liver and GI Flashcards
what are the functions of vit b12
forms rbc
develops nerve cells
forms DNA
how is b12 absorbed?
IF in the terminal ileum
what causes scurvy
lack of collagen synthesis due to vit c deficiency
functions of vit A
rhodopsin production
spermatogenesis
prevention of foetal resorption
growth
antioxidant
source of vit A
meat milk and carotenes
functions of Vit D
Ca absorption and reabsorption
Phosphate absorption and reabsorption
resorption and formation of bone
regulates DNA transcription of PTH
vit K functions
activation of clotting factors 2,7,9,10
vit K sources
spinach broccoli kale sunflower oil
folate functions
methylation rxns
DNA synthesis
methionine synthesis
where is folate stored
liver
what vit is folate
vit B9
how is alcohol metabolised in the liver
NOT phase 1 and phase 2 rxns
alcohol dehydrogenase enzyme converts alcohol to acetyl aldehyde which is very toxic to the liver and scars the tissue before converting it to acetyl-CoA which leads into fatty acid synthesis and causes the fatty liver
what is bile
H2O + electrolytes + bile acids + phospholipids + cholesterol + bile pigments
outline enterohepatic circulation
1) cholesterol is broken down into cholic acid and chenodeoxycholic acid
2) cholic acid and chenodeoxycholic acid are conjugated to increase hydrophilicity (so that they stay in the intestinal lumen and don’t diffuse through the membrane)
3) CCK released when food in stomach
4) release of bile by contraction of the gall bladder
5) 5% bile deconjugated and reabsorbed back to hepatocytes
6) 95% turn to bile salts and become micelles
7) micelles break down lipids into free fatty acids
8) the free fatty acids cross the intestinal lumen into the enterocytes and reform with the enterocytes as chylomicrons
9) 90% of the bile is reabsorbed in the terminal ileum via the Na/bile transporter
10) 5% of the bile excreted in faeces
outline the breakdown of Hb
1) broken into globin and heme
2) the globin is broken into its amino acids and recycled
3) the heme is broken down into iron and unconjugated bilirubin
4) the unconjugated bilirubin is carried in the blood via albumin to the liver
5) glucuronic acid conjugates bilirubin so that it can’t be absorbed by enterocytes
6) in the distal ileum intestinal bacteria turn the conjugated bilirubin into urobilinogen
7)
- 5% taken to liver and incorporated in bile
- 5% taken to kidneys –> yellow urobilinogen (colour of pee)
- 90% excreted in faeces as stercobilin (gives brown colour to poo)
how is cholesterol secreted?
only via the biliary pathway
what is the surface marking of the fundus of the gallbladder?
the tip of the 9th costal cartilage; where the right midclavicular line intersects the right costal margin
what are the 3 surfaces of the hepatocytes? and their functions
canalicular surface –> where bile is secreted
sinusoidal surface –> where the blood runs towards the central hepatic vein
intercellular surface –> between 2 hepatocytes
draw the biliary system from canaliculi to the entrance of bile into the duodenum
1) the canaliculi form the right and left hepatic ducts
2) the right and left hepatic ducts join into the common hepatic duct
3) the common hepatic duct also receives the cystic duct from the gall bladder
4) after the cystic duct the common hepatic duct turns into the bile duct
5) the bile duct travels posterior to the duodenum and the head of the pancreas
6) the bile duct joins with the pancreatic duct to form the hepatopancreatic ampulla
7) the hepatopancreatic ampulla empties its contents into the duodenum through a small opening called the major duodenal papilla
what is the blood supply of the gallbladder
right and left cystic arteries from the right hepatic artery
what are the components of the portal triad
hepatic portal vein
hepatic artery proper
bile duct
what LFTs give an index of liver function
bilirubin
albumin
prothrombin time
what causes jaundice (in terms of what causes the yellow colour)
raised serum bilirubin
what is cholestasis
a condition where the normal flow of bile is obstructed or reduced
explain the different types of jaundice and the type of bilirubin that they present with
pre-hepatic jaundice - due to haemolysis; increased unconjugated bilirubin levels
Hepatic jaundice - impaired liver function; elevated unconjugated and conjugated bilirubin
post-hepatic jaundice - obstruction of bile flow from liver to intestine; accumulation of conjugated bilirubin in the bloodstream
name 2 acuses of prehepatic jaundice
haemolysis and gilbert’s syndrome
pre hepatic vs post hepatic jaundice symptoms (urine, stools, itching, liver tests)
pre-hepatic
urine normal
stools normal
no itching
normal liver tests
post-hepatic
urine dark
stools pale
maybe itching
liver tests abnormal
what type of jaundice is this?
urine dark
stools pale
maybe itching
liver tests abnormal
post-hepatic/hepatic
what is Biliary Colic
A self-limiting pain in the RUQ/epigastrium associated with gallstones
what is Acute Cholecystitis
Acute inflammation of the gallbladder, most commonly caused by gallstones
what is Acute Cholangitis
Infection of the biliary tree, commonly due to an obstructing stone in the common bile duct
what is Choledocholithiasis
Gallstones within the biliary tree
what are risk factors for gall stones
female
age
white caucasian, native americans and hispanic
high cholesterol
Extravascular haemolysis, haemolytic anaemia, sickle cell, hereditary spherocytosis
Liver disease
Rapid weight loss/prolonged fasting
Diabetes
Medications - eg Oestrogen HRT, ceftriaxone, octreotide
Crohn’s disease
Rapid Weight Loss/Prolonged Fasting:
where does pain from gall stones manifest and where can it radiate
right upper quadrant
radiating into right shoulder
What is the commonest serious infection in cirrhosis
Spontaneous bacterial peritonitis
what test do you run in a patient with jaundice
Liver enzymes: AST/ALT
Ultrasound: 90% have dilated intrahepatic bile ducts on ultrasound
if the ducts are dilates you need further imaging: - CT - Magnetic resonance cholangioram MRCP
- Endoscopic retrograde cholangiogram ERCP
what are some factors contributing to gallstone formation?
Increased Ca
Haemolysis
Increased cholesterol
Biliary stasis
Infection
what are the different types of gallstones that you can develop
cholesterol stones –> vast majority of cases
Black pigment stones –> due to too much billirubin
brown pigment stones –> mixed stones
symptoms of biliary colic
Localised RUQ pain
worse after fatty meal
symptoms of acute cholecystitis
RUQ/Epigastric Pain - may radiate to right shoulder if diaphragm is irritated (phrenic nerve)
Fever + rigors
Nausea + Vomiting
RUQ tenderness
Murphy’s Sign positive
Occasionally mildly deranged LFTs - esp. If Mirizzi syndrome
Raised inflammatory markers
Ultrasound can show inflamed gallstones and pericholecystic fluid
what is murphy’s sign
Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand, Murphy’s sign is positive.
symptoms and signs of acute cholangitis
Charcot’s triad:
1. RUQ pain
2. Fever
3. Jaundice
if sepsis is very severe Reynold’s Pentad:
Charcot’s triad + Hypotension + confusion
RUQ tenderness
Raised inflammatory markers
Raised bilirubin, ALT, ALP
Duct dilation on ultrasound
what is the difference in the blood tests between acute cholangitis and acute cholecystitis
in acute cholangitis you will have raised bilirubin, ALT and ALP as the biliary tree is inflamed, whereas in acute cholecystits you do not.
if ultrasound shows acute cholangitis what tests do you order
CT or MRCP
what is pyrexia
fever
what are common drugs which cause drug induced liver injury
32-45% Antibiotics (Augmentin, Flucloxacillin, Erythromycin, Septrin, TB drugs)
15% CNS Drugs (Chlorpromazine, Carbamazepine Valproate, Paroxetine,
5% Immunosupressants
5-17% Analgesics/musculskeletal
(Diclofenac…)
10% Gastrointestinal Drugs (PPIs…)
10% Dietary Supplements
PARACETAMOL
Statins
explain what ALP, ALT, GGT and AST are
these are some of the liver function tests
ALT = alanine aminotransferase –> important in protein breakdown
- more specific for liver than AST
AST - aspartate aminotransferase –> indicates protein metabolism and is not as specific as ALT
ALP - alkaline phosphatase –> enzyme found specifically and bile duct in bone so indicates acute cholangitis
GGT - gamma-glutamyl transferase –> enzyme found in bile duct cells; more specific than ALP
explain paracetamol metabolism
paracetamol is also known as acetaminophen
There are 2 pathways for paracetamol metabolism:
A
most paracetamol is metabolised like this:
1) acetaminophen is conjugated with glucuronic acid
2) acetaminophen more hydrophilic now so easily excreted through urine
B
in case of OD or liver damage paracetamol is metabolised to a toxic compound which can further damage the liver
1) CYP2E1 converts acetaminophen to the intermediate NAPQI
2) NAPQI is toxic and causes hepatocyte damage
what investigations would you do for drug-induced liver disease
LFTs
Viral testing
FBC
CRP
ESR
Drug screens
CT
Social and medical history are very important; any new changes in prescriptions or meds?
how do you manage paracetamol poisoning?
give N acetyl Cysteine
supportive treatment for other complications of the OD:
- coagulation factors
- fluids, electrolytes
- maintain acid-base balance
- check for hypoglycaemia
- check for encephalopathy
what complication would you be worried about in someone with drug-induced liver damage?
renal failure
what is the difference between chronic liver disease and cirrhosis?
Chronic liver disease is progressive liver dysfunction that if treated could still be reversed
cirrhosis is the end result of chronic liver disease which couldn’t be saved –> irreversible remodelling of the liver; irreversible liver damage
what is Alpha-1-Antitrypsin Deficiency
genetic disorder where you don’t produce antitrypsin so you have too much trypsin which just diugests proteins
results in liver and lung damage
what is Wilson’s disease
Wilson’s disease is a rare genetic disorder characterized by the abnormal accumulation of copper in various tissues, particularly the liver, brain, and cornea of the eyes.
what is hereditary haemochromatosis?
Hereditary hemochromatosis is a genetic disorder characterized by the excessive absorption and accumulation of iron in the body.
Uncontrolled intestinal iron absorption with deposition in liver, heart and pancreas
how do you treat hereditary haemochromatosis?
weekly therapeutic phlebotomy –> kind of like dialysis for blood
a certain amount of blood is withdrawn at regular intervals (usually weekly initially) to reduce iron levels.
what is steatosis
excess fat deposition
explain the pathogenesis of ascites
decreased oncotic pressure cuz of no more albumin synthesis
portal vein hypertension
reduced blood flow to kidneys –> triggers RAAS and leads to water retention
inflammation from cirrhosis increases blood vessel permeability
what are the complications of cirrhosis?
Coagulopathy - reducing clotting factor synthesis: evidence of bruising and deranged coagulation tests.
Jaundice - impaired breakdown of bilirubin: yellow appearance of the skin and sclera
Encephalopathy - poor detoxification of harmful substances: confusion
Ascites - poor albumin synthesis and increased portal pressure due to scarring: accumulation of fluid in the abdominal cavity
Gastrointestinal bleeding - increase portal pressure causing varices
what is caput medusae
Distended and engorged superficial epigastric veins around the umbilicus
sign of chronic liver disease and portal hypertension
what is Palmar Erythema
Red discolouration of palms especially over the hypothenar eminence
High oestrogen causes vasodilation
what is Dupuytren’s Contracture
Thickening of the palmar fascia; painless fixed flexion of fingers at the MCP joints (especially ring finger)
what is Leuconychia
Appearance of white lines/dots in nails - sign of hypoalbuminaemia
what is Gynaecomastia
Development of breast tissue in males - reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen
what is Spider Naevi
Dilated capillary with central red papule and fine red lines extending radially - due to excess oestrogen - usually found in the distribution of the superior vena cava
what is the gold standard investigation for chronic liver disease?
liver biopsy
how do you treat ascites?
diuretics - spironolactone ± furosemide
restrict water and sodium
paracentesis + albumin
Trans-jugular intrahepatic portosystemic shunt
how do you treat bleeding
give vit k and fresh frozen plasma
how do you treat hepatic encephalopathy?
lactulose (decreases ammonia), antibiotics, and enemas (stops flora making NH3)
Lactulose is an osmotic laxative which helps reduce ammonia
what is the pathophysiology of alcoholic liver disease
1) Fatty Liver: Accumulation of fat in liver cells (steatosis).
2) Alcoholic Hepatitis: Inflammation of the liver tissue.
3) Alcoholic Cirrhosis: Advanced scarring of the liver tissue; irreversible stage.
what are the risk factors for non-alcoholic fatty liver
obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia. Drugs (NSAIDs, amiodarone)
what is pruritus
itching
Hep A
transmission
prevention
name of virus
type of virus (dna/rna)
symptoms
faeco-oral
pre- and post-exposure immunisation –> Inactivated hepatitis A virus
Picorna virus
RNA
cholestasis (slowing of bile flow through the biliary system)
pruritus
significant jaundice
dark urine and pale stools.
Hep B
transmission
prevention
name of virus
type of virus (dna/rna)
symptoms
blood/sex
pre- and post-exposure immunisation + sexual education and behavioral change (condoms)
Hepadnavirus
DNA
Abdominal pain
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
RUQ pain
Malaise
Myalgia
Hep C
transmission
prevention
name of virus
type of virus (dna/rna)
blood/sex
blood donor screening + condoms
Flavivirus
RNA
Hep D
transmission
prevention
type of virus (dna/rna)
treatment
blood/sex
HBV (Hep B virus) immunisation + Condoms
(Hep D requires Hep B for its replication → you can get Hep B vaccine to prevent Hep D)
RNA
Pegylated interferon alpha
Hep E
transmission
type of virus (dna/rna)
faeco-oral
clean drinking water
RNA
Hep B management
1) Screen for other viral infections (e.g., HIV, hepatitis A, C and D)
2) Referral to gastroenterology, hepatology or infectious diseases
3) Avoid alcohol
4) Education about reducing transmission
5) informing potential at-risk contacts
6) Testing for complications (e.g., for cirrhosis and hepatocellular carcinoma)
7) Antiviral medication can be used to slow the progression of the disease and reduce infectivity
8) Liver transplantation for liver failure (fulminant hepatitis)
why do people with chronic liver diseases have raised levels of estrogen in their body
Estrogen is normally broken down in the liver, and its metabolites are excreted in bile. In liver diseases, this process is compromised, leading to elevated circulating levels of estrogen.
reduced hepatic clearance of androgens leads to peripheral conversion to oestrogen
what symptoms of chronic liver disease are due to raised estrogen in the blood
palmar erythema
gynaecomastia
spider naevi
what can cause C diff diarrhoea and why
antibiotic use –> disrupts the normal balance of the gut microbiota –> opportunity for C. difficile to proliferate and flourish.
what does watery diarrhoea tell you about where the patient has pathology
proximal small bowel problem
what kind of bacteria and viruses cause watery diarrhoea
BACTERIA
vibrio cholerae
E.coli
bacillus cereus (rice)
Clostridium perfringens (meats)
Staph aureus
VIRUSES
rotavirus and norovirus
what foods are clostridium perfringens found in
cooked meats
what does bloody and mucoid diarrhoea tell you about the cause of diarrhoea and the location of the pathology
inflammatory cause - inflammatory bowel disease
problem in colon
possible colon cancer
bacterial infection
what bacteria cause bloody and mucid diarrhoea
shigella
e coli
salmonella
clostridium difficile
campylobacter jejuni
what would you suspect if a patient presented with floating stools
high fat content in stools
malabsorption disease like coeliac or irritable bowel syndrome
what is the most common cause of diarrhoea in the UK
rotavirus/norovirus
what is traveller’s diarrhoea
Occurs within 2 weeks of arrival in new country
3 or more unformed stools per day plus one of the following:
Abdominal pain
Cramps
Nausea
Vomiting
Dysentery
Caused by organisms such as enterotoxigenic e.coli, campylobacter, shigella, non-typhoidal salmonella, viral, protozoal, cholera
what is melaena
dark black, tarry feces that are associated with upper gastrointestinal bleeding
what are the 3 big signs that someone has internal GI bleeding
haematemesis - vomiting blood
melaena - dark tarry stool
coffee ground vomiting - With coffee ground emesis, the blood is not fresh or bright red. By the time your vomiting reflex was triggered, the blood had been in your GI tract long enough to begin to dry, congeal, and turn to a darker color.
what are the 2 medications that you can use for a variceal bleed and why
Antibiotics
- most patients die of sepsis because if they have a cirrhosed liver they are already immunocompromised and GI bacteria can translate to blood and to liver more easily
Terlipressin
- Terlipressin is a synthetic analog of vasopressin (antidiuretic hormone) that is used for its vasoconstrictive effects. When patient has esophageal bleeding you give terlipressin for vasoconstriction and because it will help the kidneys retain more water (avoid hypovolemia from bleed)
what score do you use to decide if you admit someone whom you suspect of a GI bleed?
Glasgow-Blatchford score
with what medications do you treat a non-variceal bleed
Consider proton pump inhibitors.
name 2 conditions which could cause upper GI bleeding
esophageal varices
peptic ulcers
what is an intramural obstruction?
the obstruction of the wall of the bowel –> obstruction is not in lumen, it is in the wall
what is diaphragm disease?
obstruction of the intestinal lumen due to fibrous scarring from NSAIDS
what are the causes of intramural obstructions?
Chron’s disease
diverticulitis
tumours
neural
where do you get diverticulitis
sigmoid colon
what could cause extraluminal obstructions
adhesions
volvulus
tumours; peritoneal deposits
explain the Glasglow-Blatchford score
The Glasgow-Blatchford score is used at the initial presentation in suspected upper GI bleed. It estimates the risk of the patient having an upper GI bleed. A score above 0 indicates a high risk for an upper GI bleed. The NICE guidelines (updated 2016) suggest considering early discharge in patients with a score of 0.
The easiest way to calculate the score is using an online calculator. It takes into account:
Haemoglobin (falls in upper GI bleeding)
Urea (rises in upper GI bleeding)
Systolic blood pressure
Heart rate
Presence of melaena (black, tarry stools)
Syncope (loss of consciousness)
Liver disease
Heart failure
if a patient presents with diarrhoea what red flags would you look out for
Dehydration
Electrolyte imbalance
Renal failure
Immune compromise
Severe abdominal pain
Cancer risk factors
Over 50
Chronic diarrhoea
Weight loss
Blood in stool
how do you manage diarrhoea
fluids
electrolyte monitoring and replacement
antiemetics
antimotility agents - not in inflammatory diarrhoea
DO NOT give broad spectrum antibiotics
what is chron’s disease
A chronic inflammatory disorder affecting any part of the GI tract from the mouth to the anus characterised by patchy, transmural inflammation of intestinal mucosa
(transmural = layers that make up the wall of the intestine)
what are the features of the bowel in chron’s disease
C cobblestone appearance
R rosethorn ulcers
O obstruction
H Hyperplasia of lymph nodes
N narrowing of lumen
S skip lesions
what are possible causes of chron’s disease
genetic
smoking
western diets
antibiotics
contraceptives
where is chron’s most common location
distal ileum
symptoms of chron’s
Diarrhoea
Abdominal pain
Weight loss
Fever
Fatigue
Intestinal complication - due to wall thickening, lumen narrowing and ulceration
signs of chron’s
Pyrexia
Dehydration
Angular stomatitis → inflammation of one or both corners of the mouth
Aphthous ulcers → shallow and painful sores in the mouth
Pallor → pale colour of skin; due to anaemia
Tachycardia
Hypotension
Abdominal pain, mass and distension
name 2 inflammatory bowel diseases
chron’s
ulcerative colitis
what are some complications of chron’s disease
Arthritis → inflammation in crohn’s can extend beyond the gut leading to joint inflammation
Erythema nodosum → painful red nodules under the skin - systemic inflammation
Pyoderma Gangrenosum → rare skin condition characterised by painful, ulcerating skin lesions
Episcleritis, Uveitis, Conjunctivitis – inflammation of the eyes’ episclera and uvea
Aphthous Ulcers
Fatty liver disease → Chronic inflammation associated with Crohn’s disease can contribute to insulin resistance → can lead to increased hepatic lipogenesis, promoting the accumulation of fat in liver cells.
Gallstones and kidney stones → chron’s affects formation of bile acid
Pulmonary disease → also due to systemic inflammation
Venous thrombosis → systemic inflammation triggers clotting cascade more readily
Osteoporosis
B12 deficiency
Anaemia
how do you diagnose chron’s disease
endoscopy + biopsy of inflammation
what investigations would you do in a patient presenting with chron’s like symptoms
FBC
TFT
LFT
U&E
CRP
Faecal Calprotectin - very specific to IBD
Endoscopy + biopsy –> GOLD STANDARD
Colonoscopy
Barium enema
what protein you can measure in blood which indicates IBD
Faecal Calprotectin
what is the gold standard investigation for IBD
ENDOSCOPY + BIOPSY
how do you treat chron’s disease
oral corticosteroids: budesonide and prednisolone
IV hydrocortisone in severe flareups
Anti-TNF antibodies if no improvement: infliximab
immunosuppressants if things get really bad: methotrexate or azathioprine
can surgery cure chron’s disease
no
name an anti-TNF antibodies
Infliximab
name an immunosuppressant
methotrexate
what is the first line of treatment of chron’s disease
oral corticosteroids: BUDESONIDE AND PREDNISOLONE
how do you monitor chron’s disease and why
colonoscopies because of increased risk of colorectal cancer
what is ulcerative colitis
mucosal inflammation affecting the rectum and progressing proximally and continuously through the colon
what is the most common form of IBD
ulcerative colitis
what ethnicity is more predisposed to ulcerative colitis
jewish
what is the effect of smoking on ulcerative colitis
decreases risk
what are risk factors for ulcerative colitis
being jewish
milk consumption
bacterial microflora alteration
NSAIDs
what is a possible cause of ulcerative colitis
Potential abnormal immunological response to normal intestinal microflora
what are proctitis, pancolitis and left-sided disease
these are different presentations of ulcerative colitis
proctitis in inflammation limited to the rectum
left-sided disease is when the inflammation extends from rectum to sigmoid colon (on the left side of the body)
pancolitis is when inflammation extends throughout the entire colon (from rectum to caecum)
presentation of ulcerative colitis (symptoms and signs)
Symptoms
Bloody diarrhoea and rectal bleeding
Acutely unwell - hypovolemic shock
Abdominal pain
Weight loss
Fatigue
Loose stools
Tenesmus (constantly feeling like you need to poop even if your bowel is already empty)
Signs
Febrile
Pale
Dehydrated
Abdominal tenderness
Abdominal distension/mass
Tachycardic, hypotensive
where do you tend to see erythema nodosum
on shins
what is spondyloarthropathy and with what GI condition would you see it
a group of inflammatory rheumatic diseases that primarily affect the joints of the spine (spondylo-) and may involve other joints as well
would expect to see it in severe cases of ulcerative colitis
what is a major complication of ulcerative colitis
toxic megacolon
why is a toxic megacolon very problematic
Thin colon wall can be perforated → release of bowel contents in abdominal cavity and sepsis
Compromised blood flow to surrounding structures and to colon wall
Can cause severe dehydration and electrolyte imbalance
with what scoring system can you assess the severity of UC and what points does it include
TRUELOVE AND WITTS
stool frequency
bleeding
pulse rate
temperature
what investigations would you carry out for UC
Routine bloods - FBC, TFT, LFT, U&E
CRP
Faecal Calprotectin
ENDOSCOPY + BIOPSY
Colonoscopy - asses colon and terminal ileum plus biopsy w/ PPV of 100%
Sigmoidoscopy - alternative test
Take care during acute flares as risk of perforation
Abdominal X-Ray - observe dilatation of bowel and perforations. Dilatation present if (rule of 3s)
Small bowel: diameter > 3cm
Large bowel: diameter > 6cm
Caecum: diameter > 9cm
what parts of the GI wall do ulcerative colitis and chron’s disease affect
UC - mucosa only
Chron’s - transmural (affects multiple layers - mucosa, submucosa, muscularis propria, serosa/adventitia (depending if you are intraperitoneal or retroperitoneal))
which one is intraperitoneal and which one is retroperitoneal: serosa and adventitia
serosa - intra
adventitia - retro
what is diverticulitis
Diverticulitis is a condition characterized by inflammation or infection of small pouches (diverticula) that can develop along the walls of the colon (large intestine). These pouches, known as diverticula, are formed when weak spots in the colon wall give way under pressure, causing the mucosa to protrude through the submucosa and if very severe through the muscularis propria.
if it fully goes through muscularis propria you get peritonitis
what is the difference between diverticulitis and diverticular disease
diverticulitis is infection of diveriticulum where diverticular disease is diverticulum with no infection yet
how do you treat diverticular disease
Increased fibre diet and bulk-forming laxatives eg ispaghula husk
*Avoid stimulant laxative like Senna
surgery if indicated
what segment of the bowel can commonly turn into volvulus
sigmoid colon
how does the epithelium change in GORD
from stratified squamous to columnar
what is the difference between NAFL (non-alcoholic fatty liver) and NASH (non-alcoholic steatohepatitis)
NAFL is just a simple fatty liver whereas NASH involves more liver damage (INFLAMMATION, FAT, HEPATOCELLULAR INJURY, FIBROSIS)
how do you distinguish between NAFL (non-alcoholic fatty liver) and NASH (non-alcoholic steatohepatitis)
biopsy
how do you treat non-alcoholic fatty liver disease
treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL). Medication: pioglitazone, vitamin E, statins, ACEi.
what is terlipressin
a synthetic analog of vasopressin (antidiuretic hormone) that is used for its vasoconstrictive effects. When patient has esophageal bleeding you give terlipressin for vasoconstriction and because it will help the kidneys retain more water (avoid hypovolemia from bleed)
what is a problem with taking too many NSAIDs
NSAID induced gastric ulcer
with what type of patient history would you be concerned about a non-variceal upper GI bleed
NSAIDs, anticoagulation or antiplatelet use
peptic ulcers history
which is more common: small or large bowel obstruction
small
causes of small bowel obstruction
adhesions form previous abdominal, colorectal or pelvic surgeries
hernias
malignancies
chron’s disease
causes of large bowel obstruction
colorectal malignancy - most common
volvulus
how do chron’s and coeliac disease lead to bowel obstruction
formation of strictures –> narrowing of the intestine
explain the pathophysiology of mechanical bowel obstructions
mechanical means due to hernias, adhesions, and malignancies
Obstruction of the bowel 🡪 bowel distension above the block and results in increased fluid secretion into the distended bowel + swallowed air in small bowel
More dilatation 🡪 decreased absorption and mucosal wall oedema
Increased pressure with intramural vessels becoming compressed in distal intestine
Untreated obstruction leads to
Ischaemia
Necrosis
Perforation
symptoms and signs of small bowel obstruction
Pain – initially colicky (starts and stops then diffuse)
Pain is higher in abdomen than in LBO
Vomiting following pain – occurs earlier in SBO compared to LBO
Nausea
Anorexia
Obstipation - constipation with no passage of wind
Increased bowel sounds
Tympanic percussion –> where obstruction is the sound of percussion will be more resonant cuz of trapped air
Tenderness – suggests strangulation
Less distension as compared to LBO (since more distal the obstruction, the greater the distension)
symptoms and signs of large bowel obstruction
Abdominal pain – more constant than in SBO
Vomiting – more faecal like
Acute presentation – on average 5 days of symptoms
Abdominal distension
Palpable mass – hernia, distended bowel loop or caecum
Constipation
Fullness/bloating
why do large bowel obstruction symptoms appear later and more acute than small bowel obstructions
Large bowel has a larger lumen 🡪 the ability of large bowel to distend is much greater 🡪 symptoms present slower and later than in SBO
what investigations do you do for a small bowel obstruction
AXR
CT (abdominal)
FBC
what investigations do you do for a large bowel obstruction
AXR
DRE - Digital rectal exam
FBC
CT/MRI
how do you treat bowel obstructions
Aggressive fluid resuscitation
Bowel decompression
Analgesia and anti-emetic
Antibiotics
Surgery
what do you call constipation without farts
obstipation
what is the difference between primary sclerosing cholangitis and primary biliary cholangitis
PSC affects bile ducts inside and outside the liver
PBC affects bile ducts inside of the liver
PSC also is very common in IFD, whereas PBC is not
to diagnose PSC you need Magnetic resonance cholangiopancreatography (MRCP)
to diagnose PBC you can use blood tests which show elevated ALP
PSC can’t be treated
PBC can be treated
PSC increases your risk of colon cancer
what is a closed loop obstruction
two points of obstruction along the bowel - leading to a middle section sandwiched between two points of obstruction
what is coeliac disease
Autoimmune T cell mediated inflammation of the mucosa of the small bowel, and malabsorption, following exposure to gluten
what are risk factors for coeliac disease
other autoimmune conditions
IgA deficiency
familial link
what type of hypersensitivity is coeliac disease
type 4
explain the pathophysiology of coeliac disease
Gluten breaks down to gliadin which triggers the immune system to produce IgA autoantibodies such as anti-tissue transglutaminase (anti-tTG), and anti-endomysial (anti-EMA) which target the epithelial cells of the small bowel causing villous atrophy, crypt hyperplasia, intraepithelial lymphocytes.
villous atrophy leads to malabsorption
where is iron absorbed in the GI
duodenum and jejunum
what are the symptoms of someone with coeliac disease
anaemia –> malabsorption of Fe, B12, Folate
steatorrhea and diarrhoea
dermatitis herpetiformis
abdominal pain
fatigue and weakness
what are signs of coeliac disease
Angular stomatitis, mouth ulcers, weight loss, failure to thrive (in children), osteopenia (Ca2+ and Vit D malabsorption), bloating
what is the 1st line investigation for coeliac disease
Raised anti-tissue transglutaminase tTG antibodies
raised anti-endomysial EMA antibodies
Total IgA antibodies raised –> possible false negative for coeliac in IgA deficient patients as IgA will come back low)
what is the gold standard investigation for coeliac disease
Endoscopy and duodenal biopsy (villous atrophy, crypt hyperplasia, intraepithelial lymphocytes)
what are the 3 structural changes to the bowel in coeliac disease
villous atrophy
crypt hyperplasia
intraepithelial lymphocytes
if a patient is diagnosed with coeliac what further tests would you do to monitor the condition. what other things would you be interested in
FBC –> Hb, iron, B12, folate
DEXA bine scan
genetic testing
DDx for coeliac disease
IBD, IBS, lactose intolerance. Tropical sprue (chronic inflammation of bowel associated with travel. Jejunal biopsy = incomplete villous atrophy vs coeliac with complete atrophy)
management of coeliac disease
gluten free diet
replace vitamin deficiencies
complications of coeliac disease
Osteopenia, anaemia, malignancy (T cell lymphoma, NHL), vitamin deficiency
define gastritis
Inflammation of the stomach mucosal lining
causes of gastritis
autoimmune
alcohol
H. Pylori
bacterial reflux
NSAIDs
stress
how does alcohol lead to gastritis
Alcohol increases gastric acid and irritates stomach.
how do NSAIDS lead to gastritis
NSAIDs inhibit COX which inhibits prostaglandin synthesis which decreases mucus protective barrier production.
explain the physiology of autoimmune gastritis
Autoimmune gastritis attacks parietal cells and forms intrinsic factor antibodies which reduces B12 absorption.
symptoms of gastritis
Epigastric pain, nausea and vomiting, dyspepsia (indigestion), anorexia/loss of appetite
what is dyspepsia
indigestion
what are the 1st line and the gold standard investigation for coeliac disease
1st line –> helicobacter pylori urea breath test + H. Pylori stool antigen test
gold standard –> endoscopy and biopsy
how do you manage gastric ulcers caused by H. pylori
triple therapy: PPI + 2 antibiotics for 7 days
PPI: omeprazole
antibiotics: amoxicillin 1g, clarithromycin 500mg. if penicillin allergy, swap amoxicillin for 400mg metronidazole
how do you treat gastritis caused by NSAIDs or alcohol
you stop consuming NSAID or alcohol
PPI
how do you treat autoimmune gastritis
PPI
IM vit B12
what are complications of gastritis
Peptic ulcers
Achlorhydria → low HCl in stomach
bleeding and anaemia
MALT lymphoma → Non-Hodgkin Mucosa-Associated Lymphoid Tissue Lymphoma
gastric cancer
define peptic ulcers
A break in the mucosal lining of the stomach or duodenum forming ulcers. 2 types: duodenal (most common) and gastric
where is peptic ulcers most common in the GI
duodenum
what are causes of peptic ulcers
H. Pylori, NSAIDS
Zollinger Ellison syndrome → a condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas causes overproduction of gastric acid
what is the physiology of peptic ulcers
NSAIDS and H. Pylori break down the gastric mucus barrier
gastric acid then forms an ulceration in the lining
what drinks increase stomach acid
alcohol and caffein
in what area of the stomach is gastric ulcers more common
lesser curvature of antrum
what are the symptoms of peptic ulcers
epigastric pain
dyspepsia
nausea
vomiting
haematemesis (if artery is perforated)
melanea
weight loss
1st line investigation for peptic ulcers
H. Pylori urea breath test or stool antigen test, FBC (anaemia or high platelet count)
gold standard investigations for peptic ulcers
Endoscopy and biopsy (if red flags) – presence of ulcer
DDx of peptic ulcers
Oesophageal cancer, gastric cancer, GORD, biliary colic
treatment for peptic ulcers
stop NSAIDS/alcohol
triple therapy for H pylori
omeprazole (PPI) + 2 antibiotics (amoxicillin/metronidazole + clarithromycin)
complications of peptic ulcers
Bleeding, perforation, gastric outflow obstruction, malignancy
what is dysphagia
swallowing difficulties
what is Plummer-Vinson syndrome?
syndrome which causes oesophageal webs, dysphagia, glossitis, iron deficiency anaemia
usually associated with precancerous oesophagus
what are the types of oesophageal cancer and what portion of the GI do they affect
squamous cell carcinoma –> upper 2/3 of oesophagus
adenocarcinoma –> lower 1/3 of oesophagus
what are causes of squamous cell carcinoma oesophageal cancer
smoking
alcohol
achalasia
hot foods and beverages
plummer-vinson syndrome
black and asian minority ethnicity
what are causes of adenocarcinomas
barret s oesophagus
GORD
obesity
smoking
hernias
older age
male
caucasian
what are the symptoms of oesophageal cancer
progressive dysphagia –> KEY PRESENTATION
vomiting
weight loss
anorexia
lymphadenopathy
what are the signs of oesophageal cancer
hoarse voice
odynophagia
cough
melaena
heartburn
A patient presents with red flags indicating possible oesophageal, gastric or bowel cancer. What are the red flags and how would you proceed?
red flags are anaemia, loss of weight, anorexia, melanea, haematemesis, dysphagia and recent progressive symptoms.
urgent 2 week endoscopy referral
what is the 1st line and gold standard investigation for oesophageal cancer
Oesophagogastroduodenoscopy and biopsy (w/ barium swallow)
CT/MRI of chest/abdomen (metastases and staging)
what is achalasia
muscles of oesophageal tube which are right above the stomach are unable to relax; makes swallowing both liquids and solids difficult
DDx for oesophageal cancer
Achalasia (not progressive dysphagia – difficulty swallowing both solids and liquids), oesophageal strictures, Barrett’s oesophagus
what is the difference between achalasia and oesophageal strictures
In achalasia, dysphagia usually occurs with both solid and liquid food, whereas in esophageal strictures, dysphagia typically occurs only with solid food and not liquids, until very late in the progression of the stricture.
achalasia is a problem with the functioning of the oesophagus
strictures are a problem with the structure of the oesophagus
how do you treat oesophageal cancer
surgical resection with adjuvant radiotherapy/chemotherapy.
Palliative care
what is the most common benign oesophageal tumour
Leiomyomas = smooth muscle tumours in oesophageal wall
They are slow growing and usually asymptomatic. Generally found by mistake in barium swallow
what is the most common type of bowel cancer
colorectal cancer
what are the causes of colorectal cancer
IBD
sporadic mutations
Hereditary:
- Familial adenomatous polyposis
- Hereditary nonpolyposis colorectal cancer
what is Familial adenomatous polyposis
Familial adenomatous polyposis (FAP). Mutation in APC tumour suppressor gene causing high polyp formation → potential of cancer before age 40
what is hereditary nonpolyposis colorectal cancer
hereditary nonpolyposis colorectal cancer. Mutation in DNA mismatch repair genes (genese which should identify mistakes in DNA and fix them)
what are risk factors of colorectal cancer
Family history
IBD - especially UC
Age
Diet - high in red/processed meat, low in fibre
Obesity and sedentary lifestyle
Smoking
Alcohol
Low fibre diet (butyrate)
Genetics
Diabetes mellitus
what type of cancer are most colorectal cancers (histology point of view)
adenocarcinomas
what are the most common sites of metastasis of colorectal cancer
liver and lungs
right sided vs left sided carcinoma in colorectal cancer
RIGHT:
- from appendix and caecum to the first 2/3 of the transverse colon
- usually asymptomatic until patient presents with iron deficiency anaemia from bleeding
- weight loss
- abdominal pain
LEFT:
- from last 1/3 of colon to anus
- blood and mucus in stools
- diarrhoea alternating with constipation
- tenesmus –> specific for rectal carcinoma
- thinner stools –> spoecific for rectal carcinoma
what are the indicators of metastases in colorectal cancer
hepatomegaly
jaundice
lymphadenopathy
what is the criteria for referring someone with suspected rectal cancer
over 40yr + abdominal pain + unexplained weight loss
over 50yr + unexplained rectal bleeding
over 60yr + change in bowel habit/iron deficiency anaemia
what is the first line investigation for bowel cancer
Faecal Immunohistochemical Tests (FIT)
digital rectal exam
double contrast barium enema
what is the gold standard investigation for bowel cancer
colonoscopy and biopsy
DDx of colorectal cancer
IBS, IBD, haemorrhoids, anal fissure, anal prolaose, diverticulitis
what is the 1st line treatment for colorectal cancer
surgical resection depending on affected area, chemotherapy (fluorouracil), radiotherapy
what does bowel cancer screening consist of and how often is it done
offer screening every 2 years between the ages of 60 and 74. We are gradually extending this age range, and people aged 56 are now being invited as part of this proces
home testing kit –> faecal immunohistochemical test (FIT)
how do you stage any type of cancer
CT chest abdomen and pelvis –> look at metastasis and spread for staging
how do you stage colon cancer
Duke stage
explain duke staging
used for colon cancer
A – cancer only in mucosa
95% 5 year survival
B - cancer has gone through muscularis
75% 5 year survival
C - spread to regional lymoh nodes
35% 5 year survival
D - distal lymph node involvement and metastasis
25% 5 year survival
what are the different types of gastric cancer
type 1 –> intestinal metaplasia/differentiated
type 2 –> diffuse/undifferentiated; signet ring cells
in what ethnicities is gastric cancer most prevalent
east asian and eastern europe
what are causes of gastric cancer
H. Pylori, smoking, pernicious anaemia (chronic gastritis), mutations
which type of gastritis is the most common
type 1
type 1 vs type 2 gastritis
type 1: intestinal; gland forming cells; differentiated
type 2: diffuse; poorly differentiated cells, signet ring cells, linitis plastica (leather bottle appearance with thickened gastric wall)
what is the appearance of type 2 gastritis ( i want the medical term)
linitis plastica (leather bottle appearance with thickened gastric wall)
risk factors for gastric cancer
Intestinal: male, older age, H. Pylori, chronic/atrophic gastritis
Diffuse: female, younger age (<50), blood type A, genetic, H. Pylori
what are the key presentations and symptoms of gastric cancer
Virchow’s node
sister mary joseph node
Severe epigastric pain
dysphagia
Metastatic signs –>
jaundice → indicates liver mets
Krukenberg tumour → ovaries
Weight loss, vomiting, anorexia, epigastric pain, tired all the time
what are the signs of gastric cancer
Dysphagia, melaena/haematemesis, anaemia
investigations for gastritis
Gastroscopy with biopsy →2-week endoscopy referral if dysphagia or age>55 with upper abdo pain, reflux or dyspepsia
Endoscopy ultrasound → shows depth of tumour invasion and nodal involvement
CT/MRI of the chest and abdomen (Tumour Node staging and metastases)
FBC (normal or anaemia)
DDx of gastic cancer
Peptic ulcer disease, achalasia, oesophageal stricture
what is the 1st line management for gastric cancer
surgical resection (total or sub-total gastrectomy) + adjuvant radiotherapy/chemotherapy (fluorouracil/cisplatin)
which type of gastric cancer has worse prognosis
type 2
explain the TNM staging
colorectal cancer staging
Looks at:
T → tumour size and extent
T1: Tumor in submucosa.
T2: Tumor in muscularis propria (muscle layer).
T3: Tumor in the serosa (outermost layer).
T4: Tumor in adjacent structures
N → involvement of nearby lymph nodes
N0: No regional lymph node involvement.
N1: Involvement of 1-3 regional lymph nodes.
N2: Involvement of 4 or more regional lymph nodes
M→ presence or absence of distant metastasis
M0: No distant metastasis.
M1: Distant metastasis present
Prognosis after surgery
R0 (Complete Resection): the entire tumor was successfully removed
R1 (Microscopic Involvement): there is microscopic tumour left on the surgical margin
R2 (Macroscopic Involvement): there is macroscopic (visible) tumour left on the surgical margin
define chronic pancreatitis
Persistent chronic inflammation of the pancreas resulting in irreversible fibrosis and reduced function of the pancreas
causes of chronic pancreatitis
Alcohol consumption
Progression from acute pancreatitis
Trauma
Chronic kidney disease
Cystic fibrosis
Pancreatic cancer
Hypertriglyceridemia
risk factors of chronic pancreatitis
Alcohol, smoking, coeliac disease
pathophysiology of chronic pancreatitis
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.
what are the key presentations of chronic pancreatitis
Severe pain in epigastric region which can radiate to back
Jaundice
loss of exocrine function (no pancreatic enzymes secreted in GI tract, especially lipase) → steatorrhea
loss of endocrine function (lack of insulin causing diabetes)
signs of malabsorption
what vitamins are you most likely to be deficient of in chronic pancreatitis
Fat soluble vitamin deficiency → ADEK
what are the 1st line investigations for chronic pancreatitis
Faecal-elastase 1 → enzyme involved in fat digestion (low)
faecal fat (high)
pancreatic function tests (decreased function) → A combination of tests including amylase, lipase, glucose, and other markers to assess overall pancreatic function.
Secretin-Stimulated Pancreatic Function Test: Measures pancreatic secretion in response to the hormone secretin, helping evaluate overall pancreatic function.
ERCP for visualisation of ducts
what is the gold standard investigation for chronic pancreatitis
X-ray/CT/MRI scan shows calcification of pancreas and dilated ducts
causes of acute pancreatitis
I GET SMASHED:
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs (diuretics)
management of chronic pancreatitis
1st line – control pain (analgesia, NSAIDs) and risk factors (less alcohol, less smoking, obesity)
Replace pancreatic enzymes in deficiency (lipase), vitamin supplements. Insulin for diabetes. ECRP with stenting. Surgery to drain bile ducts
what are the 3 most common causes of acute pancreatitis
gallstones, alcohol, post-ERCP
explain the physiology of autoimmune pancreatitis
pancreas releases exocrine enzymes which auto digest the pancreas.
key presentations of acute pancreatitis
Severe epigastric pain radiating to the back
Vomiting
abdominal tenderness
Hypocalcaemia → The activated lipase, in particular, breaks down triglycerides (fats) into free fatty acids. These free fatty acids, in turn, bind to calcium ions in the bloodstream to form calcium soaps → less available free calcium in the blood
do you get abdominal tenderness in chronic pancreatitis
no
what are the signs of acute pancreatitis
jaundice
tachycardia
Chvostek sign
grey turner (flank bruising)
Cullen sign (periumbilical bruising)
signs of hypovolemia
pleural effusion
cullen’s sign vs grey turner
cullen –> periumbilical bruising
grey turner –> flank bruising
symptoms of acute pancreatitis
Dyspnoea, fever, nausea and vomiting, epigastric pain radiating to back
1st line investigations for acute pancreatitis
Serum amylase raised (3 times the upper limit level)
FBC: leucocytosis (increase WBC count) with left shift (increase in immature WBCs)
raised haematocrit → dehydration from vomiting (decreased plasma so more blood cells to plasma ratio)
raised CRP
Raised urea → kidney dysfunction, a potential complication of severe acute pancreatitis.
low calcium
Imaging: chest x-ray, abdominal USS (gallstones), CT scan (inflammation, necrosis, effusions)
how do you establish diagnosis of acute pancreatitis
Diagnosis needs 2 of 3: acute abdominal pain, elevated pancreatic enzymes (amylase/lipase), abnormal imaging
what is the gold standard investigation for acute pancreatitis
Serum lipase raised (3 times the upper limit level)
how do you score the severity of pancreatitis. detail
Glasgow score (severity of pancreatitis):
PANCREAS mnemonic
PaO2 low
Age >55
Neutrophils raised
Calcium low
uRea raised
Enzymes raised
Albumin low
Sugar raised
DDx for acute pancreatitis
Abdominal aortic aneurysm, peptic ulcer disease, cholangitis, oesophageal spasm
treatment for acute pancreatitis
1st line –> IV fluids, analgesia, nil by mouth, oxygen, antibiotics, electrolyte replacement.
ERCP for gallstones, treat complications
complications of acute pancreatitis
Acute Respiratory Distress Syndrome – leading cause of death
Sepsis
Pancreatic pseudocyst
Hypovolaemic shock from ruptured vessels
DIC → coagulation factors released as inflammatory response → thrombosis
Renal failure
what is IBS
Functional bowel disorder characterised by recurrent bouts of abdomen pain and abnormal bowel motility. No organic cause
epidemiology of IBS
More females, younger people
what is the cause of IBS
there is no cause
what are the risk factors for IBS
GI infections, previous severe and long-term diarrhoea, psychological (anxiety, depression, stress, trauma, abuse), eating disorders
what are the 3 types of IBS
IBS-C (constipation), IBS-D (diarrhoea), IBS-M (mixed, both D + C)
what are the key presentations of IBS
Abdominal pain, abnormal bowel motility, bloating, pain relieved by defaecation, altered stool form (diarrhoea, constipation), worse after eating, urgency, passage of mucus with stool
how do you diagnose IBS
BY EXCLUSION
Clinical diagnosis requires:
a)abdominal pain + 2 of:
- relieved by defaecation
- altered stool form
- altered bowel frequency.
b) exclusion of:
- infection (normal FBC, ESR/CRP)
- IFD (Negative faecal calprotectin)
- coeliac disease (no anti-TTG or anti-EMA)
- Exclude cancer
treatment of IBS
1) Conservative: education, diet modification (small regular meals, increase fluids, avoid caffeine, low FODMAP diet, increase/decrease fibre for constipation/diarrhoea.
FODMAP diet → a dietary approach designed to manage symptoms of IBS
2) Laxatives for constipation (senna, macrogol)
Loperamide for diarrhoea
Antispasmodics (buscopan, mebeverine) for pain and bloating
3) Severe IBS: tricyclic antidepressants (amitriptyline). Or SSRIs if they don’t work. Consider CBT
FODMAPs = Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols → these are carbohydrates that can ferment in the gut and cause symptoms such as bloating, gas, abdominal pain, and altered bowel habits in some individuals.
The low FODMAP diet involves restricting high-FODMAP foods for a specified period, followed by a structured reintroduction phase to identify specific triggers. Once trigger foods are identified, the diet can be personalized to include well-tolerated FODMAPs and avoid problematic ones.
what is charcot’s triad
key signs of acute cholangitis
RUQ pain
Jaundice
Fever
what is Reynold’s pentad
key signs of very severe sepsis from acute cholangitis
RUQ pain
Jaundice
Fever
Confusion
hypotension
what type of carcinoma are most pancreatic cancers
Majority are adenocarcinoma of exocrine pancreas of ductal origin.
where are the majority of the pancreatic adenocarcinomas located in the pancreas
head of the pancreas or neck
what are risk factors to pancreatic cancer
Smoking, alcohol, diabetes, chronic pancreatitis, family history
key presentations of pancreatic cancer
Courvoisier sign = painless palpable gallbladder and jaundice → suggests that the jaundice is not due to gallstone but to obstruction
pale stool and dark urine → high bilirubin that can’t be eliminated in poo
Pruritis = itching to the elevated bilirubin in the blood
Weight loss.
Trousseau sign of malignancy = blood clots felt as small lumps under skin → indicates a hypercoagulable state which is often seen in malignancies
what is trousseau’s sign of malignancy
blood clots felt as small lumps under skin → indicates a hypercoagulable state which is often seen in malignancies
what is courvoiser’s sign
sign of pancreatic cancer
painless palpable gallbladder and jaundice → suggests that the jaundice is not due to gallstone but to obstruction
what are the 1st line and gold standard investigations for pancreatic cancer
1st line: Abdominal ultrasound + Pancreatic CT protocol (pancreatic mass)
gold standard: biopsy
what is the management of pancreatic cancer?
1st line – surgical resection (Whipple)
Palliative therapy
what is GORD and what is the pathophysiology
Reflux of gastric contents into the stomach due to reduced pressure across the lower oesophageal sphincter causing inflammation of the oesophagus
Decreased pressure across lower oesophageal sphincter makes it easier for gastric contents and acid to pass up into the oesophagus
causes of GORD
Obesity, pregnancy, hiatal hernia, smoking, NSAIDs, caffeine, alcohol
key presentations of GORD
Heartburn
epigastric or retrosternal pain
acid regurgitation (worse when lying down, related to meals, relieved by antacids)
Dysphagia
dyspepsia (indigestion)
chronic cough, nocturnal asthma, laryngitis, dental erosion
what are the red flags for GORD
dysphagia
age >55
weight loss
upper abdominal pain/reflux
treatment-resistant dyspepsia
nausea and vomiting
low haemoglobin
raised platelet count
1st line treatment of GORD
go straight to PPI if no red flags
if there are red flags: ENDOSCOPY
what is the gold standard treatment for GORD
24-hour pH ambulatory monitor (pH <4 more than 4% of the time = abnormal)
what test can you do to assess the functioning of the oesophagal sphincter and the oesophagal muscles?
oesophageal manometry –> catheter passed into the oesophagus and detects oesophageal and sphincter contractions
management of GORD
- Conservative – stop smoking, stop alcohol, lose weight, eat smaller meals, avoid eating 3-4 hours before sleep, change sleeping position (more upright)
- Medical – proton pump inhibitor (omeprazole, lansoprazole), H2 receptor antagonist (antihistamine which reduces stomach acid, e.g., ranitidine). Over-the-counter alginates (Gaviscon) for symptom relief
- Surgery – Nissen fundoplication (tying the fundus of the stomach around the LOS to narrow it)
what can Barret’s oesophagus lead to
oesophageal adenocarcinoma
what is a Mallory Weiss tear?
Tear of the oesophageal mucosal membrane due to sudden increases in intra-abdominal pressure
what are risk factors to mallory weiss tear
Forceful vomiting (alcoholism, bulimia), chronic coughing, weightlifting, hiatal hernia, retching
key presentations of mallory wiess tear
Haematemesis after retching Hx, melaena, hypovolemic shock (hypotension, dizziness), dysphagia. No Hx of liver disease or portal hypertension
where is McBurney’s point?
2/3 of the distance between the umbilicus and the ASIS
what are the causes of appendicitis and explain the pathophysiology
most commonly due to obstruction of the lumen of the appendix by FAECOLITH (calcified faecal deposits), or infection and inflammation of the lymphoid tissue (LYMPHOID HYPERPLASIA, IBD)
it can also be due to foreign bodies
PATHOPHYSIO: Obstruction of the lumen of the appendix leads to stasis > bacterial overgrowth > inflammation. Obstruction leads to increased pressure in the appendix which can cause rupture.
what are the physical exams for appendicitis
Rovsing’s Sign: palpation (pressing down) on the left lower quadrant of the abdomen causes pain in the right lower quadrant.
Psoas Sign: Pain in the right lower quadrant is elicited when the patient extends the right hip against resistance or when the right hip is passively extended → The psoas is right next to the appendix
Obturator Sign: Pain in the right lower quadrant is felt when the right hip is flexed and internally rotated. → the obturator is right next to the appendix
Guarding: Involuntary tensing or contraction of the abdominal muscles in response to palpation or movement.
Rebound Tenderness: Pain is experienced when pressure is released after palpating the abdomen → suggests peritoneal inflammation
what is Rovsing’s sign
sign of appendicitis
palpation (pressing down) on the left lower quadrant of the abdomen causes pain in the right lower quadrant.
what is the gold standard investigation for appendicitis?
Abdominal CT with contrast
how do you manage appendicitis?
antibiotics and laparoscopic appendectomy
what is normal portal venous pressure
5-10mmHg
what cells play a role in the fibrosis and scarring of the liver
hepatic stellate cells
what are the 3 types of portal venous hypertension, give examples
Pre-hepatic: portal vein obstruction (thrombus)
Intrahepatic: cirrhosis, sarcoidosis, schistosomiasis
Post-hepatic: right heart failure, constrictive pericarditis, Budd Chiari syndrome (hepatic vein obstruction)
what is schistosomiasis
freshwater parasite which affects liver, urinary bladder, intestines etc.
what is sarcoidosis
multisystem inflammatory disorder characterised by the formation of granulomas
how does portal hypertension lead to hepatic encephalopathy
Venous blood accumulates in the portal system, raising pressure above 5-10mmHg.
This leads to the formation of portosystemic shunts where blood is directed away from the portal system and into systemic veins → liver receives less blood → reduced liver function (increased toxic products in the blood like ammonia which can cross BBB and cause hepatic encephalopathy).
name 2 portosystemic shunts in portal hypertension
oesophageal veins –> oesophageal varices
paraumbilical veins
key presentations of portal hypertension
Ascites
caput medusae → paraumbilical veins close when you are born and turn into ligaments but in the presence of portal hypertension they may reopen to offer an alternative pathway to bypass the liver
GI bleeding from esophageal varices
Haemoptysis
melaena/hematochezia (passage of bright red blood through the rectum)
Jaundice
Pruritus
hepatic encephalopathy (asterixis, altered consciousness, lethargy, seizure, coma)
Gynecomastia
Palmar erythema
Spider naevi
Splenomegaly
1st line and gold standard investigation for portal hypertension
1st line
Liver USS (nodules = cirrhosis), CT/MRI scan (ascites, cirrhosis, splenomegaly), endoscopy (oesophageal varices). Labs (FBC, LFT, serology may identify cause)
gold standard
Hepatic venous pressure gradient measurement (difference in pressure between IVC and portal vein)
how can you treat ascites invasively
paracentesis
management of portal hypertension
Treat underlying disease → lifestyle modifications
Beta blockers → to reduce portal pressure; they reduce HR so they reduce CO and the consequential pressure on the venous system
Management of esophageal varices: sclerotherapy or endoscopic variceal ligation
Diuretics
Management of hepatic encephalopathy (lactulose, enemas, antibiotics)
Transjugular intrahepatic portosystemic shunt
complications of portal hypertension
Hepatic encephalopathy, spontaneous bacterial peritonitis, Ascites, bleeding (oesophageal varices), caput medusae, diminished liver function, enlarged spleen
what is the marker for hepatocellular carcinoma
Alpha-fetoprotein → marker for liver cancer
causes of ascites
Cirrhosis, congestive heart failure, peritonitis, malignancy, nephrotic syndrome
pathophysiology of ascites
Excessive build-up of fluid in the peritoneal cavity. Poor liver function = low albumin = low blood oncotic pressure = fluid loss into the peritoneal cavity
key presentations of ascites
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
1st line investigations for ascites and gold standard
1st line
Shifting dullness on examination.
WBC count
Ascites tap: abdominal paracentesis → for protein measurement
gold standard
Abdominal ultrasound (fluid in peritoneal cavity)
explain why you do an ascites tap in ascites and what information this gives you
Ascites tap: abdominal paracentesis → for protein measurement
If Protein <25g/dL:
Indicates a low protein concentration in the ascitic fluid.
Typically associated with transudative ascites.
Implies that there is not enough protein being synthesized by the liver.
Possible causes: cirrhosis and heart failure
If Protein >25g/dL:
Indicates a higher protein concentration in the ascitic fluid.
Typically associated with exudative ascites.
Suggests that proteins, including inflammatory markers, have leaked from blood vessels into the peritoneal cavity due to increased permeability.
Possible causes: nephrotic syndrome
Peritonitis
Malignancy
TB
what is the difference between transudate and exudate
transudate is due to decreased oncotic pressure or increased hydrostatic pressure and results in plasma leaking in body cavities –> associated with portal hypertension, hypoalbuminea, heart failure
exudate is due to inflammation which causes leaky capillaries so you get fluid full of proteins and vessel contents in body cavities –> associated with infections, cancers, inflammation, autoimmune conditions
management of ascites
Management of Ascites
Fluid and salt restriction
Diuretics: spironolactone ± furosemide (can be given together because spironolactone causes hyperkalemia and furosemide causes hypokalemia → they cancel each other out)
Large-volume paracentesis
Albumin
Trans-jugular intrahepatic portosystemic shunt
what is a major complication of ascites
spontaneous bacterial peritonitis
what is a major cause of acute liver failure in the UK and how do you treat it
paracetamol OD
N-acetylcysteine
causes of chronic/acute liver disease, including metabolic and vascular causes
Acute liver disease is most common cause
Non-alcoholic fatty liver disease.
Drugs: paracetamol, alcohol.
Viral infection: hepatitis, Epstein Barr virus.
Autoimmune hepatitis.
Neoplastic: hepatocellular or metastatic carcinoma.
Metabolic: Wilson’s disease, alpha 1 antitrypsin, haemochromatosis, NAFL.
Vascular:
Budd-Chiari syndrome → blockage of hepatic vein by a thrombus (hepatic vein thrombosis) which leads to liver congestion
Congestive hepatopathy → Liver damage resulting from congestive heart failure
risk factors for acute liver injury
Chronic alcohol abuse, female, chronic hepatitis
risk factors for chronic liver injury
Alcohol, obesity, T2DM, drugs, metabolic disease
pathogenesis of ascites
decreased synthesis of albumin → lower oncotic pressure
Portal hypertension → triggers vasodilation of splanchnic circulation (intestinal circulation) to redistribute blood away from liver → more fluid in abdominal vessels coupled with decreased oncotic pressure from decreased albumin
Reduced blood flow to kidneys → activated RAAS → water retention
Generalised inflammation increases blood vessel permeability
compensated vs decompensated liver disease
compensated, with some preserved liver function → asymptomatic
decompensated which causes end-stage liver failure. → patient gets COAGULOPATHY, JAUNDICE, ENCEPHALOPATHY, ASCITES, UPPER GI BLEEDING
the 5 signs of decompensated liver disease
COAGULOPATHY, JAUNDICE, ENCEPHALOPATHY, ASCITES, UPPER GI BLEEDING
key presentations of liver disease
Jaundice
Ascites → due to less albumin synthesis
abnormal bleeding
hepatic encephalopathy (confusion, altered mood, asterixis (liver flap), comatose)
low serum albumin
Hepatomegaly
the 3 stages of chronic liver disease
Inflammation
Fibrosis → reversible damage
Cirrhosis → irreversible damage
signs and symptoms of chronic liver disease
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) → presence of certain sulfur-containing compounds that are produced in the intestines by bacteria due to impaired liver function; bacteria have to take over metabolism of ammonia
Dupuytren’s contracture
Malaise
Nausea
Vomiting
abdominal pain
Pruritis
bleeding
1st line investigations for chronic and acute liver disease
LFTs (all raised):
Bilirubin
PT/INR
serum AST + ALT
AST/ALT Ratio
AST/Platelet Ratio
NH3 → liver should convert NH3 to urea
GGT all raised → enzyme in liver and bile duct (inidcates inflammation of liver and bile)
Serum albumin and glucose decreased.
FBC:
Anaemia
Thrombocytopenia → liver helps make thrombopoietin
leukopenia
U&E:
urea and creatinine raised → severe liver injury can impair blood flow to kidneys
deranged electrolytes
Bilirubin - hyperbilirubinemia in decompensated cirrhosis
what is the most specific lab finding for diagnosing liver cirrhosis in chronic liver disease
thrombocytopenia
acute and chronic liver injury gold standard investigations
Liver biopsy (distortion of liver parenchyma)
what additional tests would you order for acute liver injury if you are worried about a drug OD or an infection
blood cultures
toxicology screen
management of chronic liver injury
1st line – prevent progression, lifestyle monitoring (less alcohol, reduce BMI)
Antiviral therapy in viral hepatitis
liver transplant (MELD score – model for end-stage liver disease. Assesses severity and transplant likelihood
Manage complications:
hepatic encephalopathy –> lactulose
ascites –> diuretics
bleeding –> vit K
cerebral oedema –> mannitol
Hyperglycaemia –> dextrose
how do you treat hyperglycaemia in chronic liver disease
dextrose + possible diabetes management
how do you treat cerebral oedema
mannitol
complications of chronic/acute liver disease
Malnutrition - increased use of muscle tissue as fuel (impaired glycogen storage and gluconeogenesis) + reduced protein available (form impaired liver metabolism)
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma
Hyponatraemia
Cerebral oedema → mannitol
AKI → acute kidney injury
Acute-on-chronic liver failure
Coagulopathy (Vit K def)
how do you manage acute liver disease
1st line – intensive care management, ABCDE, fluids analgesia. Assessment for liver transplant.
Treat underlying causes and complications, e.g., paracetamol overdose with N-acetylcysteine
what score is used to asses suitability for liver transplant in patients with chronic or acute liver disease
UKELD
how do you manage coagulopathy due to chronic or acute liver disease
Vit K + FFP (fresh frozen plasma)
what are the most common causes of liver cirrhosis
Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C
what is the gold standard investigation for liver cirrhosis
liver biopsy
what is the score which assesses the severity and prognosis of cirrhosis and what does it take in to account
Child-Pugh score
Involves - bilirubin, albumin, INR, ascites, encephalopathy.
what is the MELD score
MELD score: model for end-stage liver disease. Gives 3 month mortality estimate and liver transplant advice
explain why liver patients are immuno-compromised
Pathogens enters body via GI → liver is first filter to infections → needs a lot of leukocytes so that it can eliminate the pathogens effectively
liver patients have an impaired reticulo-endothelial function and reduced opsonic activity and leucocyte function
what is autoimmune liver disease
Chronic inflammatory liver disorder which causes a chronic relapsing hepatitis
what are the autoimmune liver diseases
PBC, PSC, Autoimmune hepatitis
risk factors for autoimmune hepatitis
Female, genetic predisposition, immune dysfunction, other autoimmune conditions, HLA loci → HLA-DR3/DR4
what are the different types of autoimmune hepatitis
Type 1: occurs in adults, typically women.
Type 2: occurs in children.
what are the autoantibodies formed in type 1 autoimmune hepatitis
Anti-nuclear antibodies → Antibodies targeted against nuclear proteins and/or DNA
anti-smooth muscle antibodies → Antibodies targeted against actin, tubulin and other proteins
anti-soluble liver antigen
what are the autoantibodies formed in type 2 autoimmune hepatitis
Anti-liver kidney microsomes-1. → Antibodies targeted against subcellular vesicles that are derived from the endoplasmic reticulum (ER). They contain various enzymes involved in drug metabolism and detoxification, particularly the cytochrome P450 enzymes.
Anti-liver cytosol antigen type-1.
key presentations in autoimmune hepatitis
25% asymptomatic
the rest present with either acute hepatitis or chronic liver disease
rarely they can present directly with acute liver failure
acute hep presentation:
Jaundice
RUQ pain
Hepatomegaly
Malaise
fatigue
fever
chronic liver disease presentation:
Non-specific features: anorexia, nausea, weight loss, amenorrhoea, arthralgia or arthritis, acne, unexplained fever
Stigmata of chronic liver disease: hepatomegaly, splenomegaly, palmar erythema, spider naevi
Complications of cirrhosis (i.e. decompensation): ascites, hepatic encephalopathy, jaundice, GI bleeding
acute liver failure presentation:
Jaundice + Confusion + Coagulopathy in absence underlying liver disease
key presentation of acute hepatitis
Jaundice
RUQ pain
Hepatomegaly
Malaise
fatigue
fever
acute liver failure presentation
Jaundice + Confusion + Coagulopathy in absence underlying liver disease
what are other autoimmune conditions which are associated with autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
Inflammatory bowel disease
Coeliac disease
Thyroiditis
Rheumatoid arthritis
Other connective tissue diseases
diagnosis and investigations for autoimmune hepatitis
use of IAIHG scoring system
it includes:
1) Gender: female more likely
2) ALP/AST ratio → indicator of cholestatic liver damage because ALP is marker for bile duct enzymes and bone whereas AST is general marker for liver damage and damage to other tissues. AST should generally be higher than ALP because it is in more tissue. If ALP is higher it indicates bile obstruction or primary biliary cholangitis. If the ratio is normal it simply excludes bile duct involvement
3) Serum immunoglobulins + Serum IgG → marker for the activation of the immune system and antibodies against liver; IgG is quite specific for liver antibodies
4) Antibodies:
Type 1 autoimmune hepatitis (adult):
ANA: antinuclear antibodies
SMA: anti smooth muscle antibodies
Type 2 (kid):
LKM: anti liver-kidney microsomes
5) Drug use history
6) Average daily alcohol intake
7) Histological findings from liver biopsy → liver biopsy done with percutaneous or transjugular approach
8) Other autoimmune disease
9) AMA → antimitochondrial antibodies → highly specific for PBC
10) Hepatitis viral markers → to exclude viral hepatitis
how do you manage autoimmune hepatitis
1st line
immunosuppression with corticosteroid and immunosuppressant
prednisolone + azathioprine
2nd line
liver transplant
what do you monitor patients with autoimmune hepatitis for? they are very susceptible to developing other complications
hepatocellular carcinoma
osteoporosis due to steroids: DEXA scan
what is PBC
autoimmune T-cell mediated attack of interlobular bile ducts which results in inflammation
what is more common: PBC or PSC
also mention what genders are associated with PBC or PSC
PBC more common
females
PSC - males
risk factors for PBC
Female, age 45-60, smoking, other autoimmune disease, rheumatoid diseases
what is xanthelasma
cholesterol deposits in the skin (xanthelasma)
pathophysiology of PBC
Immune system attacks small interlobular 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.
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.
key presentations of PBC, signs and symptoms
Pruritis, fatigue, Jaundice, xanthelasma
signs: Pale stools, signs of cirrhosis (hepatomegaly, ascites, spider naevi)
symptoms: Abdominal pain, joint pain
1st line and gold standard investigations for PBC
1st line
LFT
bilirubin
ALP
ALT
GGT
albumin
ultrasound
gold standard: AMA –> anti-microbial antibodies
management of PBC 1st line and others
1st line: Ursodeoxycholic acid (bile acid analogue reduces intestinal absorption of cholesterol).
Cholestyramine (bile acid sequestrant) for pruritis.
Cholestyramine binds to bile acids in the intestine, forming complexes that are then excreted in the feces → decreases bile acid reabsorption → liver uses more cholesterol to synthesise new bile acids (less xanthelasma) + reduces bile acids overall and decreases itching
Liver transplant if severe
complications of PBC
Liver cirrhosis, portal hypertension, steatorrhea, osteoporosis, hypercholesterolaemia
what is PSC
Inflammation and fibrosis of intrahepatic and extrahepatic bile ducts, resulting in strictured ‘beaded’ appearance of bile ducts.
risk factors for PSC
Male, aged 40-50, heavily associated with IBD especially ulcerative colitis
which autoimmune liver disorder is associated with UC
PSC
Pathophysiology of PSC
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 pruritus and jaundice.
Ongoing strictures eventually lead to fibrosis, cirrhosis, and liver failure.
key presentations of PSC
Pruritus, fatigue
Charcot’s triad: RUQ abdominal pain, fever, jaundice
hepatomegaly, IBD signs and symptoms
what is ascending cholangitis and what are the three most key presentations
an acute infection of the bile ducts. In ascending cholangitis, bacteria from the intestines can ascend into the bile ducts, causing infection, inflammation, and obstruction.
the three most key symptoms are from Charcot’s triad: fever, RUQ pain, jaundice
1st line and gold standard investigations for PSC
1st line
LFTs: raised bilirubin, ALP, AST and ALT, GGT. Decreased albumin.
Serology: no antimicrobial antibodies (AMA), maybe pANCA antibodies
gold standard
MRCP (magnetic resonance cholangiopancreatography) – shows bile duct strictures or lesions
MRCP is required for diagnosis!!!
management of PSC
cholestyramine for pruritus
Liver transplant
complications of PSC; what are you especially worried about that you might want to monitor
Portal hypertension, cirrhosis, cholangiocarcinoma, colorectal cancer (risk from IBD), hepatic encephalopathy
especially worried about cholangiocarcinoma and colorectal cancer
which one of PBS or PSC could be treated
PBS
PSC can’t be treated
definition and stages of NAFL
Metabolic 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
causes of NAFL
Metabolic syndrome: obesity, hypertension, diabetes, hypertriglyceridemia, hyperlipidaemia
key presentations
either asymptomatic or with very severe symptoms of liver failure
hepatomegaly
jaundice
ascites
RUQ pain absence of chronic alcohol consumption
1st line and gold standard investigations for NAFL
mention score used to assess chance of cirrhosis
1st line
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)
gold standard
Liver biopsy (steatosis, inflammation, fibrosis)
Child Pugh score
management of NAFL
1st line – treat underlying cause and reduce risks (lose weight, exercise, smoking, control diabetes, LDL).
Medications:
Pioglitazone → improves insulin sensitivity (improves fat levels in the blood which is a concern)
vitamin E → excess fat can cause oxidative damage in NAFL, and vit E is an antioxidant
Statins
ACEi.
end stage: liver transplant
what is the main cause of liver disease and failure
Main cause of liver disease and failure
key presentations of alcoholic liver disease
asymptomatic in early stages
later: abdominal pain, hepatomegaly, jaundice, spider naevi (cluster of minute blood vessels under skin), alcohol dependency
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
1st line and gold standard investigations for alcoholic liver disease
1st line:
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
gold standard:
Liver biopsy: steatosis, inflammation, Mallory bodies
what specific finding would you get from a liver biopsy from an alcoholic liver disease patient
Mallory bodies
what screening tools can you use to assess alcohol dependence
CAGE
AUDIT
management of alcoholic liver disease
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)
complications of alcoholic liver disease
Wernicke-Korsakoff syndrome (thiamine deficiency), hepatic encephalopathy, renal failure, hepatocellular carcinoma, portal hypertension
how much paracetamol are you allowed per day
400mg
which hepatitis is associated with blood transfusions
Hep B
what is secondary haemochromatosis
haemochromatosis as a result of transfusions, hep B and C, NAFLD
how is iron mainly excreted in the body
mainly FAECES
other ways include bleeding (sloughing of intestinal cells, menstruation etc.)
explain what the presence of Hep A IgG antibodies in the blood and absence of IgM means and why
indicates past Hep A infection or vaccination
IgM Antibodies:
Early Infection Marker: IgM antibodies are often the first antibodies to appear in response to a new infection.
The presence of IgM antibodies suggests an acute or recent infection.
IgG Antibodies:
Late Infection Marker: IgG antibodies usually appear later in the course of an infection.
The presence of IgG antibodies, especially in the absence of IgM antibodies, may suggest a past or resolved infection.
IgG antibodies can persist in the bloodstream for a more extended period, providing a marker of previous exposure or vaccination.
hepatic encephalopathy vs Wernicke’s encephalopathy
hepatic:
Brain infection due to toxic metabolites (especially ammonia) not removed by the liver due to liver dysfunction
can be due to liver cirrhosis and liver failure
Wernicke’s: it is specifically due to thiamine (vit B1) deficiency
is due to excess alcohol, malnutrition or impaired absorption of thiamine
pathophysiology of alcohol-induced Wernicke’s encephalopathy
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
pathophysiology of hepatic encephalopathy
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 mean that ammonia bypasses the liver and enters systemic circulation directly.
key presentations of hepatic encephalopathy
Reduced consciousness, confusion, stupor, coma, changes to personality mood and memory.
Asterixis → clinical sign that describes the inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements
rigidity, hypokinesia.
investigations and management of hepatic encephalopathy
investigations
Blood ammonia raised, abnormal LFTs, EEG (decrease in brain wave frequency and amplitude), U&E (maybe hyponatraemia or hypokalaemia)
management
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
key presentations of Wernicke-korsakoff encephalopathy
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
what can Wernicke’s encephalopathy progress into
korsakoff syndrome
investigations and management of Wernike’s encephalopathy
investigations:
thiamine levels decreased, LFTs deranged, MRI degeneration of mammillary bodies
management:
IV thiamine infusion (pabrinex). Can be given with glucose, magnesium, and multivitamins
1st line and gold standard investigations for peritonitis
1st line Bloods, urine dipstick (rule out UTI), serum amylase + lipase (rule out pancreatitis), ECG if heart suspicion.
Gold standard CT abdomen
investigations used for malabsorption
FBC
Increased/decreased MCV
Decreased calcium/iron/B12 and folate
Increased INR
Stool sample microscopy
Coeliac tests
what is tropical sprue
severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition
usually happens to residents or visitors to tropical areas
a 75-year-old man presents with severe RUQ pain, rigours and fever. He has RUQ tenderness but a negative Murphy’s sign. Blood tests show high CRP and bilirubin. What is the next most appropriate test?
Abd ultrasound
71 yr old man admitted to hospital with pneumonia. He is treated with co-amoxiclav. after 1 week he starts having severe diarrhoea (with no blood), and feels unwell and dehydrated. what is the most likely organism that caused the diarrhoea?
C diff
man with cirrhosis presents with black stools, is apyrexial and jaundiced. bloods show anaemia and raised urea. what treatment will reduce mortality risk:
a) tranexamic acid
b) co-amoxiclav
c) metoclopramide
d) iron infusion
B
most patients die of sepsis because if they have a cirrhosed liver they are already immunocompromised and GI bacteria can translate to blood and to liver more easily
1st line treatment is: terlipressin (vasoconstriction) + co-amoxiclav
a man with a history of liver transplant presented with deranged LFTs after eating raw pork meat on holiday. what is the most likely cause of the deranged LFTs
Hep A, B, C, D or E
Hep E
man presents to GP with fatigue and deranged LFTs (raised ALT and ALP)
normal liver ultrasound
hepatitis screen negative
AMA positive
what is the diagnosis
PBC
patient shows up with liver cancer and mets in GI lymph nodes. What Duke stage is he?
Dukes D
a patient has abdominal pain which can be relieved by defecation. She also has loose stools and is 19yr old. what is the most likely diagnosis
IBS
what costal cartilage does the subcoastal line pass through
10th costal cartilage
at what vertebral level in the intertubercular line
L5
where is the transpyloric plane and what does it intersect
transpyloric plane: between left and right 9th costal cartilages
crosses the pylorus of the stomach, the gallbladder, the pancreas and the hila of the kidney
where is the intercristal plane
between the right and left iliac crests
what nerves innervate the anterior abdominal wall and what kind of innervation do they receive
somatic
T7-T11
subcostal nerve (T12)
Iliohypogastric and ilioingunal nerve from L1
which were the retroperitoneal components (not only organs)
adrenal glands, aorta, kidneys, oesophagus, ureters, pancreas, duodenum, ascending and descending colon, rectum
what are the medial umbilical folds a remnant of
umbilical arteries
name all of the hiatuses of the diaphragm and stat their vertebral level
oesophageal hiatus - T10
IVC - T8
Aorta - T12
what is the blood supply and venous drainage of the oesophagus?
oesophageal arteries from aorta + left gastric arteries
drainage: left gastric vein azygous veins
draw/name the branches of the SMA and IMA
SMA
jejunal artery
ileal artery
ileocolic artery
right colic
middle colic
IMA
left colic artery –> anastomoses with the middle colic via marginal artery
sigmoid artery
superior rectal artery
explain how the portal venous system looks
spelling vein joins inferior mesenteric veins which then join the superior mesenteric and form the portal vein which breaks into smaller and smaller veins. all of the central veins then join into the hepatic vein which joins the IVC
what is the innervation of the stomach?
parasympathetic: vagus
sympathetic: T5-T9
what is the blood supply of the duodenum?
1st half from the coeliac trunk (gastro-duodenal artery) and the second half from SMA (inferior pancreatico-duodenal artery)
(this is because the duodenum has 2 embryological origins; first half is from the foregut and the second half is from the midgut)
what is the difference between the jejunum and ileum
Jejunum
- lots of plicae circulares; ileum also has but much less
Ileum
- payer’s patches (submucosal lymph nodes)
what is meckel’s diverticulum
embryological remnant of the connection between the midgut and the yolk sac –> how the baby was fed
(remnant of the vitelline duct)
what were the three anatomical features of the large intestine?
haustra, taeniae coli, epiploic appendages
what is the phenicolic ligament
ligament between transverse colon and diaphragm at the splenic flexure
what is the innervation of the foregut, midgut and hindgut
foregut
sympathetic + visceral sensory- great splanchnic from T5-T9
parasympathetic - vagus
midgut
s + vs- lesser splanchnic T10-11
p - vagus
hindgut
s + vs - least T12
p - pelvic splanchnic S2-4
what is the epiploic foramen?
the entrance to the lesser sac; lies behind the portal triad and the lesser omentum
what is ligamentum teres remnant of and where is it
it is at the end of the falciform ligament inferior to the liver and it is the remnant of the umbilical vein
what is does the ductus venosus turn into and what was the function of ductus venosus
ductus venosus becomes the ligamentum venosum in the adult
function of the ductus venosus is to shunt blood from umbilical vein straight to the IVC instead of through the liver because the umbilical vein carries very oxygenated blood from the mother –> you want to take that blood to systemic circulation and bypass the liver
blood supply of pancreas
gastroduodenal artery from coeliac trunk splits into the anterior and posterior superior pancreaticoduodenal arteries
the SMA has the inferior anterior and posterior pancreatico-duodenal branches
the splenic artery from the coeliac supplies the body of the pancreas
what is the sphincter of oddi
the circular muscle around the hepatopancreatic ampulla which leads to the major duodenal papilla
papilla vs sphincter vs ampulla
papilla = lump
sphincter = muscle
ampulla = opening
what are the cartilages which form the nasal septum?
vomer
ethmoid
septal cartilage
