GI + liver Flashcards
What is gastritis?
gastric mucosal inflammation
What is the most common cause of acute non-erosive gastritis?
Helicobacter Pylori infection
What can cause erosive gastritis?
Chronic NSAID or alcohol use/misuse
Reflux of bile salts from pyloric dysfunction (e.g. gastric surgery)
Aetiology of gastritis
H.pylori infection
Chronic NSAID or alcohol use/misuse
Reflux of bile salts into stomach
Autoimmune disorders
Bacterial invasion of gastric wall
Risk factors for gastritis
Helicobacter pylori infection
non-steroidal anti-inflammatory drug (NSAID) use
alcohol use/toxic ingestions
previous gastric surgery
critically ill patients
autoimmune disease
Symptoms of gastritis
Dyspepsia
Nausea, vomiting
Loss of appetite
Epigastric discomfort
What investigations would be carried out for suspected gastritis?
H pylori urea breath test (first line)
H pylori faecal antigen test
FBC
endoscopy
gastric mucosal histology
serum vitamin B12
What are some differentials of gastritis?
Peptic ulcer disease (PUD)
Gastro-oesophageal reflux disease (GORD)
Non-ulcer dyspepsia
Gastric lymphoma
Gastric carcinoma
How would you treat gastritis caused by H.pylori?
PPI + 2 antibiotics
can also do PPI + bismuth + 2 antibiotics
How would you treat erosive gastritis
Reduce exposure, e.g. discontinue NSAIDS, limit alcohol
How would you treat gastritis caused by bile reflux?
rabeprazole or sucralfate
How would you manage autoimmune gastritis?
more at risk for b12 deficiency
check levels and if needed treat with IM cyanocobalamin
Complications of gastritis
Peptic ulcer
Gastric carcinoma
Achlorhydria (decreased/absent production of hydrochloric acid)
Vitamin b12 deficiency
What are the 2 main types of IBD?
Ulcerative colitis
Crohn’s
What is ulcerative colitis
type of IBD that involves chronic inflammation of the colonic mucosa
confined to colon + rectum
follows a relapsing + remitting course
What is peritonitis?
Inflammation of the peritoneum
What are the 2 main types of peritonitis?
Spontaneous bacterial peritonitis
Secondary peritonitis
What is ascites?
a pathological collection of fluid in the peritoneal cavity
What is the most common cause of ascites?
cirrhosis
What are some non-peritoneal causes of ascites?
Portal hypertension: cirrhosis, CHF, alcoholic liver disease, hepatitis
Hypo-albuminaemia: nephrotic syndrome
Other causes are ovarian tumours, surgical trauma
What are some peritoneal causes of ascites?
Infectious causes, e.g. TB
Malignancy
SLE
What is a more common cause of ascites? (non-peritoneal or peritoneal)
Non-peritoneal (portal hypertension)
What is portal hypertension?
Increased BP in the portal system
Portal pressure more than 5mmHg than pressure in IVC
What is the most common cause of portal hypertension?
Cirrhosis
How can you sample ascitic fluid to help find cause?
abdo paracentesis
What does the serum-ascitic albumin gradient compare?
compares albumin concentration in the ascitic fluid and the serum albumin concentration
What is a high SAAG and what does that suggest?
High SAAG ≥ 1.1g/dL
fluid is pushed out of circulation, causing increase of serum albumin, but ascitic albumin is lower
hydrostatic pressure imbalance, e.g. portal hypertension
What is ascites with a high SAAG usually caused by?
Portal hypertension
e.g. cirrhosis, CHF, budd-chiari syndrome
What is ascites with a low SAAG usually caused by?
Infections
Peritoneal malignancy
Pancreatitis
Nephrotic syndrome
How would you treat asicites with a high SAAG?
diuretics (spironolactone) + low salt diet
paracentesis with albumin infusion
main points: treat underlying cause, relieve symptoms, prevent complicat
How would you treat low SAAG ascites?
repeated paracentesis + treatment of underlying cause
What are the presentations of ascites?
Abdo distension
Fluid and shifting dullness on exam
Differentials of ascites
Hepatitis
Alcoholic liver disease
Congestive heart failure
Nephrotic syndrome
Pancreatitis
Clinical features of ascites
Abdominal distension
Abdominal discomfort
Weight gain
Shortness of breath
Reduced appetite
What is exudative ascites?
Protein concentration above 25 gm/l
What is transudative ascites?
Protein concentration below 25 gm/l
How can portal hypertension cause ascites?
(pathophysiology)
- Endothelial cells lining blood vessels release more nitric oxide
- Vasodilation, Bp drops, aldosterone released
- Kidneys retain more sodium and water
- Plasma volume increases and fluid is pushed into tissues and peritoneal cavity
How can portal hypertension cause oesophageal varices?
Venous blood accumulates in hepatic portal system
Blood backs up into systemic veins
Portal hypertension leads to formation of portosystemic shunts
In oesophagous
What is gastro-oesophageal reflux disease?
& epidemiology
reflux of gastritic contents through lower oesophagel sphincter into oesophagus causing irritation of the lining and symptoms
common condition affecting all ages groups
What are the risk factors for developing GORD?
Family hx of GORD
Hiatus hernia
Obesity
Smoking
NSIADs
Diet: caffeine, carbonated drinks, chocolate, citrus, spicy
What is the pathophysiology of GORD?
lower oesophageal sphincter relaxes more frequently and contents from stomach can reflux into the oesophagus.
The oesophageal lining is stratified squamous epithelium and is more irritated and damaged.
Scar tissue can form and lead to oesophageal stenosis
Barrett’s oesophagus can also occur
What is Barrett’s oesophagus?
occurs with chronic GORD
an oesophagus in which any portion of the normal distal squamous epithelial lining has been replaced by metaplastic columnar epithelium through metaplasia
increases risk of neoplastic (cancerous) changes
What are the main features of GORD?
Heartburn and acid regurgitation typically after meals
Relief with an antacid
diagnosis is made clinically
What are the extra-oesophageal symptoms of GORD?
Cough
laryngitis
asthma
dental erosion
How does reflux induced asthma occur?
chronic aspiration of reflux contents and vasovagal bronchoconstriction
What are the alarm symptoms in patients presenting with “GORD”?
anaemia,
dysphagia
haematemesis- vomiting fresh blood
melaena- black tarry stools from upper GI bleeding
persistent vomiting
involuntary weight loss
What are some possible differentials of GORD?
ACS
Stable angina
Functional heartburn or dyspepsia
Achalasia
Peptic ulcer disease
Eosinophilic oesophagitis
Malignancy
Laryngopharyngeal reflux
Non-acid reflux
How is GORD managed?
PPI: omeprazole 20mg once daily
Lifestyle changes
What are the possible complications of GORD?
oesophageal ulcer, haemorrhage, or perforation
oesophageal stricture
Barrett’s oesophagus
adenocarcinoma of the oesophagus
What is coeliac disease?
A systemic autoimmune disease triggered by dietary gluten peptides.
common, about 1 in 100
What common grains is gluten found in?
Wheat
Rye
Barley
What are the 3 autoantibodies present in coeliac disease?
Anti-tissue transglutaminase antibodies (anti-TTG)
Anti-endomysial antibodies (anti-EMA)
Anti-deamidated gliadin peptide antibodies (anti-DGP)
What is the pathophysiology of coeliac disease?
Gluten peptide triggers immune response and autoantibodies against tissue transglutaminase and anti-EMA
Autoantibodies cause inflammation particularly in the jejunum and cause atrophy of the villi, leading to malabsorption
What are the 2 major histocompatibility complex class-II molecules associated with coeliac disease?
HLA-DQ2
HLA-DQ8
What typically causes coeliac disease?
genetic predisposition (HLA-DQ2 and -DQ8) and environmental trigger
What are the symptoms of coeliac disease?
GI: diarrhoea, abdo discomfort, bloating
dermatitis herpetiformis
fatigue
weight loss
failure to thrive in kids
may be asymptomatic
Which patients should be screened for coeliac disease?
Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease
What are some risk factors for coeliac disease?
family hx of coeliac disease
IgA deficiency
T1DM
autoimmune thyroid disease
Down’s syndrome
Turner’s syndrome
What investigations should be run for coeliac?
MUST CONTINUE EATING GLUTEN DURING TESTING
Quantitative IgA: normal/low
IgA tissue transglutaminase: raised
Small bowel histology: intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia
What’s the gold standard test for coeliac disease?
Small bowel histology: intra-epithelial lymphocytes, villous atrophy, and crypt hyperplasia
What’s the management for coeliac disease?
strict lifelong gluten-free diet
supplements for any deficiencies
What are some differentials for coeliac disease?
Crohn’s
Enteropathy
Non-coeliac gluten sensitivity
What are the possible complications of coeliac disease?
Osteoporosis/penia
Vitamin deficiencies
Malignancy, e.g. intestinal lymphoma
What’s the most common form of IBD?
Ulcerative colitis
What’s the aetiology for IBD?
Exact is unclear but a genetic predisposition + environmental trigger cause an abnormal inflammatory response to gut bacteria
Where does ulcerative colitis typically affect?
Begins distally at rectum
Can only affect rectum and colon
L sided affects up to splenic flexure
If whole colon is affected = pancolitis (extensive UC)
What are the risk factors for UC?
and what ages is it often diagnosed?
Family hx of IBD
HLA-B27 positive
Infection risking a relapse
peak around 20-40 but increasily diagnosed in the over 60s now
What is proctitis?
inflammation confined to the rectum
What is the cardinal feature of UC?
Bloody diarrhoea
What are the symptoms of UC?
BLOODY DIARRHOEA
Blood in stool/ rectal bleeding
feeling of incomplete defecation (tenesmus)
Increased stool frequency and urgency
Abdominal pain
What histological changes would be seen on a biopsy for UC?
Crypt abscess formation
Reduced goblet cells
Non-granulomatous
What would be visible on a colonscopy for UC?
Continuous inflammation (proximal from rectum)
Pseudopolyps
Superficial ulceration
What criteria is used to grade UC from mild to severe?
Truelove and Witts
What investigations and results would show for UC?
Stool culture: negative
Faecal calprotectin: elevated
Sigmoidoscopy/ileocolonoscopy + biopsy: crypt abscesses, non-granulomatous
What are the possible differentials for UC?
Crohn’s
IBS
Colitis
Diverticulitis
What is mild UC?
passage of ≤4 stools per day (with or without blood)
absence of any systemic illness
normal levels of inflammatory markers (ESR)
What is moderate UC?
passage of >4 stools per day
minimal signs of systemic toxicity
What is the classification for severe UC?
passage of ≥6 bloody stools daily + one of:
HR: 90+ bpm
temp 37.5ºC
Hb <10.5 g/dL
ESR of at least 30 mm/hour
What is the management for mild to severe UC?
Mild: Aminosalicylate: mesalazine
Moderate to severe: corticosteroid: prednisolone
Acute severe: IV hydrocortisone
What are some possible complications of UC?
Toxic megacolon
Perforation
Infection
Inflammatory pseudopolyps
What is Crohn’s disease?
what ages does it affect?
A type of IBD characterised by transmural inflammation of the GI tract
all ages, diagnosis peaks 15-30yrs
What happens in the GI tract in Crohn’s?
transmural inflammation (affecting all layers of the bowel) in the affected region of bowel, producing deep ulcers and fissures (cobblestoning)
Inflammation is not continuous, forming skip lesions throughout the bowel
What is the hallmark appearance of Crohn’s disease on biopsy/colonoscopy?
Cobblestoning
Non-caseating granulomas
Skip lesions
transmural ulcers
Where in the GI tract can Crohn’s affect?
Anywhere from mouth to anus
Terminal ileum and R colon often affected
What are some conditions associated with IBD?
Erythema nodosum
Pyoderma gangrenosum (rapidly enlarging, painful skin ulcers)
Enteropathic arthritis
Primary sclerosing cholangitis (particularly with UC)
Red eye conditions (e.g., episcleritis, scleritis and anterior uveitis)
What are some of the risk factors for Crohn’s?
white ethnicity and Ashkenazi Jewish ancestry
age 15-40 or 50-60 years
family history of CD
smoking
oral contraceptive pill + NSAIDs may also increase risk
How might Crohn’s disease present?
chronic diarrhoea
weight loss
R lower quadrant abdominal pain
Fever
Fatigue
Some blood in stool
extra-intestinal manifestations (e.g., erythema nodosum or pyoderma gangrenosum)
perianal lesions
episodic
What investigations should be run for suspected Crohn’s?
colonoscopy with ileoscopy and tissue biopsy
FBC
Comprehensive metabolic panel
Serum iron, b12, folate
Stool microscopy + culture: negative
CRP and ESR: raised
What are the differentials for Crohn’s disease?
UC
Colitis
Acute appendicitis
Diverticular disease
Colorectal cancer
What is the first line treatment of Crohn’s?
Inducing remission
- Oral prednisolone
- Enteral nutrition if concerns about corticosteroids, e.g. in kids
Maintaining remission
- Azathioprine
What are the possible complications of Crohn’s disease?
Intestinal obstruction
Malabsorption related, e.g. anaemia
What’s going wrong in IBS?
Disturbance in gut/brain interaction
Functional so no underlying disease causing symptoms
What are the 4 subtypes of IBS?
IBS with diarrhoea
IBS with constipation
Mixed IBS
Unspecified
What criteria is used to classify IBS and how does it define IBS?
Rome IV
presence of abdominal pain related to defecation, associated with a change in stool frequency and/or stool form
What are the risk factors for IBS?
Family hx of IBS
age <50 years
female sex
previous enteric infection
stress
How may IBS present?
Recurrent abdominal pain often relieved by defecation
Changes in bowel habits
Bloating
Flatulence
Urgency
Mucus with stools
Sensation of incomplete emptying
What investigations could be run to exclude differentials in IBS?
- Full blood count for anaemia
- Inflammatory markers (e.g., ESR and CRP)
- Coeliac serology (e.g., anti-TTG antibodies)
- Faecal calprotectin for IBD
- CA125 for ovarian cancer
What are the differentials for IBS?
IBD
Colitis
Colon cancer
Coeliac disease
Bowel infection
What is required for an IBS diagnosis?
at least 6 months of abdo pain/discomfort with at least one of:
- Pain or discomfort relieved by opening the bowels
- Bowel habit abnormalities (more or less frequent)
- Stool abnormalities (e.g., watery, loose or hard)
and 2 of straining, bloating, worse after eating, passing mucus
How does the Rome IV criteria diagnosis IBS?
Recurrent abdominal pain, at least 1 day per week in the last 3 months and associated with 2+:
- Related to defecation
- Associated with a change in stool frequency
- Associated with a change in stool form
What are some dietary modifications that can be made in IBS?
- Reduce caffeine, alcohol and fizzy drinks
- Have regular meals
- Drink lots of fluids
- Low FODMAP diet
- Adjust fibre intake depending on symptoms
What are the possible pharmacological treatments for IBS?
Diarrhoea: loperamide
Constipation: laxative
Pain or bloating: antispasmodics, e.g. dicycloverine
What is appendicitis and which age group has the highest incidence rate?
inflammation of the appendix
highest incidence rate in children and adolescents
How can appendicitis lead to peritonitis?
There is a single opening to the appendix that connects it to the bowel
Pathogens can get trapped where appendix meets bowel.
Leads to infection and inflammation.
Inflammation may proceed to gangrene and rupture
Faecal contents and infective material released into the peritoneal cavity
Peritonitis
What is the main cause of appendicitis?
Obstruction of the lumen of the appendix, via
- Faecolith (a hard mass of faecal matter)
- normal stool
- lymphoid hyperplasia
When should you suspect appendicitis?
Any patient with:
- Acute severe right iliac fossa pain
- Poorly localised central abdominal pain that becomes localised to the right lower quadrant
- Anorexia, nausea, and vomiting
What is the most common presentation of acute appendicitis?
poorly localised central abdominal pain that becomes localised to the right lower quadrant as inflammation progresses
How might acute appendicitis present?
poorly localised central abdominal pain that localises to R lower quadrant
Tenderness at McBurney’s point
Anorexia – almost always present
Nausea and vomiting
Loose stool or constipation
What investigations should be run for suspected appendicitis?
FBC: leukocytosis
CRP: elevated
CT or ultrasound
Possible differentials for appendicitis
Mesenteric adenitis
Viral gastroenteritis
Meckel’s diverticulitis
Crohn’s
Peptic ulcer disease
R sided ureteric stone
Ectopic pregnancy
What is the treatment for acute appendicitis?
Removal of the inflamed appendix (appendicectomy)
What are the main complications of appendicitis?
Perforation
Peritonitis
What is achalasia?
an oesophageal motor disorder characterised by a loss of oesophageal peristalsis and failure of the lower oesophageal sphincter to relax in response to swallowing
incidence increases with age, mean age 53
What causes achalasia?
progressive destruction of the ganglion cells in the myenteric plexus
possible triggers include infection, autoimmunity, and genetic factors
How does achalasia present?
dysphagia to solids and liquids, regurgitation, and retrosternal pain
slowly progressive over months to years
What investigations are done for achalasia?
endoscopy to exclude malignancy
barium swallow
high-resolution oesophageal manometry
What are some differentials for achalasia?
Oesophageal carcinoma
Reflux oesophagitis
Connective tissue disorders (e.g., systemic sclerosis)
Pseudoachalasia
What would be seen on oesophageal manometry for achalasia?
Absence of oesophageal peristalsis
Failure of relaxation of the lower oesophageal sphincter
High resting lower oesophageal sphincter tone
Management options for achalasia
no interventions that can restore oesophageal peristalsis
CCBs: nifedipine
Surgery: pneumatic dilatation
What is a peptic ulcer?
A break in the mucosal lining of the stomach or duodenum more than 5 mm in diameter, with depth to the submucosa
What are the 2 sites that can be affected by peptic ulcers?
mucosa of the stomach (gastric ulcer), most often on lesser curvature of stomach
proximal duodenum (duodenal ulcer)
What are the risk factors for peptic ulcer disease?
H.pylori infection
NSAID use
Smoking
Increasing age
Personal or family hx of peptic ulcers
How does H.pylori cause ulceration?
Survive in the stomach by creating an alkaline microenvironment
Induces an inflammatory response in the mucosa leading to ulceration
How can NSAIDs cause a peptic ulcer?
inhibiting COX and prostaglandin synthesis, resulting in a reduced secretion of glycoprotein, mucus, and
mucosa more susceptible to damage
What are the 2 main causes of peptic ulcers?
H.pylori
NSAIDs
What is acid secretion like in gastric or duodenal ulcers?
Gastric: normal to low
Duodenal: hypersecretion, often in response to H.pylori in stomach
What’s the typical presentation of a patient with a peptic ulcer?
chronic, upper abdominal pain related to eating a meal (dyspepsia)
epigastric tenderness
nausea and vomiting
What are the signs of an upper GI bleed?
Haematemesis (vomiting blood)
Coffee ground vomiting
Melaena (black, tarry stools)
Fall in haemoglobin on a full blood count
How is a peptic ulcer diagnosed?
Endoscopy
Urea breath test for H.pylori
What are the differentials for peptic ulcer disease?
GI cancer
GORD
Gastroparesis
Acute pancreatitis
Functional dyspepsia
Coeliac
IBS
What’s the management for peptic ulcer disease?
Treat underlying cause: stop NSAIDs, treat H.pylori infection with amoxicillin
PPIs: omeprazole, lansoprazole
repeat endoscopy 6 to 8 weeks after beginning treatment
What are the possible complications of peptic ulcers?
Penetration
Perforation
Gastric obstruction
Upper GI bleed
How can peptic ulcers be avoided in people who require NSAIDs?
Prescribe them with a PPI
What are the 3 types of ischaemic bowel disease?
acute mesenteric ischaemia
chronic mesenteric ischaemia
colonic ischaemia
What’s the arterial blood supply of the bowel?
Small intestine blood from: coeliac artery and superior mesenteric artery
Colon: SMA and inferior MA
Rectum: internal iliac artery
What typically causes ischaemic bowel?
embolism
thrombus
non-occlusive cause, e.g. hypoperfusion
How does acute mesenteric ischaemia present?
abdominal pain out of proportion to examination
nausea/vomiting
rectal bleeding
abdo bruit
What investigations should be done for ischaemic bowel?
CT scan with contrast
FBC: leukocytosis, anaemia
ABG + serum lactate: acidosis
What is diverticular disease?
any clinical state caused by symptoms pertaining to colonic diverticula
What are diverticula?
outpouchings of the bowel wall
How do diverticula form?
Bowel is surrounded by circular muscle.
Bowel is weakened in areas where blood vessels penetrate and over time.
Increased pressure inside the lumen over time, can cause a gap to form in these areas of the circular muscle.
Gaps allow the mucosa to herniate through the muscle layer and pouches to form (diverticula)
Why don’t diverticula form in the rectum?
it has an outer longitudinal muscle layer that completely surrounds the diameter of the rectum
adding extra support
What are some predisposing factors for diverticular disease?
low fibre
decreased physical activity
obesity
increased red meat consumption
smoking
excessive alcohol and caffeine intake
steroids
NSAIDs
How does diverticular disease present?
In left lower quadrant:
- guarding
- tenderness
- abdo pain
rectal bleeding
constipation
bloating
What are the symptoms of acute diverticulitis?
acute abdominal pain, sharp, localised in the left iliac fossa pain, worsened by movement.
Localised tenderness
decreased appetite
pyrexia
nausea
What would a CT for diverticulitis show?
thickening of the colonic wall
pericolonic fat stranding
abscesses
localised air bubbles or free air
What investigations should be run for suspected diverticular disease?
FBC: polymorphonuclear leukocytosis
U&E: uraemia and elevated creatinine
C-reactive protein: elevated
CT abdomen-pelvis scan
What are the differentials for diverticular disease?
IBD
Endometriosis
Colorectal cancer
UTI
Appendicitis
Example of an antispasmodic which helps abdo cramping
dicycloverine
How is diverticulosis treated?
increased fibre in the diet
bulk-forming laxatives if constipated
How is diverticulitis managed?
Uncomplicated diverticulitis: oral co-amoxiclav if unwell, analgesia (not NSAIDs), avoid solid food for a few days
Complicated diverticulitis: IV co-amoxiclav + fluids, low residue diet, surgery
What is the rule of 2s in Meckel’s diverticulum?
Present in 2% of the population
symptomatic in 2% of those with it
children are usually less than 2 years old
males are 2x as common as female
found approximately 2 feet proximal to the ileocaecal valve
it is 2 inches long or less
has 2 types of ectopic tissue (gastric and pancreatic)
What is the commonest congenital malformation of the small bowel?
Meckel’s diverticulum
What is meckel’s diverticulum?
congenital abnormality
the remnants of the vitello-intestinal duct
How might meckel’s diverticulum present?
GI bleeding
Small bowel obstruction
Abdo pain and cramps
Nausea and vomiting
asymptomatic in most patients
How might meckel’s diverticulum be diagnosed?
FBC
CT/ultrasound of abdomen
Meckel’s scan
What is the management of meckel’s diverticulum?
Asymptomatic no treatment
Symptomatic: surgical resection of the diverticulum
What is a mallory-weiss tear?
A superficial tear of the oesophageal mucosa in the region of the gastroesophageal junction and gastric cardia
What are the risk factors for a mallory-weiss tear?
condition predisposing to retching, vomiting, and/or straining
chronic cough
hiatal hernia
endoscopy or other instrumentation
heavy alcohol use
What are some typical causes of a MWT?
mallory-weiss tear
coughing
retching
vomiting
binge drinking
How does a MWT typically present?
small and self-limiting episodes of haematemesis after a bout of retching, vomiting, coughing, straining, or blunt trauma
What are the initial investigations for a suspected MWT?
Upper GI endoscopy
FBC
What are the differentials of a MWT?
Spontaneous oesophageal perforation (Boerhaave’s syndrome)
Cameron erosions
Peptic ulcer disease
Oesophageal varices
How is a MWT managed?
Resus and ensure haemodynamically stable
Mostly self-limiting so treatment is supportive
What’s meant by bowel obstruction?
a mechanical blockage of the bowel, whereby a structural pathology physically blocks the passage of intestinal contents
What are the risk factors for developing small bowel obstruction?
previous abdominal surgery
malrotation
Crohn’s disease
hernia
appendicitis
What can cause small bowel obstruction?
Previous surgery
Inguinal hernia with incarceration
Crohn’s disease
Intestinal malignancy
Appendicitis
adhesions
What are the symptoms of a bowel obstruction?
intermittent abdominal pain
distention
vomiting
nausea
constipation
What are the differential diagnoses for a small bowel obstruction?
Ileus
Infectious gastroenteritis
Large bowel obstruction
Intestinal pseudo-obstruction
Acute appendicitis
Acute pancreatitis
What does obstruction in the instestine cause?
Obstruction results in a build up of gas and faecal matter before the obstruction.
This causes back-pressure, resulting in vomiting and dilatation of the intestines proximal to the obstruction
How can a bowel obstruction lead to hypovolaemia and third spacing of fluid?
The GI tract secretes fluid that is later absorbed in the colon. Obstruction means fluid can’t be reabsorbed.
Fluid loss from the intravascular space into the GI tract.
This leads to hypovolaemia and shock.
The higher up the intestine the obstruction, the greater the fluid losses as there is less bowel over which the fluid can be reabsorbed
What are the big 3 causes of bowel obstruction?
Adhesions (small bowel)
Hernias (small bowel)
Malignancy (large bowel)
What is a closed-loop obstruction in the bowel?
two points of obstruction along the bowel
meaning that there is a middle section sandwiched between two points of obstruction
What are some possible complications of a bowel obstruction?
progression to intestinal necrosis, perforation, sepsis, and death
Short bowel syndrome in a SBO
What are some risk factors for large bowel obstruction?
Colorectal adenoma or polyp
Malignancy
IBD
Diverticular disease
Hernia
What can cause large bowel obstruction?
Malignancy most common cause
Diverticular disease
Volvulus
What imaging should be used for a suspected bowel obstruction?
Contrast CT of abdomen and pelvis
How is bowel obstruction managed?
NG decompression
Emergency surgery
What is a pseudo-obstruction of the bowel?
dilatation of the colon due to an adynamic bowel, in the absence of mechanical obstruction
most commonly affects caecum and ascending colon
What are the 2 subtypes of oesophageal cancer?
Squamous cell carcinoma: upper and middle 1/3s
Adenocarcinoma: lower 1/3 of oesophagus develops from barrett’s oesophagus, more common in developed countries
Where does oesophageal cancer tend to metastasize to?
peri-oesophageal lymph nodes
liver
lungs
What are the risk factors for oesophageal cancer?
Male
Older age
Low socioeconomic status
Smoking
excessive alcohol use
GORD
Barrett’s oesophagus
obesity
What are the symptoms of oesophageal cancer?
Dysphagia
Pain when swallowing
Weight loss
Hiccups from phrenic nerve involvement
typically present quite late
What imaging may be done for suspected oesophageal cancer?
Upper GI endoscopy with biopsy
CT of chest and abdomen
What are the possible differentials for oesophageal cancer?
Benign stricture
Achalasia
Barrett’s oesophagus
What are the possible options for managing oesophageal cancer?
Chemoradiotherapy
Surgical resection
What is the most common form of gastric cancer?
Adenocarcinoma from gastric mucosa
What tumour suppressor gene can be lost in gastric cancer?
p53
What investigation is done for possible gastric cancer?
Upper GI endoscopy with biopsy
What are the risk factors for gastric cancer?
pernicious anaemia
Helicobacter pylori
N-nitroso compounds
Family hx
smoking
What are the differentials for gastric cancer?
Peptic ulcer disease
Benign oesophageal stricture
Achalasia
What’s the management for gastric cancer?
Surgical resection
Subtotal gastrectomy
Chemoradiotherapy
What’s the most common type of colorectal cancer and where does it typically affect?
Adenocarcinoma
66% of colorectal cancers in colon
What is familial adenomatous polyposis (associated with colorectal cancer)?
- autosomal dominant condition involving malfunctioning of the tumour suppressor genes called adenomatous polyposis coli (APC)
- results in many polyps (adenomas) developing along the large intestine
- polyps can become cancerous
What is hereditary nonpolyposis colorectal cancer (lynch syndrome)?
associated with colorectal cancer
- autosomal dominant condition that results from mutations in DNA mismatch repair (MMR) genes
- patients at higher risk of colorectal cancer
What does colorectal cancer typically arise from?
dysplastic adenomatous polyps
inactivation of tumour suppressor genes
mostly sporadic but can be familial, e.g. FAP or Lynch
What are common presenting symptoms of colorectal cancer?
Abdominal pain
change in bowel habit
rectal bleeding
anaemia
What are signs of advanced disease in colorectal cancer?
Abdominal distension
weight loss
vomiting
What are some of the risk factors for colorectal cancer?
increasing age
family history
APC mutation (from FAP)
Lynch syndrome
Polyposis
IBD
Obesity
What investigations should be done for colorectal cancer?
faecal immunochemical test
colonoscopy
What’s the mainstay of colorectal cancer treatment?
Surgical resection
What can cause haematemesis?
Oesophageal varices
Peptic ulcer disease
MWT
Oesophagitis
GI cancer
What are haemorrhoids?
enlarged anal vascular cushions
haemorrhoidal cushions are normal vascular structures
can be internal or external
How does haemorrhoidal disease typically present?
painless rectal bleeding
sudden onset of perianal pain with a tender palpable perianal mass
What typically causes haemorrhoids?
Excessive straining due to constipation or diarrhoea
What are some of the risk factors for developing haemorrhoidal disease?
age between 45 and 65 years
history of constipation
pregnancy
presence of a space-occupying pelvic lesion
What are the differentials for haemorrhoids?
Anal fissure
Anal fistula
Colorectal cancer
IBD
Rectal prolapse
What are some ways of managing haemorrhoids?
Increase fibre intake
Short term topical corticosteroids
Rubber band ligation/ sclerotherapy
What is an anal fissure?
a split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding
How are anal fissures treated?
Conservative therapy: high fibre diet, adequate fluid intake, topical analgesics
Consider topical diltiazem
What is a perianal fistula?
an abnormal connection between the anal canal and the perianal skin
often a complication of an anorectal abscess
managed surgically
How does an anal fistulae present?
recurrent perianal abcesses
intermittent or continuous discharge onto the perineum
What is an anorectal abscess?
an infection of the soft tissues around the anus
common in crohn’s
What are the symptoms of an anorectal abscess?
Severe perianal pain and swelling
Fever
Chills
Urinary retention
Anal fistula may be present
diagnosed through hx and clinical exam
What are the risk factors for an anorectal abscess?
anal fistula
Crohn’s disease
male sex
What are the differentials for an anorectal abscess?
Pilonidal abscess
STI
Anal fissure
How is an anorectal abscess treated?
Incision and drainage
What is pilonidal disease?
An acquired disease in which hair follicles become inserted into the skin, creating a chronic sinus tract, usually in the natal cleft
Acute infection may lead to a pilonidal abscess, requiring surgical drainage
commonly affects men age 16-35
What are the symptoms of pilonidal disease?
Sacrococcygeal
- Discharge
- Pain and swelling
- Sinus tracts
presence of hair containing cysts
What is pseudomembranous colitis?
Infection of the colon caused by C.Diff
Characterised by inflammation of the colon and the formation of pseudomembranes
Occurs in patients whose normal bowel flora has been disrupted by recent antibiotic use
How does C.Diff colitis typically present?
diarrhoea
abdominal pain
leukocytosis
hx of recent antibiotic use
can also have distension, tenderness and fever
How might C.Diff colitis be diagnosed?
Stool sample
- Faecal occult blood test
- PCR
How is C.Diff colitis treated?
discontinue the inciting antimicrobial agent and start therapy with oral fidaxomicin or vancomycin
What is acute liver failure?
a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease
very rare
What causes acute liver failure?
Paracetamol overdose
Drug-induced
Hepatitis A or B
Which LFTs show damage to liver cells?
ALT and AST show parenchymal damage
ALP and GGT are for cholestatic damage
What are the symptoms of acute liver failure?
Jaundice
Coagulopathy
abdominal pain
nausea
vomiting
malaise
signs of cerebral oedema
What investigations should be done in acute liver failure and what would they show?
LFTs: hyperbilirubinaemia, elevated liver enzymes
PT/INR: elevated INR (>1.5)
Basic metabolic panel
What are the differentials for acute liver failure?
Severe acute hepatitis
Cholestasis
Haemolysis
How should patients be managed in acute liver failure?
ICU admission and consider possible transplant
Treat paracetamol overdose if that’s cause
What are the possible complications of acute liver failure?
rapidly progressing hepatic encephalopathy
coagulopathy
infection
renal failure and haemodynamic changes
metabolic disorders
cerebral oedema
GI bleed
What is chronic liver disease?
the result of repeated damage to the liver
progressive liver dysfunction for 6 months or more
What can cause chronic liver disease?
Alcohol
Hepatitis
Alpha-1-antitrypsin deficiency
Wilson’s disease
Non-alcoholic fatty liver disease
Hepatocellular carcinoma
Toxins
Ischaemia
Budd-Chiari
What are the signs and symptoms of chronic liver disease?
jaundice
ascites
encephalopathy
Caput medusa
Splenomegaly
Spider naevi
Palmar erythema
What is the max paracetamol dose in adults over 24hours?
4g
What are the different types of paracetamol overdose?
Acute: taken in less than 1 hour, context of self-harm
Staggered: excessive amounts over longer than an hour in context of self harm
Therapeutic: excessive dose taken with intent to treat pain
What are some risk factors for paracetamol overdose?
hx of self-harm
hx of frequent/repeated use of medications for pain relief
glutathione deficiency
drugs that induce liver enzymes (cytochrome P450 inducers)
low bodyweight (<50 kg)
What is the pathophysiology of a paracetamol overdose?
After ingestion, paracetamol metabolised
About 4% of a therapeutic dose is metabolised by cytochrome P450 enzymes, mainly CYP2E1, to a potentially toxic intermediate metabolite N-acetyl-p-benzoquinone imine (NAPQI)
When the production of NAPQI exceeds the capacity to detoxify it, the excess NAPQI binds to cellular components, causing mitochondrial injury and hepatocyte death
What are the main symptoms of a paracetamol overdose?
Nausea
Vomiting
Altered consciousness level
can show signs of an AKI or metabolic acidosis (in mixed overdose)
What are the most common causes of cirrhosis?
alcohol-related liver disease
non-alcoholic fatty liver disease (NAFLD)
chronic viral hepatitis (B and C)
What are the investigations for a paracetamol overdose?
serum paracetamol concentration
liver function tests
prothrombin time and INR
blood glucose (hypo indicates acute liver injury)
How is a paracetamol overdose managed?
Immediate acetylcysteine
Activated charcoal if patient presents within an hour
What is liver cirrhosis?
pathological end-stage of any chronic liver disease
characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules
What metabolic disorders can result in cirrhosis?
NAFLD
haemochromatosis
Wilson’s disease
alpha-1 antitrypsin deficiency
What can cause liver cirrhosis?
Viral hepatitis
Alcohol use
Metabolic: NAFLD, NA steatohepatitis, haemochromatosis, alpha 1 antitrypsin deficiency, Wilson’s
Drug induced, e.g. methotrexate
Autoimmune hepatitis
Venous outflow obstruction: e.g. Budd-Chiari, occlusion
What is the pathophysiology of liver cirrhosis?
Insult causes inflammation and scarring, fibrosis
Nodules of scar tissue form + capillarisation of sinusoids
Increase in blood flow resistance leading to portal HTN
What are some signs of cirrhosis?
Leukonychia – white nails
palmar erythema
spider naevi
jaundiced sclera
caput medusa
hepatosplenomegaly
distension
muscle wasting
peripheral oedema
What disease scoring systems can be used for liver cirrhosis?
Child-Pugh-Turcotte (CPT)
Model of End-Stage Liver Disease (MELD)
What investigations should be run for cirrhosis?
LFTs
Liver biopsy
PT
FBC + electrolytes
What are the features of decompensated liver disease that may suggest transplantation is required?
A – Ascites
H – Hepatic encephalopathy
O – Oesophageal varices bleeding
Y – Yellow (jaundice)
What are the general principles of management for liver cirrhosis?
Treat underlying cause
Manage and monitor complications
Liver transplant
What are some possible complications of liver cirrhosis?
Ascites
Gastro-oesophageal varices
Bleeding and thrombosis
Hepatocellular carcinoma
What are some pre-hepatic causes of portal htn?
portal or splenic vein thrombosis
AV malformation
splenomegaly
What are some intra-hepatic causes of portal HTN?
cirrhosis (most common cause)
primary sclerosing cholangitis
schistosomiasis
What are some post-hepatic causes of portal HTN?
IVC obstruction
R heart failure
Budd-Chiari syndrome
What are the 3 stages of alcohol-related liver disease?
- fatty liver (steatosis)
- alcohol-related hepatitis (inflammation and necrosis)
- alcohol-related cirrhosis
What is the main cause of alcoholic liver disease?
chronic heavy alcohol ingestion
What happens in alcoholic fatty liver?
stage of ARLD
Drinking leads to a build-up of fat in the liver
Reversible with abstinence.
What happens in alcoholic hepatitis?
stage of ARLD
Drinking alcohol over a long period/ Binge drinking causes inflammation in the liver cells.
Mild alcoholic hepatitis is usually reversible with permanent abstinence
What is binge drinking defined as in men and women?
6 or more units for women
8 or more for men
in a single session
What are the 2 main pathways that alcohol is metabolised through in the liver?
alcohol dehydrogenase
cytochrome P-450 2E1
In ARLD what is happening in the alcohol dehydrogenase pathway?
Alcohol dehydrogenase (hepatic enzyme) converts alcohol to acetaldehyde, which is then metabolised to acetate
Dehydrogenases convert NAD to NADH.
Excessive NADH in relation to NAD inhibits gluconeogenesis and increases fatty acid oxidation, which promotes fatty infiltration in the liver
In ARLD, what is happening in the cP450-2E1 pathway of metabolism?
cP-450 2E1 pathway generates free radicals through the oxidation of NADPH to NADP.
Chronic alcohol use upregulates cytochrome P-450 2E1 and produces more free radicals
What are symptoms of severe hepatocellular failure in advanced liver disease?
Abdominal distension and weight gain (ascites)
Confusion (hepatic encephalopathy)
Haematemesis or melaena (gastrointestinal bleeding)
Asterixis
Leg swelling.
What questionnaires can be used to assess alcohol dependency?
AUDIT
CAGE
What are some signs of portal HTN?
Ascites
Splenomegaly
Venous collateral circulations
What are the risk factors for alcohol-related liver disease?
prolonged and heavy alcohol consumption
hepatitis C
female sex: develops more rapidly and at low drinking levels
What are the signs and symptoms of ARLD?
Fatigue
Anorexia
Weight loss
Jaundice
Fever
Nausea and vomiting
Right upper quadrant abdominal discomfort.
Hepatomegaly
Caput medusae
Telangiectasia
Ascites
What are some of the possible differentials for ARLD?
Hepatitis A,B,C, drug-induced, autoimmune
Cholecystitis
Hepatic vein thrombosis
Acute liver failure
Haemochromatosis
Wilson’s disease
Wernicke’s encephalopathy
Biliary obstruction
What investigations should be done for ARLD and what might they show?
LFTs: most elevated
AST/ALT ratio: ratio >2, AST elevated higher
FBC: anaemia
Liver ultrasound
Increased PT
What is the management of ARLD?
Alcohol abstinence
Nutrition supplementation
Weight reduction
Smoking cessation
Consider pred in severe alcohol-related hepatitis
What are the complications of ARLD?
hepatic encephalopathy
portal hypertension
GI bleeding
coagulopathy
renal failure
hepatorenal syndrome
How does alcoholic liver disease lead to wernicke’s encephalopathy?
Alcohol excess leads to thiamine (vitamin B1) deficiency as it’s poorly absorbed in the presence of alcohol
Thiamine deficiency leads to WE and Korsakoff syndrome.
What is steatosis?
an accumulation of fat in the liver
What is NAFLD?
evidence of steatotic liver disease in the absence of secondary causes of hepatic fat accumulation
What are the stages of NAFLD?
Non-alcoholic fatty liver disease
Non-alcoholic steatohepatitis (NASH)
Fibrosis
Cirrhosis
What are some of the metabolic comorbidities for NAFLD?
obesity, DM, HTN, dyslipidaemia, obstructive sleep apnoea, CVD, CKD
What happens in NAFLD?
accumulation of excessive triglycerides in the liver
interferes with liver cell functioning
What are the signs and symptoms of NAFLD?
Many patients asymptomatic
Hepatosplenomegaly
Fatigue
Malaise
Abdo pain
What are the risk factors for NAFLD?
obesity
insulin resistance or diabetes
dyslipidaemia
hypertension
metabolic syndrome
rapid weight loss
medications, e.g. NSAIDs, corticosteroids
total parenteral nutrition
How could NAFLD be diagnosed?
LFTs: elevated
FBC: anaemia
Abnormal metabolic panel
Liver biopsy: gold standard, but not used on every patient
exclusion of alcohol use as the cause
Enhance liver fibrosis test
What are the differentials of NAFLD?
ARLD
Hepatitis
Metabolic liver disease
Primary biliary cholangitis
Primary sclerosing cholangitis
What is the management of NAFLD?
Lifestyle modifications, e.g. weight loss, alcohol reduced, healthy diet, exercise
Consider pioglitazone + vitamin E
What is jaundice?
the result of accumulation of bilirubin in the bloodstream and subsequent deposition in the skin, sclera, and mucous membranes
When is bilirubin produced?
Breakdown of haem
What are the different mechanisms of bilirubin?
from increased bilirubin production (prehepatic)
diseases that impair hepatocyte function (hepatocellular)
obstruction of the biliary system (cholestatic/ post-hepatic)
What are the pre-hepatic causes of jaundice?
- Excessive haemolysis, e.g. haemolytic anaemia, haemolytic drugs, blood transfusions, sickle cell, thalassaemia
- impaired conjugation, e.g. gilberts
What are some causes of hepatocellular jaundice?
- Damaged hepatocytes, e.g. hepatitis + other infections, cirrhosis, hepatic carcinoma, toxins
- Metabolic liver disease: Haemochromatosis, Wilson’s disease, Alpha 1 antitrypsin deficiency
What are some causes of cholestatic/post-hepatic jaundice?
Something stopping bile flow, e.g. cholecystitis, pancreatic head carcinoma, cholangitis
What investigations should be run for jaundice?
Serum LFTs with fractionation of bilirubin
PT/INR
FBC
Patient Hx: e.g is it painful
What is Wernicke’s encephalopathy?
a neurological emergency resulting from thiamine deficiency
Where is thiamine stored and how long do stores last?
a water-soluble vitamin stored predominantly in the liver
up to 18 days
What’s the classic triad of presentation for wernicke’s encephalopathy?
not actually that common in patients, 10%
mental status changes
ophthalmoplegia
gait dysfunction
What are some symptoms of WE?
Cognitive dysfunction
Ocular motor changes
Gait disturbances
Confusion
Altered level of consciousness
What are important features of a Hx in suspected WE?
- alcohol dependence
- poor dietary intake
- vomiting, diarrhoea
- fever
- co-existing conditions
- immunodeficiency
- recent abdominal surgery
What are the risk factors for WE?
alcohol dependence
AIDS
cancer and treatment with chemotherapeutic agents
malnutrition
history of gastrointestinal surgery
What investigations should be done for WE?
Therapeutic trial of thiamine
finger-prick glucose
FBC + electrolytes
renal function
LFTs
serum ammonia
blood alcohol level
blood thiamine and its metabolites
What are some differentials for WE?
Alcohol intoxication
Alcohol withdrawal
Encephalitis
How should WE be treated?
IV thiamine ASAP
What is Korsakoff’s psychosis?
a complication of WE
disproportionate impairment of recent memory relative to other cognitive domains
What are some of the complications of WE?
ataxia and varying degrees of ophthalmoparesis
seizures
Korsakoff’s psychosis
hearing loss
if not treated early, permanent brain injury
What is haemochromatosis?
An autosomal recessive condition causing a build-up of iron levels in the body
When does haemochromatosis typically present?
usually presents after age 40 when the iron overload becomes symptomatic
It presents later in females due to menstruation
What normally causes haemochromatosis?
mutations in the HFE gene on chromosome 6
What’s a common marker for haemochromatosis?
elevated transferrin saturation
What are the cardinal symptoms of haemochromatosis?
lethargy
fatigue
loss of libido
skin bronzing
How is haemochromatosis managed?
Venesection (regularly removing blood to remove excess iron – initially weekly)
avoid iron-fortified foods or iron-containing supplements
What is Gilbert syndrome?
a genetic syndrome of mild unconjugated hyperbilirubinaemia
<102 micromol/L (<6 mg/dL)
What goes wrong in Gilbert syndrome?
Decreased UDPGT activity leads to decreased conjugation of unconjugated bilirubin
bilirubin clearance is reduced by 60%.
How does Gilbert syndrome typically present?
usually asymptomatic, with mild jaundice seen during times of fasting or physiological stress
Does Gilbert syndrome require treatment?
No treatment is needed since there is no liver injury or progression to end-stage liver disease
What features are typically present for a diagnosis of Gilbert syndrome?
- Asymptomatic healthy patient with mild unconjugated hyperbilirubinaemia (<68.4 micromol/L [<4 mg/dL])
- No evidence of haemolysis
- Normal serum transaminases and alkaline phosphatase levels
- Exclusion of medications that cause hyperbilirubinaemia
What is Wilson’s disease?
an autosomal recessive genetic condition resulting in the excessive accumulation of copper in the body tissues, particularly in the liver
What causes Wilson’s disease?
Autosomal recessive mutations in the ATP7B gene on chromosome 13
What is going wrong in Wilson’s disease?
ATP7B facilitates trans-membrane transport of copper within hepatocytes
Mutation leads to decreased copper excretion from the liver and copper overload in hepatocytes.
When hepatic storage capacity is exceeded, copper is released into the circulation and deposited in other organs
How can Wilson’s disease manifest?
liver disease (with jaundice, and possibly ascites and oedema)
neurological movement disorder (with tremor, dystonia, rigidity)
What is seen in the eye in Wilson’s disease?
Kayser-Fleischer rings surrounding iris
What investigations should be done for Wilson’s disease?
- 24-hour urine copper measurement
- ophthalmological slit-lamp examination for Kayser-Fleischer (KF) rings
- serum ceruloplasmin levels
- abnormal lfts
How is Wilson’s disease managed?
Copper chelation: Penicillamine, trientine
Zinc acetate
Restriction of copper in diet
What is alpha-1 antitrypsin (AAT) deficiency?
an autosomal codominant genetic disorder
Allele mutations cause ineffective activity of alpha-1 antitrypsin, the enzyme responsible for neutralising neutrophil elastase
How does AAT deficiency affect liver?
Alpha-1 antitrypsin is produced in the liver.
Abnormal mutant version of the protein is made that gets trapped and builds up inside the liver cells (hepatocytes).
These mutant proteins are toxic to the hepatocytes, causing inflammation. Progresses to fibrosis, cirrhosis and potentially hepatocellular carcinoma
How does AAT deficiency affect lungs?
In the lungs, the lack of a normal, functioning AAT protein leads to excess protease enzymes attacking the connective tissues.
Leads to bronchiectasis and emphysema.
Alpha-1 antitrypsin is a protease inhibitor
What causes AAT deficiency?
decreased circulating plasma levels of AAT
due to the inheritance of variant alleles of the SERPINA1 gene
How might AAT manifest?
Panacinar emphysema and associated obstructive lung disease
hepatitis and jaundice
bronchiectasis
What investigations would be done for AAT deficiency and what would the results show?
plasma AAT level: low
pulmonary function testing: reduced FEV1
Chest XR/CT: emphysematous changes
LFTs: elevated
What are the differentials for AAT deficiency?
Asthma
COPD
Bronchiectasis
Viral hepatitis
Alcohol-related liver disease
What is the basic management for AAT deficiency?
Stop smoking
Standard management for manifestations, e.g. COPD or liver disease
What is spontaneous bacterial peritonitis?
an infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory, or surgically correctable condition
Who is SB peritonitis most commonly seen in?
most commonly seen in patients with end-stage liver disease
What causes SB peritonitis?
(almost always) Monomicrobial infection of the ascitic fluid
What’s the most common pathogen causing SB peritonitis?
E.Coli
gram negative more common than positive
What are the symptoms of SB peritonitis?
Signs of ascites
abdominal pain
fever
vomiting
altered mental status
GI bleeding
What investigations should be done for SB peritonitis?
diagnostic paracentesis: ascitic fluid absolute neutrophil count >250 cells/mm³, fluid culture
FBC: leukocytosis
Blood culture
What’s the treatment for SB peritonitis?
Abx: IV 3rd-gen cephalosporin (e.g., cefotaxime, ceftriaxone), 5-7 days
What are the possible complications of SB peritonitis?
Sepsis
Tense ascites
Renal failure
What is cholestasis?
blockage to the flow of bile
What is biliary colic?
intermittent right upper quadrant pain caused by gallstones irritating bile ducts
What is cholelithiasis?
Cholelithiasis is the presence of solid concretions (stones) in the gallbladder
What is choledocholithiasis?
Gallstones exit into the bile ducts
When do symptoms occur in gallstones?
if a stone obstructs the cystic, bile, or pancreatic duct
What are the risk factors for gallstones?
increasing age
female sex
obesity, diabetes, and metabolic syndrome
family hx
gene mutations
pregnancy/exogenous oestrogen
NAFLD
prolonged fasting/rapid weight loss
4 Fs: Female, fat, forty, fertile
Why do gallstones form and what are the main types?
Gallstones form as a result of supersaturation of the bile.
Cholesterol stones (85-90%)
Pigment stones (15%)
Mixed stones – comprised of both cholesterol and bile pigments
What are the main risk factors for cholesterol gallstones forming?
obesity, poor diet, rapid weight loss after weight loss surgery
female, oestrogen
other meds: octreotide, ceftriaxone
How does biliary pain present?
gallstones causing obstruction to a duct
right upper quadrant or epigastric pain
Radiates to the right back or shoulder
Responds to analgesia
Typically occurs approximately 1 hour after eating, often in the evening, accompanied by nausea
Becomes increasingly intense and then stabilises
Typically lasts for at least 15-30 minutes, up to several hours
What investigations are done for gallstones?
LFTs
Ultrasounds
What are the management options for gallstones?
Analgesia: e.g. paracetamol or diclofenac
Elective cholecystectomy
What are some complications of gallstones?
Acute cholecystitis
Acute cholangitis
Obstructive jaundice (if the stone blocks the ducts)
Pancreatitis
What is acute cholecystitis?
acute gallbladder inflammation
major complication of cholelithiasis (gallstones)
Who does cholecystitis tend to affect?
patients with gallstones, at least 90% of patients with cholecystitis have gallstones
What normally causes acute cholecystitis?
caused by complete cystic duct obstruction usually due to an impacted gallstone
stops gallbladder from draining
What is acalculous cholecystitis?
dysfunction in gallbladder emptying is caused by something other than gallstones
Gallbladder is not being stimulated by food to regularly empty, resulting in a build-up of pressure
How do gallstones cause acute cholecystitis?
Fixed obstruction of gallstones into the gallbladder neck or cystic duct causes bile to become trapped in gallbladder
Irritation and pressure increases in gallbladder.
Stimulates prostaglandin synthesis and inflammatory response
Can result in secondary bacterial infection leading to necrosis and gallbladder perforation
What are some signs/symptoms of acute cholecystitis?
Upper R quadrant pain and tenderness
Murphy’s sign
Fever
Nausea/vomiting
What would be seen on an abdo ultrasound for acute cholecystitis?
Pericholecystic fluid
Distended gallbladder
Thickened gallbladder wall (>3 mm)
Gallstones
Positive sonographic Murphy’s sign
What can be used to visualise the biliary tree in more detail if a common bile duct stone is suspected but not seen on an ultrasound?
magnetic resonance cholangiopancreatography
What are some differentials for acute cholecystitis?
Acute cholangitis
Chronic cholecystitis
Peptic ulcer disease
Acute pancreatitis
Sickle cell crises
Appendicitis
Right lower lobe pneumonia
What’s the management of acute cholecystitis?
Nil by mouth
IV fluids
Antibiotics (as per local guidelines)
Cholecystectomy
What is gallbladder empyema? And how is it treated?
infected tissue and pus collecting in the gallbladder
IV Abx + either gallbladder drain or removal
What are some complications of acute cholecystitis?
Sepsis
Gallbladder empyema
Gangrenous gallbladder
Perforation
How does acute cholangitis lead to sepsis?
As the obstruction progresses, the bile duct pressure increases.
Forms a pressure gradient that promotes extravasation of bacteria into the bloodstream.
If not recognised and treated, this will lead to sepsis
What is acute cholangitis?
infection and inflammation of the biliary tree, most commonly caused by obstruction of common bile duct
What are the main causes of acute cholangitis?
cholelithiasis leading to choledocholithiasis and biliary obstruction
Iatrogenic biliary duct injury, i.e. surgical injury
Sclerosing cholangitis
What’s the epidemiology of acute cholangitis?
relatively uncommon, presenting as a complication in less than 10% of patients admitted to hospital with cholelithiasis
average age 50-60 years
What are the most common organisms causing acute cholangitis?
Escherichia coli
Klebsiella species
Enterococcus species
What are the 3 main features of acute cholangitis? (Charcot’s triad)
Right upper quadrant pain
Fever
Jaundice
How does acute cholangitis occur?
Obstruction leads to bile stasis and bile sludge, bacterial seeding
Bacteria can breed in bile sludge and travel from duodenum up biliary tree
What are the risk factors for acute cholangitis?
Gallstones
Over 50
After endoscopic retrograde cholangiopancreatography
Stricture
Hx of sclerosing cholangitis
What symptoms may be present in acute cholangitis?
Charcot’s triad: Right upper quadrant pain, Fever, Jaundice
Pale stool
Pruritus
Altered mental status
Hypotension
What investigations should be done for acute cholangitis?
FBC: raised WBC
LFTs: raised ALP + transaminases
CRP: raised
Blood cultures
Transabdominal ultrasound: dilated bile duct
ERCP, often done following an MRCP
How is acute cholangitis managed?
Broad spectrum IV Abx
IV fluids
Biliary decompression via ERCP
What is primary biliary cholangitis?
Chronic, autoimmune condition where the immune system attacks the small intrahepatic bile ducts, causing bile duct damage and loss
What’s the pathophysiology of primary biliary cholangitis?
Reduced immune tolerance
inflammation and damage to the epithelial cells of the small intrahepatic bile ducts
Over time, this can lead to obstruction of bile flow through these ducts and cholestasis
The back-pressure of bile and disease process ultimately lead to liver fibrosis, cirrhosis and failure
What patient population is most commonly affected by primary biliary cholangitis?
females, 9:1 f:m ration
middle age, peaks at 40
What is the aeitology of primary biliary cholangitis?
Autoimmune disease, with characteristic antimitochondrial antibody
What are some signs and symptoms of primary biliary cholangitis?
Xanthoma and xanthelasma (cholesterol deposits)
Hepatomegaly
Signs of liver cirrhosis and portal hypertension
Fatigue, sleep disturbance
Pruritus (itching)
Gastrointestinal symptoms and abdominal pain
Jaundice
Pale, greasy stools
Dark urine
Dry eyes and mouth
often asymptomatic and detected in LFTs
What is the diagnostic cirteria for primary biliary cholangitis?
LFTs: ALP and GGT elevated
Autoantibody profile: antimitochondrial antibody
Liver biopsy: bile duct lesions, granuloma formation
How is primary biliary cholangitis treated?
ursodeoxycholic acid: hydrophilic bile acid that protects cholangiocytes, makes bile less harmful
Obeticholic acid (where UDCA is inadequate or not tolerated
What are some complications of primary biliary cholangitis?
Hypercholesterolaemia
Cirrhosis and portal HTN
What is primary sclerosing cholangitis?
a chronic progressive cholestatic liver disease, characterised by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, resulting in diffuse, multi-focal stricture formation
causing continued destruction of the bile ducts
What is the epidemiology of primary sclerosing cholangitis?
relatively rare
typically presents between 25 and 45 years, median age of 36-39 at diagnosis
Many patients with PSC have associated IBD (typically UC)
Affects men more than women
What is the aetiology of primary sclerosing cholangitis?
Not completely clear but gen + environment
Genetic predisposition: HLA-B2/D3
What are the risk factors for PSC?
male sex
inflammatory bowel disease (IBD)
first degree relative with PSC
What are the symptoms of PSC?
Fatigue
Fever
Itching
Non-specific upper abdo pain
Jaundice
Fat-soluble vitamin deficiency
can just present with cirrhosis
Most commonly asymptomatic and found incidentally
What investigations would be done for PSC?
LFTs: elevated
Autoantibodies: anti-smooth muscle, anti-nuclear, p-ANCA
MRCP: bile duct strictures looking like beads on a string
How is PSC managed?
No definitive treatment found
- general lifestyle changes (including maintaining a healthy diet and weight, and limiting alcohol use)
- colestyramine for pruritus relief
- liver transplants in end stage, recurrence of PSC still a risk
What is acute pancreatitis?
acute inflammation of the pancreas
rapid symptom onset
What are the causes of acute pancreatitis?
I GET SMASHED
Idiopathic
Gallstones
Ethanol (alcohol)
Trauma
Steroids
Microbiological (mumps, hepatitis, tb)
Autoimmune pancreatitis
Scorpion sting
Hyperlipidaemia + hypercal
ERCP + emboli
Drugs + thiazide diuretics (furosemide), opiated, VPA
How do gallstones cause acute pancreatitis?
gallstones trapped at the end of the biliary system, blocking the flow of bile and pancreatic juice into the duodenum.
Bile refluxes into the pancreatic duct and prevents pancreatic juice from being secreted, results in inflammation in the pancreas
more common in women + older patients
How does alcohol cause acute pancreatitis?
directly toxic to pancreatic cells, resulting in inflammation
more common in men + younger patients
What are the risk factors for acute pancreatitis?
middle-aged women
young- to middle-aged men
gallstones
alcohol
hypertriglyceridaemia
use of causative drugs
endoscopic retrograde cholangiopancreatography (ERCP)
What’s the diagnostic criteria for acute pancreatitis?
Upper abdominal pain (epigastric or left upper quadrant)
Elevated serum lipase or amylase (>3 times upper limit of normal)
Characteristic findings on abdominal imaging (CT, MRCP, ultrasound).
2/3 present
How does acute pancreatitis typically present?
severe, constant upper abdominal pain, usually sudden in onset and often radiating to the back - with associated nausea/vomiting
What investigations would be done for acute pancreatitis?
Serum lipase/amylase: >3 times the upper limit of the normal range
FBC: leukocytosis
CRP: elevated
Urea: elevated
LFTs: elevated ALT
What’s the criteria for the glasgow score assessing severity of acute pancreatitis?
P – Pa02 < 8 KPa
A – Age > 55
N – Neutrophils (WBC > 15)
C – Calcium < 2
R – uRea >16
E – Enzymes (LDH > 600 or AST/ALT >200)
A – Albumin < 32
S – Sugar (Glucose >10)
0-1 – mild , 2 – moderate, 3+ – severe pancreatitis
1 point for each
What’s the management for acute pancreatitis?
IV fluid resus
Oral feeding as soon as can be tolerated
ERCP for gallstones
What are some possible complications of acute pancreatitis?
Necrosis of the pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collections
Chronic pancreatitis
Sepsis
Acute renal failure (hypovolaemia)
What’s the prognosis for acute pancreatitis?
80% have mild disease and will improve within 3 to 7 days of conservative management.
The overall mortality rate is low (approximately 5%) but this rises to 25% to 30% in severe acute pancreatitis
What is chronic pancreatitis?
chronic inflammation in the pancreas.
What can cause chronic pancreatitis?
who does it affect?
Chronic alcohol ingestion (>75%)
Idiopathic, hereditary
men twice as much as women, middle aged-older patients
What are the typical features of chronic pancreatitis?
epigastric abdominal pain radiating to the back
steatorrhoea
malnutrition
diabetes mellitus
What imaging should be done for chronic pancreatitis?
CT/MRI: pancreatic enlargement
How is chronic pancreatitis managed?
Alcohol and smoking cessation
Dietary advice and supplementation (i.e. fat soluble vitamins ADEK)
Analgesia
Pancreatic enzyme replacement therapy
What are some complications of chronic pancreatitis?
pancreatic exocrine insufficiency
diabetes mellitus
pancreatic calcifications
pancreatic duct obstruction
opiate addiction
What is hepatic encephalopathy?
brain dysfunction caused by advanced liver insufficiency and/or portosystemic shunt
What causes hepatic encephalopathy?
build-up of neurotoxic substances that affect the brain, i.e. ammonia
often as a result of cirrhosis, excessive nitrogen load, benzos, SBP or hyponatraemia/kalaemia
What is the pathophysiology of hepatic encephalopathy?
hepatocytes are less capable of metabolising waste product + shunts may have formed so ammonia bypasses liver
Blood containing nitrogenous compounds (ammonia) moves into IVC
Ammonia crosses BBB and leads to increased glutamine and oncotic pressure in astrocytes, swelling of astrocytes
What are type A,B,C of hepatic encephalopathy?
Type A: HE associated with acute liver failure
Type B: HE associated predominantly with portosystemic bypass or shunting
Type C: HE associated with cirrhosis
What are the risk factors for hepatic encephalopathy?
hypovolaemia
GI bleeding
constipation
excessive protein intake
hypokalaemia, hyponatraemia
metabolic alkalosis
hypoxia
sedative or opioid use
hepatic or portal vein thrombosis
What are the symptoms of hepatic encephalopathy?
Mood, sleep and motor disturbances
positive Babinski in later stages
manifestations of underlying liver disease (ascites, jaundice)
What would be seen on investigations of hepatic encephalopathy?
Diagnosed in presence of liver disease
Serum ammonia: elevated
What’s the management of hepatic encephalopathy?
Lactulose (aiming for 2-3 soft stools daily)
Abx (e.g., rifaximin) to reduce the number of intestinal bacteria producing ammonia
Nutritional support
What is hepatitis?
inflammation of the liver
Which forms of viral hepatitis are RNA/DNA viruses?
A,C,D,E are RNA
B is DNA
What is the most common liver infection?
Hep B
How are the different forms of viral hepatitis transmitted?
A: faecal-oral route, not associated with chronic liver disease
B: blood/ bodily fluids
C: blood
D: attaches itself to the HBsAg and cannot survive without (hep b)
E: faecal-oral route
Which viral hepatitis can cause acute/chronic disease?
A: acute
B: acute and chronic
C: acute and chronic
D: acute and chronic
E: mostly acute and self-limiting, can be chronic immunosuppressed
all viral hep are notifiable
How does viral hepatitis present?
Abdominal pain (RUQ)
Hepatosplenomegaly
Fatigue
Flu-like illness
Pruritus (itching)
Muscle and joint aches
Nausea and vomiting
Jaundice
What would LFTs show for viral hepatitis?
hepatitic picture
high transaminases (AST and ALT) with proportionally less of a rise in ALP
high bilirubin
What viral markers are present for hepatitis B?
Surface antigen (HBsAg) – active infection
E antigen (HBeAg) – a marker of viral replication and implies high infectivity
Core antibodies (HBcAb) – implies past or current infection
Surface antibody (HBsAb) – implies vaccination or past or current infection
Hepatitis B virus DNA (HBV DNA) – a direct count of the viral load
Which antigen is present for Hepatitis A?
IgM antibodies to HAV
How is hep C diagnosed?
HCV antibody test
HCV RNA testing
What are some of the complications of Hep B and C?
B: cirrhosis, hepatocellular carcinoma
C: rheumatological complications, cirrhosis, hepatocellular carcinoma
Why is Hep D often linked with Hep B?
attaches itself to the HBsAg and cannot survive without this protein
increases severity and complications
How is hepatitis D diagnosed?
Anti-HDV antibodies + HDV RNA
presence of HBV
How is hep A treated?
supportive, mild analgesia
How is hep C treated?
direct-acting antiviral therapy, e.g. sofosbuvir/velpatasvir
How is hep b treated?
supportive care, antiviral therapy in chronic
How is hep D treated?
supportive
liver transplant if liver failure occurs
peginterferon alfa and/or bulevirtide in chronic
How is hepatitis E diagnosed?
serum antibody to HEV
HEV RNA
Who can be more affected by Hep E?
Can cause acute liver failure in pregancy or become chronic in immunosuppressed
Which viral hepatitis’ have vaccines?
A: vaccine, post-exposure prophylaxis
B: vaccine
C: no vaccine
D: no vaccine but hep b vaccine is protective
E: no vaccine
When do hernias occur?
weak point in a cavity wall (usually affecting the muscle or fascia)
Body organ (e.g., bowel) normally be contained within that cavity to pass through the cavity wall
How does an abdo hernia typically present?
A soft lump protruding from the abdominal wall
The lump may be reducible
The lump may protrude on coughing or standing
Aching, pulling or dragging sensation
What’s a femoral hernia?
herniation of the abdominal contents through the femoral canal
What’s a hiatus hernia?
and risk factors
protrusion of intra-abdominal contents into the thoracic cavity through an enlarged oesophageal hiatus of the diaphragm
obesity, increased age, increased intra-abdo pressure
What’s an umbilical hernia and who does it typically affect?
hernias occur around the umbilicus due to a defect in the muscles around umbilicus
Neonates, closes by age 4-5 without treatment normally
How can you differentiate between an indirect and direct hernia?
When an indirect hernia is reduced and pressure is applied to the deep inguinal ring, the hernia will remain reduced
What are the inguinal hernias?
Inguinal:
- Indirect: hernia sac comes through the internal (deep) inguinal ring
- Direct: hernia protrudes directly through the abdominal wall
What are incisional hernias?
hernias occur at the site of an incision from previous surgery
How can diarrhoea be defined?
3 or more loose stools across a day
Stools that are more frequent than what is normal for the individual lasting <14 days
Stool weight greater than 200 g/day
How is diarrhoea classifed based on duration?
Acute (≤14 days)
Persistent (>14 days)
Chronic (>4 weeks)
What is primary liver cancer?
Cancer that starts in the liver
Main one is hepatocellular carcinoma
What is secondary liver cancer?
Secondary liver cancer originates outside the liver and metastasises to the liver
What are the main risk factors for primary liver cancer?
Liver cirrhosis caused by:
* Alcohol-related liver disease
* Non-alcoholic fatty liver disease (NAFLD)
* Hepatitis B
* Hepatitis C
* Rarer causes (e.g., primary sclerosing cholangitis)
How is liver cancer screened for?
Ultrasound
Alpha-fetoprotein
every 6 months for liver cirrhosis patients
What investigations are done for liver cancer?
Alpha-fetoprotein (tumour marker for hepatocellular carcinoma)
Liver ultrasound is the first-line imaging investigation
CT and MRI scans are used for further assessment and staging of the cancer
Biopsy is used for histology
What are the symptoms of liver cancer?
Weight loss
Abdominal pain
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Upper abdominal mass on palpation
What are the management options for hepatocellular carcinoma?
Surgical resection or transplant
Radiofrequency or microwave ablation
Transarterial chemoembolisation (TACE)
Radiotherapy
Targeted drugs (e.g., kinase inhibitors and monoclonal antibodies)
What are some criteria for a liver transplant?
Cancer isolated to liver
Alcohol free for 6 months
What is a cholangiocarcinoma?
a type of cancer that originates in the bile ducts.
majority are adenocarcinomas
What is the most common site for a cholangiocarcinoma?
perihilar region, where the right and left hepatic ducts have joined to become the common hepatic duct
What is the tumour marker for cholangiocarcinoma?
CA19-9
What are the symptoms of obstructive jaundice?
Pale stools
Dark urine
Generalised itching
What are the majority of pancreatic cancers and where are they found?
adenocarcinomas found in head of pancreas
Where do pancreatic cancers tend to metastasise to?
tend to spread and metastasise early, particularly to the liver, then to the peritoneum, lungs and bones
What does Courvoisier’s law state?
palpable gallbladder along with jaundice is unlikely to be gallstones
pancreatic cancer or cholangiocarcinoma
What is Trousseau’s sign of malignancy?
migratory thrombophlebitis as a sign of malignancy, particularly pancreatic adenocarcinoma.
Thrombophlebitis is where blood vessels become inflamed with an associated blood clot (thrombus) in that area.
How does pancreatic cancer typically present?
Painless obstructive jaundice
Non-specific upper abdominal or back pain
Unintentional weight loss
Palpable mass in the epigastric region
Change in bowel habit
Nausea or vomiting
New-onset diabetes or worsening of type 2 diabetes
What investigations can be done for pancreatic cancer?
CT thorax, abdomen and pelvis
CA 19-9 tumour marker
MRCP and ERCP
Biopsy
What is the main differential for pancreatic cancer?
cholangiocarcinoma
What are the management options for pancreatic cancer?
Surgery (Whipple)
Stent to relieve symptoms
Chemo and radiotherapy (palliative)
What are oesophageal varices?
dilations of the porto-systemic anastomoses
What typically causes oesophageal varices?
portal hypertension secondary to liver cirrhosis
most commonly ARLD
