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
