GI Fifth yr Flashcards
(151 cards)
1
Q
Features of acute liver failure?
A
Jaundice
Coagulopathy
Hypoalbuminaemia
Hepatic encephalopathy
Renal failure (hepatorenal syndrome)
2
Q
Management of variceal bleeding?
A
ABC
Correct clotting - FFP, vitamin K
Terlipressin and prophylactic ABx at presentation (before endoscopy)
Band ligation for oesophageal varices. Injections of N-butyl-2-cyanoacrylate for gastric varices.
Sengstaken-Blakemore tube if uncontrolled haemorrhage
TIPS if not controlled with above measures
Prophylaxis - propranolol
3
Q
LFTS for alcoholic liver disease
A
GGT elevated
AST:ALT normally >2, ratio >3 is suggestive of acute alcoholic hepatitis
4
Q
Management of alcoholic hepatitis
A
Glucocorticosteroids during acute episodes (pt’s who will benefit determined by Maddrey’s discriminant function - using prothrombin time and bilirubin concentration)
Pentoxyphylline sometimes used
5
Q
Causes of ascites with serum-ascites albumin gradient (SAAG) <11g/L
A
Hypoalbuminaemia (nephrotic syndrome, severe malnutrition, e.g., Kwashiorkor)
Malignancy (peritoneal carcinomatosis)
Infections (tuberculous peritonitis)
Pancreatitis
Bowel obstruction
Biliary ascites
Postop lymphatic leak
Serositis in CTD
6
Q
Causes of ascites with serum-ascites albumin gradient (SAAG) >11g/L
A
Indicates portal hypertension
Liver disorders are most common cause (cirrhosis/alcoholic liver disease, acute liver failure, liver metastases)
Cardiac (right HF, constrictive pericarditis)
Budd-Chiari syndrome
Portal vein thrombosis
Veno-occlusive disease
Myxoedema
7
Q
Management of ascites
A
Reduce dietary sodium
Fluid restriction if serum Na+ <125mmol/L
Aldosterone antagonists (+/- top diuretics)
Drainage if tense ascites - requires albumin cover to prevent paracentesis induced circulatory dysfunction
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
TIPS in some pt’s
8
Q
Epidemiology of autoimmune hepatitis
A
Young females
Associations with other autoimmune disorders, hypergammaglobulinaemia, HLA B8, DR3
9
Q
Three types of autoimmune hepatitis
A
Type 1 - ANA and anti-SMA, affects both adults and children
Type 2 - Anti-liver/kidney microsomal type 1 antibodies (LKM1), Affects children only
Type 3 - Soluble liver-kidney antigen, Affects adults in middle-age
10
Q
Investigations for autoimmune hepatitis
A
LFTs
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
11
Q
Management of autoimmune hepatitis
A
Steroids
Other immunosuppressants (e.g., azathioprine)
Liver transplantation
12
Q
Causes of raised levels of unconjugated bilirubin
A
Overproduction - Haemolysis (autoimmune, Hb disordrers, RBC enzyme disorders, RBC membrane disorders, myeloproliferative neoplasms)
Reduced uptake (eg. drugs, port systemic shunt)
Hepatocyte dysfunction
Conjugation dysfunction - GGT deficiency (Gilberts, Crigler-Najjar syndrome)
13
Q
Causes of raised levels of conjugated bilirubin
A
Predominantly elevated AST & ALT - viral hepatitis, AI hepatitis, toxin/drug related hepatitis, haemochromatosis, ischaemic hepatitis, alcoholic hepatitis
Normal AST, ALT and ALP - Defective excretion of bilirubin (Dubin-Johnson syndrome)
Predominantly elevated ALP - cholestasis of pregnancy, malignancy (pancreas), cholangiocarcinoma, PBC, PSC, choledocholithiasis
14
Q
Summary of Budd-Chiari (causes, features, Ix)
A
Hepatic vein thrombosis - usually in haematological disease or procoagulant condition
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
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
15
Q
Sx of gallstones?
A
colicky right upper quadrant pain
occurs postprandially
symptoms are usually worst following a fatty meal - when cholecystokinin levels are highest and gallbladder contraction is maximal.
16
Q
Ix and Tx of gallstones?
A
abdominal ultrasound
LFTs
stones in bile duct - MRCP or intraoperative imaging
Tx - laparoscopic cholecystectomy
17
Q
Features and Tx of acute cholecystitis?
A
Right upper quadrant pain
Pain may radiate to back or right shoulder
Fever
Murphys sign on examination
Occasionally mildly deranged LFT’s (especially if Mirizzi syndrome)
Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation) (2)
18
Q
Features and Tx of gallbladder abscess?
A
Usually prodromal illness and right upper quadrant pain
Swinging pyrexia
Patient may be systemically unwell
Generalised peritonism not present
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
19
Q
Features and Tx of gallbladder abscess?
A
Patient severely septic and unwell
Jaundice
Right upper quadrant pain
Fluid resuscitation
Broad-spectrum intravenous antibiotics
Correct any coagulopathy
Early ERCP
20
Q
Features and Tx of gallbladder abscess?
A
Patients may have a history of previous cholecystitis and known gallstones
Small bowel obstruction (may be intermittent)
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.
21
Q
Features and Tx of acalculous cholecystitis?
A
Patients with intercurrent illness (e.g. diabetes, organ failure)
Patient of systemically unwell
Gallbladder inflammation in absence of stones
High fever
If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy
22
Q
Features and Tx of Gilbert’s syndrome?
A
autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase
prevalence is approximately 1-2% in the general population.
Sx
unconjugated hyperbilirubinaemia (i.e. not in urine)
jaundice may only be seen during an intercurrent illness, exercise or fasting
Investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid
No treatment required
23
Q
What is haemochromatosis?
A
autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene. prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis
24
Q
Features of haemochromatosis?
A
early symptoms (non-specific) 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)
25
Complications of haemochromatosis?
Reversible:
Cardiomyopathy
Skin pigmentation
Irreversible:
Liver cirrhosis
DM
Hypogonadotrophic hypogonadism
Arthropathy
26
Ix for haemochromatosis?
general population:
transferrin saturation is considered the most useful marker, ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
testing family members:
genetic testing for HFE mutation
Iron study profile:
transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
LFTS
molecular genetic testing for the C282Y and H63D mutations
MRI is generally used to quantify liver and/or cardiac iron
liver biopsy is now generally only used if suspected hepatic cirrhosis
27
Management of haemochromatosis?
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
28
Aetiology of hepatic encephalopathy?
excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut
acute and chronic liver disease
TIPS may precipitate
29
Features of hepatic encephalopathy?
confusion, altered GCS
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)
30
Grading of hepatic encephalopathy?
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
31
Precipitating factors for hepatic encephalopathy?
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
32
Management of hepatic encephalopathy?
treat any underlying precipitating cause
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
other options include embolisation of portosystemic shunts and liver transplantation in selected patients
33
Summary of hepatitis B serology?
surface antigen (HBsAg) - causes the production of anti-HBs
Anti-HBs implies immunity (either exposure or immunisation). It is negative in chronic disease
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)
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
HbeAg results from breakdown of core antigen from infected liver cells as is, therefore, a marker of infectivity. Marker of HBV replication and infectivity
Example results:
previous immunisation: anti-HBs positive, all others negative
previous hepatitis B (> 6 months ago), not a carrier: anti-HBc positive, HBsAg negative
previous hepatitis B, now a carrier: anti-HBc positive, HBsAg positive
34
Features of viral hepatitis?
nausea and vomiting, anorexia
myalgia
lethargy
right upper quadrant (RUQ) pain
RFs - recent travel, IVDU
34
Features of viral hepatitis?
nausea and vomiting, anorexia
myalgia
lethargy
right upper quadrant (RUQ) pain
RFs - recent travel, IVDU
35
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
36
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
37
Risk factors for hepatocellular carcinoma?
iver cirrhosis, for example secondary to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis.
Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.
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
38
Features of hepatocellular carcinoma?
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
Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
- patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
- men with liver cirrhosis secondary to alcohol
39
Management of hepatocellular carcinoma?
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
40
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
Other causes:
viral hepatitis
glandular fever
malaria
abscess: pyogenic, amoebic
hydatid disease
haematological malignancies
haemochromatosis
primary biliary cirrhosis
sarcoidosis, amyloidosis
41
Pathophysiology of hepatorenal syndrome?
vasoactive mediators cause splanchnic vasodilation
in turn reduces the systemic vascular resistance
results in 'underfilling' of the kidneys.
This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.
42
Types 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
43
Management of hepatorenal syndrome?
vasopressin analogues, for example terlipressin - work by causing vasoconstriction of the splanchnic circulation
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shunt
44
Inherited causes of jaundice?
Unconjugated hyperbilirubinaemia:
Gilbert's syndrome - AR, mild deficiency of UDP-glucuronyl transferase
Crigler-Najjar syndrome - AR, type 1 = absolute deficiency of UDP-glucuronosyl transferase, do not survive to adulthood, type 2 = less severe, may improve with phenobarbital
Conjugated hyperbilirubinaemia:
Dubin-Johnson syndrome - AR, mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin, results in a grossly black liver
Rotor syndrome - autosomal recessive, defect in the hepatic uptake and storage of bilirubin
45
Summary of ischaemic hepatitis?
diffuse hepatic injury resulting from acute hypoperfusion (sometimes known as 'shock liver')
diagnosed in the presence of an inciting event (e.g. a cardiac arrest) and marked increases in aminotransferase levels (exceeding 1000 international unit/L or 50 times the upper limit of normal).
Often occurs in conjunction with acute kidney injury (tubular necrosis) or other end-organ dysfunction.
46
Diagnosis of liver cirrhosis
traditionally a liver biopsy was used - however associated with adverse effects such as bleeding and pain
other techniques such as transient elastography 'Fibroscan' and acoustic radiation force impulse imaging are increasingly used
for patients with NAFLD, NICE recommend using the enhanced liver fibrosis score to screen for patients who need further testing
Further investigations
NICE recommend doing an upper endoscopy to check for varices in patient's with a new diagnosis of cirrhosis
liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
47
Screening for liver cirrhosis?
Offer transient elastography to:
people with hepatitis C virus infection
men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months
people diagnosed with alcohol-related liver disease
48
Summary of NAFLD
describes a spectrum of disease ranging from:
steatosis - fat in the liver
steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH)
progressive disease may cause fibrosis and liver cirrhosis
hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis.
thought to affect around 3-4% of the general population.
Associated factors
obesity
type 2 diabetes mellitus
hyperlipidaemia
jejunoileal bypass
sudden weight loss/starvation
49
Features of NAFLD
usually asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on ultrasound
50
Investigations for NAFLD
no evidence to support screening
based on incidental finding of NAFLD
NICE recommends the use of the enhanced liver fibrosis (ELF) blood test to check for advanced fibrosis
FIB4 score or NALFD fibrosis score
FibroScan
advanced fibrosis should be referred to a liver specialist. They will then likely have a liver biopsy to stage the disease more accurately
51
Management of NAFLD
lifestyle changes (particularly weight loss) and monitoring
?gastric banding and insulin-sensitising drugs (e.g. metformin, pioglitazone)
52
Summary of pancreatic cancer?
Often diagnosed late due to non-specific presentations
80% of pancreatic tumours are adenocarcinomas which typically occur at the head of the pancreas.
Associations:
increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation
53
Features of pancreatic cancer?
classically painless jaundice
pale stools, dark urine, and pruritus
cholestatic liver function tests
Courvoisier's law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
however, patients typically present in a non-specific way with anorexia, weight loss, epigastric pain
loss of exocrine function (e.g. steatorrhoea)
loss of endocrine function (e.g. diabetes mellitus)
atypical back pain is often seen
migratory thrombophlebitis (Trousseau sign) is more common than with other cancers
54
Ix for pancreatic cancer?
USS
high-resolution CT scan - 'double duct' sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
55
Management of pancreatic cancer?
less than 20% are suitable for surgery at diagnosis
a Whipple's resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple's include dumping syndrome and peptic ulcer disease
adjuvant chemotherapy is usually given following surgery
ERCP with stenting is often used for palliation
56
Summary of primary biliary cholangitis?
typically seen in middle-aged females (female:male ratio of 9:1)
autoimmune condition
Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis
"itching in middle-aged woman"
Associations: Sjogrens, RA, systemic sclerosis, thyroid disease
Complications:
cirrhosis > portal HTN > ascites, vatical haemorrhage
osteomalacia, osteoporosis
^ risk of hepatocellular carcinoma
57
Features of PBC
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
58
Diagnosis of PBC
immunology:
anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
smooth muscle antibodies in 30% of patients
raised serum IgM
imaging:
required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)
59
Management of PBC
first-line: ursodeoxycholic acid
(slows disease progression and improves symptoms)
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem
60
Summary of primary sclerosis cholangitis?
biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts
Associations
ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC
Crohn's (much less common association than UC)
HIV
Complications
cholangiocarcinoma (in 10%)
increased risk of colorectal cancer
61
Features of PSC
cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue
62
Ix of PSC
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
there is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as 'onion skin'
63
Most common organisms in pyogenic liver abscess?
A liver abscess can develop from several different sources, including a blood infection, an abdominal infection, or an abdominal injury which has been become infected.
Staphylococcus aureus in children
Escherichia coli in adults.
64
Management of pyogenic liver abscess?
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
65
Scoring systems for liver cirrhosis?
Previously Child-Pugh classification (bilirubin, albumin, PT, encephalopathy, ascites)
Model for End-Stage Liver Disease (MELD) has been increasingly used, particularly patient's who are on a liver transplant waiting list (bilirubin, creatinine, INR)
66
Summary of spontaneous bacterial peritonitis?
form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis
Sx = ascites, abdominal pain, fever
Dx = paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Tx = IV cefotaxime
ABx prophylaxis to those 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
67
Summary of Wilson's disease?
AR
Excess copper deposition in tissues
increased copper absorption from the small intestine and decreased hepatic copper excretion.
defect in the ATP7B gene located on chromosome 13.
onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease
68
Features of Wilsons disease?
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
69
Ix and Tx of Wilsons disease?
Ix:
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
Tx:
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
70
What is coeliac disease? including S+S
autoimmune condition caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption.
S+S:
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
Rarely neuro Sx - peripheral neuropathy, cerebellar ataxia, epilepsy
71
Conditions associated with coeliac disease?
Autoimmune thyroid disease
Dermatitis herpetiformis
Irritable bowel syndrome
Type 1 diabetes
First-degree relatives (parents, siblings or children) with coeliac disease
Autoimmune hepatitis
PBC/PSC
strongly associated with HLA-DQ2 and HLA-DQ8
72
Complications of 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
73
Investigations of coeliac disease?
reintroduce gluten for at least 6 weeks prior to testing
Serology:
TTG antibodies (IgA)
endomyseal antibody (IgA) - need to look for selective IgA deficiency, which would give a false negative coeliac result
anti-DGPs
Endoscopic intestinal biopsy:
'gold standard' for diagnosis
typically duodenum
Findings: villous atrophy, crypt hyperplasia, increase in intraepithelial lymphocytes, lamina propria infiltration with lymphocytes
74
Management of coeliac disease?
gluten-free diet (bread, pasta, pastry, beer, rye, oat, rice, potatoes, corn)
immunisation - degree of functional hyposplenism, so offered pneumococcal vaccination and booster every 5 years
75
Risk factors for gastric cancer?
Helicobacer pylori
triggers inflammation of the mucosa → atrophy and intestinal metaplasia
atrophic gastritis
diet
salt and salt-preserved foods
nitrates
smoking
blood group
male predominance (2:1)
Older people (half of patients are >75)
76
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)
77
Ix and management of gastric cancer?
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
staging: CT
surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy
78
What is diverticular disease?
diverticular disease - symptomatic
diverticulosis - presence of multiple outpouchings of bowel wall
herniation of colonic mucosa through the muscular wall of the colon. The usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa
Sx - altered bowel habit, rectal bleeding, abdo pain
RF - ^ age, low fibre diet
79
Complications of diverticular disease?
Diverticulitis
Haemorrhage
Development of fistula
Perforation and faecal peritonitis
Perforation and development of abscess
Development of diverticular phlegmon
80
Diagnosis and management of diverticular disease?
colonoscopy, CT cologram or barium enema
Hinchey classification - I-IV (para-colonic abscess to faecal peritonitis)
Tx:
increase dietary fibre
mild diverticulitis - ABx
peri colonic abscess - drained
recurrent episodes requiring hospitalisation - surgical resection
Hinchey Iv - resection and stoma
81
Sx of diverticulitis?
left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)
82
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
83
Complications of diverticulitis?
abscess formation
peritonitis
obstruction
perforation
84
Summary of Plummer-Vinson syndrome?
Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia
Treatment includes iron supplementation and dilation of the webs
85
Summary of Mallory-Weiss syndrome?
Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics
86
Summary of Boerhaave syndrome?
Severe vomiting → oesophageal rupture
87
Types of oesophageal cancer?
Adenocarcinoma
Lower third - near the gastroesophageal junction
RFs: GORD, Barrett's oesophagus, smoking, obesity
Squamous cell cancer:
Upper two-thirds of the oesophagus
RF: smoking, alcohol, achalasia, Plummer-Vinson syndrome, diets rich in nitrosamines
88
Features of oesophageal cancer?
dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough
89
Dx and Tx of oesophageal cancer?
UGI endoscopy with biopsy
Endoscopic US for loco regional staging
CTAP - initial staging
Tx:
Surgical resection - risk of anastomosis resulting in mediastinitis
Adjuvant chemotherapy
90
What is Barrett's oesophagus?
metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium - goblet cells, brush border
^ risk of adenocarcinoma
short (<3cm) and long (>3cm)
91
RF for Barrett's?
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
92
Management of Barrett's?
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
93
Ix for GORD?
if red flags:
age > 55 years
symptoms > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss
upper abdo pain
low Hb
raised platelet
94
What is GORD?
where acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.
squamous epithelial lining making it more sensitive to the effects of stomach acid
Sx: heartburn. acid regurgitation, retrosternal or epigastric pain, bloating, nocturnal cough, hoarse voice
95
Management of GORD?
Lifestyle advice - reduce tea, coffee, alcohol, WL, avoid smoking, smaller lighter meals, avoid heavy meals before bed, stay upright after meals
Acid neutralising meds - gaviscon, Rennie
PPIs - omeprazole, lansoprazole
Ranitidine - H2 receptor antagonist
Surgery - laparoscopic fundoplication
96
How to test for H. Pylori?
Gram -ve aerobic bacteria. Causes damage to the epithelial lining of the stomach resulting in gastritis, ulcers and increasing the risk of stomach cancer
Off PPIs 2 weeks before
Urea breath test using radiolabelled carbon 13
Stool antigen test
Rapid urease test can be performed during endoscopy.
97
H. Pylori eradication therapy?
involves triple therapy with a proton pump inhibitor (e.g. omeprazole) plus 2 antibiotics (e.g. amoxicillin and clarithromycin) for 7 days.
The urea breath test can be used as a test of eradication after treatment. This is not routinely necessary.
98
What is achalasia?
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
middle-aged pt
M=F
99
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
100
Ix and Tx of achalasia?
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
Tx:
pneumatic (balloon) dilation is increasingly the preferred first-line option
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
101
Causes of dysphagia?
Oesophageal cancer
Oesophagitis
Oesophageal candidiasis
Achalasia
Pharyngeal pouch
Systemic sclerosis
Myasthenia gravis
Globus hystericus
Can separate into extrinsic, oesophageal wall, intrinsic and neurological
101
Causes of dysphagia?
Oesophageal cancer
Oesophagitis
Oesophageal candidiasis
Achalasia
Pharyngeal pouch
Systemic sclerosis
Myasthenia gravis
Globus hystericus
Can separate into extrinsic, oesophageal wall, intrinsic and neurological
102
3 main conditions of ischaemia to the GIT?
acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis
103
Common features in bowel ischaemia?
Common predisposing factors = increasing age, AF, other causes of emboli (endocarditis, malignancy), CVD RF's (smoking, HTN, DM), cocaine
Common features - abdo pain, rectal bleeding, diarrhoea, fever, bloods (elevated WBC and lactic acidosis)
CT investigation of choice
104
Summary 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
Classically - Hx of AF
Features - severe, sudden onset and out of keeping with physical exam findings
Tx - urgent surgery (laparotomy) required, poor prognosis, especially if surgery delayed
105
Summary of chronic mesenteric ischaemia?
Rare clinical diagnosis due to non-specific features
'Intestinal angina'
Colicky, intermittent abdominal pain
106
Summary of ischaemic colitis?
describes an acute but transient compromise in the blood flow to the large bowel
may lead to inflammation, ulceration and haemorrhage
occurs in 'watershed areas' like splenic flexure, that are at the border of territory (superior and inferior mesenteric arteries)
Ix - thumb printing seen on abdominal x-ray due to mucosal oedema/haemorrhage
Tx - supportive, surgery if conservative measures fail - if generalised peritonitis, perforation or ongoing haemorrhage
107
Summary of carcinoid tumour?
rare, slow-growing neuroendocrine tumors arising from the enterochromaffin cells disseminated throughout the gastrointestinal and bronchopulmonary systems
usually occurs when mets are present in the liver and release serotonin into systemic circulation. may also occur with lung carcinoid
Sx - flushing, diarrhoea, bronchospasm, hypotension, right heart valvular stenosis (left heart can be affected in bronchial carcinoid), paraneoplastic (ACTH and GHRH), pellagra as tryptophan diverted to serotonin by tumour
Ix - urinary 5-HIAA, plasma chromogranin A y
Tx - somatostatin analogues (octreotide), diarrhoea (cyproheptadine can help)
108
Pathophysiology of appendicitis?
inflammation of the appendix.
peak age 10-20
appendix is a small, thin tube arising from the caecum. It is located at the point where the three teniae coli meet
Pathogens can get trapped due to obstruction at the point where the appendix meets the bowel - leading to infection and inflammation - can lead to gangrene and rupture
When the appendix ruptures, faecal contents and infective material are released into the peritoneal cavity. This leads to peritonitis, which is inflammation of the peritoneal lining.
109
Features of appendicitis?
This typically starts as central abdominal pain that moves down to the right iliac fossa (RIF) within the first 24 hours, eventually becoming localised in the RIF.
On palpation of the abdomen, there is tenderness at McBurney’s point. McBurney’s point refers to a specific area one third of the distance from the anterior superior iliac spine (ASIS) to the umbilicus.
Loss of appetite - anorexia
N+V
Low-grade fever
Rovsing's sing (palpation of LIF causes pain in RIF)
psoas sign: pain on extending hip if retrocaecal appendix
Guarding on abdominal palpation
Rebound tenderness in RIF
Percussion tenderness
110
Ix for appendicitis?
Clinical presentation and raised inflammatory markers
neutrophil-predominant leucocytosis is seen in 80-90%
CT - to confirm
USS - esp in women to rule out gynae pathology + in children
Observation can be used also - repeated investigations
Clinical presentation but Ix -ve - diagnostic laparoscopy
111
Tx of appendicitis?
suspected appendicitis need emergency admission to hospital under the surgical team.
Appendicectomy - ideally laparoscopic
administration of prophylactic intravenous antibiotics reduces wound infection rates
Complications - Bleeding, infection, pain and scars
Damage to bowel, bladder or other organs
Removal of a normal appendix
Anaesthetic risks
Venous thromboembolism (deep vein thrombosis or pulmonary embolism)
112
DDx for appendicitis?
Ectopic
Ovarian cysts
Meckels diverticulum
Mesenteric adenitis
Appendix mass - occurs when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa. This is typically managed conservatively with supportive treatment and antibiotics, followed by appendicectomy once the acute condition has resolved.
113
Micro and macro pathological hallmarks of UC?
Macro:
inflammation extends proximally from rectum - defined as proctitis, left-sided colitis, pan-colitis
- mucosa reddened, inflamed and bleeds easily
- extensive ulceration
Micro:
- superficial inflammation of mucosa
- chronic inflammatory cell infiltrate in lamina propria
- crypt abcesses
- goblet cell depletion
114
How to classify severely acute colitis?
Truelove and Witts criteria
more than 6 bloody stools per day (often nocturnal) and one of:
temp >37.8 on 2/4 days
Hb <10.5
ESR >30
Pulse >90
Colon dilated >5.5
115
Extra intestinal manifestations of UC?
Mouth ulcers
Erythema nodosum
Uveitis/episcleritis
Arthropathy
Pyoderma granulosum
Primary sclerosis cholangitis
116
Complications of ulcerative colitis?
Acute - toxic megacolon
Primary sclerosing cholangitis
Colorectal carcinoma (colonoscopy at 10 years)
Pouchitis after colectomy (w/ relapsing remitting course)
Osteoporosis from steroid therapy
117
Why check TPMT levels in ulcerative colitis?
Thiopurine methyltransferase (TPMT) is involved in the metabolism of thiopurines (metcaptopurine and azathioprine)
To avoid fatal administration to patient with no or low TPMT levels
118
Features of Crohn's?
Diarrhoea - bloody and/or chronic
Abdominal pain
WL
Malaise, anorexia, fever
Poor growth or delayed puberty in kids
Mouth ulcers
Abdominal tenderness, distension, palpable masses
Anal/perianal skin tags, fissures, fistulas
119
Extra-intestinal manifestations of Crohn's?
Arthritis
Conjunctivitis/uveitis/episcleritis
Erythema nodosum
Pyoderma granulosum
Clubbing
120
Macro and microscopic features of Crohn's disease?
Macro
Distribution - 20% colonic, 30% ileocaecal, 40% small bowel
Bowel thickened and narrowed
Deep fissures and ulcers in mucosa - cobblestone
Fistulae, abacuses and strictures
Skip lesions
Mouth ulcers and ana;/peri-anal disease
Micro:
Transmural inflammation
Increase in chronic inflammatory cells
Granulomata - not caveating
121
Complications of Crohn's disease?
Toxic megacolon and perforation
Stricturing and bowel obstruction
Fistulae
Small bowel cancer
Iron, folate, B12 deficiencies
Osteoporosis from steroid therapy
Short-bowel syndrome and malabsorption
122
Oesophageal causes of acute UGIB?
Varices
Oesophagitis
Cancer
Mallory Weiss tear
123
Summary of oesophageal varices?
Varices - usually large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common.
124
Summary of mallory weiss tear?
brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Melena rare. Usually ceases spontaneously
125
Summary of oesophagitis?
Small volume of fresh blood, often streaking vomit. Malena rare. Often ceases spontaneously.
Usually history of antecedent GORD type symptoms.
126
Gastric causes of acute UGIB?
Gastric ulcer
Gastric cancer
Dieulafoy lesion
Diffuse erosive gastritis
127
Summary of gastric ulcer?
Small low volume bleeds > iron deficiency anaemia
Torsion into significant vessel - considerable haemorrhage and haemateemsis
128
Summary of gastric cancer?
Frank haemateemsis or altered blood mixed with vomit
Usually prodromal features of: dyspepsia, constitutional Sx
Erosion of major vessel - considerable haemorrhage
129
Summary of dieulafoy lesion?
Usually no prodromal features prior to haematemesis and melena - AV malformation may produce quite a considerable haemorrhage
May be difficult to detect endoscopically
130
Summary of diffuse erosive gastritis?
Causes haemateemsis and epigastric discomfort.
Usually underlying cause - recent NSAID usage
Large volume haemorrhage may occur with considerable haemodynamic compromise
131
Duodenal cause of UGIB?
Duodenal ulcer
Aorto-enteric fistula - previous AAA surgery
132
Summary of duodenal ulcer?
posteriorly sited, may erode gastroduodenal artery
Pain hours after eating
133
Management of acute UGIB?
Glasgow-Blatchford score - first assessment - outpatient or not? 0 - early discharge
Resuscitation - A-E, IV access, platelet transfusion if needed, FFP if fibrinogen low, PCC if taking warfarin
Endoscopy - after resuscitation - have within 24 hours
No PPIs before endoscopy if non-variceal bleed
Variceal bleed - terlipressin and ABx given at presentation, band ligation, injections of N-butyl-2-cyanoacrylate, TIPS
Rockall - after endoscopy - % risk of rebreeding and mortality
134
RFs for peptic ulcer disease?
Helicobacter pylori
Drugs - NSAIDs, SSRIs, corticosteroids, bisphosphonates
Zollinger-Ellison syndrome - excessive levels of gastrin (usually from gastrin secreting tumour)
135
Features of peptic ulcer disease?
Epigastric pain
Nausea
Duodenal - more common than gastric, epigastric pain when hungry, relieved by eating
Gastric ulcers - epigastric pain worsened by eating
136
Ix for peptic ulcer disease?
H. Pylori - urea breast test or stool antigen
137
Tx of peptic ulcer disease?
if Helicobacter pylori is negative then proton pump inhibitors (PPIs) should be given until the ulcer is healed
if Helicobacter pylori is positive then eradication therapy should be given:
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin
138
Ix of colorectal cancer?
FBC - iron deficiency anaemia
Colonoscopy - flexible sigmoidoscopy if significant bleeding
If unfit - CT angio
FIT
CEA
Staging CT AP
139
RFs for colorectal cancer?
FHx - FAP, HNPCC (Lynch)
IBD
Increasing age
Diet - red + processed meat, low fibre
Obesity
Sedentary lifestyle
Smoking
Alcohol
140
How to classify colorectal cancer?
Duke's classification (A-D) now replaced by TNM
141
When to refer (2ww) for colorectal cancer?
>40yrs - unexplained WL + abdo pain
>50yrs - unexplained rectal bleeding
>60 - IDA or change in bowel habit
Occult blood in faeces
Urgent - rectal/abdominal mass, unexplained anal mass/ulceration
Pt >50 with rectal bleeding and: abdo pain, or change in bowel habit, or WL or IDA
142
Management of colorectal cancer?
MDT - surgeons, oncologists, radiologists, histopathologists, specialist nurses
Surgical resection, chemo, radio, palliative care
Palliative adjuncts - stents, surgical bypass, diversion stomas
Resections tailored around lymphatic drainage - oleo-colic pedicle for R sided tumours
143
Similarities in UC and Crohns?
Diarrhoea
Arthritis
Erythema Nodosum
Pyoderma gangrenosum
144
Mnemonic for Crohns?
SISTER
Skip lesion
Ileum (MC affected)
Strictures
Transmural
Extra fibrosis and fistula formation
Radiological signs - Kantors string sign, rectum spared
145
Mnemonic for UC?
ULCCCERS
Ulcers
Large intestine
Continuous
Colorectal Ca
Crypt abscesses
Extends proximally
Red diarrhoea
Sclerosing cholangitis
146
Management of Crohns?
General - stop smoking
Inducing remission - 1 - glucocorticosteroids (budesonide), 2 - 5-ASA drugs (mesalazine), azathioprine/mercaptopurine as add-on.
Infliximab in refractory disease + fistulating Crohns
Metronidazole for isolated peri-anal disease
Maintaing remission - 1 - azathioprine/mercaptopurine, 2 - methotrexate
Surgery - stricturing terminal ileum = ileocaecal resection, stricturoplasty
- perianal fistulae - MRI, metronidazole, anti-TNF agents (infliximab), draining seton
- perianal abscess - incision + drainage, ABx therapy, draining seton
147
Complications of Crohns?
Fistulae/abscess
Small bowel cancer
Colorectal cancer
Osteoporosis
148
Management of UC?
Inducing remission:
proctitis/proctosigmoiditis + left sided UC - topical ASA, then oral ASA, oral steroid/topical steroid
Severe - 1- IV steroids, 2 - ciclosporin
Maintaining remission:
- proctitis - topical ASA, or oral and topical ASA
- left-sided + extensive - low maintenance dose of oral ASA
- severe relapse or >2 exacerbation in 1 yr - oral azathioprine/mercaptopurine
149
Triggers for UC flares?
Stress
Medications (NSAIDs, ABx)
Smoking cessation
