatic: right heart failure, constrictive pericarditis, Budd Chiari syndrome (hepatic vein obstruction)

Answer 161

Venous blood accumulates in portal system, raising pressure to 5-10mmHg. This leads to the formation of portosystemic shunts where blood is directed away from portal system and into systemic veins. This means the liver receives less blood causing reduced liver function and blood detoxification, leading to increased toxic products in the blood, e.g., ammonia which can cross BBB and cause hepatic encephalopathy. One of the portosystemic shunts is at the oesophagus causing oesophageal varices which can rupture causing upper GI bleed.

Answer 162

Asymptomatic until complications occur: ascites, caput medusa, GI bleeding from oesophageal varices, haemoptysis, melaena/haematochezia, jaundice, hepatic encephalopathy (asterixis, altered consciousness, lethargy, seizure, coma)

Answer 163

Hepatic venous pressure gradient measurement (difference in pressure between IVC and portal vein)

Answer 164

Liver USS (nodules = cirrhosis), CT/MRI scan (ascites, cirrhosis, splenomegaly), endoscopy (oesophageal varices). Labs (FBC, LFT, serology may identify cause)

Answer 165

1st line – beta blockers to reduce portal venous pressure. Treat complications: ascites (reduce salt, diuretics), prevent oesophageal varices bleeding etc.

Answer 166

Hepatic encephalopathy, spontaneous bacterial peritonitis, Ascites, bleeding (oesophageal varices), caput medusae, diminished liver function, enlarged spleen

Answer 167

Dilated collateral blood vessels which are a direct complication of portal hypertension and liver cirrhosis

Answer 168

Portal hypertension and cirrhosis

Answer 169

Portal hypertension leads to formation of portosystemic shunts where blood is diverted away from portal venous system and into systemic system. One of the portosystemic shunts is at the oesophagus which causes oesophageal varices, which are enlarged oesophageal veins. They are very fragile and can easily rupture causing an upper GI bleed.

Answer 170

Upper GI bleeding: Haematemesis, melaena, haematochezia, splenomegaly

Answer 171

Gastroscopy (presence of varices)

Answer 172

FBC: anaemia, thrombocytopenia. LFTs: raised AST, ALT, ALP, bilirubin. U&Es: hyponatraemia

Answer 173

Mallory Weiss tear, hiatal hernia, gastric varices, peptide ulcer disease

Answer 174

Stop bleeding: terlipressin/octreotide, endoscopic banding variceal ligation, balloon tamponade, TIPPS (trans-jugular intrahepatic portosystemic shunt – decrease portal pressure by diverting blood to other veins). Prevent bleeding: non-selective beta blocker, endoscopic banding variceal ligation, TIPPS

Answer 175

Spontaneous bacterial peritonitis, oesophageal stricture, bleeding

Answer 176

Haematemesis is simply defined as “vomiting blood”. It is caused by bleeding from part of the upper portion of the gastrointestinal tract. It may be bright red or look like coffee grounds. (Upper GI tract bleeds may also present as malaena - dark sticky poo)

Answer 177

Common: - Peptic ulcers - Mallory-Weiss tear - Oesophageal varices - Gastritis/gastric erosions - Drugs - Oesophagitis - Duodenitis - Malignancy Rare: - Bleeding disorders - Portal hypertensive gastropathy - Aorto-enteric fistula - Angiodysplasia - Haemobilia - Dieulafoy lesion - Meckel's diverticulum - Peutz-Jegher's syndrome - Osler-Weber-Rendu syndrome

Answer 178

- FBCs - LFTs - U&Es - OGD - Chest X-ray - CT abdomen

Answer 179

- Rapid ABCDE assessment - High flow O2 - Fluid resus if needed - Correct clotting abnormalities For suspected varices: - Terlipressin +IV antibiotics Peptic ulcer bleeds: - achieve endoscopic haemostasis. Start IV PPI. Treat if positive for H.Pylori.

Answer 180

Inflammation of the liver due to viral infection. Hepatitis A is an RNA virus spread by the faecal-oral route (through contamination food or water). It is acute.

Answer 181

Very common hepatitis worldwide but rare in UK, common in Africa. Common in travellers

Answer 182

RNA virus spread through faecal-oral route (via contaminated food and water)

Answer 183

Living in endemic region, travel to endemic region, overcrowding, shellfish

Answer 184

Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.

Answer 185

Acute. Fever, malaise, nausea + vomiting, jaundice

Answer 186

Signs: Cholestasis (slowing of bile through biliary system), dark urine, pale stools, hepatomegaly Symptoms: Fatigue, headache, muscle aches, pruritis, abdominal pain

Answer 187

Gold Standard HAV serology: HAV IgM = active. HAV IgG = recovery or vaccination

Answer 188

Serum ALT and AST raised, bilirubin raised, ESR raised

Answer 189

Differential diagnosis Acute hepatitis B, acute hepatitis C, hepatitis E, EBV, CMV

Answer 190

1st line – supportive therapy, resolves by itself. Incubation period 2 weeks then self-limiting for 1-3 months. Vaccine available. It is a notifiable disease.

Answer 191

Acute liver failure, acute kidney injury, pancreatitis

Answer 192

Hepatitis is inflammation of the liver caused by viral infection. Hepatitis B is an enveloped DNA virus transmitted by blood and bodily fluids. Acute and chronic.

Answer 193

Most common liver infection globally. Only 20% of cases become chronic. 50% of chronic hepatitis B in children under 6y.o.

Answer 194

Viral transmission by blood and bodily fluid (needles – needlestick injury, IVDU, tattoo. Vertical transmission to child, unprotected sex, contaminated household products (toothbrush), contact of minor cuts or abrasions

Answer 195

Unprotected sex, MSM, IVDU, healthcare workers, infected mother to child

Answer 196

Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver

Answer 197

Fever, N+V, jaundice, ascites, hepatomegaly

Answer 198

Signs: Jaundice, dark urine and pale stools, ascites, hepatosplenomegaly, urticaria, arthralgia Symptoms: Fever, fatigue, malaise, nausea + vomiting, muscle aches, abdominal pain, pruritis

Answer 199

HBV DNA (direct count of viral load) and Serology: HBV surface antigen – HBsAg = active infection Core antigen in core of HBV – HBcAg = active infection E antigen – HBeAg. Secreted by infected cells = active acute infection and replication. Correlates with infectivity. IgM antibodies to core antigen - HBcAb = current or past infection. IgM = active infection (high in acute, low in chronic). IgG = past infection where HBcAg is negative. IgG antibodies to surface antigen - HBsAb = current or past infection, or vaccination

Answer 200

LFTs: AST and ALT raised, bilirubin raised, alkaline phosphatase raised

Answer 201

Liver imaging

Answer 202

Acute hepatitis A C E, chronic hepatitis C, EBV hepatitis, CMV hepatitis

Answer 203

1st line – peginterferon alpha 2a subcutaneous injection, or tenofovir (inhibits viral replication) Vaccination with HBV surface antigen (HBsAg). HBV is a notifiable disease.

Answer 204

Liver failure, cirrhosis, hepatocellular carcinoma, HBV reactivation

Answer 205

Inflammation of the liver due to viral infection. Hepatitis C is an RNA and is transmitted through blood and bodily fluids. It is acute and chronic.

Answer 206

¼ fight off virus. ¾ it becomes chronic.

Answer 207

Viral transmission through blood and bodily fluids – unprotected sex, vertical transmission in childbirth, needlestick injury, sharing needles

Answer 208

IVDU, unsafe medical practices, unprotected sex, blood transfusion or organ transplant

Answer 209

Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.

Answer 210

Asymptomatic in acute. Chronic = jaundice, ascites, hepatosplenomegaly,

Answer 211

Fever, malaise, nausea and vomiting, fatigue, pruritis, muscle aches, abdominal pain

Answer 212

HCV RNA test (PCR) – indicates current or past infection. Viral RNA decreasing = recovery. Viral level same = chronic

Answer 213

HCV antibody Enzyme immunoassay – HCV IgG (positive indicates current infection), aminotransferases elevated

Answer 214

Chronic hepatitis B, alcoholic liver disease, steatohepatitis

Answer 215

1st line – direct acting antivirals (ribavirin, sofosbuvir). It is a notifiable disease. No vaccine available.

Answer 216

Liver cirrhosis, hepatocellular carcinoma, cardiovascular disease

Answer 217

Hepatitis is inflammation of the liver caused by viral infection. Hepatitis D is an RNA which only survives in patients who also have Hepatitis B. It is spread via blood and bodily fluids. Hepatitis D attaches itself to the surface antigen of Hepatitis B and cannot survive without this protein.

Answer 218

Hepatitis B patients. Hepatitis D increases the complications and severity of Hepatitis B.

Answer 219

Viral transmission via blood and bodily fluids.

Answer 220

Hepatitis B: needlestick injury, IVDU, MSM, unprotected sex, vertical transmission

Answer 221

Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver. Hepatitis D attaches itself to the surface antigen of Hepatitis B and cannot survive without this protein.

Answer 222

Fever, malaise, nausea and vomiting, jaundice, hepatomegaly

Answer 223

Signs: Jaundice, dark urine and pale stools, ascites, hepatosplenomegaly, urticaria, arthralgia Symptoms: Fever, fatigue, malaise, nausea + vomiting, muscle aches, abdominal pain, pruritis

Answer 224

Serology: HDV IgM or IgG = active infection. HVD RNA in serum

Answer 225

1st line LFTs: AST and ALT raised, bilirubin raised, alkaline phosphatase raised

Answer 226

Liver imaging

Answer 227

Acute hepatitis A C E, chronic hepatitis C, EBV hepatitis, CMV hepatitis

Answer 228

1st line – no specific treatment. Treat hepatitis B – SC pegylated interferon alpha 2a or tenofovir. It is a notifiable infection.

Answer 229

Cirrhosis, hepatocellular carcinoma

Answer 230

Hepatitis is inflammation of the liver caused by viral infection. Hepatitis E is an RNA virus spread by the faecal-oral route (via contaminated food and water, dogs, and pigs). It is acute

Answer 231

Viral transmission via faecal-oral route (food, contaminated water, undercooked seafood and pork)

Answer 232

Undercooked seafood and pork, contaminated water, pregnant

Answer 233

Virus infected cells undergo cytotoxic killing and apoptosis by the immune system. Hepatocytes undergoing apoptosis are called councilman bodies. Cytotoxic killing causes inflammation of the liver.

Answer 234

Acute. Fever, malaise, nausea + vomiting, jaundice, hepatomegaly

Answer 235

Signs: Jaundice, dark urine, and pale stools Symptoms: Pruritis, abdominal pain, muscle aches and pain

Answer 236

HEV serology: HEV IgM antibodies = active infection. HEV IgG antibodies = recovery. HEV RNA = current infection

Answer 237

Serum ALT and AST raised, bilirubin raised, ESR raised

Answer 238

Acute hepatitis B, acute hepatitis C, EBV, CMV

Answer 239

1st line – no treatment. Very mild illness which is self-limiting within a month. It is a notifiable disease. No vaccine available.

Answer 240

Chronic hepatitis, liver failure (especially in pregnant women), cirrhosis, hepatocellular carcinoma

Answer 241

25% mortality in pregnant women

Answer 242

Inflammation of the liver due to it being attacked by the body’s own cells.

Answer 243

Young women

Answer 244

Female, genetic predisposition, immune dysfunction, other autoimmune conditions, HLA DR3/DR4

Answer 245

T cells recognise liver cells as harmful and alert the immune system to attack the liver. Type 1: occurs in adults, typically women. Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-soluble liver antigen Type 2: occurs in children. Anti-liver kidney microsomes-1. Anti-liver cytosol antigen type-1.

Answer 246

Asymptomatic or Malaise, fatigue, jaundice, fever, hepatosplenomegaly

Answer 247

Liver biopsy

Answer 248

Increased transaminases AST and ALT (higher ALT since it is more associated with the liver). Decreased albumin. Prolonged prothrombin time. Serology: Type 1 - Anti-nuclear antibodies, anti-smooth muscle antibodies, anti-soluble liver antigen. Type 2 - Anti-liver kidney microsomes-1. Anti-liver cytosol antigen type-1.

Answer 249

Chronic hepatitis B C D, systematic lupus erythematous

Answer 250

1st line – corticosteroid (prednisolone). Plus, immunosuppressant (azathioprine) Liver transplant if resistant to medication

Answer 251

Cirrhosis, acute liver failure, corticosteroid complications (hypertension, osteoporosis, diabetes mellitus, growth impairment)

Answer 252

Also called icterus, jaundice is yellowing of skin and eyes due to accumulation of conjugated or unconjugated bilirubin. 3 types: pre-hepatic, intra-hepatic, post-hepatic

Answer 253

Pre-hepatic: unconjugated hyperbilirubinemia due to excessive red blood cell breakdown which overwhelms the liver’s ability to conjugate bilirubin. Causes: Haemolytic anaemia, Gilbert’s syndrome, Criggler-Najjar syndrome.

Answer 254

Intrahepatic: dysfunction of hepatic cells, liver loses ability to conjugate bilirubin, both conjugated and unconjugated bilirubin in blood. Causes: alcoholic liver disease, hepatitis, hepatocellular carcinoma, hepatotoxic medication

Answer 255

Post-hepatic: obstruction of biliary drainage causing increase in conjugated bilirubin. Causes: gallstones, cholangiocarcinoma, pancreatic cancer,

Answer 256

RBCs are broken down by reticuloendothelial macrophages in spleen, haemoglobin is broken down to heme and globin. Heme is broken down to Fe2+ and biliverdin. Biliverdin reductase converts biliverdin to unconjugated bilirubin which is water insoluble. Unconjugated bilirubin travels in the blood bound to albumin, to the liver. In the liver, enzyme UGT conjugates bilirubin making it water soluble. Conjugated bilirubin is stored in gallbladder and excreted into small intestine as bile and converted to urobilinogen by colonic bacteria. Some urobilinogen is converted to stercobilin, giving faeces its brown colour. Some urobilinogen is recycled in the enterohepatic circulation, and some goes to the kidneys where it is oxidised to urobilin which makes urine yellow. Jaundice occurs when this pathway is disrupted.

Answer 257

Yellow skin and sclera. Pre-hepatic (normal urine and stool). Intrahepatic (dark urine, normal stool). Post hepatic (dark urine, pale stool). Pruritis

Answer 258

Pre-hepatic: conjugated bilirubin normal, unconjugated bilirubin increased, urobilinogen increased, ALP AST and ALT normal, urine conjugated bilirubin not present Intrahepatic: conjugated bilirubin increased, unconjugated bilirubin increased, urobilinogen decreased, ALP increased, AST and ALT very increased, urine conjugated bilirubin present Post-hepatic: conjugated bilirubin increased, unconjugated bilirubin normal, urobilinogen decreased, ALP highly increased, AST and ALT increased, urine conjugated bilirubin present

Answer 259

Abdominal USS

Answer 260

Depends on underlying cause

Answer 261

Wernicke-Korsakoff syndrome is caused by thiamine deficiency (vitamin B1). Wernicke’s encephalopathy is the acute, medical emergency reversible stage before progressive to Korsakoff syndrome which is the chronic, irreversible stage.

Answer 262

Excess alcohol (alcohol reduces thiamine levels), inadequate intake (malnutrition, anorexia), impaired absorption (stomach cancer, IBD)

Answer 263

Thiamine deficiency impairs glucose metabolism, decreasing cellular energy. Brain is vulnerable to impaired glucose. Alcohol reduces thiamine by interfering with thiamine conversion to its active form, preventing absorption, causes cirrhosis which interferes with thiamine storage in liver

Answer 264

Wernicke’s: confusion, apathy, difficulty concentrating, ophthalmoplegia weakness and paralysis of eye muscles, ataxia – difficulty with coordinated movement. Korsakoff: severe memory impairment (anterograde and retrograde), confabulation (creates stories to fill in memory gaps), behavioural changes

Answer 265

Clinical diagnosis, thiamine levels decreased, LFTs deranged, MRI degeneration of mammillary bodies

Answer 266

Alcohol intoxication, alcohol withdrawal, viral encephalitis

Answer 267

1st line – IV thiamine infusion (pabrinex). Can be given with glucose, magnesium, and multivitamins

Answer 268

Korsakoff’s syndrome, ataxia, ophthalmoplegia, hearing loss

Answer 269

Collection of fluid in the peritoneal cavity

Answer 270

Cirrhosis, congestive heart failure, peritonitis, malignancy, nephrotic syndrome

Answer 271

Excessive build-up of fluid in the peritoneal cavity. Poor liver function = low albumin = low blood oncotic pressure = fluid loss into the peritoneal cavity

Answer 272

Distended large abdomen, shifting dullness: percuss abdomen and observe dullness over fluid and resonance over air. Supine = central abdomen resonant as bowel floats, flanks dull as fluid collects. Lying on side = flank resonant as fluid moves to other side

Answer 273

Abdominal ultrasound (fluid in peritoneal cavity)

Answer 274

Alcoholic liver disease, hepatitis C, congestive heart failure

Answer 275

1st line – treat underlying cause. Diuretic (spironolactone and furosemide) to drain fluid. Low sodium diet. Paracentesis.

Answer 276

Dyspnoea, abdominal infections (SBP), kidney failure

Answer 277

Metabolic disease caused by genetic abnormality of protein alpha 1 antitrypsin

Answer 278

Autosomal recessive mutation of protease inhibitor gene on chromosome 14

Answer 279

Young/middle aged male, smoking

Answer 280

A1AT is a protease inhibitor which inactivates elastase, an enzyme which breaks down elastin. Deficiency of normal A1AT means elastase is not inactivated so it breaks down elastin unchecked. Liver: A1AT is produced in liver. Mutated protein damages liver causing fibrosis, cirrhosis, HCC. Lungs: protease enzymes attack connective tissue in lungs, damaging alveoli walls causing emphysema and bronchiectasis.

Answer 281

Lung – shortness of breath, chronic cough, wheeze, mucus production, emphysema, COPD like symptoms Liver – jaundice, cirrhosis (+ complications: HE, oesophageal varices), hepatitis, hepatomegaly

Answer 282

Serum alpha 1 antitrypsin low

Answer 283

Serum alpha 1 antitrypsin low, reduced pulmonary function tests (spirometry obstruction FEV:FVC <0.7), # chest x-ray/CT: hyperinflated chest, panacinar emphysema and bronchiectasis, LFTs: elevated bilirubin, aminotransferase, ALP. Liver biopsy (cirrhosis and periodic acid Schiff pink staining A1AT mutant globules Other: genetic testing

Answer 284

Asthma, COPD, bronchiectasis, viral hepatitis

Answer 285

1st line - no curative treatment: stop smoking, A1AT infusions, standard COPD treatment (inhalers, oxygen), standard liver disease treatment (lactulose for HE)

Answer 286

Hepatocellular carcinoma, COPD, cirrhosis

Answer 287

Metabolic disorder where body absorbs too much iron leading to increase total body iron and iron deposition into tissues which can poison the tissues (liver, pancreas, heart, pituitary)

Answer 288

Autosomal recessive mutation of human haemochromatosis protein (HFE) on chromosome 6

Answer 289

Family history, male (because women lose iron in menstruation), age >50

Answer 290

Mutation in HFE causes increased iron absorption. Iron is deposited into other tissues, process called hemosiderosis (liver, pancreas, heart, pituitary, joints, skin). Extra iron leads to organ damage through free radical production which cause cellular damage > cell death > fibrosis

Answer 291

Chronic tiredness, joint pain, pigmentation (bronze/slate-grey discolouration), hair loss, hypogonadism, erectile dysfunction, amenorrhoea, cognitive symptoms (memory and mood disturbance)

Answer 292

Signs: Chronic liver disease, cirrhosis, heart failure, arrhythmias Symptoms: Fatigue, weakness, lethargy, joint pain

Answer 293

Liver biopsy (brown spots of iron deposited in hepatocytes. Prussian blue stain shows iron as blue)

Answer 294

FBC: high transferrin saturation, high iron, high serum ferritin, decreased total iron binding capacity. LFTs: raised aminotransferases Other: genetic testing, MRI

Answer 295

Secondary haemochromatosis (from transfusions), hepatitis B and C, NAFLD

Answer 296

1st line – phlebotomy/venesection to decrease serum iron, ferritin, and iron saturation. Done weekly. 2nd line – iron chelation (desferrioxamine). Lifestyle modification

Answer 297

Cirrhosis, diabetes mellitus, hepatocellular carcinoma, hypogonadism

Answer 298

Metabolic disease which causes excessive accumulation of copper in body and tissues which can lead to tissue damage.

Answer 299

Autosomal recessive mutation of ATP7B gene on chromosome 13

Answer 300

Young <20, family history

Answer 301

Autosomal recessive defect in ATP7B copper-binding protein which leads to copper building up in hepatocytes and production of free radicals. Excess copper and free radicals damage injures the hepatocytes and copper spills out into blood where it circulates to other tissues causing free radical damage (e.g., brain, basal ganglia, cornea, liver)

Answer 302

Liver: hepatitis, cirrhosis Neurological: Parkinsonism (tremor, bradykinesia, rigidity), dysarthria (speech difficulties), dystonia (abnormal muscle tone,) concentration and coordination difficulties, dementia Psychiatric: depression, psychosis Eyes: Kayser-Fleischer rings in cornea (brown circles of copper deposits in Descemet’s membrane)

Answer 303

Hepatosplenomegaly, renal disease, osteopenia, haemolytic anaemia

Answer 304

Liver biopsy (increased copper, hepatitis)

Answer 305

Serum copper and ceruloplasmin reduced (copper in tissues not blood), 24hour urinary copper excretion high, abnormal LFTs

Answer 306

Slit-lamp examination (Kayser-Fleischer rings), MRI brain, genetic testing

Answer 307

Hepatitis B and C, haemochromatosis, alpha 1 antitrypsin deficiency

Answer 308

1st line – copper chelation with penicillamine (or trientene) 2nd – zinc salts, decrease copper diet (reduce liver, chocolate, nuts, mushrooms, shellfish), liver transplant if cirrhosis

Answer 309

Brain infection due to toxic metabolites (especially ammonia) not removed by the liver due to liver dysfunction.

Answer 310

Liver cirrhosis

Answer 311

Ammonia is produced by intestinal bacteria when they break down proteins and is absorbed in the gut. Ammonia builds up in the blood in patients with cirrhosis because liver impairment prevents hepatocytes from metabolising ammonia into harmless waste products, and collateral vessels between the portal and systemic circulation means that ammonia bypasses the liver and enters systemic circulation directly.

Answer 312

Reduced consciousness, confusion, stupor, coma, changes to personality mood and memory. Asterixis, rigidity, hypokinesia. Signs of chronic liver failure.

Answer 313

Blood ammonia raised, abnormal LFTs, EEG (decrease in brain wave frequency and amplitude), U&E (maybe hyponatraemia or hypokalaemia)

Answer 314

Laxatives (e.g., lactulose) promote excretion of ammonia from gut before it is absorbed. Antibiotics (e.g., rifaximin) reduce the number of intestinal bacteria which produce ammonia. Nutritional support, e.g., nasogastric feeding

Answer 315

Infection of ascitic fluid caused by bacterial infection. Not attributed to any intra-abdominal, ongoing inflammatory or surgically correctable condition.

Answer 316

E. coli most common causative organism. Most common infection in cirrhosis.

Answer 317

Gram negative: E. coli, klebsiella. Gram positive: staph aureus

Answer 318

Cirrhosis, liver failure, GI bleeding

Answer 319

Severe abdominal pain with shock and collapse, fever, ascites, guarding (rigidify helps pain, pain eased when pressing hands on abdomen, lying still)

Answer 320

Signs: hypothermia, hypotension, tachycardia Symptoms: Nausea and vomiting, confusion

Answer 321

Ascitic fluid absolute neutrophil count (ANC) raised >250cells/mm3

Answer 322

1st line FBC: leucocytosis, anaemia. Raised CRP/ESR. Blood cultures and ascitic tap (show causative microorganism) hCG test (exclude pregnancy). Abdominal x-ray (exclude bowel obstruction). Chest x-ray (air below diaphragm)

Answer 323

Renal colic, secondary peritonitis, chemical peritonitis, tuberculosis peritonitis

Answer 324

1st line – IV antibiotics: piperacillin/tazobactam. Cephalosporins (cefotaxime) are also used. Consider vancomycin (better coverage), IV albumin, large volume paracentesis. Peritoneal lavage (surgical cleaning of peritoneal cavity)

Answer 325

Sepsis, renal failure, death

Answer 326

Excessive ingestion of paracetamol. Serious toxicity >150mg/kg in a 24-hour period. In adults the maximum dose in 24 hours if 4g.

Answer 327

Most common cause of acute liver failure

Answer 328

In an overdose there are not enough glutathione stores in the liver so toxic NAPQI (toxic by-product of paracetamol) builds up and damages the liver.

Answer 329

Nausea, vomiting, anorexia, right upper quadrant pain, jaundice, coma

Answer 330

Serum paracetamol concentration (very high), LFTs (elevated ALT), prolonged prothrombin time, hypoglycaemia

Answer 331

1st line – activated charcoal within 1 hour of ingestion. Plus, N-acetylcysteine (increases availability of glutathione)

Answer 332

Liver failure, multiorgan failure, death

Answer 333

Genetic condition of mild unconjugated hyperbilirubinemia

Answer 334

Autosomal recessive condition. Main cause of inherited jaundice

Answer 335

Decreased UDPGT activity leads to decreased conjugation of bilirubin > unconjugated hyperbilirubinemia

Answer 336

Short episodes of jaundice. Asymptomatic between episodes.

Answer 337

Unconjugated bilirubin elevated. Exclude other causes of unconjugated hyperbilirubinemia.

Answer 338

No treatment

Answer 339

Majority are adenocarcinoma of exocrine pancreas. Usually in head or neck of pancreas.

Answer 340

Genetic mutations in ductal epithelial cells

Answer 341

Smoking, alcohol, diabetes, chronic pancreatitis

Answer 342

Courvoisier sign (painless palpable gallbladder and jaundice) with pale stool and dark urine. Pruritis, weight loss. Trousseau sign of malignancy (blood clots felt as small lumps under skin)

Answer 343

Pancreatic CT protocol (pancreatic mass)

Answer 344

Abdominal ultrasound (pancreatic mass, dilated bile ducts)

Answer 345

1st line – surgical resection (Whipple)

Answer 346

Primary liver that originates in the liver, arising from hepatocytes in predominantly cirrhotic liver. 90% of primary liver cancers

Answer 347

Viral hepatitis (B and C), alcoholic liver disease, NAFLD,

Answer 348

Metastasises to lymph nodes, bones, and lungs through haematogenous spread (hepatic/portal vessels)

Answer 349

Chronic liver disease signs: jaundice, ascites, hepatic encephalopathy, hepatomegaly. Weight loss, tired all the time (TATT), RUQ pain

Answer 350

Raised serum alpha-fetoprotein (HCC tumour marker). 1st line abdominal USS, GS = CT scan

Answer 351

1st line – surgical resection of tumour. Also: liver transplant

Answer 352

Primary liver cancer which originates from bile ducts. Least common primary liver cancer after hepatocellular carcinoma

Answer 353

Age >50, parasitic flukeworms, primary sclerosing cholangitis

Answer 354

Courvoisier’s sign (painless jaundice and palpable gallbladder), weight loss, abdominal pain, fever, malaise, pruritis

Answer 355

CA19-9 raised (tumour marker for cholangiocarcinoma), CEA raised (carcinoembryonic antigen), LFTs: raised bilirubin, ALP 1st line – abdominal USS and CT. GS = ERCP (endoscopic retrograde cholangiopancreatography)

Answer 356

1st line – surgical resection or ERCP can be used to stent in the bile duct that the cholangiocarcinoma is compressing, to drain bile and relieve symptoms

Answer 357

Hernia: bowel protrusion through defect in wall of its cavity. Epigastric: in upper abdomen epigastric area

Answer 358

Painful swelling of upper abdomen

Answer 359

Clinical diagnosis, ultrasound

Answer 360

Surgical repairDes

Answer 361

Incarceration, obstruction and strangulation

Answer 362

Hernia: protrusion of bowel through a defect in the wall of its cavity Femoral: bowel comes through femoral canal

Answer 363

High risk of incarceration, obstruction, and strangulation due to narrow opening and rigid femoral canal borders. Femoral canal: potential space medial to femoral vein

Answer 364

Painful swelling in medial upper thigh, pointing down. Lateral and inferior to pubic tubercle. May be cough impulse

Answer 365

Clinical diagnosis, Ultrasound, CT, MRI

Answer 366

Surgical repair

Answer 367

Incarceration, obstruction, strangulation

Answer 368

Hernia: bowel protrusion through defect in the wall of its cavity Hiatal: herniation of stomach through the diaphragm hiatus

Answer 369

Obesity, increasing age and pregnancy

Answer 370

20% - rolling: gastroesophageal junction stays in abdomen, other parts of stomach, e.g., fundus folds around and up through diaphragm aperture, alongside the oesophagus. 80% - sliding: stomach slides up through the diaphragm with the gastroesophageal junction passing through the diaphragm.

Answer 371

Heartburn/GORD, dyspepsia (indigestion), bowel sounds in chest, dysphagia,

Answer 372

Chest x-ray, barium swallowing, endoscopy, oesophageal manometry

Answer 373

1st line – surgical repair or conservative treatment of gastric acid reflux (proton pump inhibitor)

Answer 374

Hernia: bowel protrusion due to defect in wall of its cavity incisional: tissues protrude through surgical scar due to weakness of muscles and tissues following closure from surgery

Answer 375

Painful swelling in area of incision

Answer 376

Clinical diagnosis, ultrasound

Answer 377

Surgical repair or left alone

Answer 378

Hernia: protrusion of organ through a defect in the wall of its containing cavity. Inguinal: protrusion of abdominal contents through inguinal canal. spermatic cord herniates through inguinal canal in males.

Answer 379

Male, heavy lifting, chronic coughing, past abdominal surgery

Answer 380

Presents superior and medial to pubic tubercle. Direct: 20%, directly through abdominal wall in Hesselbach’s triangle. RIP: rectus abdominis medial border, inferior epigastric arteries, Poupart’s (inguinal) inferior border ligament. Indirect: 80%, bowel herniates through inguinal canal

Answer 381

Painful swelling in groin, when an indirect hernia is reduced, and pressure applied to deep inguinal ring it will remain reduced. When pressure is applied to a direct hernia it will not stop the herniation.

Answer 382

Clinical diagnosis. Also: ultrasound, CT, MRI

Answer 383

1st line – surgical repair (laparoscopic, tension-free mesh repair)

Answer 384

Incarceration (cannot be reduced, trapped in herniated position), obstruction (blocks faeces passage), strangulation (ischaemia)

Answer 385

Hernia: obstruction of bowel through a defect in the wall of its cavity. Umbilical hernias occur around the umbilicus

Answer 386

Muscle weakness around umbilicus. Common in children

Answer 387

Asymptomatic, bulge at umbilicus, pain can occur on straining abdominal wall

Answer 388

Clinical diagnosis, Ultrasound

Answer 389

1st line – spontaneous resolution or surgical repair.

Answer 390

Incarceration, obstruction, strangulation

Hepatobiliary Flashcards

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