Gastroenterology Flashcards
definition of achalasia
Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus
clinical features of achalasia
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
investigation findings in achalasia
oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing
barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray
wide mediastinum
fluid level
treatment of achalasia
pneumatic (balloon) dilation
surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
intra-sphincteric injection of botulinum toxin - high surgical risk
causes of abdominal pain
infective
inflammatory
vascular
traumatic
metabolic
causes of RUQ pain
biliary colic
acute cholecystitis - fever, raised inflammatory markers
ascending cholangitis - RUQ pain, fever, jaundice
causes of epigastric or central pain
acute pancreatitis - tenderness, ileus, fever
peptic ulcer disease
ruptured AAA - shock
mesenteric ischaemnia - metabolic acidosis, diarrhoea, rectal bleeding
intestinal obstruction - tinkling bowels, vomiting
causes of iliac fossa pain
ectopic pregnancy
appendicitis
acute diverticulitis - LLQ - diarrhoea, fever, raised inflammatory markers
causes of loin pain
renal colic - may cause haematuria
acute pyelonephritis - fever, rigors, vomiting
causes of acute liver failure
rapid onset of hepatocellular dysfunction leading to a variety of systemic complications
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’)
how to manage acute upper GI bleed
ABC
platelet transfusion if active bleeding and platelets <50
FFP if fibrinogen <1g/l or prothrombin 1.5x normal
prothrombin complex if bleeding and on warfarin
endoscopy - immediately in severe bleed, <24h for all pt
variceal bleeding - terlipressin and prophylactic antibiotics
band ligation
ransjugular intrahepatic portosystemic shunts
clinical features of upper GI bleeding
haematemesis - bright red or coffee ground
melena - passage of altered blood PR, black and tarry
urea++ due to protein meal
scoring systems used in acute upper GI bleeding
the Glasgow-Blatchford score 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
features of alcoholic ketoacidosis
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
infusion of saline & thiamine
investigation findings in alcoholic hepatitis
gamma-GT is characteristically elevated
the ratio of AST:ALT is normally > 2
management of alcoholic hepatitis
acute - glucocorticoids (e.g. prednisolone)
moa of aminosalicylate drugs
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory
features of angiodysplasia
vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia
Features
anaemia
gastrointestinal (GI) bleeding
if upper GI then may be melena
if lower GI then may present as brisk, fresh red PR bleeding
diagnosis and management of angiodysplasia
diagnosis
colonoscopy
mesenteric angiography if acutely bleeding
management
endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid
causes of high SAAG >11g/L ascites
high SAAG = portal hypertension
liver disorder - cirrhosis/alcoholic liver disease
acute liver failure
liver metastases
cardiac - RHF, constrictive pericarditis
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema
causes of low SAAG <11g/L ascites
Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)
Malignancy
peritoneal carcinomatosis
Infections
tuberculous peritonitis
Other causes
pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases
managing ascites
reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
aldosterone antagonists
drainage if tense ascites - large volume paracentesis
prophylactic cipro to reduce the risk of spontaneous bacterial peritonitis
features of autoimmune hepatitis
commonly seen in young females
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
type I AI hepatitis antibodies
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)
Affects both adults and children
type II AI hepatitis antibodies
Anti-liver/kidney microsomal type 1 antibodies (LKM1)
Affects children only
type III AI hepatitis antibodies
Soluble liver-kidney antigen
Affects adults in middle-age
RF for barrett’s oesophagus
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
management of barrett’s oesophagus
high-dose proton pump inhibitor - ability to suppress progression limited
endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
if dysplasia identified - endoscopic intervention (radiofrequency ablation, endoscopic mucosal resection)
causes of bile acid malabsorption
primary - due to excessive production of bile acid
secondary - due to an underlying gastrointestinal disorder ( ileal disease e.g., crohn’s, cholecystectomy, coeliac disease)
management of bile acid malabsorption
bile acid sequestrants e.g. cholestyramine
can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
definition and causes of budd-chiari syndrome
hepatic vein thrombosis - due to underlying haem disease or procoagulant condition
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
features of budd-chiari syndrome
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
ultrasound with Doppler flow studies
diagnosis of carcinoid tumours
usually occurs with liver metastases releasing serotonin into the systemic circulation or lung carcinoid as mediators are not ‘cleared’ by the liver
check urinary 5-HIAA
features of carcinoid syndrome
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
management of carcinoid syndrome
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help
side effects of cholestyramine
abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides
features of clostroidiodes difficile
anaerobic gram-positive, spore-forming, toxin-producing bacillus transmitted via faecal oral route, releases exotoxins causing colitis
Features
diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop
diagnosis and management of c diff
detecting C. difficile toxin (CDT) in the stool
C. difficile antigen positivity only shows exposure to the bacteria
management
oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
recurrent - <12w - fidaxomicin, >12 oral vanc
life threatening - oral vanc and IV metronidazole
isolation period for c diff patients
until no diarrhoea for 48h
all staff should wear disposable gloves and an apron during any contact with patients known to have C. difficile
hand washing is also essential
pathophysiology of coeliac disease
autoimmune condition caused by sensitivity to the protein gluten
Repeated exposure leads to villous atrophy which in turn causes malabsorption
features of coeliac disease
Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia
complications in coeliac disease
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
investigation findings in coeliac disease
tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
endomyseal antibody (IgA) - for selective IgA deficiency
Endoscopic duodenal biopsy
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
management of coeliac disease
gluten free diet - no wheat, barley, rye, oats
5 yearly pneumococcal infection
types of colon cancer
sporadic (95%)
hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
familial adenomatous polyposis (FAP, <1%)
features of lynch syndrome (HNPCC)
autosomal dominant condition
most common form of inherited colon cancer - 90% develop cancer, proximal colon, poorly differentiated and highly aggressive
The most common genes involved are:
MSH2 (60% of cases)
MLH1 (30%)
increased risk of endometrial cancer
amsterdam criteria
aids diagnosis of lynch syndrome HNPCC
at least 3 family members with colon cancer
the cases span at least two generations
at least one case diagnosed before the age of 50 years
features of familial adenomatous polyposis
rare autosomal dominant condition
leads to the formation of hundreds of polyps by the age of 30-40
inevitably develop carcinoma
due to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC) Chr5
also at risk from duodenal tumours
features of gardner’s syndrome
osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
management of constipation
investigate and exclude any secondary causes, consider red flag symptoms
exclude any faecal impaction
advice on lifestyle measures
first-line laxative: bulk-forming laxative first-line, such as ispaghula
second-line: osmotic laxative, such as a macrogol
features of crohns syndrome
form of inflammatory bowel disease
commonly affects the terminal ileum and colon
inflammation occurs in all layers, down to the serosa - strictures, fistulas and adhesions
pt present with non-specific sx, diarrhoea (crohns colitis - bloody diarrhoea), abdo pain, perianal disease, extra-intestinal features
investigation findings in crohns disease
raised CRP
anaemia
low vitamin B12 and vitamin D
increased faecal calprotectin
colonoscopy - deep ulcers, skip lesions
histology - goblet cells, granulomas
small bowel enema
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae
management of crohns disease
induce remission
glucocorticoids
enteral feeding
5-ASA - second line to glucocorticoids
azathioprine/mercaptopurine - add on to induce remission
maintaining
stop smoking
azathioprine, mercaptopurine to maintain remission
surgery
causes of diarrhoea
acute - gastroenteritis, diverticulitis, abx, constipation overflow
chronic - IBS, IBD, colorectal cancer, coeliac
features of diverticulitis
left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)
Complications of diverticulitis include:
abscess formation
peritonitis
obstruction
perforation
management of diverticulitis
mild attacks can be treated with oral antibiotics
more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given
drugs which may induce liver disease
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
drugs which cause cholestasis
combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine
indications for urgent referral to endoscopy
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
indications for non-urgent referral to endoscopy
Patients with haematemesis
Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
managing patients with undiagnosed dyspepsia
- Review medications for possible causes of dyspepsia
- Lifestyle advice
- Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
(carbon-13 urea breath test or a stool antigen test)
causes of dysphagia
Extrinsic
Mediastinal masses
Cervical spondylosis
Oesophageal wall
Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter
Intrinsic
Tumours
Strictures
Oesophageal web
Schatzki rings
Neurological
CVA
Parkinson’s disease
Multiple Sclerosis
Brainstem pathology
Myasthenia Gravis
role of ferritin
binds iron and stores it to be released in a controlled fashion at sites where iron is required
may be synthesised in increased quantities in situations with inflammation
causes of increased ferritin
> 300 µg/L in men/postmenopausal women and > 200 µµg/L in premenopausal women
ferritin++ with iron overload (10%) - primary iron overload (hereditary haemochromatosis), secondary iron overload (following repeated transfusions)
ferritin++ without iron overload - Inflammation (due to ferritin being an acute phase reactant)
Alcohol excess
Liver disease
Chronic kidney disease
Malignancy
action of transferrin
best test to see whether iron overload is present is transferrin saturation
normal transferrin of < 45% in females and < 50% in males exclude iron overload.
Transferrin is a protein produced by the liver. It regulates the absorption of iron into the blood. TIBC relates to the amount of transferrin in your blood that’s available to attach to iron
investigating gallstones
colicky right upper quadrant pain that occurs postprandially
abdominal ultrasound - may be repeated
liver function tests
for bile duct stones - MRCP, intraoperative imaging
managing gallstones
asymptomatic gallstones in gallbladder - common, dont require treatment
symptomatic gallstones - lap cholecystectomy
bile duct stones - surgical management - ERCP
features of gastric cancer
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)
investigation findings of gastric cancer
diagnosis: oesophago-gastro-duodenoscopy with biopsy - signet ring cells
staging - CT
management of gastric cancer
surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy
management for oesophagitis on endoscopy
full dose proton pump inhibitor (PPI) for 1-2 months
if response then low dose treatment as required
if no response then double-dose PPI for 1 month
features of gilbert syndrome
autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase
unconjugated hyperbilirubinaemia
jaundice if intercurrent stress
investigations and management of gilberts syndrome
rise in bilirubin following prolonged fasting or IV nicotinic acid
no treatment required
definition and features of haemochromatosis
autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation - HFE gene, Ch6
fatigue, erectile dysfunction and arthralgia
‘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)
complications of haemochromatosis
reversible
Cardiomyopathy
Skin pigmentation
irreversible
Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy
iron profile in haemochromatosis
transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
transferrin saturation - most useful marker
management of haemochromatosis
venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation kept below 50%, serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line
eradication of helicobacter pylori
eradication may be achieved with a 7-day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
tests used in helicobacter pylori
urea breath test - consume a drink containing carbon isotope 13 enriched urea
rapid urease test (CLO) - mix biopsy sample with urea and pH indicator
serum antibody - positive after eradication
culture of gastric biopsy
stool antigen test
features of hepatic encephalopathy
confusion, altered GCS (see below)
asterix: ‘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)
grades of hepatic encephalopathy
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
management of hepatic encephalopathy
treat any underlying precipitating cause
lactulose first-line (promotes excretion of ammonia)
addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
hepatitis b serology
HBsAG - acute disease
HBsAG >6m - chronic disease
anti HBs - implies immunity, negative in chronic disease
anti HBc - previous or current infection
HbeAg - marker of HBV replication and infectivity
features of biliary colic
RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.
features of acute cholecystitis
Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder.
The patient may be pyrexial and Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)
features of ascending cholangitis
fever (rigors are common)
RUQ pain
jaundice
features of cholangiocarcinoma
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
features of acute pancreatitis
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
features of hepatocellular carcinoma
ends 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
risk factors for developing hepatocellular carcinoma
liver cirrhosis, for example secondary to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
aflatoxin
drugs: oral contraceptive pill, anabolic steroids
management of hepatocellular carcinoma
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
causes of hepatomegaly
Cirrhosis: if early disease, later liver decreases in size. 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
definition of hepatorenal syndrome
vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance causing underfilling of kidneys, activating RAAS, causing renal vasoconstriction
classification of hepatorenal syndrome
type 1
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
Slowly progressive
Prognosis poor, but patients may live for longer
management of hepatorenal syndrome
vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shunt
main differences between crohns and UC
crohns - weight loss, upper GI symptoms, gallstones, fistulas, perianal signs, increased goblet cells, granulomas, deep ulcers, skip lesions
UC - bloody diarrhoea, LLQ pain, tenesmus, PSC, colorectal ca risk, continuous disease, no inflammation beyond submucosa, crypt abscesses , pseudopolyps
inherited causes of jaundice
Unconjugated hyperbilirubinaemia
Gilbert’s syndrome
Crigler-Najjar syndrome
Conjugated hyperbilirubinaemia Dubin-Johnson syndrome
Rotor syndrome
iron studies interpretation
Total iron binding capacity (TIBC)
transferrin
raised in iron deficiency anaemia (IDA)
raised in pregnancy and by oestrogen
Transferrin saturation
calculated by serum iron / TIBC
Ferritin
raised in inflammatory disorders
low in IDA
features of acute mesenteric ischaemia
typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery
hx AF
abdo pain severe, of sudden onset and out-of-keeping with physical exam findings.
management of acute mesenteric ischaemia
urgent surgery is usually required
poor prognosis, especially if surgery delayed
features of 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.
features of ischaemic colitis
cute but transient compromise in the blood flow to the large bowel - may lead to inflammation, ulceration and haemorrhage.
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.
‘thumbprinting’ on AXR due to mucosal oedema/haemorrhage
supprotive management
cause of ischaemic hepatitis
diffuse hepatic injury resulting from acute hypoperfusion
has inciting event e.g., cardiac arrest
market increase in aminotransferase >1000
diagnosis of liver cirrhosis
transient elastography - fibroscan - measures the ‘stiffness’ of the liver which is a proxy for fibrosis
fibroscan offered to:
people with hepatitis C virus infection
men drinking >50 units of alcohol per week
women drinking >35 units of alcohol per week
people diagnosed with alcohol-related liver disease
upper endoscopy - check for varices in new cirrhosis diagnoses
liver USS + AFP every 6m to check for HCC
definition of 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
screening using MUST
management of malnutrition
dietician support if the patient is at 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
what is melanosis coli
disorder of pigmentation of the bowel wall.
Histology demonstrates pigment-laden macrophages.
It is associated with laxative abuse, especially anthraquinone compounds such as senna
mechanism of metabolic alkalosis
activation of renin-angiotensin II-aldosterone (RAA)
aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule
ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality
features of oesophageal adenocarcinoma
most common in UK/US
affects lower third
RF -
GORD
Barrett’s oesophagus
smoking
obesity
features of oesophageal SCC
common in developing world
affects upper 2/3
RF
smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines
investigation findings of oesophageal carcinoma
Upper GI endoscopy with biopsy
Endoscopic ultrasound - for locoregional staging
CT CAP - initial staging
management of oesophageal carcinoma
operable disease T1N0M0 - managed by surgical resection
risk - anastomotic leak
adjuvant chemotherapy
features of plummer vinson syndrome
Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia
Treatment includes iron supplementation and dilation of the webs
features of pancreatic cancer
classically painless jaundice
(pale stools, dark urine, and pruritus
cholestatic liver function tests)
abdominal masses:
hepatomegaly: due to metastases
gallbladder
epigastric mass
non-specific - anorexia, weight loss, epigastric pain
loss of exocrine function - steatorrhoea
loss of endocrine function (e.g. diabetes mellitus)
investigations in pancreatic cancer
high res CT
‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
management of pancreatic cancer
a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas
adjuvant chemo
ERCP with stenting for palliation
management of acute peptic ulcer disease
presenting features include haematemesis, melaena, hypotension, tachycardia
ABC approach as with any upper gastrointestinal haemorrhage
IV proton pump inhibitor
the first-line treatment is endoscopic intervention
if this fails (approximately 10% of patients) then either:
urgent interventional angiography with transarterial embolization or
surgery
investigating perforated peptic ulcers
erect CXR - when pt presents with acute upper abdo pain
free air under diaphragm
causes of pernicious anaemia
antibodies to intrinsic factor +/- gastric parietal cells
RF - autoimmune disorders: thyroid disease, type 1 diabetes mellitus, Addison’s, rheumatoid and vitiligo, females
features of pernicious anaemia
fx of anaemia
neurological features
peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy
mild jaundice: combined with pallor results in a ‘lemon tinge’
glossitis → sore tongue
investigation findings in pernicious anaemia
macrocytic anaemia
hypersegmented polymorphs on blood film
low WCC and platelets may also be seen
a vitamin B12 level of >= 200 nh/L is generally considered to be normal
anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)
management of pernicious anaemia
IM vitamin B12 replacement
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
more frequent if with neurological features
folic acid supplementation
features of peutz-jeghers syndrome
AD condition
numerous hamartomatous polyps in the gastrointestinal tract - may cause small bowel obstruction or GI bleeds
pigmented freckles on the lips, face, palms and soles
conservative mx
features of pharyngeal pouch
dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis
seen via barium swallow combined with dynamic video fluoroscopy
pathophysiology of primary biliary cholangitis
chronic liver disorder of middle-aged females
interlobular bile ducts are damaged by chronic inflammation -> progressive cholestasis, may cause cirrhosis
assx
Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease
features of primary biliary cholangitis
early: may be asymptomatic (e.g. raised ALP on routine LFTs) 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
investigation findings in primary biliary cholangitis
anti-mitochondrial antibodies (AMA) M2
anti smooth muscle antibodies
raised serum IgM
management of primary biliary cholangitis
ursodeoxycholic acid - slows disease progression and improves symptoms
cholestyramine for pruritis
fat-soluble vitamin supplementation
liver transplant
pathophysiology of primary sclerosing cholangitis
biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.
features and investigation findings of primary sclerosing cholangitis
cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue
ERCP/MRCP show multiple biliary strictures giving a ‘beaded’ appearance
pANCA+
risk of cholangiocarcinoma
action of PPI
Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell.
management of pyogenic liver abscesses
causative organisms: Staphylococcus aureus in children, Escherichia coli in adults
management
percutaneous drainage
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
metabolic abnormalities seen in refeeding syndrome
hypophosphataemia - hallmark symptom of refeeding syndrome - causes significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
pathophysiology of refeeding syndrome
Shift from Fat to Carbohydrate Metabolism - reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism - activates insulin secretion, increases cellular uptake of glucose
IC movement of phosphate - insulin stimulates IC movement of phosphate
reduced phosphate stores - chronic malnutrition causes depletion of phosphate stores - refeeding increases demand for phosphate»_space; supply, leading to hypophosphatemia
scoring systems used in liver cirrhosis
child-pugh - bilirubin, albumin, PT, encephalopathy, ascites - to severity of liver cirrhosis
MELD - combination of a patient’s bilirubin, creatinine, and the international normalized ratio (INR) to predict survival - increasing use for those on transplant waiting list
features and diagnosis of small bowel bacterial overgrowth syndrome
excessive amounts of bacteria in the small bowel causing chronic diarrhoea, bloating, flatulence, abdo pain
diagnosed by hydrogen breath test
treat with rifamixin
features of spontaneous bacterial peritonitis
usually seen in patients with ascites secondary to liver cirrhosis
Features
ascites
abdominal pain
fever
diagnosis of spontaneous bacterial peritonitis
paracentesis - neutrophils >250 cells/ul
usually caused by E. coli - treat with IV cefotaxime
indications for spontaneous bacterial peritonitis prophylactic therapy
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’
endoscopy findings in ulcerative colitis
colonoscopy + biopsy is generally done for diagnosis - avoid if severe colitis due to perforation risk
red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent
barium enema findings in ulcerative colitis
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’
classification of severity of ulcerative colitis
The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
inducing remission in ulcerative colitis
proctitis - topical (rectal) aminosalicylate (+ oral aminosalicylate after 4w, add topical/oral corticosteroid if still not effective)
left sided - topical aminosalicylate, + high dose oral aminosalicylate after 4w, add oral corticosteroid and stop topical tx if remission not achieved
extensive - topical aminosalicylate + high dose oral aminosalicylate, add oral corticosteroid and stop topical tx if remission not achieved
severe colitis - IPT, IV steroids
maintaining remission in ulcerative colitis
Following a mild-to-moderate ulcerative colitis flare
proctitis and proctosigmoiditis -
topical aminosalicylate or
oral aminosalicylate or both
left-sided and extensive ulcerative colitis
low maintenance dose of an oral aminosalicylate
Following a severe relapse or >=2 exacerbations in the past year
oral azathioprine or oral mercaptopurine
prophylactic measures for variceal haemorrhage
propranolol
reduced rebleeding and mortality compared to placebo
endoscopic variceal band ligation (EVL)
TIPSS
managment of variceal haemorrhage
ABC
patients should be resuscitated prior to endoscopy
blood transfusion may be needed
correct clotting: FFP, vitamin K, platelet transfusions may be required
vasoactive agents: terlipressin
prophylactic IV antibiotics
give terlipressin and abx before endoscopy
endoscopic variceal band ligation
Sengstaken-Blakemore tube if uncontrolled haemorrhage
function of vitamin A and deficiency
Vitamin A is a fat soluble vitamin - retinol
Functions
converted into retinal, an important visual pigment
important in epithelial cell differentiation
antioxidant
Consequences of vitamin A deficiency
night blindness
function of vitamin B1 (thiamine) and deficiency
important in the catabolism of sugars and aminoacids
Conditions associated with thiamine deficiency:
Wernicke’s encephalopathy: nystagmus, ophthalmoplegia and ataxia
Korsakoff’s syndrome: amnesia, confabulation
dry beriberi: peripheral neuropathy
wet beriberi: dilated cardiomyopathy
function of vitamin B3 (niacin) and deficiency
a water soluble vitamin of the B complex group. It is a precursor to NAD+ and NADP+ and hence plays an essential metabolic role in cells.
Consequences of niacin deficiency:
pellagra: dermatitis, diarrhoea, dementia
function of vitamin B6 (pyridoxine) and deficiency
water soluble vitamin of the B complex group
converted to pyridoxal phosphate (PLP) which is a cofactor for many reactions including transamination, deamination and decarboxylation
Causes of vitamin B6 deficiency
isoniazid therapy
Consequences of vitamin B6 deficiency
peripheral neuropathy
sideroblastic anemia
functions of vitamin C (ascorbic acid)
antioxidant
collagen synthesis: acts as a cofactor for enzymes that are required for the hydroxylation proline and lysine in the synthesis of collagen
facilitates iron absorption
cofactor for norepinephrine synthesis
features of vitamin C deficiency
Vitamin C deficiency (scurvy) leads to defective synthesis of collagen resulting in capillary fragility (bleeding tendency) and poor wound healing
Features vitamin C deficiency
gingivitis, loose teeth
poor wound healing
bleeding from gums, haematuria, epistaxis
general malaise
features of whipple’s disease
a rare multi-system disorder caused by Tropheryma whippelii infection
Features
malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus
investigations and management of whipple’s disease
jejunal biopsy - macrophages containing Periodic acid-Schiff (PAS) granules
management - oral co-trimoxazole 1 year has lowest relapse rate
definition of wilson’s disease
autosomal recessive disorder characterised by excessive copper deposition in the tissues
increased copper absorption from the small intestine and decreased hepatic copper excretion
defect in the ATP7B gene, Chr13
features of wilson’s disease
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration - speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings - green-brown rings in iris peripheral due to copper deposition
RTA
haemolysis
blue nails
investigation findings for wilson’s disease
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 serum copper is increased
increased 24hr urinary copper excretion
the diagnosis is confirmed by genetic analysis of the ATP7B gene
treatment of wilson’s disease
penicillamine - copper chelator
features of zollinger ellison syndrome
excessive levels of gastrin secondary to a gastrin-secreting tumour, usually in 1st part of duodenum or pancreas
assx MEN type 1
multiple gastroduodenal ulcers
diarrhoea
malabsorption
investigations for zollinger ellison syndrome
fasting gastrin levels: the single best screen test
secretin stimulation test
