Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Conditions > Hepatobiliary > Flashcards

Hepatobiliary Flashcards

1
Q

Define acute liver failure

A

Liver loses its ability to repair and regenerate leading to decompensation. Decompensation is characterised by jaundice, coagulopathy, and hepatic encephalopathy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the epidemiology of acute liver failure

A

ALF is the primary indication for liver transplantation in around 8% of cases within Europe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the aetiology of acute liver failure

A

Drugs: paracetamol, alcohol.
Viral infection: hepatitis, Epstein Barr virus. Autoimmune hepatitis.
Neoplastic: hepatocellular or metastatic carcinoma.
Metabolic: Wilson’s disease, alpha 1 antitrypsin.
Vascular: Budd Chiari

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are risk factors for acute liver failure

A

Chronic alcohol abuse, female, chronic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the pathophysiology of acute liver failure

A

Destruction of hepatocytes leads to inflammation and fibrosis. The destruction of the architecture of the nodules of the liver means it cannot perform its functions properly, repair or regenerate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the key presentations for acute liver failure

A

Jaundice, abnormal bleeding, hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the signs and symptoms for acute liver failure

A

Malaise, nausea, vomiting, confusion, abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the gold standard investigation for acute liver failure

A

LFTs: bilirubin, PT/INR, serum AST + ALT, NH3 all raised. Albumin and glucose decreased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the first line investigations for acute liver failure

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are further investigations for acute liver failure

A

Toxicology screen, abdominal USS, blood cultures, EEG for HE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the differential diagnosis for acute liver failure

A

Acute hepatitis, drug or alcohol intoxication, viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the management for acute liver failure

A

1st line – intensive care management, ABCDE, fluids analgesia. Assessment for liver transplant.
Treat underlying causes and complications, e.g., paracetamol overdose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What monitoring is done for acute liver failure

A

Fluids - urinary and central venous cannulas

Bloods - daily FBC, U&E, LFT and INR

Glucose - 1-4hr + administer IV glucose if needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are complications for acute liver failure

A

Hepatic encephalopathy (lactulose), ascites (diuretics), cerebral oedema (IV mannitol), bleeding (vitamin K), sepsis (sepsis 6, antibiotics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the prognosis for acute liver failure

A

Survival from ALF is greater than 60% and around 55% of patients will have spontaneous recovery without need for liver transplantation.

The overall one year survival following emergency liver transplantation is around 80%.

Worst prognosis if grade III-IV encephalopathy, age >40 years, low albumin, high INR, DILI. Late onset hepatic failure worse than fulminant failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the role of the liver

A
  • Storage(i.e. glycogen, iron, vitamins)
  • Breakdown(i.e. drugs, toxins, ammonia, bilirubin)
  • Synthesis(i.e. bile, cholesterol, coagulation factors, growth factors)
  • Immune function(i.e. innate immune protein production, resident immune cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define chronic liver disease

A

Chronic liver disease is caused by repeated insults to the liver, which can result in inflammation, fibrosis and ultimately cirrhosis.

CLD is generally defined as progressive liver dysfunction for six months or longer. The end result of chronic liver disease is cirrhosis, which describes irreversible liver remodelling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the epidemiology of chronic liver disease

A
  • CLD represents the fourth commonest cause of years of life lost in those aged under 75.
  • In England and Wales an estimated 600,000 patients have CLD.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the aetiology of CLD

A

Acute liver disease is most common cause, non-alcoholic fatty liver disease.

Acute causes which progress to chronic:
Drugs: paracetamol, alcohol.
Viral infection: hepatitis, Epstein Barr virus. Autoimmune hepatitis. Neoplastic: hepatocellular or metastatic carcinoma.
Metabolic: Wilson’s disease, alpha 1 antitrypsin.
Vascular: Budd Chiar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the risk factors of CLD

A

Alcohol, obesity, T2DM, drugs, metabolic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the pathophysiology of CLD

A

Destruction of hepatocytes leads to inflammation (hepatitis) which leads to fibrosis (reversible damage). This can progress to cirrhosis - scarring of liver caused by long term liver damage which is irreversible. Cirrhosis can be compensated, with some preserved liver function, or decompensated which causes end-stage liver failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the key presentations of CLD

A

Jaundice, ascites, abnormal bleeding, hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose), low serum albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the clinical manifestations of CLD

A

Signs
Portal hypertension, oesophageal varices (enlarged veins), caput medusae (cluster of swollen veins in abdomen), spider naevi, palmar erythema, gynecomastia, clubbing, fetor hepatis (sweet musty rotten egg garlic breath), Dupuytren’s contracture, hepatomegaly

Symptoms
Malaise, nausea, vomiting, abdominal pain, pruritis, bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the gold standard investigation for CLD

A

Liver biopsy (distortion of liver parenchyma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the first line investigations of CLD

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are other investigations for CLD

A

Abdominal ultrasound, ascites tap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the differential diagnosis for CLD

A

Budd Chiari, portal vein thrombosis, constrictive pericarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the management for CLD

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What monitoring may be done for CLD

A
  • Hepatocellular Carcinoma -
    • Six monthly surveillance with ultrasound +/- AFP (tumour marker) as patients with cirrhosis are at high risk of HCC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are potential complications with CLD

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the prognosis for CLD

A

2 years without transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the breakdown of RBCs

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe the properties of unconjugated bilirubin

A
  • Unconjugated bilirubin is abreakdown product of haemfrom senescent red blood cells
  • Unconjugated bilirubin isnot water-solubleand requiresconjugationfor excretion in bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How is unconjugated bilirubin conjugated

A
  • 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 andstored in the gallbladderas a component of bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What happens to conjugated bilirubin

A
  • When it is released into the intestinal tract, conjugated bilirubin is broken down intourobilinogenand thenstercobilinby bacteria
  • Stercobilin is excreted infaeces, 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 theurine, giving it a yellow colour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Define cholelithiasis (gallstones)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the epidemiology of gallstones

A
  • 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%).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the aetiology of gallstones

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the risk factors for gallstones

A

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

Family history, rapid weight loss, diabetes and medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Describe the clinical manifestations of gallstones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the gold standard investigation for gallstones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the primary investigations for gallstones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the differential diagnosis for gallstones

A

Pancreatitis, peptic ulcer disease, gallbladder cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is the management for gallstones

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the complications of gallstones

A

Gallstones > cholecystitis > cholangitis. Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the prognosis for gallstones

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Define biliary colic

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe the epidemiology of biliary colic

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are risk factors for biliary colic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe the pathophysiology of biliary colic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the clinical manifestations of biliary colic

A
  • 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the first line investigations for biliary colic

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the differential diagnosis for biliary colic

A
  • Cholecystitis
  • Ascending cholangitis
  • Common bile duct stone
  • Gastritis
  • Peptic ulcer disease
  • IBS
  • Carcinoma on right side of colon
  • Renal colic
  • Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe the management for biliary colic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Describe the complications of biliary colic

A
  • 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 infever,rightupperquadrantpain(usually > 6 hours) and positiveMurphy’s sign
  • Ascending cholangitis:infection of the biliary tree results in ‘Charcot’s triad’ (rightupperquadrantpain,feverandjaundice)
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Define acute cholecystitis

A

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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the epidemiology of acute cholecystitis

A

Acute cholecystitis occurs in 10% of patients with symptomatic gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the risk factors for acute cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Describe the pathophysiology of acute cholecystitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the clinical manifestations for acute cholecystitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is the gold standard investigation for acute cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe the first line investigations for acute cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the differential diagnosis for acute cholecystitis

A
  • Pancreatitis
  • Peptic ulcer disease
  • Cholangitis
  • Appendicitis
  • Basal pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Describe the management for acute cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are the complications of acute cholecystitis

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the prognosis for acute cholecystitis

A

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%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What does positive Murphy’s sign mean

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe chronic cholecystitis

A

Chronic inflammation of the gallbladder +/- colic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Describe the pathophysiology of chronic cholecystitis

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Describe the clinical manifestations of chronic cholecystitis

A
  • Flatulent dyspepsia
  • Abdominal discomfort - RUQ pain (esp after meal)
  • Distension
  • Nausea
  • Fat intolerance (fat stimulates cholecystokinin release and gallbladder contraction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the investigations for chronic cholecystitis

A
  • Ultrasound - to image stone and assess CBD diameter
  • MRCP - used to find CBD stones
  • X-ray - may show porcelain gallbladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are the differential diagnosis of chronic cholecystitis

A
  • If symptoms persist post-treatment, consider:
    • Hiatus hernia
    • IBS
    • Peptic ulcer
    • Chronic pancreatitis
    • Tumour
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Describe the management for chronic cholecystitis

A
  • Cholecystectomy
    • ERCP + sphincterectomy prior to surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the complications for chronic cholecystitis

A

Increased risk of gallbladder cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Define acute cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe the epidemiology of acute ascending cholangitis

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe the aetiology of acute ascending cholangitis

A
  • Choledocholithiasis
  • Benign stricture
  • Malignant stricture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the risk factors for acute cholangitis

A
  • Gallstones:the most common predisposing factor
  • Stricture of the biliary tree:benign or malignant
  • Post-procedure injuryof the bile ducts e.g. post-ERCP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe the pathophysiology of ascending cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What are the key presentations of ascending cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is the gold standard investigation for ascending cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the first line investigations for ascending cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What are the differential diagnosis for ascending cholangitis

A
  • Acute cholecystitis
  • Peptic ulcer disease
  • Pancreatitis
  • Hepatic abscess
  • Appendicitis
  • Biliary colic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Describe the management for ascending cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the complications for ascending cholangitis

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the prognosis for ascending cholangitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Define primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Describe the epidemiology of primary biliary cholangitis

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Describe the aetiology of primary biliary cholangitis

A

Unknown. Genetic predisposition and environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe the risk factors for primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Describe the pathophysiology of primary biliary cholangitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe the key presentations of primary biliary cholangitis

A

Pruritis, fatigue, Jaundice, xanthelasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Describe the clinical manifestations of primary biliary cholangitis

A

Signs:
Pale stools, signs of cirrhosis (hepatomegaly, ascites, spider naevi)

Symptoms:
Abdominal pain, joint pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the gold standard investigation for primary biliary cholangitis

A

Anti-microbial antibodies (AMA) present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the first line investigations for primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What are further investigations for primary biliary cholangitis

A

Liver biopsy (bile duct lesions and granuloma formation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are the differential diagnosis for primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Describe the management for primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What monitoring needs to be done for primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What are the complications with primary biliary cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the prognosis for primary biliary cholangitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Define primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Describe the epidemiology of primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Describe the risk factors for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Describe the pathophsyiology of primary sclerosing cholangitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Describe the key presentations for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the gold standard investigation for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the first line investigations for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What are the differential diagnosis for primary sclerosing cholangitis

A

Primary biliary cholangitis/cirrhosis, secondary sclerosing cholangitis, hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the management for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are potential complications for primary sclerosing cholangitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Describe the prognosis for primary sclerosing cholangitis

A

Theaverage survivalof patients newly diagnosed with PSC is9.3 to 18 years. Despite the rare nature of this disease, PSC is the5thleading indication for liver transplantationin the USA. For those who receive aliver transplantation, the 5-year survival rate is approximately85%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Define acute pancreatitis

A

Sudden and rapid onset inflammation of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Describe the epidemiology of acute pancreatitis

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Describe the aetiology of acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Describe the risk factors for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Describe the pathophysiology of acute pancreatitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What are the key presentations for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the clinical manifestations for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is the gold standard investigation for acute pancreatitis

A

Serum lipase raised (3 times the upper limit level)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What are the first line investigations for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What are the further investigations for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the differential diagnosis for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Describe the management for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What are the complications for acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Describe the prognosis for acute pancreatitis

A

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%).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is necrotising pancreatitis

A

A severe subtype of acute pancreatitis

  • Necrosis presents within thefirst 24-48 hoursresulting in the death of portions of the pancreas
  • It should be suspected in those who continue to haveabdominal pain, nausea and feverdespite supportive management of acute pancreatitis
  • Thekey diagnostic factoris non-enhancing low attenuating pancreatic tissue onCT imaging, which signifies necrosis
  • Some hospitals performfine-needle aspirationto 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;earlynecrosectomy has ahigh mortality rate
  • Despite the above, the presence of sepsis and multi-organ dysfunction may warrantearly surgery
  • It carries apoor prognosisand has a high risk of becoming infected
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Define chronic pancreatitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Describe the epidemiology of chronic pancreatitis

A
  • 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%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Describe the aetiology of chronic pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What are risk factors for chronic pancreatitis

A
  • Alcohol excess
  • Smoking
  • Family history
  • Ductal obstruction e.g. gallstones, tumours, structural abnormalities
  • Genetic - cystic fibrosis and haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Describe the pathophysiology of chronic pancreatitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are the key presentations for chronic pancreatitis

A

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),

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are other symptoms of chronic pancreatitis

A

Weight loss, nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What is the gold standard investigation for chronic pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What are the first line investigations for chronic pancreatitis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What are the differential diagnosis for chronic pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is the management for chronic pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What monitoring is done for chronic pancreatitis

A

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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What complications occur with chronic pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What is the prognosis for chronic pancreatitis

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Define alcoholic liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Describe the epidemiology of alcoholic liver disease

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe the aetiology of alcoholic liver disease

A

Chronic heavy alcohol consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Describe the pathophysiology of alcoholic liver disease

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Describe the key presentations for alcoholic liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Describe the clinical manifestations for alcoholic liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

What is the gold standard investigation for alcoholic liver disease

A

Liver biopsy: steatosis, inflammation, Mallory bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What are the first line investigations for alcoholic liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What are other investigations for alcoholic liver disease

A

Ultrasound, CT, alcohol dependence (CAGE and AUDIT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What are the differential diagnosis for alcoholic liver disease

A

Hepatitis A B C, acute liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

What is the management for alcoholic liver disease

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What are complications for alcoholic liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

What is the prognosis for alcoholic liver disease

A

Good if you stop alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Define non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is the epidemiology of non-alcoholic fatty liver disease

A
  • Commonest liver disorder in industrialised western countries
  • Affects around 3/4’s of all obese individuals
  • Individuals with metabolic syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Describe the aetiology of non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What are the risk factors for non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Describe the pathophysiology of non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Describe the key presentations for non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What are the symptoms of non-alcoholic fatty liver disease

A

Fatigue, malaise, nausea, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What is the gold standard investigation for non-alcoholic fatty liver disease

A

Liver biopsy (steatosis, inflammation, fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What are the first line investigations of non-alcoholic fatty liver disease

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What are the other investigations for non-alcoholic fatty liver disease

A

Assess risk of fibrosis with fibrosis score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What are the differential diagnosis for non-alcoholic fatty liver disease

A

Alcoholic liver disease, hepatitis BC, Wilson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What is the management for non-alcoholic fatty liver disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

What are the complications for non-alcoholic fatty liver disease

A

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

168
Q

What is the prognosis for non-alcoholic fatty liver disease

A

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.

169
Q

Define liver cirrhosis

A

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)

170
Q

Describe the epidemiology of liver cirrhosis

A
  • 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.
171
Q

Describe the aetiology of liver cirrhosis

A

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

172
Q

Describe the risk factors for liver cirrhosis

A

Alcohol misuse, IV drug use, unprotected sex, obesity

173
Q

Describe the pathophysiology of liver cirrhosis

A

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.

174
Q

Describe the key presentations for liver cirrhosis

A

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

175
Q

Describe the clinical manifestations of liver cirrhosis

A

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

176
Q

What is the gold standard investigation for liver cirrhosis

A

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

177
Q

What are the first line investigations for liver cirrhosis

A

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)

178
Q

What are other investigations for liver cirrhosis

A

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

179
Q

What are the differential diagnosis for liver cirrhosis

A

Budd Chiari, portal vein thrombosis, constrictive pericarditis

180
Q

What is the management for liver cirrhosis

A

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

181
Q

What are the complications for liver cirrhosis

A

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

182
Q

What is the prognosis for liver cirrhosis

A

2 years without transplant

183
Q

Define portal hypertension

A

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

184
Q

Describe the aetiology for portal hypertension

A

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)

185
Q

Describe the pathophysiology of portal hypertension

A

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.

186
Q

Describe the key presentations of portal hypertension

A

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

187
Q

What is the gold standard investigation for portal hypertension

A

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

188
Q

What are the first line investigations for portal hypertension

A

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

189
Q

What is the management for portal hypertension

A

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

190
Q

What are the complications for portal hypertension

A

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

191
Q

Define oesophageal varices

A

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

192
Q

Describe the aetiology of oesophageal varices

A

Portal hypertension and cirrhosis

193
Q

Describe the pathophysiology of oesophageal varices

A

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.

194
Q

Describe the key presentations of oesophageal varices

A

Upper GI bleeding: Haematemesis, melaena, haematochezia, splenomegaly

195
Q

What is the gold standard investigation for oesophageal varices

A

Gastroscopy (presence of varices)

196
Q

What are other investigations for oesophageal varices

A

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

197
Q

What are the differential diagnosis for oesophageal varices

A

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

198
Q

What is the management for oesophageal varices

A

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

199
Q

What are the complications for oesophageal varices

A

Spontaneous bacterial peritonitis, oesophageal stricture, bleeding

200
Q

Define haematesis

A

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)

201
Q

Describe the aetiology of haematamesis

A

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

202
Q

What are the primary investigations for haematamesis

A
  • FBCs
  • LFTs
  • U&Es
  • OGD
  • Chest X-ray
  • CT abdomen
203
Q

Describe the management for haematamesis

A
  • 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.

204
Q

Define hepatitis A

A

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.

205
Q

Describe the epidemiology of hepatitis A

A

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

206
Q

Describe the aetiology of hepatitis A

A

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

207
Q

Describe the risk factors for hepatitis A

A

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

208
Q

Describe the pathophysiology of hepatitis A

A

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.

209
Q

What are the key presentations for hepatitis A

A

Acute. Fever, malaise, nausea + vomiting, jaundice

210
Q

What are the clinical manifestations of hepatitis A

A

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

211
Q

What is the gold standard investigation for hepatitis A

A

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

212
Q

What are the first line investigations for hepatitis A

A

Serum ALT and AST raised, bilirubin raised, ESR raised

213
Q

What are the differential diagnosis for hepatitis A

A

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

214
Q

What is the management for hepatitis A

A

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.

215
Q

Describe the complications of hepatitis A

A

Acute liver failure, acute kidney injury, pancreatitis

216
Q

Define hepatitis B

A

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.

217
Q

Describe the epidemiology of hepatitis B

A

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

218
Q

Describe the aetiology of hepatitis B

A

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

219
Q

Describe the risk factors for hepatitis B

A

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

220
Q

Describe the pathophysiology of hepatitis B

A

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

221
Q

What are the key presentations for hepatitis B

A

Fever, N+V, jaundice, ascites, hepatomegaly

222
Q

What are the clinical manifestations for hepatitis B

A

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

223
Q

What is the gold standard investigation for hepatitis B

A

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

224
Q

What are the first line investigations for hepatitis B

A

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

225
Q

What are further investigations for hepatitis B

A

Liver imaging

226
Q

What are the differential diagnosis for hepatitis B

A

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

227
Q

What is the management for hepatitis B

A

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

228
Q

What are the complications for hepatitis B

A

Liver failure, cirrhosis, hepatocellular carcinoma, HBV reactivation

229
Q

Define hepatitis C

A

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.

230
Q

Describe the epidemiology of hepatitis C

A

¼ fight off virus. ¾ it becomes chronic.

231
Q

Describe the aetiology of hepatitis C

A

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

232
Q

Describe the risk factors for hepatitis C

A

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

233
Q

Describe the pathophysiology of hepatitis C

A

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.

234
Q

Describe the key presentations for hepatitis C

A

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

235
Q

What are the clinical manifestations for hepatitis C

A

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

236
Q

What is the gold standard investigation for hepatitis C

A

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

237
Q

What are the first line investigations for hepatitis C

A

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

238
Q

What are the differential diagnosis for hepatitis C

A

Chronic hepatitis B, alcoholic liver disease, steatohepatitis

239
Q

What is the management for hepatitis C

A

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

240
Q

What are the complications for hepatitis C

A

Liver cirrhosis, hepatocellular carcinoma, cardiovascular disease

241
Q

Define hepatitis D

A

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.

242
Q

Describe the epidemiology of hepatitis D

A

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

243
Q

Describe the aetiology of hepatitis D

A

Viral transmission via blood and bodily fluids.

244
Q

Describe the risk factors for hepatitis D

A

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

245
Q

Describe the pathophysiology of hepatitis D

A

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.

246
Q

What are the key presentations for hepatitis D

A

Fever, malaise, nausea and vomiting, jaundice, hepatomegaly

247
Q

Describe the clinical manifestations for hepatitis D

A

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

248
Q

What is the gold standard investigation for hepatitis D

A

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

249
Q

What are the first line investigations for hepatitis D

A

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

250
Q

What are further investigations for hepatitis D

A

Liver imaging

251
Q

What are the differential diagnosis for hepatitis D

A

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

252
Q

What is the management for hepatitis D

A

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

253
Q

What are the complications for hepatitis D

A

Cirrhosis, hepatocellular carcinoma

254
Q

Define hepatitis E

A

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

255
Q

Describe the aetiology of hepatitis E

A

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

256
Q

Describe the risk factors for hepatitis E

A

Undercooked seafood and pork, contaminated water, pregnant

257
Q

Describe the pathophysiology of hepatitis E

A

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.

258
Q

Describe the key presentations of hepatitis E

A

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

259
Q

Describe the clinical manifestations of hepatitis E

A

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

260
Q

What is the gold standard investigation for hepatitis E

A

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

261
Q

Describe the first line investigations for hepatitis E

A

Serum ALT and AST raised, bilirubin raised, ESR raised

262
Q

What are the differential diagnosis for hepatitis E

A

Acute hepatitis B, acute hepatitis C, EBV, CMV

263
Q

Describe the management for hepatitis E

A

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

264
Q

Describe the complications for hepatitis E

A

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

265
Q

Describe the prognosis for hepatitis E

A

25% mortality in pregnant women

266
Q

Define autoimmune hepatitis

A

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

267
Q

Describe the epidemiology of autoimmune hepatitis

A

Young women

268
Q

Describe the aetiology of autoimmune hepatitis

269
Q

Describe the risk factors for autoimmune hepatitis

A

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

270
Q

Describe the pathophysiology of autoimmune hepatitis

A

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.

271
Q

Describe the key presentations for autoimmune hepatitis

A

Asymptomatic or Malaise, fatigue, jaundice, fever, hepatosplenomegaly

272
Q

What is the gold standard investigation for autoimmune hepatitis

A

Liver biopsy

273
Q

Describe the first line investigations for autoimmune hepatitis

A

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.

274
Q

What are the differential diagnosis for autoimmune hepatitis

A

Chronic hepatitis B C D, systematic lupus erythematous

275
Q

Describe the management for autoimmune hepatitis

A

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

276
Q

Describe the complications for autoimmune hepatitis

A

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

277
Q

Define jaundice

A

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

278
Q

Describe the aetiology of pre-hepatic jaundice

A

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.

279
Q

Describe the aetiology of intrahepatic jaundice

A

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

280
Q

Describe the aetiology of post-hepatic jaundice

A

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

281
Q

Describe the pathophysiology of jaundice

A

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.

282
Q

What are the key presentations for jaundice

A

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

283
Q

What are the first line investigations for jaundice

A

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

284
Q

What are the further investigations for jaundice

A

Abdominal USS

285
Q

Describe the management for jaundice

A

Depends on underlying cause

286
Q

Define Wernicke’s encephalopathy and korsakoff syndrome

A

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.

287
Q

Describe the aetiology of Wernicke’s encephalopathy and Korsakoff syndrome

A

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

288
Q

Describe the pathophysiology of Wernicke’s encephalopathy and Korsakoff syndrome

A

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

289
Q

What are the key presentations for Wernicke’s encephalopathy and korsakoff syndrome

A

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

290
Q

Describe the first line investigations for Wernicke’s encephalopathy and Korsakoff syndrome

A

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

291
Q

What are the differential diagnosis for Wernicke’s encephalopathy and Korsakoff syndrome

A

Alcohol intoxication, alcohol withdrawal, viral encephalitis

292
Q

What is the management for Wernicke’s encephalopathy and Korsakoff syndrome

A

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

293
Q

What are the complications with Wernicke’s encephalopathy and Korsakoff syndrome

A

Korsakoff’s syndrome, ataxia, ophthalmoplegia, hearing loss

294
Q

Define ascites

A

Collection of fluid in the peritoneal cavity

295
Q

Describe the aetiology of ascites

A

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

296
Q

Describe the pathophysiology of ascites

A

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

297
Q

Describe the key presentations for ascites

A

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

298
Q

What is the gold standard investigation for ascites

A

Abdominal ultrasound (fluid in peritoneal cavity)

299
Q

What are the differential diagnosis for ascites

A

Alcoholic liver disease, hepatitis C, congestive heart failure

300
Q

What is the management for ascites

A

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

301
Q

What are the complications with ascites

A

Dyspnoea, abdominal infections (SBP), kidney failure

302
Q

Define alpha 1 antitrypsin deficiency

A

Metabolic disease caused by genetic abnormality of protein alpha 1 antitrypsin

303
Q

Describe the aetiology of alpha 1 antitrypsin deficiency

A

Autosomal recessive mutation of protease inhibitor gene on chromosome 14

304
Q

What are the risk factors for alpha 1 antitrypsin deficiency

A

Young/middle aged male, smoking

305
Q

Describe the pathophysiology for alpha 1 antitrypsin deficiency

A

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.

306
Q

What are the key presentations for A1AT deficiency

A

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

307
Q

What is the gold standard investigation for A1AT deficiency

A

Serum alpha 1 antitrypsin low

308
Q

What are the first line investigations for A1AT deficiency

A

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

309
Q

What are the differential diagnosis for A1AT deficiency

A

Asthma, COPD, bronchiectasis, viral hepatitis

310
Q

What is the management for A1AT deficiency

A

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

311
Q

Describe the complications of A1AT deficiency

A

Hepatocellular carcinoma, COPD, cirrhosis

312
Q

Define haemochromatosis

A

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)

313
Q

Describe the aetiology of haemochromatosis

A

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

314
Q

Describe the risk factors for haemochromatosis

A

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

315
Q

Describe the pathophysiology of haemochromatosis

A

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

316
Q

What are the key presentations for haemochromatosis

A

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

317
Q

What are the clinical manifestations of haemochromatosis

A

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

318
Q

What is the gold standard investigation for haemochromatosis

A

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

319
Q

What are the first line investigations for haemochromatosis

A

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

Other: genetic testing, MRI

320
Q

What are the differential diagnosis for haemochromatosis

A

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

321
Q

What is the management for haemochromatosis

A

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

322
Q

What are the complications for haemochromatosis

A

Cirrhosis, diabetes mellitus, hepatocellular carcinoma, hypogonadism

323
Q

Define Wilson’s disease

A

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

324
Q

Describe the aetiology of Wilson’s disease

A

Autosomal recessive mutation of ATP7B gene on chromosome 13

325
Q

What are the risk factors for Wilson’s disease

A

Young <20, family history

326
Q

Describe the pathophysiology of Wilson’s disease

A

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)

327
Q

Describe the key presentations of Wilson’s disease

A

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)

328
Q

What are the signs of Wilson’s disease

A

Hepatosplenomegaly, renal disease, osteopenia, haemolytic anaemia

329
Q

What is the gold standard investigation for Wilson’s disease

A

Liver biopsy (increased copper, hepatitis)

330
Q

What are the first line investigations for Wilson’s disease

A

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

331
Q

What are further investigations for Wilson’s disease

A

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

332
Q

What are the differential diagnosis for Wilson’s disease

A

Hepatitis B and C, haemochromatosis, alpha 1 antitrypsin deficiency

333
Q

Describe the management for Wilson’s disease

A

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

334
Q

What are the complications of Wilson’s disease

335
Q

Define hepatic encephalopthy

A

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

336
Q

Describe the aetiology of hepatic encephalopathy

A

Liver cirrhosis

337
Q

Describe the pathophysiology of hepatic encephalopathy

A

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.

338
Q

Describe the key presentations for hepatic encephalopathy

A

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

339
Q

Describe the first line investigations for hepatic encephalopathy

A

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

340
Q

Describe the management for hepatic encephalopathy

A

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

341
Q

Define spontaneous bacterial peritonitis

A

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

342
Q

Describe the epidemiology of spontaneous bacterial peritonitis

A

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

343
Q

Describe the aetiology of spontaneous bacterial peritonitis

A

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

344
Q

Describe the risk factors of spontaneous bacterial peritonitis

A

Cirrhosis, liver failure, GI bleeding

345
Q

Describe the key presentations of spontaneous bacterial peritonitis

A

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

346
Q

Describe the clinical manifestations of spontaneous bacterial pericarditis

A

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

347
Q

What is the gold standard investigation of spontaneous bacterial peritonitis

A

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

348
Q

Describe the first line investigations for spontaneous bacterial peritonitis

A

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)

349
Q

What are the differential diagnosis for spontaneous bacterial peritonitis

A

Renal colic, secondary peritonitis, chemical peritonitis, tuberculosis peritonitis

350
Q

Describe the management for spontaneous bacterial peritonitis

A

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)

351
Q

What are the complications of spontaneous bacterial peritonitis

A

Sepsis, renal failure, death

352
Q

Define paracetamol overdose

A

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

353
Q

Describe the epidemiology of paracetamol overdose

A

Most common cause of acute liver failure

354
Q

Describe the pathophysiology of paracetamol overdose

A

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.

355
Q

What are the key presentations of paracetamol overdose

A

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

356
Q

Describe the first line investigations for paracetamol overdose

A

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

357
Q

Describe the management for paracetamol overdose

A

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

358
Q

Describe the complications for paracetamol overdose

A

Liver failure, multiorgan failure, death

359
Q

Describe Gilbert’s syndrome

A

Genetic condition of mild unconjugated hyperbilirubinemia

360
Q

Describe the aetiology of Gilbert’s syndrome

A

Autosomal recessive condition. Main cause of inherited jaundice

361
Q

Describe the pathophysiology of Gilbert’s syndrome

A

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

362
Q

What are the key presentations of Gilbert’s syndrome

A

Short episodes of jaundice. Asymptomatic between episodes.

363
Q

Describe the first line investigations for Gilbert’s syndrome

A

Unconjugated bilirubin elevated. Exclude other causes of unconjugated hyperbilirubinemia.

364
Q

Describe the management for Gilbert’s syndrome

A

No treatment

365
Q

Define pancreatic cancers

A

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

366
Q

Describe the aetiology of pancreatic cancers

A

Genetic mutations in ductal epithelial cells

367
Q

Describe the risk factors for pancreatic cancers

A

Smoking, alcohol, diabetes, chronic pancreatitis

368
Q

Describe the key presentations for pancreatic cancer

A

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)

369
Q

What is the gold standard investigation for pancreatic cancer

A

Pancreatic CT protocol (pancreatic mass)

370
Q

Describe the first line investigations for pancreatic cancer

A

Abdominal ultrasound (pancreatic mass, dilated bile ducts)

371
Q

Describe the management for pancreatic cancer

A

1st line – surgical resection (Whipple)

372
Q

Define hepatocellular carcinoma

A

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

373
Q

Describe the risk factors for hepatocellular carcinoma

A

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

374
Q

Describe the pathophysiology of hepatocellular carcinoma

A

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

375
Q

What are the key presentations for hepatocellular carcinoma

A

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

376
Q

What are the first line investigations for hepatocellular carcinoma

A

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

377
Q

Describe the management for hepatocellular carcinoma

A

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

378
Q

Define cholangiocarcinoma

A

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

379
Q

Describe the risk factors of cholangiocarcinoma

A

Age >50, parasitic flukeworms, primary sclerosing cholangitis

380
Q

What are the key presentations of cholangiocarcinoma

A

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

381
Q

Describe the first line investigations of cholangiocarcinoma

A

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)

382
Q

Describe the management for cholangiocarcinoma

A

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

383
Q

Define an epigastric hernia

A

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

384
Q

What are the key presentations for an epigastric hernia

A

Painful swelling of upper abdomen

385
Q

Describe the first line investigations for an epigastric hernia

A

Clinical diagnosis, ultrasound

386
Q

Describe the management for an epigastric hernia

A

Surgical repairDes

387
Q

Describe the complications for an epigastric hernia

A

Incarceration, obstruction and strangulation

388
Q

Define a femoral hernia

A

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

389
Q

Describe the pathophysiology of a femoral hernia

A

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

390
Q

What are the key presentations of a femoral hernia

A

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

391
Q

Describe the first line investigations for a femoral hernia

A

Clinical diagnosis, Ultrasound, CT, MRI

392
Q

Describe the management for a femoral hernia

A

Surgical repair

393
Q

Describe the complications of a femoral hernia

A

Incarceration, obstruction, strangulation

394
Q

Define hiatal hernia

A

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

395
Q

Describe the risk factors for hiatal hernias

A

Obesity, increasing age and pregnancy

396
Q

Describe the pathophysiology of hiatal hernias

A

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.

397
Q

Describe the key presentations of hiatal hernias

A

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

398
Q

Describe the first line investigations for hiatal hernias

A

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

399
Q

Describe the management for hiatal hernias

A

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

400
Q

Define incisional hernia

A

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

401
Q

What are the key presentations for incisional hernia

A

Painful swelling in area of incision

402
Q

Describe the first line investigations for incisional hernia

A

Clinical diagnosis, ultrasound

403
Q

Describe the management for incisional hernias

A

Surgical repair or left alone

404
Q

Define inguinal hernia

A

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.

405
Q

Describe the aetiology of inguinal hernias

A

Male, heavy lifting, chronic coughing, past abdominal surgery

406
Q

Describe the pathophysiology of inguinal hernias

A

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

407
Q

Describe the key presentations of inguinal hernias

A

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.

408
Q

Describe the first line investigations for inguinal hernias

A

Clinical diagnosis. Also: ultrasound, CT, MRI

409
Q

Describe the management for inguinal hernias

A

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

410
Q

Describe the complications for inguinal hernias

A

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

411
Q

Define umbilical hernias

A

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

412
Q

Describe the pathophysiology of umbilical hernias

A

Muscle weakness around umbilicus. Common in children

413
Q

What are the key presentations for umbilical hernias

A

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

414
Q

Describe the first line investigations for umbilical hernias

A

Clinical diagnosis, Ultrasound

415
Q

Describe the management for umbilical hernias

A

1st line – spontaneous resolution or surgical repair.

416
Q

Describe the complications for umbilical hernias

A

Incarceration, obstruction, strangulation

Conditions (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions