Gastroenterology Flashcards
How do you make a diagnosis of C diff infection and how do you determine severity?
Diagnose by detecting CDT (toxin) in stool
WCC to determine severity
Risk factors for C diff?
abx and PPIs
esp cephalosporins
What is the tx stepladder for C diff infections?
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy/ in life- threatening cases: oral vancomycin +/- IV metronidazole
What drugs must be stopped before a urea breath test?
no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks
What is achalasia?
Most important diagnostic test?
What cancer does it increase the risk of?
How is it treated?
Definition: Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated.
Presents with dysphagia of both solids and liquids from onset
Key test: Oesophageal manometry
- also shows grossly expanded oesophagus, fluid level and ‘bird’s beak’ appearance on barium swallow
increases the risk of squamous cell carcinoma of the oesophagus
First line: pneumatic (balloon) dilation
Surgical management when comorbidites/recurrence : Heller cardiomyotomy
How is appendicitis diagnosed?
Thin young male patients with a high likelihood of appendicitis (classic central abdominal pain that localises to the right iliac fossa) can be diagnosed clinically w/o a scan
Often do an USS in women for pelvic pathology
Raised inflammatory markers (e.g. CRP) and neutrophil predominant leucocytosis can aid in diagnosis
May be psoas sign positive- unable to stand on one leg comfortably and pain on hip extension
Best way to measure liver function in people with established disease?
Liver enzymes are a poor way to look at liver function - they are usually low in end-stage cirrhosis whereas coagulation e.g. prothrombin time and albumin are better measures
What is fetor hepaticus?
sweet and fecal breath, it is a sign of liver failure
Causes of acute liver failure?
paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
Features of acute liver failure?
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)
Raised urea + normocytic anaemia= ?
How much does urea need to be raised to be a significant case?
Upper GI bleed!
- a haemorrhage with an origin proximal to the ligament of Treitz
Urea is from protein meal (digestion of RBCs)
Urea of 15.4 mmol/l on a background of normal renal function is a significant bleed
Management of Upper GI bleed?
All patients with suspected upper GI bleed require an endoscopy within 24 hours of admission
IV PPIs given AFTER endoscopy (never before) if evidence of recent variceal haemorrhage
Repeated endoscopic intervention with no success (more acute bleeds) = surgical intervention
How is risk stratified in Upper GI bleeding?
the Glasgow-Blatchford score used at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not
the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
Eq for alcohol units?
Alcohol units = volume (ml) * ABV / 1,000
Cause of metabolic acidosis in non-diabetic alcoholics? Tx?
Alcoholic ketoacidosis
- Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation and ketone production
Will likely have normal or low blood glucose
treatment is an infusion of saline & thiamine
AST/ALT ratio in alcoholic hepatitis?
2:1
Management of alcoholic hepatitis?
glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
Maddrey’s discriminant function (DF) is often used to determine who would benefit from glucocorticoid therapy
- its calculated using prothrombin time and bilirubin concentration
pentoxyphylline is also sometimes used
Key investigation in unwell patient taking aminosalicylates?
A patient who is taking aminosalicylates and becomes unwell with a sore throat, fever, fatigue or bleeding gums needs an urgent full blood count to rule out agranulocytosis.
What do Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) with raised IgG suggest?
Type 1 autoimmune hepatitis- common in young women, often also see secondary amenorrhea, tx with steroids
When is endoscopic intervention ( endoscopic mucosal resection or radiofrequency ablation) offered with Barrett’s oesophagus?
When dysplasia is seen
If not pts can be managed with endoscopic surveillance every 3-5 years and a high dose PPI
how does Budd-Chiari present and how is it investigated?
Budd-Chiari syndrome (hepatic vein thrombosis):
Presents with the triad of sudden onset abdominal pain, ascites, and tender hepatomegaly
Can do a Serum - Ascites Albumin Gradient (a raised SAAG (>11g/L) indicates that it is portal hypertension that has caused the ascites and makes Budd-Chiari more likely)
Investigate with doppler USS
For carcinoid syndrome (release of serotonin into systemic circulation), outline the presentation, test and tx
carcinoid syndrome-
Sx: flushing, diarrhoea, bronchospasm, hypotension, and weight loss
Caused by lung carcinoid or more commonly mets in the liver
Test urinary 5-HIAA
Give somatostatin analogues e.g. octreotide
Features of coeliac?
Coeliac disease:
- non specific symptoms like fatigue, anaemia and weight loss
- low ferritin/folate
- raised white cells/CRP due to inflammation
- raised tissue transglutaminase (TTG) antibody
- grey frothy stool
Coeliac disease increases the risk of developing enteropathy-associated T cell lymphoma
How long before testing should coeliac patients eat gluten? What is being tested for in serology?
6 weeks
tissue transglutaminase (TTG) antibodies (IgA)
How is disease progression monitored in Crohn’s and how is it managed?
ESR can be used to assess disease progression
first-line management strategy for the induction of remission is glucocorticoids
Azathioprine or mercaptopurine is used first-line to maintain remission
Managing complications:
MRI is the investigation of choice for suspected perianal fistulae- provides visualisation of the course
Wound swab can be used for recurrent abscesses
Management of ‘undiagnosed’ dyspepsia?
Patient with dyspepsia who does not meet referral criteria:
do a full work up before anything else e.g bloods and review meds for common drug-induced causes such as NSAIDs and aspirin
give lifestyle advice
trial PPI for one month
If PPI fails for reflux and upper GI symptoms test for H.pylori
When is urgent referral required for dyspepsia?
All patients who’ve got dysphagia
All patients who’ve got an upper abdominal mass consistent with stomach cancer
Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia
What tests are needed in a pt with GORD being considered for surgery?
oesophageal pH and manometry studies- measures pressure in oesophageal sphincter to confirm diagnosis
Sign on biopsy in gastric cancer?
Signet ring cells - more = worse prognosis
What is Gilbert’s syndrome and how does it present?
autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase
An isolated rise in bilirubin in response to physiological stress (e.g. onset of jaundice exclusively while ill, exercising or fasting) is typical
No treatment required
Describe presentation, investigation and management of hereditary haemochromatosis
Haemochromatosis : aut. dom. disorder of iron absorption
Presentation:
bronze/ slate grey colouration
fatigue and cognitive sx
joint pain - can have secondary osteoarthritis (hook-like osteophytes at the 2nd and 3rd digits at MCPJ)
hair loss
erectile dysfunction
Investigation:
general population: transferrin saturation > ferritin
family members: HFE genetic testing
(can also do liver biopsy w Perl’s stain)
Management:
venesection
Ferritin and transferrin saturation are used to monitor treatment
Describe presentation and tx of hepatic encephalopathy
Hepatic encephalopathy:
Liver disease -> build up of ammonia and glutamine ( liver cell impairment prevents adequate metabolism and portosystemic anastomoses mean blood can bypass the liver altogether)
Presentation: altered GCS, acute confusion, asterixis (hepatic flap) and triphasic slow waves on ECG
Graded 1- 4 : Irritability -> confusion -> incoherence -> coma
Tx: lactulose first line to excrete ammonia , then rifaximin to alter gut flora and breakdown of ammonia there
What is indicated by:
1. HBsAG
2. Anti-HBc
3. Anti-HBc IgM
4. Anti-HBc IgG
5. Anti-HBs
6. HbeAg
- first surface antigen to be produced in response to infection, represents acute hepatitis infection if less than 6mo or chronic if present for over 6mo. If it is negative they are not currently infected.
- anti hepatitis core antibody is produced in response to infection- c for caught- currently or has previously caught hepatitis
- IgM- acute infection
- IgG- chronic infection, remains indefinitely even if hepatitis is cleared (IgM are produced in initial infection and are gradually replaced with IgG over months)
- immunisation (in a healthy individual who has been vaccinated this is the only one that is raised)
- results from breakdown of core antigen from infected liver cells. Marker of HBV replication and infectivity
What is the Sister Mary Joseph node?
a palpable nodule in the umbilicus due to metastasis of malignant cancer within the pelvis or abdomen
Describe the nature of hepatomegaly in:
Early cirrhosis
Malignancy
RHF
Hepatomegaly:
Cirrhosis (in early disease): Associated with a non-tender, firm liver
Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular liver edge
Right heart failure: firm, smooth, tender liver edge. May be pulsatile
Most common disease pattern in UC and Crohn’s?
UC- proctitis
Crohn’s- ileitis
Tx of IBS?
IBS Tx:
pain: antispasmodic agents
constipation: laxatives but avoid lactulose ( first line isphagula husk, linaclotide can be used as an alternative to conventional laxatives if nothing else works for 12 months)
diarrhoea: loperamide is first-line
Features and test for acute mesenteric ischaemia (occlusion of blood flow to small bowel)
Common features
abdominal pain - often of sudden onset, severe and not inkeeping with physical exam findings
fever
rectal bleeding and diarrhoea
often have a hx of AF
Investigation:
Venous blood gas first line to look for raised lactate
What is ischemic colitis? Sign on Xray?
Transient compromise in blood flow to large bowel
Often occurs in watershed areas like splenic flexure
Thumb-printing seen on xray
Give 3 causes of liver cirrhosis. Investigation of choice?
Causes:
alcohol
non-alcoholic fatty liver disease (NAFLD)
viral hepatitis (B and C)
Transient elastography is now the investigation of choice
What is Melanosis coli?
Melanosis coli is the abnormal pigmentation of the large bowel due to the presence of pigment-laden macrophages. It is most commonly due to laxative abuse
Briefly differentiate between Mallory Weiss, Plummer Vinson Syndrome and Boerhaave Syndrome
Mallory-Weiss syndrome
Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics
Plummer-Vinson syndrome:
triad of dysphagia, glossitis and iron-deficiency anaemia
(dysphagia is due to post cricoid webs)
tx is iron supplements and dilation of webs
Boerhaave syndrome:
Severe vomiting → oesophageal rupture
Chest pain and subcut emphysema also feature
key investigation for a suspected perforated peptic ulcer?
Erect CXR to look for pneumoperitoneum
Difference between duodenal and gastric ulcers?
Duodenal ulcers characteristically cause pain when hungry, and are relieved by eating
Gastric ulcers are worse with food
Outline presentation and tx of pernicious anaemia
Pernicious anaemia: autoimmune disorder that causes B12 deficiency
antibodies to IF
middle/old age patients, more common in females
anaemia features (headache, fatigue, pallor)
neuro features - peripheral neuropathy, psychiatric changes
Can have pancytopenia
Tx= IM Vit B12
Vitamin B12 1mg IM three times/week then 1mg IM every 3 months
folate should never be replaced before vitamin B12 due to the risk of precipitating subacute combined degeneration of the cord. (Think BeFore: B before F to remember).
What is Peutz Jehgers syndrome?
Aut. dom condition
Hamartomatous polyps in GI tract (often presents with small bowel obstruction)
Pigmented freckles on lips, palms and soles
Dysphagia, aspiration pneumonia, halitosis (bad breath) →
pharyngeal pouch
Investigate with barium swallow
Outline presentation and management of primary biliary cholangitis
Chronic autoimmune condition, bile ducts damaged by inflammation, often presents with itching or jaundice or raised ALP on routine bloods
Imaging required to rule out extra-hepatic biliary obstruction
Management : ursodeoxycholic acid 1st line, then cholestyramine for itching
What is SBBO? Give risk factors, diagnostic test and tx.
Small bowel bacterial overgrowth syndrome:
excessive bacteria in SI
presents w chronic diarrhoea and flatulence
scleroderma and diabetes are risk factors, as well as neonates w congenital GI issues
hydrogen breath test to diagnose
treat with rifaximin
For SBP, give the presentation, diagnostic test and tx.
Features:
ascites, abdominal pain, fever
Diagnosis is by paracentesis. Confirmed by neutrophil count >250 cells/ul
Managed with IV cefotaxime (E.coli infection)
what should you do when there is evidence of systemic disturbance and increase in bloody stool in patient with UC?
abdo xray to look for toxic megacolon
Outline tx of flares in UC
In a mild-moderate flare of distal ulcerative colitis, the first-line treatment is topical (rectal) aminosalicylates e.g. mesasalazine and if no response then it should be given orally
(In a mild-moderate flare extending past the left-sided colon, oral aminosalicylates should be added to rectal as enemas only reach so far)
A severe flare of ulcerative colitis (e.g. tachycardic and febrile) should be treated in hospital with IV corticosteroids
Give tx for:
- prophylaxis of variceal bleeding
- acute variceal bleeding
- uncontrolled variceal haemorrhage
- non selective BB e.g. propanolol
- terlipressin
- A Sengstaken-Blakemore tube
What supplement is routinely recommended in alcoholism?
Thiamine
Give the 4 Ds of pellagra (Vit B deficiency )
Dermatitis (sunburn like), diarrhoea, dementia/delusions, leading to death
Describe presentation and tx of Wilson’s disease
Wilsons disease- aut. dom. reduced serum copper (deposited in tissues)
Presentation:
Usually 10-25
Presents with liver disease in kids and neuro issues in adults
can appear like a mental illness e.g. schizophrenia
brown rings in the eyes (Kayser-Fleischer rings), blue nails, dystonia
reduced serum copper and reduced caeruloplasmin (binds copper)
Tx: penicillamine
What is Zollinger-Ellison syndrome? Give features and screening test
Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome
Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption
Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test
What can you do to reduce mortality when doing a high vol ascitic drain?
give IV human albumin solution
What is the M rule for primary biliary cholangitis?
Primary biliary cholangitis - the M rule
IgM raised
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
Causes of drug-induced cholestasis?
COCP
antibiotics
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas and fibrates
What do hypersegmented polymorphs show?
Early sign of megaloblastic anaemia
Most common cause of hepatocellular carcinoma?
How does it present?
hepatitis B most common cause worldwide
hepatitis C most common cause in Europe
Occurs secondary to liver cirrhosis
Presents late with features of liver disease e.g. jaundice and raised alpha fetoprotein on bloods
Investigation of choice in pancreatic cancer?
High-resolution CT scanning
May see double duct sign caused by dilation of the common bile duct and pancreatic duct in response to the tumour
What is seen on histology in Crohn’s?
Inflammation in all layers from mucosa to serosa
increased goblet cells
granulomas
What is seen on histology in UC?
No inflammation beyond submucosa
crypt abscesses
depletion of goblet cells and mucin
A 62-year-old presents with upper abdo pain. She has recently been discharged from hospital where she underwent an ERCP to investigate cholestatic liver function tests. The pain is severe. On examination she is apyrexial and has a pulse of 96 / min. Likely diagnosis?
Acute pancreatitis- Pancreatitis may develop following an ERCP.
Acute cholecystitis→ abdo pain, distension and vomiting=
Gallstone ileus- small bowel obstruction secondary to an impacted gallstone
How are perianal fistulae managed in Crohn’s disease?
patients with symptomatic perianal fistulae are usually given oral metronidazole
anti-TNF agents such as infliximab may also be effective in closing them
a draining seton is used for complex fistulae-
it is a piece of surgical thread that’s left in the fistula for several weeks to keep it open so it doesn’t heal up with pus inside and form an abscess
Ulcerative colitis + cholestatis (e.g. jaundice, raised ALP) →
? primary sclerosing cholangitis
What is the gold standard for diagnosis of coeliac disease?
Endoscopic intestinal biopsy- e.g. jejunal biopsy
What are the associations of primary sclerosing cholangitis (PSC) ? How does it present?
ulcerative colitis: 80% of patients with PSC have UC
Crohn’s (much less common association than UC)
HIV
cholestasis - jaundice, pruritus, raised bilirubin + ALP
right upper quadrant pain
fatigue
How is PSC diagnosed?
endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
p-ANCA may be positive
What are the complications of Primary Sclerosing Cholangitis?
cholangiocarcinoma (in 10%)
increased risk of colorectal cancer
What are the complications of Primary Biliary Cholangitis?
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
What should be given before endoscopy in patients with suspected variceal haemorrhage?
terlipressin and antibiotics
What is the TIPSS procedure? Common complication?
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) is a last line tx in variceal bleeding
connects the hepatic vein to the portal vein
exacerbation of hepatic encephalopathy is a common complication- inadequate metabolism of nitrogenous waste products by the liver
Right-sided tenderness on PR exam→
appendicitis
triad of CVD, high lactate and soft but tender abdomen =
mesenteric ischaemia
If NAFLD is found incidentally, what blood test should be performed to look for more severe disease? How should it be managed?
enhanced liver fibrosis (ELF) testing is recommended to aid diagnosis of liver fibrosis
Weight loss is the best first line management
How do you differentiate between iron deficiency anaemia and anaemia of chronic disease on bloods?
Total Iron Binding Capacity is high in IDA, and low/normal in anaemia of chronic disease
What is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease?
Thrombocytopenia (platelet count <150,000 mm^3)
What are the primary care investigations for IBS?
full blood count
ESR/CRP
coeliac disease screen (tissue transglutaminase antibodies)
Give some symptoms and signs of iron deficiency anaemia
Symptoms:
Fatigue
SOB on exertion
Palpitations
Signs:
Pallor
Hair loss
Koilonychia
Angular stomatitis and glossitis
Tachycardia/systolic murmur - compensation
What are the main causes of iron deficiency anaemia?
Excessive blood loss: often menorrhagia in pre-menopausal women and GI bleeding in men (always suspect colon cancer) and post-menopausal women.
Malabsorption: coeliac, Crohn’s, diverticular disease
Inadequate dietary intake: esp in vegetarians and vegans (However dark green leafy vegetables are another good source of iron)
Increased iron requirements: Growing children and pregnant women (needs to supply baby with iron and also dilutional deficiency)
Investigations in iron deficiency anaemia?
Who should be referred to a gastroenterologist within 2 weeks?
Full hx: changes in diet, medication history, menstrual history, weight loss, change in bowel habit
FBC : hypochromic microcytic anaemia
Serum ferritin: low (However ferritin can be raised during states of inflammation; so a raised ferritin does not necessarily rule out iron deficiency anaemia)
Total iron-binding capacity (TIBC) : high
Blood film : anisopoikilocytosis (red blood cells of different sizes and shapes) , target cells, ‘pencil’ poikilocytes
Endoscopy to rule out malignancy, males and post-menopausal females who present with unexplained iron-deficiency anaemia should be considered for further gastrointestinal investigations.
Post-menopausal women with a haemoglobin level ≤10 and men with a haemoglobin level ≤11 should be referred to a gastroenterologist within 2 weeks.
How should iron deficiency anaemia be managed?
Ensure malignancy is excluded first
Oral ferrous sulfate: patients should continue taking for 3 months after the deficiency has been corrected in order to replenish iron stores. Common side effects of iron supplementation include nausea, abdominal pain, constipation, diarrhoea
Iron-rich diet: this includes dark-green leafy vegetables, meat, iron-fortified bread
What are the commonest causes of pyogenic liver abscesses? How should they be managed?
Staphylococcus aureus in children and Escherichia coli in adults.
Management
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
What can be seen on small bowel enema in Crohn’s?
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae
Outline the management of ascites
reducing dietary sodium is first line
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone
drainage if tense ascites (therapeutic abdominal paracentesis)
prophylactic antibiotics to reduce the risk of SBP - oral ciprofloxacin or norfloxacin with an ascitic protein of 15 g/litre or less
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
Classical patient presentation:
Colicky abdominal pain, worse postprandially, worse after fatty foods
Give the diagnosis and management
Biliary colic
Do abdo USS and LFTs
If imaging shows gallstones and history compatible then laparoscopic cholecystectomy
Classical patient presentation:
Right upper quadrant pain
Murphys sign on examination (pain on inspiration while palpating RUQ)
Fever
Occasionally mildly deranged LFT’s (especially if Mirizzi syndrome)
Give the diagnosis and management
Acute cholecystitis
Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)
Classical patient presentation:
Usually prodromal illness and right upper quadrant pain
Swinging pyrexia
Patient may be systemically unwell
Generalised peritonism not present
Give the diagnosis and management
Gallbladder abscess
Imaging with USS +/- CT Scanning
Ideally surgery (although subtotal cholecystectomy may be needed if Calot’s triangle is hostile)
In unfit patients, percutaneous drainage may be considered
Classical patient presentation:
Patient severely septic and unwell
Jaundice
Right upper quadrant pain
Give the diagnosis and management
Cholangitis
Fluid resuscitation
Broad-spectrum intravenous antibiotics
Correct any coagulopathy
Early ERCP
Classical patient presentation:
Small bowel obstruction (may be intermittent)
Patients may have a history of previous cholecystitis and known gallstones
Give the diagnosis and management
Gallstone ileus
Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.
Classical patient presentation:
Gallbladder inflammation in absence of stones
Systemically unwell with high fever
Patients with intercurrent illness (e.g. diabetes, organ failure)
Give the diagnosis and management
Acalculous cholecystitis
If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy
Give the key causes of Budd Chiari syndrome (hepatic vein thrombosis)
polycythaemia rubra vera
thrombophilia
pregnancy
COCP: accounts for around 20% of cases
What is seen on histology in Coeliac disease?
villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
A triad of severe, colicky post-prandial abdominal pain, weight loss, and an abdominal bruit points towards…?
Intestinal angina (or chronic mesenteric ischaemia)
What can be seen on barium enema in UC?
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’
Classical presentation of UC?
Bloody diarrhoea more common
Abdominal pain in the left lower quadrant
Tenesmus
Classical presentation of Crohn’s?
Diarrhoea usually non-bloody
Weight loss more prominent
Upper gastrointestinal symptoms, mouth ulcers, perianal disease
Abdominal mass palpable in the right iliac fossa
Which artery is at risk of damage in duodenal ulceration?
Gastroduodenal artery is at risk with duodenal ulcers on the posterior wall
Give some oesophageal causes of acute upper GI bleeding and how they present
Oesophageal varices - Large volume of fresh blood. Sometimes malena due to swallowed blood. Often associated with haemodynamic compromise.
Oesophagitis - Small volume of fresh blood, often streaking vomit. Malena rare. Usually history of GORD type symptoms.
Cancer - Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often dysphagia and constitutional symptoms such as weight loss.
Mallory Weiss tear - brisk bright red blood following a bout of repeated vomiting. Malena rare.
Give some gastric causes of acute upper GI bleeding and how they present
Gastric ulcer- tends to present as iron deficiency anaemia due to repeated small bleeds. Erosion into a significant vessel may produce considerable haematemesis.
Gastric cancer - frank haematemesis or altered blood mixed with vomit. Usually dyspepsia and may have constitutional symptoms.
Dieulafoy lesion (AV malformation)- Often no prodromal features prior to haematemesis and melena. May produce considerable haemorrhage and may be difficult to detect endoscopically
Diffuse erosive gastritis - Usually haematemesis and epigastric discomfort. Usually underlying cause such as NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise
Give 2 duodenal causes of acute upper GI bleeding and how they present
Duodenal ulcer- haematemesis, melena and epigastric discomfort.
Aorto-enteric fistula - In patients with previous AAA surgery, can cause major haemorrhage associated with high mortality.
Hepatorenal syndrome is thought to come about when vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance and causes underfilling of the kidneys.
Describe the 2 types
Type 1 HRS
Rapidly progressive
Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks
Very poor prognosis
Type 2 HRS
Slowly progressive
Prognosis poor, but patients may live for longer
How is hepatorenal syndrome managed?
vasopressin analogues, for example terlipressin (they work by causing vasoconstriction of the splanchnic circulation)
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shunt
How is remission maintained in UC after a severe relapse?
Following a severe relapse or 2 exacerbations in the past year : tx is oral azathioprine or oral mercaptopurine
What key investigation is done to diagnose UC?
colonoscopy + biopsy is generally done for UC diagnosis
however in patients with severe colitis colonoscopy should be avoided due to the risk of perforation - a flexible sigmoidoscopy is preferred
Define malnutrition
a Body Mass Index (BMI) of less than 18.5;
or
unintentional weight loss greater than 10% within the last 3-6 months;
or
a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
How should malnutrition be managed?
Stratify risk using the MUST score
dietician support if the patient is high-risk
a ‘food-first’ approach with clear instructions (e.g. ‘add full-fat cream to mashed potato’), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
if ONS are used they should be taken between meals, rather than instead of meals
Which patients are at an increased risk of developing hepatotoxicity after paracetamol overdose?
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John’s Wort)
malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days
Acute alcohol intake is not associated with an increased risk of developing hepatotoxicity and may actually be protective.
How should paracetamol overdose be managed?
Activated charcoal if presents within 1 hour
Acetylcysteine should be given if:
there is a staggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration;
or
the plasma concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
What is the major potential adverse affect of acetylcysteine and how is this mitigated?
Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate.
Acetylcysteine is now infused over 1 hour (rather than the previous 15 minutes) to reduce the number of adverse effects.
What are the criteria for liver transplant following paracetamol overdose?
Arterial pH < 7.3, 24 hours after ingestion
or all of the following:
prothrombin time > 100 seconds
creatinine > 300 µmol/l
grade III or IV encephalopathy
How can you quickly screen for alcohol abuse in a history?
CAGE
Cut down - ever thought you should?
Annoyed- do you get annoyed at others commenting on your drinking?
Guilty- do you ever feel guilty about drinking?
Eye opener- ever drink in the morning to help your hangover or nerves?
Key investigations to order in acute liver failure?
liver function tests
prothrombin time/INR
basic metabolic panel
FBC
What is the Mackler triad for Boerhaave syndrome?
vomiting, thoracic pain, subcutaneous emphysema
What do ALT and ALP show?
ALT is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury.
ALP is particularly concentrated in the liver, bile duct and bone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ALP is a useful indirect marker of cholestasis.
Give some causes of an isolated rise in ALP
Bony metastases or primary bone tumours (e.g. sarcoma)
Recent bone fractures
Vitamin D deficiency
Renal osteodystrophy
Causes of an isolated rise in bilirubin?
Gilbert’s syndrome: the most common cause.
Haemolysis: check a blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.
How can you investigate the liver’s synthetic function?
Serum bilirubin
Serum albumin
Prothrombin time (PT)
Serum blood glucose
What can cause albumin levels to fall?
- Liver disease resulting in a decreased production of albumin (e.g. cirrhosis).
- Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin.
- Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome.
most common inheritable form of colorectal cancer?
HNPCC (Lynch syndrome)
What therapy is used for H.pylori eradication?
PPI + amoxicillin + clarithromycin, or
PPI + metronidazole + clarithromycin
Sign on barium swallow in oesophageal cancer?
‘apple core sign’
