Gastroenterology Flashcards
Peptic ulcer disease
What is it relieved by?
Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating
Gastric ulcers: epigastric pain worsened by eating
Appendicitis
Site
Symptoms
Examinations
sign
Pain initial in the central abdomen before localising to the right iliac fossa
Anorexia is common
Tachycardia, low-grade pyrexia, tenderness in RIF
Rovsing’s sign: more pain in RIF than LIF when palpating LIF
Acute pancreatitis
2 main Causes
Site of pain
Symptoms
Examination
Sign
Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare
Biliary colic
Site
Symptoms
Causes
Pain in the RUQ radiating to the back and interscapular region, may be following a fatty meal. Slight misnomer as the pain may persist for hours
Obstructive jaundice may cause pale stools and dark urine
It is sometimes taught that patients are female, forties, fat and fair although this is obviously a generalisation
Acute cholecystitis
Site
Symptom
Signs
History of gallstones symptoms (see above)
Continuous RUQ pain
Fever, raised inflammatory markers and white cells
Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)
Diverticulitis
Site
Symptom
Colicky pain typically in the LLQ
Fever, raised inflammatory markers and white cells
Abdominal aortic aneurysm
Site
Symptom
Severe central abdominal pain radiating to the back
Presentation may be catastrophic (e.g. Sudden collapse) or sub-acute (persistent severe central abdominal pain with developing shock)
Patients may have a history of cardiovascular disease
Achalasia
Symptom
Can it cause a malgnant change?
Clinical features
dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients
Achaelsia Ix
oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing
considered the most important diagnostic test
barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray
wide mediastinum
fluid level
Achalesia Tx
pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients should be a low surgical risk as surgery may be required if complications occur
surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects
Acute liver failure
Causes:
PAVA
Causes
paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
Acute liver failure
Features*
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’
‘liver function tests’ do not always accurately reflect the synthetic function of the liver.
What is the best way?
This is best assessed by looking at the prothrombin time and albumin level.
IX for acute pancreatitis
Investigations:
serum amylase
raised in 75% of patients - typically > 3 times the upper limit of normal
levels do not correlate with disease severity
specificity for pancreatitis is around 90%. Other causes of raised amylase include: pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis
serum lipase
more sensitive and specific than serum amylase
for acute pancreatitis
and another benefit
serum lipase
more sensitive and specific than serum amylase
it also has a longer half-life than amylase and may be useful for late presentations > 24 hours
Imaging for Acute pancreatitis
a diagnosis of acute pancreatits can be made without imaging if characteristic pain + amylase/lipase > 3 times normal level
however, early ultrasound imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction
other options include contrast-enhanced CT
Severe pancreatitis include:
severe pancreatitis include:
age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST
Causes of Acute Pancreatitis
GET SMASHED
Gallstones
Ethanol
Trauma
Steroids
Mumps (other viruses include Coxsackie B)
Autoimmune (e.g. polyarteritis nodosa), Ascaris infection
Scorpion venom
Hypertriglyceridaemia, Hyperchylomicronaemia, Hypercalcaemia, Hypothermia
ERCP
Drugs (azathioprine, mesalazine*, didanosine, bendroflumethiazide, furosemide, pentamidine, steroids, sodium valproate)c
UGIB most common cause
most commonly due to either oesophageal varices or peptic ulcer disease.
features OF UGIB
clinical features
haematemesis
the most common presenting feature
often bright red but may sometimes be described as ‘coffee ground’
melena
the passage of altered blood per rectum
typically black and ‘tarry’
a raised urea may be seen due to the ‘protein meal’ of the blood
Management of non-variceal bleeding
NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
if further bleeding then options include repeat endoscopy, interventional radiology and surgery
Management of variceal bleeding
terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
UGIB Tx
Resuscitation
ABC, wide-bore intravenous access * 2
platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
prothrombin complex concentrate to patients who are taking warfarin and actively bleeding
Alcoholic Ketoacidosis presenting pattern
who gets it
Treatment
Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation. Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones. Hence the patient develops a ketoacidosis.
It typically presents with a pattern of:
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.
Alcoholic liver disease covers a spectrum of conditions:
name 3
Selected investigation findings: in the blood
Alcoholic liver disease covers a spectrum of conditions:
alcoholic fatty liver disease
alcoholic hepatitis
cirrhosis
Selected investigation findings:
gamma-GT is characteristically elevated
the ratio of AST:ALT is normally > 2, a ratio of > 3 is strongly suggestive of acute alcoholic hepatitis
Aminosalicylate drugs
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis
Sulphasalazine
a combination of sulphapyridine (a sulphonamide) and 5-ASA
many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
other side-effects are common to 5-ASA drugs (see mesalazine)
Mesalazine
a delayed release form of 5-ASA
sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis
Olsalazine
two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria
Selected management notes for alcoholic hepatitis:
Selected management notes for alcoholic hepatitis:
glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis
Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
it is calculated by a formula using prothrombin time and bilirubin concentration
pentoxyphylline is also sometimes used
Anal Ca presentation
Patients typically present with a subacute onset of:
Perianal pain, perianal bleeding
A palpable lesion
Faecal incontinence
A neglected tumour in a female may present with a rectovaginal fistula.
RF and feature’s of ana; fissure
Risk factors
constipation
inflammatory bowel disease
sexually transmitted infections e.g. HIV, syphilis, herpes
Features
painful, bright red, rectal bleeding
around 90% of anal fissures occur on the posterior midline.
if the fissures are found in alternative locations then other underlying causes should be considered e.g. Crohn’s disease
Management of an acute anal fissure (< 1 week)
Management of an acute anal fissure (< 1 week)
soften stool
dietary advice: high-fibre diet with high fluid intake
bulk-forming laxatives are first-line - if not tolerated then lactulose should be tried
lubricants such as petroleum jelly may be tried before defecation
topical anaesthetics
analgesia
Management of a chronic anal fissure
the above techniques should be continued
topical glyceryl trinitrate (GTN) is first-line treatment for a chronic anal fissure
if topical GTN is not effective after 8 weeks then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin
Angiodysplasia - brief what is it
Angiodysplasia is a vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia.
There is thought to be an association with aortic stenosis, although this is debated. Angiodysplasia is generally seen in elderly patients
Angiodysplasia features
Features
anaemia
gastrointestinal (GI) bleeding
if upper GI then may be melena
if lower GI then may present as brisk, fresh red PR bleeding
Angiodysplasia diagnosis
Diagnosis
colonoscopy
mesenteric angiography if acutely bleeding
Angiodysplasia Mx
Management
endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid
oestrogens may also be used
Charcot’s triad
ascending cholangitis Investigation
Charcot’s triad of right upper quadrant (RUQ) pain, fever and jaundice occurs in about 20-50% of patients
fever is the most common feature, seen in 90% of patients
RUQ pain 70%
jaundice 60%
hypotension and confusion are also common (the additional 2 factors in addition to the 3 above make Reynolds’ pentad)
Other features
raised inflammatory markers
Investigation
ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones
Management of ascending cholangitis
Management
intravenous antibiotics
endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction
Ascities mx
Management
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists: e.g. spironolactone
loop diuretics are often added. Some authorities only add loop diuretics in patients who don’t respond to aldosterone antagonists whereas other authorities suggest starting both types of diuretic on the first presentation of ascites
drainage if tense ascites (therapeutic abdominal paracentesis)
large-volume paracentesis for the treatment of ascites requires albumin ‘cover’. Evidence suggests this reduces paracentesis-induced circulatory dysfunction and mortality
paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
ALT/AST: INFLAMATION IN LIVER
ALP: PATHOLOGY IN BILE DUCT
Autoimmune hepatitis predominantly involves inflammation in the liver and thus ALT / AST are likely to be raised. A markedly raised ALP would suggest pathology involving the bile duct although slight elevation can be present.
Autoimmune hepatitis
features
Antibodies
liver biopsy
management
Features
may present with signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
Management
steroids, other immunosuppressants e.g. azathioprine
liver transplantation
Barrett’s refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium
Barrett’s refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, e
Histological features
the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
Barrest Oesophagus RF
Risk factors
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
Barrest Oesophagus Mx
Management
high-dose proton pump inhibitor
whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
if dysplasia of any grade is identified endoscopic intervention is offered. Options include:
radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
endoscopic mucosal resection
Bile acid malabsorption
a cause of chronic diarrhoea. This may be primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
Investigation and management
Investigation
the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
Management
bile acid sequestrants e.g. cholestyramine
Bile acid malabsorption
a cause of chronic diarrhoea. This may be primary, due to excessive production of bile acid, or secondary to an underlying gastrointestinal disorder causing reduced bile acid absorption. It can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
Secondary causes:
Secondary causes are often seen in patients with ileal disease, such as with Crohn’s. Other secondary causes include:
cholecystectomy
coeliac disease
small intestinal bacterial overgrowth
Budd-Chiari syndrome
Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.
Causes
Causes
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases
Budd-Chiari syndrome
Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.
Features
Investigation
The features are classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly
Investigations
ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
Carcinoid tumours
Carcinoid syndrome
usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
Features
flushing (often the earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
Investigation
urinary 5-HIAA
plasma chromogranin A y
Management
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help
Carcinoid tumours
Carcinoid syndrome
usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
IX
Mx
Investigation
urinary 5-HIAA
plasma chromogranin A y
Management
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help
Cholangiocarcinoma is the medical term for bile duct cancer.
Primary sclerosing cholangitis is the main risk factor for cholangiocarcinoma
Features
persistent biliary colic symptoms
associated with anorexia, jaundice and weight loss
a palpable mass in the right upper quadrant (Courvoisier sign)
periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen
raised CA 19-9 levels
often used for detecting cholangiocarcinoma in patients with primary sclerosing cholangitis
Clostridioides difficile is a Gram positive rod often encountered in hospital practice. It produces an exotoxin which causes intestinal damage leading to a syndrome called pseudomembranous colitis.
What abx causes#
Other than antibiotics, risk factors include:
C. difficile develops when the normal gut flora are suppressed by broad-spectrum antibiotics. Clindamycin is historically associated with causing C. difficile but the aetiology has evolved significantly over the past 10 years. Second and third-generation cephalosporins are now the leading cause of C. difficile.
Other than antibiotics, risk factors include:
proton pump inhibitors
c diff transmission
transmission: via the faecal-oral route by ingestion of spores
C diff features
Features
diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop
C diff
1ST
SECOND
THRID LINE
First episode of C. difficile infection
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
Life-threatening C. difficile infection
Life-threatening C. difficile infection
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered
Conditions associated with coeliac diseasE
Conditions associated with coeliac disease include dermatitis herpetiformis (a vesicular, pruritic skin eruption) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-DQ8 (80%).
COMPLICATIONS OF CEOLIAC DISEASE
Complications
anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)
hyposplenism
osteoporosis, osteomalacia
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies
iMMUNISATION IN cEOLIAC
WHY IS THIS ?
Patients with coeliac disease often have a degree of functional hyposplenism
For this reason, all patients with coeliac disease are offered the pneumococcal vaccine
Coeliac UK recommends that everyone with coeliac disease is vaccinated against pneumococcal infection and has a booster every 5 years
Crohns affects which part?
It commonly affects the terminal ileum and colon but may be seen anywhere from the mouth to anus.
Crohns mX
Inducing remission
glucocorticoids (oral, topical or intravenous) are generally used to induce remission. Budesonide is an alternative in a subgroup of patients
enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective
azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy. Methotrexate is an alternative to azathioprine
infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
metronidazole is often used for isolated peri-anal disease
Crohns maintaining remission
azathioprine or mercaptopurine is used first-line to maintain remission
Cancer asscoatiated with crohns , patients are also at risk of:
As well as the well-documented complications described above, patients are also at risk of:
small bowel cancer (standard incidence ratio = 40)
colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
osteoporosis
Dubin-Johnson syndrome
Dubin-Johnson syndrome
Dubin-Johnson syndrome is a benign autosomal recessive disorder
resulting in hyperbilirubinaemia (conjugated, therefore present in urine). It is due to a defect in the canillicular multispecific organic anion transporter (cMOAT) protein. This causes defective hepatic bilirubin excretion
Pharyngeal pouch
More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough. Halitosis may occasionally be seen
Globus hystericus
Globus hystericus There may be a history of anxiety
Symptoms are often intermittent and relieved by swallowing
Usually painless - the presence of pain should warrant further investigation for organic causes
Gastric Cancer RF
Risk factors
Helicobacer pylori
triggers inflammation of the mucosa → atrophy and intestinal metaplasia → dysplasia
pernicious anaemia, atrophic gastritis
diet
salt and salt-preserved foods
nitrates
ethnicity: Japan, China
smoking
blood group A
Gastric Cancer FEATURES
Features
abdominal pain
typically vague, epigastric pain
may present as dyspepsia
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
overt upper gastrointestinal bleeding is seen only in a minority of patients
if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)
Gastric Ca diagnosis
Investigations
diagnosis: oesophago-gastro-duodenoscopy with biopsy
signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis
Indications for upper GI endoscopy: for GORD
Indications for upper GI endoscopy:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss
If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
eNZYMES Gastro
Amylase is present in saliva and pancreatic secretions. It breaks starch down into sugar
The following brush border enzymes are involved in the breakdown of carbohydrates:
maltase: cleaves disaccharide maltose to glucose + glucose
sucrase: cleaves sucrose to fructose and glucose
lactase: cleaves disaccharide lactose to glucose + galactose
Gilbert’s syndrome is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase. The prevalence is approximately 1-2% in the general population.
Features
unconjugated hyperbilirubinaemia (i.e. not in urine)
jaundice may only be seen during an intercurrent illness, exercise or fasting
Investigaruon
Investigation and management
investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid
no treatment required
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*
features
Presenting features
early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)
Haemochromtisis Treatment
Outline
venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line
f hepatic encephalopathy treatment
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
hepatic encephalopathy
Features
Features
confusion, altered GCS (see below)
asterixis: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)
HCC RF
The main risk factor for developing HCC is liver cirrhosis, for example secondary* to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis. Other risk factors include:
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
aflatoxin
drugs: oral contraceptive pill, anabolic steroids
porphyria cutanea tarda
male sex
diabetes mellitus, metabolic syndrome
HCC FEATURES
Features
tends to present late
features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly
possible presentation is decompensation in a patient with chronic liver disease
raised AFP
The most common cause of biliary disease in patients with HIV is
The most common cause of biliary disease in patients with HIV is sclerosing cholangitis due to infections such as CMV, Cryptosporidium and Microsporidia
Hydatid cysts are endemic in Mediterranean and Middle Eastern countries. They are caused by the tapeworm parasite ____________
An outer fibrous capsule is formed containing multiple small daughter cysts. These cysts are allergens which precipitate a type 1 hypersensitivity reaction.
Echinococcus granulosus.
Inherited causes of jaundice
There are 4 inherited causes of jaundice you need to be aware of: Gilbert’s syndrome, Crigler-Najjar syndrome, Dubin-Johnson syndrome and Rotor’s syndrome.
It is important for the exam to be able to classify them according to whether they cause
conjugated or unconjugated hyperbilirubinaemia:
Unconjugated hyperbilirubinaemia
Gilbert’s syndrome:
autosomal recessive
mild deficiency of UDP-glucuronyl transferase
benign
Crigler-Najjar syndrome:autosomal recessive
absolute deficiency of UDP-glucuronosyl transferase
do not survive to adulthood
Conjugated hyperbilirubinaemia
Dubin-Johnson syndrome:autosomal recessive. Relatively common in Iranian Jews
mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
results in a grossly black liver
benign
Rotor syndrome:
autosomal recessive
defect in the hepatic uptake and storage of bilirubin
benign
schaemia to the lower gastrointestinal tract can result in a variety of clinical conditions. Whilst there is no standard classification it can be useful to separate cases into 3 main conditions
acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis
Acute mesenteric ischaemia
Acute mesenteric ischaemia
Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery. Classically patients have a history of atrial fibrillation.
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.
Management
urgent surgery is usually required
poor prognosis, especially if surgery delayed
Chronic mesenteric ischaemia
Chronic mesenteric ischaemia
Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it’s non-specific features and may be thought of as ‘intestinal angina’. Colickly, intermittent abdominal pain occurs.
Ischaemiac colitis
Ischaemiac colitis
Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage. It is more likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.
Investigations
‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage
Management
- usually supportive
- surgery may be required in a minority of cases if conservative measures fail. Indications would include generalised peritonitis, perforation or ongoing haemorrhage
Jejunal villous atrophy
Whilst coeliac disease is the classic cause of jejunal villous atrophy there are a number of other causes you need to be aware of
Causes
coeliac disease
tropical sprue
hypogammaglobulinaemia
gastrointestinal lymphoma
Whipple’s disease
cow’s milk intolerance
Contraindications to percutaneous liver biopsy
Contraindications to percutaneous liver biopsy
deranged clotting (e.g. INR > 1.4)
low platelets (e.g. < 60 * 109/l)
anaemia
extrahepatic biliary obstruction
hydatid cyst
haemoangioma
uncooperative patient
ascites
Melanosis coli
Histology
CAUSE
Melanosis coli
Melanosis coli is a disorder of pigmentation of the bowel wall. Histology demonstrates pigment-laden macrophages.
It is associated with laxative abuse, especially anthraquinone compounds such as senna
Metoclopramide is a D2 receptor antagonist* mainly used in the management of nausea.
SE
Adverse effects
extrapyramidal effects
acute dystonia e.g. oculogyric crisis
this is particularly a problem in children and young adults
diarrhoea
hyperprolactinaemia
tardive dyskinesia
parkinsonism
Oesophageal cancer LoCATION
Location Lower third - near the gastroesophageal junction
Upper two-thirds of the oesophagus
Adenocarino,a
Location Lower third - near the gastroesophageal junction
Squamous cell canver
Upper two-thirds of the oesophagus
The most common organisms found in pyogenic liver abscesses are
The most common organisms found in pyogenic liver abscesses are Staphylococcus aureus in children and Escherichia coli in adults.
Management
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
refeeding syndrome
bloods
hypophosphataemia
this is the hallmark symptom of refeeding syndrome
may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
Small bowel bacterial overgrowth syndrome (SBBOS) is a disorder characterised by excessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms.
diagnisis and management
Diagnosis
hydrogen breath test
small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
clinicians may sometimes give a course of antibiotics as a diagnostic trial
Management
correction of the underlying disorder
antibiotic therapy:rifaximin is now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.
Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.
Features
ascites
abdominal pain
fever
Spontaneous bacterial peritonitis (SBP)
diagnosis and mx
Diagnosis
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Management
intravenous cefotaxime is usually given
Antibiotic prophylaxis should be given to patients with ascites if:
patients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’
what is a poor marker of prognosis in SBP
Alcoholic liver disease is a marker of poor prognosis in SBP.
UC features symptioms
The initial presentation is usually following insidious and intermittent symptoms. Features include:
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the left lower quadrant
extra-intestinal features (see below)
Fewer than four stools daily, with or without blood - Mild UC
Four to six stools a day, with minimal systemic disturbance- Mod UC
in UC what is severe
More than six stools a day, containing blood
Evidence of systemic disturbance, e.g.
fever
tachycardia
abdominal tenderness, distension or reduced bowel sounds
anaemia
hypoalbuminaemia
Severe colitis
should be treated by
Severe colitis
should be treated in hospital
IV steroids are usually given first-line
IV ciclosporin may be used if steroids are contraindicated
if after 72 hours there has been no improvement, consider adding IV ciclosporin to IV corticosteroids or consider surgery
Treating mild-to-moderate ulcerative colitis
proctitis
topical (rectal) aminosalicylate: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates
if remission is not achieved within 4 weeks, add an oral aminosalicylate
if remission still not achieved add topical or oral corticosteroid
proctosigmoiditis and left-sided ulcerative colitis
topical (rectal) aminosalicylate
if remission is not achieved within 4 weeks, add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
if remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid
extensive disease
topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
if remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid
Villous adenoma
Villous adenomas are colonic polyps with the potential for malignant transformation. They characteristically secrete large amounts of mucous, potentially resulting in electrolyte disturbances.
vast majority are asymptomatic. Possible features:
vast majority are asymptomatic. Possible features:
non-specific lower gastrointestinal symptoms
secretory diarrhoea may occur
microcytic anaemia
hypokalaemia
Whipple’s disease is a rare multi-system disorder caused by
Its most commen in whom
Tropheryma whippelii infection.
It is more common in those who are HLA-B27 positive and in middle-aged men.
Whipples disease features
Features
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
Whipples inx and mx
Investigation
jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules
Management
guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin
Zollinger elission syn diagnosis
Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test
ZES features
Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption
Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues.
Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson’s disease is caused by a defect
in the ATP7B gene located on chromosome 13.
Features result from excessive copper deposition in the tissues,
especially the brain, liver and cornea:
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Wilsons inx
Investigations
slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene
Wilsons mx
Management
penicillamine (chelates copper) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
tetrathiomolybdate is a newer agent that is currently under investigatio
what feature in haemochromatosis may be reversible with treatment?
In haemochromatosis, cardiomyopathy and skin pigmentation are reversible with treatment
Irreversible complications of haemchromotoasis
Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy
Clinical features
early in PBC may be asymptomatic
or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
Primary biliary cholangitis - the M rule
IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females
e.g. raised ALP on routine LFTs)
What cardiac abnormalities are associated with this cARCINOID TUMOUR
Carcinoid syndrome can affect the right side of the heart. The valvular effects are tricuspid insufficiency and pulmonary stenosis
Diagnosing chronic pancreatitis
CT pancreas is the preferred diagnostic test for chronic pancreatitis - looking for pancreatic calcification
Screening for haemochromatosis
general population: transferrin saturation > ferritin
family members: HFE genetic testing
low TIBC
ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
test recommended for H. pylori post-eradication therapy
Urea breath test is the only test recommended for H. pylori post-eradication therapy
diagnose small bowel bacterial overgrowth syndrome
hydrogen breath test is used to diagnose small bowel bacterial overgrowth syndrome
The following drugs tend to cause a hepatocellular picture:
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
The following drugs tend to cause cholestasis (+/- hepatitis):
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
Liver cirrhosis causing drugs
methotrexate
methyldopa
amiodarone
How to work out SAAG
A high SAAG indiactes+____
To calculate SAAG, we subtract the ascitic albumin value from the serum albumin value
Ascites: a high SAAG gradient (> 11g/L) indicates portal hypertension
alcoholism
Which of these abnormalities is attributable chronic excessive alcohol use without being secondary to liver decompensation?
Macrocytic anaemia
Neutrophilia
Thrombocytopenia
Deranged clotting
Hypoalbuminaemia
Macrocytosis is common in patients with alcoholism,
Anti-HBs
Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease
Anti-HBc
Anti-HBc implies previous (or current) infection. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months. IgG anti-HBc persists
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
HBsAg
HBsAg normally implies acute disease (present for 1-6 months)
if HBsAg is present for > 6 months then this implies chronic disease (i.e. Infective)
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
Ongoing diarrhoea in Crohn’s patient post-resection with normal CRP →
cholestyramine
Adverse effects
abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides
GORD DIAGNOSIS
If endoscopy is negative consider 24-hr oesophageal pH monitoring (the gold standard test for diagnosis)
TPMT activity should be assessed before offering azathioprine or mercaptopurine therapy in Crohn’s disease
Thiopurine methyltransferase (TPMT) is an enzyme involved in the metabolism of azathioprine and mercaptopurine. Some people have a deficiency of TPMT due to genetic mutations, and these people are at a greater risk of experiencing severe side effects from conventional doses of azathioprine or mercaptopurine. TPMT activity should therefore be assessed before offering azathioprine or mercaptopurine therapy. Such medications should not be commenced if TPMT is very low or absent. If TPMT activity is below normal, but not deficient, azathioprine or mercaptopurine can be commenced at a lower dose.
Diarrhoea, weight, arthralgia, lymphadenopathy, ophthalmoplegia ?
Whipple’s disease
Diarrhoea + hypokalaemia →
villous adenoma
PPIs are a cause of microscopic colitis, which can present with chronic diarrhoea,
ix
colonoscopy and biopsy should be considered when patients present in this way and are taking a PPI
Familial adenomatous polyposis - once diagnosed patients typically have
a total proctocolectomy with ileal pouch anal anastomosis due to the extremely high risk of developing colorectal cancer
CCK
I cells in upper small intestine
Secretin
S cells in upper small intestine
VIP
Small intestine, pancreas
Somatostatin
D cells in the pancreas & stomach
