GI and Liver Flashcards
What is GORD
Gastro-oesophageal reflux disease
What is the pathology of GORD
Caused by reflux of stomach contents into the oesophagus.
What are 7 causes of GORD
Lower oesophageal sphincter hypotension
Hiatus hernia
Oesophageal dysmotility
Obesity
Gastric acid hypersecretion
Delayed gastric emptying
Smoking, alcohol, pregnancy, drugs.
What are the 5 oesophageal clinical manifestations of GORD
Heartburn (burning, retrosternal discomfort after meals)
Belching
Acid brash (acid regurgitation)
Waterbrash
Odynophagia (swallowing pain)
What are the 4 extra-oesophageal clinical manifestations of GORD
Nocturnal asthma
Chronic cough
Laryngitis
Sinusitis
What are 2 differential diagnoses for GORD
Oesophagitis from corrosives, NSAIDs, herpes
Duodenal or gastric ulcers
What are 3 investigations for GORD
Endoscopy if dysphagia
24h oesophageal pH monitoring
Manometry help diagnose GORD when endoscopy is normal
What are the lifestyle changes for management of GORD
Weight loss
Smoking cessation
Small, regular meals
Reduce hot drinks, alcohol, citrus fruits, tomatoes, onions, fizzy drinks
What are 3 types of drugs used for GORD
Antacids
H2 receptor antagonists e.g. ranitidine
Proton pump inhibitor – lansoprazole
What is peptic ulceration
A break in the inner lining of the stomach, first part of the small intestine or sometimes the lower oesophagus.
What are 2 pathological causes of Peptic ulceration
Inflammation caused by the bacteria H.pylori
Erosion from stomach acids.
What are the 6 clinical manifestations of peptic ulceration
Epigastric pain often related to hunger, specific foods, or time of day
Fullness after meals
Heart burn (retrosternal pain)
Tender epigastrium
ALARM symptoms
Swallowing difficulty
What are the ALARM symptoms
for peptic ulceration
Anaemia
Loss of weight
Anorexia
Recent onset
Melaena/haematemesis (vomit/ faeces containing blood)
What are the tests for h.pylori
Urea breath test, serology, stool antigen test
What is the treatment for h.pylori
appropriate Proton Pump Inhibitor and 2 antibiotic combination
e.g.
Lansoprazole with clarithromycin and metronidazole.
What are the 5 risk factors for duodenal ulcer
H.pylori, drugs
increased gastric acid secretion and emptying, blood group O
What are 4 symptoms and signs for Duodenal ulcer
Asymptomatic
Epigastric pain
Weight loss
Epigastric tenderness
What are the tests for duodenal ulcer
Upper GI endoscopy
Test for H. pylori
What are 2 differential diagnoses for duodenal ulcers
Non-ulcer dyspepsia
Duodenal Crohn’s
What are 4 risk factors for gastric ulcers
H.pylori, smoking, NSAIDs
Age
What are 3 symptoms for gastric ulcer
Asymptomatic
Epigastric pain
Weight loss
What is the investigation for gastric ulcer
Upper GI endoscopy to exclude malignancy
What is the treatment for gastric ulcer
Proton pump inhibitors
What is the overall treatment for peptic ulcers
Lifestyle: decrease alcohol and tobacco use
H.pylori eradication
Drugs to reduce acid: Proton pump inhibitors are effective e.g. lansoprazole
Drug-induced ulcers: stop drug if possible.
what are Oesophago-gastric varices
Submucosal venous dilatations secondary to high portal pressures.
What is the complication of Oesophago-gastric varices
Bleeding can be brisk, particularly if underlying coagulopathy secondary to loss of hepatic synthesis of clotting factors.
What are 3 causes of oesophago-gastric varices
Cirrhosis
Thrombosis
Parasitic infection
What is a pre-hepatic cause of portal hypertension
thrombosis (portal or splenic vein)
What are 5 intra-hepatic causes of portal hypertension
cirrhosis, schistosomiasis, sarcoid, myeloproliferative diseases, congenital hepatic fibrosis
What are 4 post-hepatic causes of portal hypertension
Budd-Chiari syndrome, right heart failure, constrictive pericarditis, veno-occlusive disease
What are 3 Risk factors for variceal bleeds
High portal pressure
Variceal size
Endoscopic features of the variceal wall and advanced liver disease
What are 4 symptoms of oesophago-gastric varices
Only symptomatic if they bleed;
Vomiting large amounts of blood
Black, tarry or bloody stools
Light headedness
Loss of consciousness in severe cases
What are 3 prevention methods for Oesophago-gastric varices
Don’t drink alcohol
Healthy diet and weight
Reduce risk of hepatitis – don’t share needles or have unprotected sex
What are the 2 management options for Oesophago-gastric varices
Endoscopic banding or sclerotherapy
What is haematemesis
vomiting of blood. It may be bright red or look like coffee grounds.
What is malaena
black motions, often like tar, and has a characteristic smell of altered blood
What are 4 common and 3 rare causes for upper GI bleeds
Peptic ulcers
Oesophageal varices
Mallory-Weiss tear
Gastritis/ oesophagitis
Bleeding disorders
Portal hypertensive gastropathy
Meckel’s diverticulum
What is a Mallory- Weiss tear
a tear in the mucous membrane where the oesophagus meets the stomach
What is the cause of a Mallory-Weiss tear
Persistent vomiting/retching causes haematemesis via an oesophageal mucosal tear.
What is the management of a mallory-weiss tear
Endoscopy to stop the bleeding.
Endoscopic haemostasis: 2 of clips, cautery, adrenaline.
What is Gastritis
Inflammation of the lining of the stomach.
What are 4 causes of gastritis
Irritation due to excessive alcohol use, chronic vomiting, stress, or the use of certain medications such as aspirin.
Helicobacter pylori
Bile reflux: a backflow of bile into the stomach from the bile tract
Infections caused by bacteria and viruses
what are 4 risk factors for gastritis
Alcohol
NSAIDs
H.pylori
Reflux hernia
4 symptoms of gastritis
Epigastric pain
Vomiting
Indigestion (dyspepsia)
Abdominal bloating
3 investigations for gastritis
Upper GI endoscopy
Blood tests: anaemia and H.pylori infection
Faecal occult blood tests – presence of blood in your stool.
3 management options for gastritis
H2 receptor antagonists e.g. ranitidine
Proton pump inhibitors
Avoid hot and spicy foods
what is Coeliac disease
A disease in which the small intestine is hypersensitive to gluten, leading to difficulty in digesting food.
pathology of coeliac disease
T-cell responses to gluten in the small bowel causes villous atrophy and malabsorption.
9 clinical manifestations of coeliac disease
Stinking stools/steatorrhea
Diarrhoea
Bloating
Abdominal pain
Nausea and vomiting
Aphthous ulcers
Angular stomatitis
Weight loss, fatigue, weakness
Dermatitis herpetiformis
3 investigations for coeliac disease
Low Hb, B12 and ferritin
Antibodies: anti-transglutaminase is single preferred test – check IgA levels to exclude subclass deficiency.
Where serology positive or high index of suspicion proceed to duodenal biopsy while on a gluten-containing diet; expect subtotal villous atrophy
4 management options for coeliac disease
Lifelong gluten-free diet – rice, maize, soya, potatoes, and sugar are OK
Limited consumption of oats may be tolerated in patients with mild disease.
Gluten-free biscuits, flour, bread and pasta are prescribeable.
Monitor response by symptoms and repeat serology.
3 complications of coeliac disease
Anaemia
Dermatitis herpetiformis
Osteopenia/ osteoporosis
what is malabsorption
The small intestine can’t absorb enough of certain nutrients and fluids. Malabsorption of protein, fat and carbohydrate leads to weight loss and malnutrition.
5 causes of malabsorption
Coeliac disease – reduced surface area
Chronic pancreatitis
Crohn’s disease
Pancreatic insufficiency – poor intraluminal digestion
Infection – lymphatic obstruction
5 symptoms of malabsorption
Diarrhoea
Weight loss
Lethargy
Steatorrhea
Bloating
4 signs of malabsorption
Anaemia
Bleeding disorders (low vit K)
Oedema
Metabolic bone disease
3 investigations for malabsorption
FBC: low Ca2+, Fe, B12 and folate
Lipid profile: coeliac tests
Stool: Sudan stain for fat globules
2 management steps for malabsorption
Correction of nutritional deficiencies
Treatment of causative diseases
What is Inflammatory bowel disease
Inflammatory bowel disease is a term mainly used to describe two conditions: ulcerative colitis and Crohn’s disease. These are long term conditions that involve inflammation of the gut.
What is the main difference between crohns and ulcerative colitis
Crohn’s disease favours the ileum, but can occur anywhere along the intestinal tract.
Ulcerative colitis affects the colon (large intestine) only.
What is crohns disease
A chronic inflammatory disease characterised by transmural granulomatous inflammation affecting any part of the gut from mouth to anus (especially terminal ileum).
What are skip lesions
unaffected bowel between areas of active disease (crohns)
pathology of crohns
An inappropriate immune response against the gut flora in a genetically susceptible individual. Smoking increases the risk.
4 symptoms of crohns
Diarrhoea
Abdominal pain
Weight loss/failure to thrive
Systemic symptoms: fatigue, fever, malaise, anorexia
5 signs of crohns
Bowel ulceration
Abdominal tenderness/mass
Perianal abscess/fistulae/skin tags
Anal strictures
Clubbing, skin, joint and eye problems
5 complications of crohns
Small bowel obstruction
Toxic dilatation
Abscess formation
Fistulae
Malnutrition
first line investigations for crohns
FBC: raised WCC, platelets, CRP&ESR, anaemia. Faecal calprotectin raised (indicates IBD). pANCA negative. Stool samples (rule out infection). LFTs: hypoalbuminemia. Low iron, vitamin B12 and folate (B9) levels.
2 lifestyle management options for crohns
Quit smoking
Optimise nutrition
management plan for mild-moderate crohns
Prednisolone PO, plan maintenance therapy
Azathioprine
Biologics
Nutrition
Surgery
management plan for severe crohns
Admit for IV hydration/ electrolyte replacement; IV steroids e.g. hydrocortisone
Monitor pulse, BP, temperature, record stool frequency/character
Physical examination daily, and FBC, ESR, CRP, AXR
Consider need for blood transfusion
What is ulcerative colitis
A relapsing and remitting inflammatory disorder of the colonic mucosa.
It may affect just the rectum or extend to involve part of the colon or the entire colon.
Cause of UC
Inappropriate mucosal immune response to luminal bacteria. Smoking appears to decrease the risk of UC.
pathology of UC
Hyperaemic/ haemorrhagic colonic mucosa +/- pseudopolyps formed by inflammation.
5 symptoms of UC
Episodic or chronic diarrhoea
Crampy abdominal discomfort
Bowel frequency relates to severity
Urgency/tenesmus – proctitis
Systemic symptoms: fever, malaise, anorexia, weight loss
6 signs of UC
May be none
Acute, severe UC – fever, tachycardia, tender distended abdomen
Extra-intestinal signs:
Clubbing
Aphthous oral ulcers
Conjunctivitis
3 investigations for UC
Blood: FBC, ESR, CRP, U&E, LFT, blood culture
Stool: to exclude Campylobacter, C.difficile
Faecal calprotectin: a simple, non-invasive test for GI inflammation with high sensitivity.
2 complications of acute UC
Toxic dilatation of colon with risk of perforation
Venous thromboembolism
2 complications of chronic UC
Colonic cancer
Neoplasms in mucosa
Management of mild UC
Mesalamine is the mainstay for remission-induction/maintenance
Prednisolone
management of moderate UC
Induce remission oral prednisolone
management of severe UC
IV hydration/ electrolyte replacement
Monitor pulse, BP, temperature, record stool frequency/character
Physical examination daily, and FBC, ESR, CRP, AXR
What is IBS
Irritable bowel syndrome
A mixed group of abdominal symptoms for which no organic cause can be found.
Most are probably due to disorders of intestinal motility, enhanced visceral perception or microbial dysbiosis.
5 clinical manifestations of IBS
Urgency
Abdominal bloating/distension
Worsening of symptoms after food
Symptoms are chronic >6 months and often exacerbated by stress, menstruation or gastroenteritis.
Examination may be normal but general abdominal tenderness is common
3 investigations for IBS
FBC, CRP, ESR, U&E
Coeliac screen
Faecal calprotectin
Diagnosis criteria for IBS
Only diagnose IBS if recurrent abdominal pain associated with at least 2 of:
Relief by defecation
Altered stool form
Altered bowel frequency (constipation/diarrhoea)
3 differential diagnoses for IBS
Colonic cancer
Inflammatory bowel disease – Crohn’s, UC
Coeliac disease
What is the overall management plan for IBS
Should focus on controlling symptoms, initially using lifestyle/dietary measures, then cognitive therapy or pharmacotherapy if required
treatment of constipation in IBS
ensure adequate water and fibre intake and promote physical activity.
treatment of diarrhoea in IBS
avoid sorbitol sweeteners, alcohol and caffeine. Reduce dietary fibre content, encourage patients to identify their own trigger foods.
Treatment of Colic/bloating in IBS
oral antispasmodics. Combination probiotics in sufficient doses may help flatulence or bloating. Less alcohol intake.
treatment of Psychological symptoms/visceral hypersensitivity for IBS
emphasize the positive. Sinister pathology has been excluded and symptoms tend to improve over time. Consider CBT and hypnosis.
What are Gastro-intestinal infections (gastroenteritis)
diarrhoea +/- vomiting due to enteric infection with viruses, bacteria or parasites.
What is Norovirus
Single-stranded RNA virus. Highly infectious. Transmission by contact with infected people, environment, food.
Most common cause of infectious GI disease in England.
Presents 12-48hr after exposure, lasting 24-72h.
4 symptoms of norovirus
Acute-onset vomiting, watery diarrhoea, cramps, nausea.
2 investigations for norovirus
clinical, stool sample reverse transcriptase PCR
3 treatments for norovirus
supportive, anti-motility agents, usually self-limiting.
What is rotavirus
Double-stranded RNA virus.
Commonest cause of gastroenteritis in children.
Presentation of rotavirus
incubation 2day. Watery diarrhoea and vomiting for 3-8d, fever, abdominal pain
2 investigations for rotavirus
clinical, antigen in stool
2 treatments for rotavirus
supportive. Routine vaccination in UK
What is Enterotoxigenic E.coli
Gram -ve anaerobe
Disease due to heat-stable or heat labile toxin which stimulates Na+, Cl- and water efflux into gut lumen
presentation of Enterotoxigenic E.coli
incubation 1-3days. Watery diarrhoea, cramps lasts 3-4 days
2 investigations for Enterotoxigenic E.coli
clinical, identification of toxin from stool culture.
treatment for Enterotoxigenic E.coli
supportive, self-limiting
Prevention of travellers diarrhoea
boil water, cool thoroughly, peel fruit and vegetables. Avoid ice, salads, shellfish. Drink with a straw.
presentation of E.coli
watery diarrhoea preceded by cramps and nausea
presentation of giardia lamblia
upper GI symptoms e.g. bloating, belching
presentation of Campylobacter jejuni and Shigella
colitic symptoms, urgency, cramps.
Diagnosis criteria for travellers diarrhoea
3 or more unformed stools per day plus one of the following:
Abdominal pain
Cramps
Nausea
Vomiting
Dysentery
3 treatment steps for travellers diarrhoea
Oral rehydration. Clear fluid or oral rehydration salts.
Antimotility agents e.g. loperamide
Antibiotics
define Acute diarrhoea
3 episodes partially formed or watery stool/day for <14d
define dysentry
infectious gastroenteritis with bloody diarrhoea
define Persistent diarrhoea
acutely starting diarrhoea lasting >14d
define Traveller’s diarrhoea
Traveller’s diarrhoea: starting during, or shortly after, foreign travel
define Food poisoning
disease caused by consumption of food/wate
What is campylobacter
Gram -ve, spiral-shaped rod
7 infective causes of diarrhoea
Rotavirus/norovirus most common in the UK
Campylobacter
Shigella
Salmonella
S.aureus
E.coli
C.diff
presentation of campylobacter
incubation 1-10d. Bloody diarrhoea, pain, fever, headache.
5 complications of camylobacter
bacteraemia, hepatitis, pancreatitis, miscarriage, reactive arthritis
2 investigations for campylobacter
stool culture. PCR/enzyme immunoassay.
treatment plan for campylobacter
supportive. Antibiotics only in invasive cases, refer to local sensitivities.
6 key points of history for diarrhoea
Onset/duration
Characteristics of stool
Food/drink
Travel
Fresh water/ swimming
Medications
how does onset/duration change diagnosis of diarrhoea
Acute – viral/bacterial
Chronic – parasites and non-infectious causes
how does Characteristics of stool change diagnosis of diarrhoea
Floating: fat content – malabsorption, coeliac
Blood or mucus: inflammatory/invasive infection/ cancer
Watery: small bowel infection
how does food/drink affect diagnosis of diarrhoea
Meat – campylobacter
Rice – bacillus cereus
Poultry – salmonella
Shellfish – norovirus, v.parahaemolyticus
how does travel history change diarrhoea diagnosis
No cholera in the UK – traveller’s diarrhoea
how does fresh water/swimming change diarrhoea diagnosis
crypto, giardia, aeromonas
how does medication history change diarrhoea diagnosis
Recent antibiotics – C.diff or side effects
4 cancer risk factors with diarrhoea
Over 50
Chronic diarrhoea
Weight loss
Blood in stool
what are 3 investigations for diarrhoea
Stool tests
Blood tests
Lower GI endoscopy
what is looked at in stool tests for diarrhoea
Microscopy
Culture
Ova, cysts and parasites
Toxin detection
what is looked at in blood tests for diarrhoea
Blood culture
Inflammatory markers
ESR/ CRP
mechanism of watery diarrhoea
non-inflammatory
(enterotoxin or superficial adherence/invasion)
mechanism of bloody/mucoid diarrhoea
inflammatory
(invasion/cytotoxin)
location of watery diarrhoea
proximal small bowel
location of bloody/mucoid diarrhoea
colon
bacterial causes of watery diarrhoea
vibrio cholerae
e.coli (ETEC)
c.diff
bacillus cereus
s.aureus
bacterial causes of bloody/mucoid diarhoea
shigella
e.coli (EIEC,EHEC)
Salmomella enteritidis
v.parahaemolyticus
c.diff
campylobacter jejuni
viral causes of watery diarrhoea
rotavirus
norovirus
parasitic causes of watery diarrhoea
giardia
cryptosporidium
parasitic cause of bloody, mucoid diarrhoea
entamoeba histolytica
management of diarrhoea
Treat cause.
Food handlers – no work until stool samples are -ve. If a hospital outbreak, wards may need closing
Oral rehydration is better than IV, but if sustained diarrhoea/vomiting then IV fluids with electrolytes may be needed.
Avoid antibiotics unless infective diarrhoea is causing systemic upset.
What is Clostridium difficile
The cause of pseudomembranous colitis. Gram positive spore forming bacteria.
What are 4 antibiotics that cause clostridium difficile
rule of Cs
Clindamycin
Ciprofloxacin
Co-amoxiclav
Cephalosporins
3 signs of C.diff
Increased temperature
Diarrhoea with systemic upset
High CRP, WCC and low albumin
3 steps of detection of C.diff
Urgent testing of suspicious stool (characteristic smell)
Two-stage process with rapid screening test for C.diff protein followed by specific ELISA for toxins.
treatment of C.diff
Stop causative antibiotic.
Barrier nursing
clinical presentation of oesophageal tumour
Dysphagia
Weight loss
Retrosternal chest pain
3 investigations for oesophageal tumours
Oesophagoscopy with biopsy
Endoscopic ultrasound
CT/ MRI for staging
describe the t1-4 stages of oesophageal cancer
T1 – invading lamina propria/ submucosa
T2 – invading Muscularis propria
T3 – invading adventitia
T4 – invasion of adjacent structures
describe the N and M stages of oesophageal cancers
N0 – no nodal spread
N1 – regional node metastases
M0 – no distant metastases spread
M1 – distal metastases
4 treatment options for oesophageal cancer
Localised T1/T2 disease – radical curative oesophagectomy may be tried
Pre-op chemo – cisplatin
Chemoradiotherapy
Palliation aims to restore swallowing with chemo/radiotherapy, stenting and laser use
6 symptoms of gastric carcinoma
Often non-specific
Dyspepsia
Weight loss
Vomiting
Dysphagia
Anaemia
4 signs of gastric carcinoma
Epigastric mass
Hepatomegaly
Jaundice
Ascites
3 investigations for gastric carcinoma
Gastroscopy and multiple ulcer edge biopsies
EUS (endoscopic ultrasound)
CT/ MRI for staging
4 treatment options for gastric carcinoma
Partial gastrectomy for distal tumours
Total gastrectomy if more proximal
Combination chemo
Surgical palliation for obstruction, pain or haemorrhage
4 presentations of left sided colorectal carcinoma
Bleeding/ mucus PR
Altered bowel habit or obstruction
Tenesmus
PR mass
4 presentations of right sided colorectal carcinoma
Weight-loss
Low Hb
Abdominal pain
Obstruction less likely
4 presentations in both left and right sided colorectal carcinoma
Abdominal mass
Perforation
Haemorrhage
Fistula
4 urgent referral criteria for colorectal carcinoma
Over 40 with PR bleeding and bowel habit change
Any age with right lower abdominal mass
Palpable rectal mass
Men/non-menstruating women with unexplained iron-deficiency anaemia
5 investigations for colorectal carcinoma
FBC – microcytic anaemia
Faecal occult blood – used for UK screening programme
Sigmoidoscopy
Barium enema or colonoscopy – or CT
Liver USS
surgical management of colorectal carcinoma
Aims to cure and increases survival by up to 50%
Different types of surgery done for different sites of cancer
radiotherapy for colorectal cancer
Used in palliation for colonic cancer
Occasionally used pre-op to allow resection
chemotherapy for colorectal cancer
Adjuvant chemo helpful
Chemo is also used in palliation of metastatic disease
5 symptoms of liver tumours
Fever
Malaise
Anorexia
Weight loss
RUQ pain
4 signs of liver tumours
Hepatomegaly
Signs of chronic liver disease and evidence of decompensation
Feel for an abdominal mass
Bruit over liver
3 investigations for liver tumours
Blood: FBC, clotting, LFT, hepatitis serology, α-fetoprotein
Imaging: US/ CT to identify lesions. MRI distinguishes malignant and benign lesions
Biopsy: find primary e.g. CXR, endoscopy
what is hepatocellular carcinoma (HCC)
Primary hepatocyte neoplasia accounts for 90% of primary liver tumours
6 clinical features of HCC
Fatigue
Appetite loss
RUQ pain
Weight loss
Jaundice
Ascites
4 causes of HCC
HBV – main cause
Autoimmune hepatitis
Cirrhosis – alcohol, hemochromatosis, PBC
Non-alcoholic fatty liver
3 investigations for HCC
3 phase CT
MRI
Biopsy
3 treatments of HCC
Resecting solitary tumours
Liver transplant
Percutaneous ablation
What is Cholangiocarcinoma
Biliary tree cancer.
4 clinical presentations of cholangiocarcinoma
Fever
Abdominal pain and ascites
Malaise
Elevated bilirubin
3 treatment options for cholangiocarcinoma
Most tumours are inoperable at presentation. Most operated on recur.
Post-op complications include liver failure, bile leak and GI bleeds
Stenting of an obstructed extrahepatic biliary tree, percutaneously or via ERCP
features of haemangiomas
collection of small blood vessels
incidental finding on US or CT
No treatment required
Avoid biopsy
causes of adenomas
anabolic steroids, oral contraceptives, pregnancy
when to treat adenomas
Only treat if symptomatic or >5cm.
Pathology of pancreas carcinoma
Mostly ductal adenocarcinoma – metastasise early, present late
A few arise in ampulla of Vater or pancreatic islet cells (insulinoma, gastrinoma, glucagonomas, somatostinomas, VIPomas
2 clinical features of pancreas carcinoma
Tumours in the head of the pancreas present with painless obstructive jaundice
75% of tumours in the body and tail present with epigastric pain – radiates to back, relieved by sitting forward
4 complications of pancreas carcinoma
anorexia, weight loss, diabetes, acute pancreatitis
6 signs of pancreas carcinoma
Jaundice + palpable gallbladder
Epigastric mass
Hepatomegaly
Splenomegaly
Lymphadenopathy
Ascites
2 investigations for pancreatic carcinoma
Blood: cholestatic jaundice. Ca19-9 elevated – non-specific, but helps assess prognosis
Imaging
US or CT show pancreatic mass +/- dilated biliary tree +/- hepatic metastases
Guide biopsy and help staging prior to surgery
6 management options for pancreas carcinoma
Surgery – considering pancreaticoduodenectomy if fit and with no metastases
Post-op morbidity is high
Laparoscopic excision
Post-op chemotherapy to delay disease progression
Palliation of jaundice
Endoscopic or percutaneous stent insertion may help jaundice and anorexia
Pain – opiates or radiotherapy
what is intestinal obstruction
Blockage to the lumen of the gut. Commonly refers to blockage of intra-abdominal part of the intestine.
What is a volvulus
a twist/rotation of segment of bowel
what are bowel adhesions
sticking together (abdominal structures to one another, bowel loops or omentum, other solid organs, abdominal wall)
3 classes of mechanical classification of bowel obstruction
Mechanical (intraluminal)/ true (extraluminal)
Paralytic (pseudo obstruction)
4 classes of bowel obstruction according to pathology
Simple
Closed loop
Strangulation
Intussusception
2 common and 4 rare causes of small bowel obstruction
Adhesions (previous surgery)
Hernia
Rarer; Crohn’s, Malignancy, Volvulus, Intussusception
what is intussesception
the inversion of one portion of the intestine within another.
4 causes of large bowel obstruction
Colon carcinoma
Constipation
Diverticular stricture
Volvulus - Sigmoid
what is sigmoid volvulus
occurs when the bowel twists on its mesentery, which can produce severe, rapid, strangulated obstruction.
6 clinical manifestations of intestinal obstruction
Anorexia
Nausea
Vomiting:
Nature – forceful/ regurgitation
Content – bilious, feculent
Distension
Abdominal pain
Altered bowel habits:
Constipation
Obstipation
2 complications of intestinal obstruction
Tissue death – blood supply can be cut off to part of the intestine
Infection – peritonitis.
first line investigation for intestinal obstruction
X-ray
general principals of intestinal obstruction management
cause, site, speed of onset, and completeness of obstruction determine definitive therapy. Strangulation and large bowel obstruction require surgery; ileus and conservatively, at least initially.
immediate management of intestinal obstruction
NGT and IV fluids to rehydrate and correct electrolyte imbalance.
what further imaging is used for intestinal obstruction management
CT to establish the cause of obstruction.
which type of bowel obstruction requires emergency surgery
strangulation needs emergency surgery.
What are hernias
the protrusion of a viscus part or part of a viscus through a defect of the walls of its containing cavity into an abnormal position.
What is an irreducible hernia
contents cannot be pushed back into place
what is an obstructed hernia
bowel contents cannot pass – features of intestinal obstruction
What is a strangulated hernia
ischaemia occurs – the patient requires urgent surgery
What is an incarceration hernia
contents of the hernial sac are stuck inside by adhesions
what is the usual presentation of a hernia
Usually presents as lump and pain
pathology of femoral hernias
Bowel enters the femoral canal, presenting as a mass in the upper medial thigh or above the inguinal ligament where it points down the leg, unlike an inguinal hernia which points to the groin.
epideimiology and features of femoral hernias
Occur more often in women, middle age and elderly
Irreducible and strangulate
treatment of femoral hernias
surgical repair
What are incisional hernias and their repair
Follow breakdown of muscle closure after surgery
If obese, repair is not easy
Mesh repair – less recurrence but more infections compared to sutures
what are inguinal hernias
Indirect hernias pass through the internal inguinal ring and out through the external inguinal ring
Direct hernias push their way directly forward through the posterior wall of the inguinal canal, into a defect in the abdominal wall
4 predisposing conditions for inguinal hernias
Male sex
Chronic cough
Urinary obstruction
Past abdominal surgery
2 examinations for inguinal hernias
Is lump visible? Ensure it is not a scrotal lump
Ask patient to cough – should appear above and medial to pubic tubercle
Do direct or indirect inguinal hernias strangulate
Indirect hernias
repair of inguinal hernias
Lose weight and stop smoking pre-op
Hernias may recur
Mesh techniques – polypropylene mesh reinforces posterior wall
what is ischaemic colitis
Inflammation and injury of the large intestine resulting from inadequate blood supply.
pathology of ischaemic colitis
Usually follows low flow in the inferior mesenteric artery territory and it ranges from mild to gangrenous.
2 clinical manifestations of Ischaemic colitis
Lower left-sided abdominal pain
May have bloody diarrhoea
2 investigations for ischaemic colitis
CT may be helpful but lower GI colonoscopy is gold-standard.
management of ischaemic colitis
Treatment – usually conservative with fluid replacement and antibiotics
Most recover but subsequent development of ischaemic strictures is common
Gangrenous ischaemic colitis requires prompt resuscitation followed by resection of the affected bowel and stoma formation. Mortality is high.
what is mesenteric ischaemia
Injury to the small intestine occurs due to inadequate blood supply.
7 causes of acute mesenteric ischaemia
Superior mesenteric artery thrombosis/embolism
Mesenteric vein thrombosis
Non-occlusive disease
Trauma,
vasculitis,
radiotherapy
strangulation.
what is the classical clinical presentation triad for acute mesenteric ischaemia
Acute severe abdominal pain
No/minimal abdominal signs
Rapid hypovolaemia – shock
pain picture for acute mesenteric ischaemia
tends to be constant, central or around the right iliac fossa (RIF)
5 investigations for acute mesenteric ischaemia
High Hb due to plasma loss
High WCC, modestly raised plasma amylase
Persistent metabolic acidosis
Abdominal X-ray shows a gasless abdomen
Laparotomy – nasty, necrotic bowel
2 main life-threatening complications secondary to acute mesenteric ischaemia
Septic peritonitis
Progression of a systemic inflammatory response syndrome to multi-organ failure.
management of acute mesenteric ischaemia
Resuscitation with fluid, antibiotics and LMW heparin are required.
If arteriography is done, thrombolytics may be attempted on potentially viable bowel.
cause of chronic mesenteric ischaemia
Typically brought about through a combination of a low-flow state with atheroma.
3 clinical presentations of chronic mesenteric ischaemia
Severe, colicky post-prandial abdominal pain
Weight loss (painful to eat)
Upper abdominal bruit may be present
2 investigations for chronic mesenteric ischaemia
CT angiography and contrast-enhanced MR angiography
treatment of chronic mesenteric ischaemia
Once diagnosis is confirmed, surgery should be considered due to the ongoing risk of acute infarction.
Percutaneous transluminal angioplasty and stent insertion has replaced open revascularisation
what is appendicitis
Inflamed and painful appendix. It is the most common surgical emergency.
pathology of appendicitis
Gut organisms invade the appendix wall after lumen obstruction by lymphoid hyperplasia, faecolith or filarial worms. This leads to oedema, ischaemic necrosis and perforation.
5 clinical manifestations of appendicitis
Classic periumbilical pain that moves to the right iliac fossa.
Tachycardia
Fever
Percussion tenderness in RIF
Pain on the right during PR examination suggests an inflamed, low lying pelvic appendix
3 specific signs for appendicitis
Rovsing’s sign: greater pain in the RIF than the LIF when the LIF is pressed
Psoas sign: pain on extending hip if retrocaecal appendix.
Cope sign: pain on flexion and internal rotation of right hip if appendix in close relation to obturator internus.
5 differential diagnoses for appendicitis
UTI
Mesenteric adenitis
Diverticulitis/ cholecystitis/ cystitis
Food poisoning
Crohn’s disease
3 investigations for appendicitis
Blood tests may reveal neutrophil leucocytosis and elevated CRP
Ultrasound may help, but appendix not always visualised
CT has high diagnosis accuracy and is useful if diagnosis is unclear
management for appendicitis
Prompt appendicectomy
Antibiotics: piperacillin
Laparoscopy: diagnostic and therapeutic advantages. Not recommended with suspected gangrenous perforation – rate of abscess formation is higher.
3 complications of appendicitis
Perforation
Appendix mass – occurs when inflamed appendix becomes covered with omentum
Appendix abscess – if an appendix mass enlarges.
pathology of gallstones
Bile contains cholesterol, bile pigments and phospholipids. If concentrations vary, different stones may form.
features of pigment gallstones
small, friable and irregular.
features of cholesterol stones
large, often solitary.
features of mixed stones
faceted (calcium salts, pigment and cholesterol).
5 Fs for gallstones
Fair
Forty
Fertile
Fat
Female
clinical manifestations for gall stones in the gall bladder
Biliary pain
Cholecystitis
maybe Obstructive jaundice
clinical manifestations for gall stones in the bile duct
Biliary pain
Obstructive jaundice
Cholangitis
Pancreatitis
management options for gallstones
Laparoscopic cholecystectomy
Bile acid dissolution therapy
Bile duct stones:
ERCP with sphincterotomy and removal (balloon)/ crushing (laser)/ stent placement
Surgery (large stones)
5 complications for gallstones in the gall bladder and cystic duct
Biliary colic
Acute and chronic cholecystitis
Carcinoma
Mirizzi’s syndrome
3 complications for gallstones in the bile ducts
Obstructive jaundice
Cholangitis
Pancreatitis
what is gallstone ileus
when a gallstone erodes through the gallbladder into the ileum, causing complications
what is biliary colic
Gallstones are symptomatic with cystic duct obstruction or if passed into the common bile duct.
RUQ pain radiating to the back
Possible jaundice
investigations for biliary colic
urinalysis, CXR and ECG
treatment for biliary colic
analgesia, rehydrate. Elective laparoscopic cholecystectomy
What is acute cholecystitis
inflammation of gallbladder
Follows stone or sludge impaction in the neck of the gallbladder, which may cause continuous epigastric or RUQ pain, vomiting, fever, local peritonism or a GB mass.
High WCC (differs it from biliary colic)
If the stone moves to the CBD, obstructive jaundice and cholangitis may occur.
3 investigations for acute cholecystitis
high WCC
ultrasound – thick-walled, shrunken GB, pericholecystic fluid.
Plain AXR only shows 10% of gallstones.
treatment of acute cholecystitis
- NBM, pain relief, IVI and antibiotics e.g. co-amoxiclav.
what is flatulent dyspepsia
Vague abdominal discomfort
Distension
Nausea
Flatulence
Fat intolerance (fat stimulates cholecystokinin release and GB contraction)
investigations for chronic cholecystitis
Ultrasound to image stones and assess CBD diameter. MRCP is used to find CBD stones.
treatment of chronic choleystitis
cholecystectomy.
pathology of acute pancreatitis
Pancreatitis is characterised by self-perpetuating pancreatic enzyme-mediated autodigestion; oedema and fluid shifts cause hypovolaemia, as extracellular fluid is trapped in the gut, peritoneum and retroperitoneum.
GET SMASHED causes for acute pancreatitis
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia/ hypothermia/ hypercalcaemia
ERCP and emboli
Drugs
symptoms of acute pancreatitis
Gradual or sudden severe epigastric or central abdominal pain. Vomiting prominent.
Pain radiates to back, sitting forward may relieve.
6 signs for acute pancreatitis
High heart rate
Fever
Jaundice
Shock
Rigid abdomen with local/general tenderness
Periumbilical bruising (Cullen’s) or flanks (Grey Turner’s) from blood vessel autodigestion
3 investigations for acute pancreatitis
Raised serum amylase – excreted renally so renal failure will increase levels.
Serum lipase is more sensitive and specific for pancreatitis – rises earlier and falls later.
CT: assess severity and complications
management of acute pancreatitis
Nil by mouth
Analgesia
Hourly pulse, BP and urine output: daily FBC, U&E, Ca2+, glucose, amylase
ERCP and gallstone removal
Repeat imaging is performed to monitor progress
3 early complications of acute pancreatitis
Shock
Renal failure
Sepsis
3 late complications of acute pancreatitis
Pancreatic necrosis and pseudocyst
Bleeding from elastase eroding a major vessel
Thrombosis may occur in splenic arteries causing bowel necrosis
what is chronic pancreatitis
A chronic inflammatory process of the pancreas, leading to irreversibly low pancreatic function.
pathology of acute pancreatitis
Chronic inflammation in the pancreas leads to the replacement of functional pancreatic tissue by fibrous scar tissue.
4 causes of chronic pancreatitis
Alcohol
Smoking
Autoimmune
Pancreatic duct obstruction
3 clinical presentations of chronic pancreatitis
Persistent upper abdominal pain and weight loss
Radiates to the back and is relieved by sitting forward or hot water bottles on epigastrium/back
Steatorrhea and diabetes mellitus occur late once most of the gland is destroyed
Brittle diabetes
4 investigations for chronic pancreatitis
Ultrasound and CT scan: pancreatic calcifications confirm the diagnosis.
MRCP, AXR – speckled calcification
3 management options for chronic pancreatitis
Drugs: give analgesia and fat-soluble vitamins
Diet: no alcohol, low fat may help
Surgery: e.g. pancreatectomy for unremitting pain/ weight loss
4 complications of chronic pancreatitis
Diabetes
Biliary obstruction
Local arterial aneurysm
Gastric varices
features of liver failure
Loss of the liver’s ability to regenerate or repair.
Liver failure may be recognised by the development of coagulopathy and encephalopathy. This may occur suddenly in the previously healthy liver (acute liver failure), but it more often occurs on a background of cirrhosis (chronic liver failure).
what is fulminant hepatic failure
a clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function.
3 infection causes of liver failure
viral hepatitis, yellow fever, leptospirosis
3 drug causes of liver failure
paracetamol overdose, halothane, isoniazid
2 toxin causes of liver failure
Carbon tetrachloride, Amanita phalloides mushroom
2 vascular causes of liver failure
Budd-Chiari syndrome, veno-occlusive disease
7 misc. causes of liver failure
alcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, haemochromatosis, autoimmune hepatitis, metabolic causes, malignancy.
what is Budd-Chiari syndrome
hepatic vein obstruction by thrombosis or tumour causes congestive ischaemia and hepatocyte damage.
pathophysiology of liver failure
Destruction of hepatocytes
Development of fibrosis in response to chronic inflammation
Destruction of the architecture of the nodules of the liver removes the ability of the liver to adequately perform functions, repair and regenerate
7 clinical presentations of liver failure
Abnormal bleeding
Ascites
Jaundice
Hepatic encephalopathy
Fetor hepaticus (sweet and musty breath)
Constructional apraxia
Mental state drowsiness and confusion, due to cerebral oedema
3 investigations of liver failure
Blood: FBC – LFTs, clotting, hepatitis, paracetamol level, ferritin
Raised bilirubin
Glucose low – no glycogenesis
Microbiology: blood culture, urine culture, neutrophils >250/mm3 indicates spontaneous bacterial peritonitis
Radiology: CXR, abdominal US, Doppler flow studies of the portal vein
8 management steps of liver failure
Beware of sepsis, hypoglycaemia, GI bleeds/ varices, encephalopathy.
Protect airway with intubation and insert a tube to avoid aspiration and remove any blood from the stomach
Insert urinary and central venous catheters to help assess fluid status
Treat the cause
Treat seizures with phenytoin
Hemofiltration/ haemodialysis
Avoid sedatives/ other drugs with hepatic metabolism
LIVER TRANSPLANT
4 complications of liver failure
Cerebral oedema, bleeding, encephalopathy, ascites
7 symptoms of acute hepatitis
Can be asymptomatic
General malaise
Myalgia
GI upset
Abdominal pain
+/- jaundice (pale stools, dark urine)
Tender hepatomegaly
6 viral causes of hepatitis
hepatitis A,B,C,D,E, herpes virus
4 non-viral causes of hepatitis
Spirochaetes
Mycobacteria
Parasites
Bacteria
3 non-infection causes of hepatitis
Alcohol
Toxins/poisoning
Autoimmune
4 signs of compensated chronic hepatitis
Dupuytren’s contracture
Spider naevi
LFTs can be normal
Compensated – liver function maintained
8 signs of decompensated chronic hepatitis
Dupuytren’s contracture
Spider naevi
LFTs can be normal
jaundice
ascites
low albumin
coagulopathy
encephalopathy
how is hepatitis A spread
faecal-oral or shellfish
incubation time of hep.A
2-6weeks
5 symptoms of hep.A
Fever
Malaise
Anorexia
Nausea
Arthralgia
3 investigations for hep.A
AST and ALT rise 22-40d after exposure, returning to normal over 5-20wks
IgM rises due to recent infection
IgG is detectable for life
treatment for Hep.A
Supportive
Monitor liver function
Fulminant hepatitis failure/ acute liver failure
how does hep.B spread
blood borne, IV drug abusers, sexual, direct contact
5 risk groups for hep.B
IV drug abusers and their sexual partners/carers, health workers, haemophiliacs, sexually promiscuous
incubation period of Hep.B
Incubation: 1-6 months
Signs for hep.B
Resemble hepatitis A but arthralgia and urticaria are commoner
2 investigations for hep.B
HBsAg (surface antigen) is present 1-6months after exposure
Antibodies imply past infection
how is vaccinations used for hep.b
high risk groups vaccinated
passive immunisation may be given to non-immune contacts after high-risk exposure
also prevents HDV
3 complications of hep.b
Fulminant hepatic failure
Cirrhosis
Membranous nephropathy
4 treatment steps for hep.b
Avoid alcohol
Immunise sexual contacts
Antivirals
Supportive
spread of hepatitis C (HCV)
blood transfusion, IV drug abuse, sexual contact
risk factors for progression of HCV
male, older, higher viral load, use of alcohol, HIV
2 investigations for HCV
LFTs
Anti-HCV antibodies confirms exposure
3 treatments for HCV
Non-structural viral protein inhibitors.
Quit alcohol
Directly acting antivirals
3 complications for HCV
Glomerulonephritis
Thyroiditis
Autoimmune hepatitis
spread of HDV
via blood and bodily fluids.
test for HDV
anti-HDV antibody
treatment of HDV
pegylated interferon-alpha. If limited success – liver transplant.
transmission of HEV
via faecal-oral route (food, contaminated water, undercooked seafood and pork)
5 acute presentations of HEV
Fever, malaise, nausea + vomiting, jaundice, hepatomegaly
investigations for HEV
Serum ALT and AST raised, bilirubin raised, ESR raised
HEV serology: HEV IgM antibodies = active infection. HEV IgG antibodies = recovery. HEV RNA = current infection
Management of HEV
1st line – no treatment. Very mild illness which is self-limiting within a month. It is a notifiable disease. No vaccine available.
4 complications of HEV
Complications Chronic hepatitis, liver failure (especially in pregnant women), cirrhosis, hepatocellular carcinoma
what is liver cirrhosis
Cirrhosis implies irreversible liver damage. Histologically, there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.
7 causes of Cirrhosis
Most common: Alcoholic liver disease, non-alcoholic fatty liver disease, hepatitis B, hepatitis C
Rarer: haemochromatosis, Wilson’s disease, alpha 1 trypsin deficiency
5 clinical manifestations of cirrhosis
Leukonychia: white nails with lunulae undermarcated, from hypoalbuminemia
Ectasias
Palmar erythema (red palms)
Hyperdynamic circulation
Hepatomegaly
5 complications of cirrhosis leading to liver failure
Coagulopathy (failure of hepatic synthesis of clotting factors)
Encephalopathy
Hypoalbuminaemia
Sepsis
Spontaneous bacterial peritonitis
3 complications of cirrhosis leading to portal hypertension
Ascites
Splenomegaly
Portosystemic shunt including oesophageal varices
3 investigations for cirrhosis
Blood: LFT – increased bilirubin, AST, ALT, ALP
Low albumin
Low WCC and platelets indicate hypersplenism
Liver ultrasound – may show a small liver or hepatomegaly, splenomegaly
MRI – increased caudate lobe size
management of cirrhosis
General:
Good nutrition is vital
Alcohol abstinence
Ascites:
Fluid restriction, low-salt diet
Transplant
what is primary biliary cholangitis
Autoimmune disease of the liver. Results from a slow, progressive destruction of the small bile ducts of the liver, causing bile and other toxins to build up in the liver (cholestasis).
Pathology of Primary biliary cholangitis
Interlobular bile ducts are damaged by chronic autoimmune granulomatous inflammation causing cholestasis (may lead to fibrosis, cirrhosis and portal hypertension).
cause of primary biliary cholangitis
Unknown environmental triggers (possibly pollutants, xenobiotics) and a genetic predisposition leading to loss of immune tolerance to self-mitochondrial proteins.
5 clinical manifestations of primary biliary cholangitis
Often asymptomatic and diagnosed after incidental finding high ALP.
Lethargy, sleepiness and pruritus (skin itching) may precede jaundice.
Jaundice
Skin pigmentation
Hepatosplenomegaly
3 investigations for primary biliarycholangitis
Blood: high ALP, mildly high AST and ALT. High bilirubin and low albumin
Ultrasound; excludes extrahepatic cholestasis
Biopsy: not usually needed but can be used to look for granulomas around bile ducts.
management of primary biliary cholangitis
For symptomatic patients try cholestyramine.
Fat-soluble vitamin prophylaxis
Monitoring: regular LFT and ultrasound twice yearly
Liver transplantation: end-stage disease
What is alcholic liver disease
Liver disease due to excessive alcohol consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with liver fibrosis or cirrhosis.
pathology of alcoholic liver disease
Alcohol metabolism in the liver generates high levels of NADH which stimulates fatty acid synthesis and production of triglycerides, leading to steatosis.
Oxidative stress from metabolism of alcohol leads to hepatocyte injury and necro-inflammatory activity (ASH – alcoholic steatohepatitis). Ongoing, this causes liver fibrosis which may progress to cirrhosis
4 clinical manifestations of alcoholic liver disease
Steatosis (fatty liver cells which disturbs metabolism) and mild ASH are usually asymptomatic but are a common cause of mildly abnormal LFTs.
Severe alcohol hepatitis following binge drinking causes malaise and fever.
Jaundice
Complications of cirrhosis e.g. ascites or ruptured oesophageal varices
how does alcohol affect the liver
Fatty liver – acute/reversible, but can progress to cirrhosis
Alcoholic hepatitis – can progress to cirrhosis
Cirrhosis – irreversible liver damage
How does alcohol affect the CNS
self neglect, decreased memory function, cortical atrophy
how does alcohol affect the gut
obesity, peptic ulcers, varices, pancreatitis, cancer
how does alcohol affect blood
high MCV, anaemia from marrow depression and GI bleeding
how does alcohol affect the heart
arrhythmias, high BP, cardiomyopathy
how does alcohol affect reproductive system
testicular atrophy
investigation for alcohol hepatitis
Blood: high WCC, low platelets, high MCV, high urea
management of alcoholic liver disease
PREVENTION – CAGE questions
ALCOHOL WITHDRAWAL – alcohol free beers may be helpful to patients with addiction to alcohol
Acamprosate may help intense anxiety, insomnia and craving after alcohol withdrawal.
CAGE questions for alcohol
Ever felt you ought to Cut down on your drinking?
Have people Annoyed you by criticising your drinking?
Ever felt Guilty about your drinking?
Ever had an Eye-opener in the morning?
What is wilsons disease
An inherited disorder of copper metabolism, leading to the accumulation of toxic levels of copper in the liver and brain.
Pathology of wilsons disease
Possession of two mutated ATP7B alleles on chromosome 13 causes disruption of normal copper transport and accumulation of toxic levels of copper in hepatocytes and basal ganglia.
5 clinical manifestations of wilsons
Most present in childhood or early adulthood with chronic liver disease or cirrhosis.
A small proportion of patients present in hepatic failure
About half of patients also develop neuropsychiatric symptoms due to copper accumulation in the brain
CNS signs
Kayser-Fleischer (KF) rings: copper in iris
4 CNS signs of wilson’s
Tremor
Dysarthria (unclear articulation of speech)
Dysphagia
Parkinson’s
6 investigations for wilsons
Urine: 24h copper excretion is high (>100mcg, normal is <40mcg)
High LFT
Serum copper - <11μmol/L
Molecular genetic testing can confirm the diagnosis
Slit lamp exam: KF rings seen in iris
Liver biopsy: raised hepatic copper
management of wilsons
Diet: avoid foods with high copper content e.g. chocolate, nuts, mushrooms.
Drugs: lifelong penicillamine
Liver transplant in severe liver failure
Screen siblings – asymptomatic homozygotes need treating.
5 side effects of penicillamine
nausea, rash, low WCC, Hb and platelets
What is hereditary haemochromatosis
An inherited disorder characterised by increased intestinal absorption of iron, leading to iron overload in multiple organs, particularly the liver and sometimes leading to organ damage
pathology of Hereditary haemochromatosis
Hepcidin controls plasma iron concentrations by inhibiting iron export by ferroportin from duodenal enterocytes and macrophages.
Deficiency of hepcidin results in raised plasma iron concentrations and accumulation in multiple organs, including the liver, pancreas, heart, joints and pituitary.
6 clinical manifestations of haemochomatosis
Early symptoms are non-specific e.g. fatigue and arthropathy
Later symptoms;
Skin pigmentation (slate-grey)
Cirrhosis
Hypogonadism
Cardiac failure
Diabetes mellitus
3 investigations for haemochromatosis
Blood: high LFT and ferritin levels are raised
Images: chondrocalcinosis (haemochromatosis causes stressed joints to deteriorate faster than resting joints, and this is visible on X-rays).
Liver and cardiac MRI
Liver biopsy: Perl’s stain quantifies iron loading and assesses severity of disease
3 management options for haemochromatosis
Venesection (removal of accumulating iron) until ferritin <50mcg/L. Iron will continue to accumulate, so maintenance venesection will be needed for life.
Diet: a well-balanced diet should be encouraged, avoiding alcohol but no need to avoid iron-rich foods. Avoid uncooked seafood.
Screening: serum ferritin, transferrin saturation.
what is α1-antitrypsin deficiency
An inherited disorder affecting the lungs (emphysema) and the liver (cirrhosis).
pathology of α1-antitrypsin deficiency
Lung A1At protects against tissue damage from neutrophil elastase. Deficiency means there is no protection and leads to emphysema in adults and liver disease in children.
It is also one of a family of serine protease inhibitors made in the liver, that control inflammatory cascades.
clinical manifestations of α1-antitrypsin deficiency
Symptomatic patients usually have the PiZZ genotype ( both parents carriers):
Dyspnoea from emphysema
Cirrhosis
Cholestatic jaundice
4 investigations for α1-antitrypsin deficiency
Serum α1-antitrypsin levels low
Lung function testing: reductions in FEV1 with obstructive pattern
Liver biopsy: periodic acid Schiff (PAS)
Phenotyping: distinguish between SZ and ZZ phenotypes
4 management options for α1-antitrypsin deficiency
Smoking cessation
Prompt treatment/ preventative vaccination for lung infections.
Liver transplanted – needed in decompensated cirrhosis
Lung transplant – improves survival
What is Ascites
Effusion and accumulation of serous fluid (protein-containing) in the abdominal cavity.
Classification of ascites
Stage 1 detectable only after careful examination/ ultrasound scan (mild)
Stage 2 easily detectable but of relatively small volume
Stage 3 obvious, not tense ascites (moderate)
Stage 4 tense ascites (large)
What is the pathology of portal hypertension ascites
A state of sodium water imbalance
Interplay of various neurohormonal agents – renin, aldosterone, sympathetic nervous system, nitric oxide
Over filling – inappropriate Na + H2O retention – no volume depletion – hypervolemia
pathology of non-portal hypertensive ascites
Malignancy
Cardiac failure
Nephrotic syndrome
pathology of Chylous ascites
Abdominal surgery/ trauma, malignancy, radiation, congenital
5 causes of ascites
Cirrhosis
Malignancy
Heart failure
TB
Pancreatitis
4 symptoms of ascites
Abdominal distension – clothes getting tighter
Nausea, loss of appetite
Constipation
Weight loss
3 signs of ascites
Flanks fullness
Fluid thrill
Shifting dullness
3 investigations for ascites
Naked eye assessment – swollen stomach
Chemistry: proteins and amylase
Ultrasound scan and abdominal CT
management of ascites
Treat underlying cause
Diuretics – spironolactone, metolazone
Salt and fluid restriction
complication of ascites
Can lead to spontaneous bacterial peritonitis.
What is peritonitis
Inflammation of the peritoneum.
what is peritonism
tensing muscles to prevent movement of peritoneum.
5 causes of peritonitis
Cholecystitis
Pancreatitis
Appendicitis
Diverticulitis
AEIOU
AEIOU causes for peritonitis
appendicitis, ectopic pregnancy, infection (TB), obstruction, ulcer.
6 inflammatory agents for peritonitis
inflamed organs, air, pus, faeces, luminal contents and blood.
pathology of 4 causes of peritonitis
Medical causes – spontaneous bacterial peritonitis, pelvic inflammatory disease, dialysis related, TB
Surgical causes – perforation of GIT e.g. trauma, appendicitis, cancer
Sterile – pancreatitis, familial Mediterranean fever
Perforation of peptic/duodenal ulcer
8 clinical manifestations of peritonitis
Abdominal pain
Diarrhoea
Swelling
Swinging fever
Prostration
Shock
Tenderness + rebound/percussion pain
Board-like abdominal rigidity
2 differential diagnoses for peritonitis
Appendicitis
Angioedema
3 investigations for peritonitis
Ultrasound/ CT scan
Ascitic tap: Raised WCC (neutropil)
Erect CXR may show gas under diaphragm
5 complications of peritonitis
Sepsis
Multi-organ failure
CV events (MI, stroke)
Respiratory complications (pneumonia, pulmonary embolus)
Surgical complications
4 surgical management options for peritonitis
Laparotomy
Laparoscopy
Treat problem – patch hole, remove organ/cause
Wash out infection
4 management options for peritonitis
Surgery
Intensive care
Support of kidneys
Physio/early mobilisation
what is a Diverticulum
an outpouching of the gut wall, usually at sites of entry of perforating arteries.
what is diverticulitis
refers to inflammation of a diverticulum.
what is diverticular disease
symptomatic diverticula
cause of diverticular disease
A diet low in fibre and high in meat is the strongest risk factor.
pathology of diverticular disease
Firm stools require higher intraluminal pressures to propel
High intraluminal pressure forces pouches of the colonic mucosa through an anatomical weak point in the muscular layer where blood vessels pass through to supply the mucosal layer.
presentation of diverticular disease
Intermittent abdominal pain, altered bowel habit, iron deficiency anaemia
Acute inflammation in a diverticulum presents with severe left iliac fossa pain
Occasionally, erosion of a large submucosal vessel can cause severe rectal bleeding.
4 investigations for diverticular disease
Diverticula are a common incidental finding at colonoscopy
CT abdomen is best to confirm acute diverticulitis and can identify extent of disease and any complications
Colonoscopy risk perforation in acute setting
AXR may identify obstruction or free air
management of diverticular disease
Try antispasmodics e.g. mebeverine
Surgical resection occasionally needed
management of diverticulitis
Mild attacks can be treated at home with bowel rest (fluids only) and antibiotics
Most attacks settle but complications include abscess formation or perforation.
What are haemorrhoids
Abnormally dilated and prolapsed anal cushions
Extremely common
Thought to be due to disruption of the normal suspensory mechanisms caused by chronic straining at stool
what are complications of haemorrhoids
Cause bright red rectal bleeding and discomfort
what are anal tags
Polypoid projections of the anal mucosa and submucosa
histology of haemorrhoids
Excised haemorrhoids examined microscopically contain large dilated blood vessels, which may show evidence of thrombosis, with an overlying hyperplastic squamous epithelium.
histology of anal tags
Microscopically composed of a fibrovascular core covered by squamous epithelium. The fibrovascular core lacks the typically ecstatic vessels of haemorrhoids
What is an anal fissure
A tear in the mucosa of the lower anal canal which is most always located posteriorly in the midline
cause of anal fissures
Cause is unclear, but chronic infection may lead to loss of the normal elasticity of the mucosa, such that passage of hard faeces may precipitate the tear
what is an anorectal abscess
A collection of pus within deep perianal tissue
A complication of infection within a deep anal gland
presentation of anorectal abscess
perianal erythema, swelling and pain
What is an anorectal fistula
An abnormal epithelial-line tract connecting the anal canal to the perianal skin
Usually the result of infection in an anal gland tracking to the skin surface
What causes anal cancer
Uncommon and invariably associated with HPV infection
what type of cancer are the majority of anal cancers
Vast majority are squamous cell carcinomas which arise from areas of squamous dysplasia known as anal intraepithelial neoplasia which is graded 1-3.
Gold standard investigations for chrons
Colonoscopy and biopsy (granulomatous transmural inflammation. Skip lesions, cobblestone appearance. Strictures “string sign”)
