Gastroenterology Flashcards

1
Q

How do you make a diagnosis of C diff infection and how do you determine severity?

A

Diagnose by detecting CDT (toxin) in stool
WCC to determine severity

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2
Q

Risk factors for C diff?

A

abx and PPIs
esp cephalosporins

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3
Q

What is the tx stepladder for C diff infections?

A

first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy/ in life- threatening cases: oral vancomycin +/- IV metronidazole

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4
Q

What drugs must be stopped before a urea breath test?

A

no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks

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5
Q

What is achalasia?
Most important diagnostic test?
What cancer does it increase the risk of?
How is it treated?

A

Definition: Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated.

Presents with dysphagia of both solids and liquids from onset

Key test: Oesophageal manometry
- also shows grossly expanded oesophagus, fluid level and ‘bird’s beak’ appearance on barium swallow

increases the risk of squamous cell carcinoma of the oesophagus

First line: pneumatic (balloon) dilation
Surgical management when comorbidites/recurrence : Heller cardiomyotomy

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6
Q

How is appendicitis diagnosed?

A

Thin young male patients with a high likelihood of appendicitis (classic central abdominal pain that localises to the right iliac fossa) can be diagnosed clinically w/o a scan

Often do an USS in women for pelvic pathology

Raised inflammatory markers (e.g. CRP) and neutrophil predominant leucocytosis can aid in diagnosis

May be psoas sign positive- unable to stand on one leg comfortably and pain on hip extension

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7
Q

Best way to measure liver function in people with established disease?

A

Liver enzymes are a poor way to look at liver function - they are usually low in end-stage cirrhosis whereas coagulation e.g. prothrombin time and albumin are better measures

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8
Q

What is fetor hepaticus?

A

sweet and fecal breath, it is a sign of liver failure

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9
Q

Causes of acute liver failure?

A

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

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10
Q

Features of acute liver failure?

A

jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)

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11
Q

Raised urea + normocytic anaemia= ?
How much does urea need to be raised to be a significant case?

A

Upper GI bleed!
- a haemorrhage with an origin proximal to the ligament of Treitz

Urea is from protein meal (digestion of RBCs)

Urea of 15.4 mmol/l on a background of normal renal function is a significant bleed

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12
Q

Management of Upper GI bleed?

A

All patients with suspected upper GI bleed require an endoscopy within 24 hours of admission

IV PPIs given AFTER endoscopy (never before) if evidence of recent variceal haemorrhage

Repeated endoscopic intervention with no success (more acute bleeds) = surgical intervention

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13
Q

How is risk stratified in Upper GI bleeding?

A

the Glasgow-Blatchford score used at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not

the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality

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14
Q

Eq for alcohol units?

A

Alcohol units = volume (ml) * ABV / 1,000

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15
Q

Cause of metabolic acidosis in non-diabetic alcoholics? Tx?

A

Alcoholic ketoacidosis
- Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation and ketone production

Will likely have normal or low blood glucose

treatment is an infusion of saline & thiamine

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16
Q

AST/ALT ratio in alcoholic hepatitis?

A

2:1

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17
Q

Management of alcoholic hepatitis?

A

glucocorticoids (e.g. prednisolone) are often used during acute episodes of alcoholic hepatitis

Maddrey’s discriminant function (DF) is often used to determine who would benefit from glucocorticoid therapy
- its calculated using prothrombin time and bilirubin concentration

pentoxyphylline is also sometimes used

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18
Q

Key investigation in unwell patient taking aminosalicylates?

A

A patient who is taking aminosalicylates and becomes unwell with a sore throat, fever, fatigue or bleeding gums needs an urgent full blood count to rule out agranulocytosis.

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19
Q

What do Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) with raised IgG suggest?

A

Type 1 autoimmune hepatitis- common in young women, often also see secondary amenorrhea, tx with steroids

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20
Q

When is endoscopic intervention ( endoscopic mucosal resection or radiofrequency ablation) offered with Barrett’s oesophagus?

A

When dysplasia is seen

If not pts can be managed with endoscopic surveillance every 3-5 years and a high dose PPI

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21
Q

how does Budd-Chiari present and how is it investigated?

A

Budd-Chiari syndrome (hepatic vein thrombosis):

Presents with the triad of sudden onset abdominal pain, ascites, and tender hepatomegaly

Can do a Serum - Ascites Albumin Gradient (a raised SAAG (>11g/L) indicates that it is portal hypertension that has caused the ascites and makes Budd-Chiari more likely)

Investigate with doppler USS

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22
Q

For carcinoid syndrome (release of serotonin into systemic circulation), outline the presentation, test and tx

A

carcinoid syndrome-

Sx: flushing, diarrhoea, bronchospasm, hypotension, and weight loss

Caused by lung carcinoid or more commonly mets in the liver

Test urinary 5-HIAA

Give somatostatin analogues e.g. octreotide

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23
Q

Features of coeliac?

A

Coeliac disease:

  • non specific symptoms like fatigue, anaemia and weight loss
  • low ferritin/folate
  • raised white cells/CRP due to inflammation
  • raised tissue transglutaminase (TTG) antibody
  • grey frothy stool

Coeliac disease increases the risk of developing enteropathy-associated T cell lymphoma

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24
Q

How long before testing should coeliac patients eat gluten? What is being tested for in serology?

A

6 weeks
tissue transglutaminase (TTG) antibodies (IgA)

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25
How is disease progression monitored in Crohn's and how is it managed?
ESR can be used to assess disease progression first-line management strategy for the induction of remission is glucocorticoids Azathioprine or mercaptopurine is used first-line to maintain remission Managing complications: MRI is the investigation of choice for suspected perianal fistulae- provides visualisation of the course Wound swab can be used for recurrent abscesses
26
Management of 'undiagnosed' dyspepsia?
Patient with dyspepsia who does not meet referral criteria: do a full work up before anything else e.g bloods and review meds for common drug-induced causes such as NSAIDs and aspirin give lifestyle advice trial PPI for one month If PPI fails for reflux and upper GI symptoms test for H.pylori
27
When is urgent referral required for dyspepsia?
All patients who've got dysphagia All patients who've got an upper abdominal mass consistent with stomach cancer Patients aged >= 55 years who've got weight loss, AND any of the following: upper abdominal pain reflux dyspepsia
28
What tests are needed in a pt with GORD being considered for surgery?
oesophageal pH and manometry studies- measures pressure in oesophageal sphincter to confirm diagnosis
29
Sign on biopsy in gastric cancer?
Signet ring cells - more = worse prognosis
30
What is Gilbert's syndrome and how does it present?
autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase An isolated rise in bilirubin in response to physiological stress (e.g. onset of jaundice exclusively while ill, exercising or fasting) is typical No treatment required
31
Describe presentation, investigation and management of hereditary haemochromatosis
Haemochromatosis : aut. dom. disorder of iron absorption Presentation: bronze/ slate grey colouration fatigue and cognitive sx joint pain - can have secondary osteoarthritis (hook-like osteophytes at the 2nd and 3rd digits at MCPJ) hair loss erectile dysfunction Investigation: general population: transferrin saturation > ferritin family members: HFE genetic testing (can also do liver biopsy w Perl's stain) Management: venesection Ferritin and transferrin saturation are used to monitor treatment
32
Describe presentation and tx of hepatic encephalopathy
Hepatic encephalopathy: Liver disease -> build up of ammonia and glutamine ( liver cell impairment prevents adequate metabolism and portosystemic anastomoses mean blood can bypass the liver altogether) Presentation: altered GCS, acute confusion, asterixis (hepatic flap) and triphasic slow waves on ECG Graded 1- 4 : Irritability -> confusion -> incoherence -> coma Tx: lactulose first line to excrete ammonia , then rifaximin to alter gut flora and breakdown of ammonia there
33
What is indicated by: 1. HBsAG 2. Anti-HBc 3. Anti-HBc IgM 4. Anti-HBc IgG 5. Anti-HBs 6. HbeAg
1. first surface antigen to be produced in response to infection, represents acute hepatitis infection if less than 6mo or chronic if present for over 6mo. If it is negative they are not currently infected. 2. anti hepatitis core antibody is produced in response to infection- c for caught- currently or has previously caught hepatitis 3. IgM- acute infection 4. IgG- chronic infection, remains indefinitely even if hepatitis is cleared (IgM are produced in initial infection and are gradually replaced with IgG over months) 5. immunisation (in a healthy individual who has been vaccinated this is the only one that is raised) 6. results from breakdown of core antigen from infected liver cells. Marker of HBV replication and infectivity
34
What is the Sister Mary Joseph node?
a palpable nodule in the umbilicus due to metastasis of malignant cancer within the pelvis or abdomen
35
Describe the nature of hepatomegaly in: Early cirrhosis Malignancy RHF
Hepatomegaly: Cirrhosis (in early disease): Associated with a non-tender, firm liver Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular liver edge Right heart failure: firm, smooth, tender liver edge. May be pulsatile
36
Most common disease pattern in UC and Crohn's?
UC- proctitis Crohn's- ileitis
37
Tx of IBS?
IBS Tx: pain: antispasmodic agents constipation: laxatives but avoid lactulose ( first line isphagula husk, linaclotide can be used as an alternative to conventional laxatives if nothing else works for 12 months) diarrhoea: loperamide is first-line
38
Features and test for acute mesenteric ischaemia (occlusion of blood flow to small bowel)
Common features abdominal pain - often of sudden onset, severe and not inkeeping with physical exam findings fever rectal bleeding and diarrhoea often have a hx of AF Investigation: Venous blood gas first line to look for raised lactate
39
What is ischemic colitis? Sign on Xray?
Transient compromise in blood flow to large bowel Often occurs in watershed areas like splenic flexure Thumb-printing seen on xray
40
Give 3 causes of liver cirrhosis. Investigation of choice?
Causes: alcohol non-alcoholic fatty liver disease (NAFLD) viral hepatitis (B and C) Transient elastography is now the investigation of choice
41
What is Melanosis coli?
Melanosis coli is the abnormal pigmentation of the large bowel due to the presence of pigment-laden macrophages. It is most commonly due to laxative abuse
42
Briefly differentiate between Mallory Weiss, Plummer Vinson Syndrome and Boerhaave Syndrome
Mallory-Weiss syndrome Severe vomiting → painful mucosal lacerations at the gastroesophageal junction resulting in haematemesis. Common in alcoholics Plummer-Vinson syndrome: triad of dysphagia, glossitis and iron-deficiency anaemia (dysphagia is due to post cricoid webs) tx is iron supplements and dilation of webs Boerhaave syndrome: Severe vomiting → oesophageal rupture Chest pain and subcut emphysema also feature
43
key investigation for a suspected perforated peptic ulcer?
Erect CXR to look for pneumoperitoneum
44
Difference between duodenal and gastric ulcers?
Duodenal ulcers characteristically cause pain when hungry, and are relieved by eating Gastric ulcers are worse with food
45
Outline presentation and tx of pernicious anaemia
Pernicious anaemia: autoimmune disorder that causes B12 deficiency antibodies to IF middle/old age patients, more common in females anaemia features (headache, fatigue, pallor) neuro features - peripheral neuropathy, psychiatric changes Can have pancytopenia Tx= IM Vit B12 Vitamin B12 1mg IM three times/week then 1mg IM every 3 months folate should never be replaced before vitamin B12 due to the risk of precipitating subacute combined degeneration of the cord. (Think BeFore: B before F to remember).
46
What is Peutz Jehgers syndrome?
Aut. dom condition Hamartomatous polyps in GI tract (often presents with small bowel obstruction) Pigmented freckles on lips, palms and soles
47
Dysphagia, aspiration pneumonia, halitosis (bad breath) →
pharyngeal pouch Investigate with barium swallow
48
Outline presentation and management of primary biliary cholangitis
Chronic autoimmune condition, bile ducts damaged by inflammation, often presents with itching or jaundice or raised ALP on routine bloods Imaging required to rule out extra-hepatic biliary obstruction Management : ursodeoxycholic acid 1st line, then cholestyramine for itching
49
What is SBBO? Give risk factors, diagnostic test and tx.
Small bowel bacterial overgrowth syndrome: excessive bacteria in SI presents w chronic diarrhoea and flatulence scleroderma and diabetes are risk factors, as well as neonates w congenital GI issues hydrogen breath test to diagnose treat with rifaximin
50
For SBP, give the presentation, diagnostic test and tx.
Features: ascites, abdominal pain, fever Diagnosis is by paracentesis. Confirmed by neutrophil count >250 cells/ul Managed with IV cefotaxime (E.coli infection)
51
what should you do when there is evidence of systemic disturbance and increase in bloody stool in patient with UC?
abdo xray to look for toxic megacolon
52
Outline tx of flares in UC
In a mild-moderate flare of distal ulcerative colitis, the first-line treatment is topical (rectal) aminosalicylates e.g. mesasalazine and if no response then it should be given orally (In a mild-moderate flare extending past the left-sided colon, oral aminosalicylates should be added to rectal as enemas only reach so far) A severe flare of ulcerative colitis (e.g. tachycardic and febrile) should be treated in hospital with IV corticosteroids
53
Give tx for: 1. prophylaxis of variceal bleeding 2. acute variceal bleeding 3. uncontrolled variceal haemorrhage
1. non selective BB e.g. propanolol 2. terlipressin 3. A Sengstaken-Blakemore tube
54
What supplement is routinely recommended in alcoholism?
Thiamine
55
Give the 4 Ds of pellagra (Vit B deficiency )
Dermatitis (sunburn like), diarrhoea, dementia/delusions, leading to death
56
Describe presentation and tx of Wilson's disease
Wilsons disease- aut. dom. reduced serum copper (deposited in tissues) Presentation: Usually 10-25 Presents with liver disease in kids and neuro issues in adults can appear like a mental illness e.g. schizophrenia brown rings in the eyes (Kayser-Fleischer rings), blue nails, dystonia reduced serum copper and reduced caeruloplasmin (binds copper) Tx: penicillamine
57
What is Zollinger-Ellison syndrome? Give features and screening test
Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome Features multiple gastroduodenal ulcers diarrhoea malabsorption Diagnosis fasting gastrin levels: the single best screen test secretin stimulation test
58
What can you do to reduce mortality when doing a high vol ascitic drain?
give IV human albumin solution
59
What is the M rule for primary biliary cholangitis?
Primary biliary cholangitis - the M rule IgM raised anti-Mitochondrial antibodies, M2 subtype Middle aged females
60
Causes of drug-induced cholestasis?
COCP antibiotics anabolic steroids, testosterones phenothiazines: chlorpromazine, prochlorperazine sulphonylureas and fibrates
61
What do hypersegmented polymorphs show?
Early sign of megaloblastic anaemia
62
Most common cause of hepatocellular carcinoma? How does it present?
hepatitis B most common cause worldwide hepatitis C most common cause in Europe Occurs secondary to liver cirrhosis Presents late with features of liver disease e.g. jaundice and raised alpha fetoprotein on bloods
63
Investigation of choice in pancreatic cancer?
High-resolution CT scanning May see double duct sign caused by dilation of the common bile duct and pancreatic duct in response to the tumour
64
What is seen on histology in Crohn's?
Inflammation in all layers from mucosa to serosa increased goblet cells granulomas
65
What is seen on histology in UC?
No inflammation beyond submucosa crypt abscesses depletion of goblet cells and mucin
66
A 62-year-old presents with upper abdo pain. She has recently been discharged from hospital where she underwent an ERCP to investigate cholestatic liver function tests. The pain is severe. On examination she is apyrexial and has a pulse of 96 / min. Likely diagnosis?
Acute pancreatitis- Pancreatitis may develop following an ERCP.
67
Acute cholecystitis→ abdo pain, distension and vomiting=
Gallstone ileus- small bowel obstruction secondary to an impacted gallstone
68
How are perianal fistulae managed in Crohn's disease?
patients with symptomatic perianal fistulae are usually given oral metronidazole anti-TNF agents such as infliximab may also be effective in closing them a draining seton is used for complex fistulae- it is a piece of surgical thread that's left in the fistula for several weeks to keep it open so it doesn't heal up with pus inside and form an abscess
69
Ulcerative colitis + cholestatis (e.g. jaundice, raised ALP) →
? primary sclerosing cholangitis
70
What is the gold standard for diagnosis of coeliac disease?
Endoscopic intestinal biopsy- e.g. jejunal biopsy
71
What are the associations of primary sclerosing cholangitis (PSC) ? How does it present?
ulcerative colitis: 80% of patients with PSC have UC Crohn's (much less common association than UC) HIV cholestasis - jaundice, pruritus, raised bilirubin + ALP right upper quadrant pain fatigue
72
How is PSC diagnosed?
endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a 'beaded' appearance p-ANCA may be positive
73
What are the complications of Primary Sclerosing Cholangitis?
cholangiocarcinoma (in 10%) increased risk of colorectal cancer
74
What are the complications of Primary Biliary Cholangitis?
cirrhosis → portal hypertension → ascites, variceal haemorrhage osteomalacia and osteoporosis significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
75
What should be given before endoscopy in patients with suspected variceal haemorrhage?
terlipressin and antibiotics
76
What is the TIPSS procedure? Common complication?
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) is a last line tx in variceal bleeding connects the hepatic vein to the portal vein exacerbation of hepatic encephalopathy is a common complication- inadequate metabolism of nitrogenous waste products by the liver
77
Right-sided tenderness on PR exam→
appendicitis
78
triad of CVD, high lactate and soft but tender abdomen =
mesenteric ischaemia
79
If NAFLD is found incidentally, what blood test should be performed to look for more severe disease? How should it be managed?
enhanced liver fibrosis (ELF) testing is recommended to aid diagnosis of liver fibrosis Weight loss is the best first line management
80
How do you differentiate between iron deficiency anaemia and anaemia of chronic disease on bloods?
Total Iron Binding Capacity is high in IDA, and low/normal in anaemia of chronic disease
81
What is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease?
Thrombocytopenia (platelet count <150,000 mm^3)
82
What are the primary care investigations for IBS?
full blood count ESR/CRP coeliac disease screen (tissue transglutaminase antibodies)
83
Give some symptoms and signs of iron deficiency anaemia
Symptoms: Fatigue SOB on exertion Palpitations Signs: Pallor Hair loss Koilonychia Angular stomatitis and glossitis Tachycardia/systolic murmur - compensation
84
What are the main causes of iron deficiency anaemia?
Excessive blood loss: often menorrhagia in pre-menopausal women and GI bleeding in men (always suspect colon cancer) and post-menopausal women. Malabsorption: coeliac, Crohn's, diverticular disease Inadequate dietary intake: esp in vegetarians and vegans (However dark green leafy vegetables are another good source of iron) Increased iron requirements: Growing children and pregnant women (needs to supply baby with iron and also dilutional deficiency)
85
Investigations in iron deficiency anaemia? Who should be referred to a gastroenterologist within 2 weeks?
Full hx: changes in diet, medication history, menstrual history, weight loss, change in bowel habit FBC : hypochromic microcytic anaemia Serum ferritin: low (However ferritin can be raised during states of inflammation; so a raised ferritin does not necessarily rule out iron deficiency anaemia) Total iron-binding capacity (TIBC) : high Blood film : anisopoikilocytosis (red blood cells of different sizes and shapes) , target cells, 'pencil' poikilocytes Endoscopy to rule out malignancy, males and post-menopausal females who present with unexplained iron-deficiency anaemia should be considered for further gastrointestinal investigations. Post-menopausal women with a haemoglobin level ≤10 and men with a haemoglobin level ≤11 should be referred to a gastroenterologist within 2 weeks.
86
How should iron deficiency anaemia be managed?
Ensure malignancy is excluded first Oral ferrous sulfate: patients should continue taking for 3 months after the deficiency has been corrected in order to replenish iron stores. Common side effects of iron supplementation include nausea, abdominal pain, constipation, diarrhoea Iron-rich diet: this includes dark-green leafy vegetables, meat, iron-fortified bread
87
What are the commonest causes of pyogenic liver abscesses? How should they be managed?
Staphylococcus aureus in children and Escherichia coli in adults. Management drainage (typically percutaneous) and antibiotics amoxicillin + ciprofloxacin + metronidazole if penicillin allergic: ciprofloxacin + clindamycin
88
What can be seen on small bowel enema in Crohn's?
strictures: 'Kantor's string sign' proximal bowel dilation 'rose thorn' ulcers fistulae
89
Outline the management of ascites
reducing dietary sodium is first line fluid restriction is sometimes recommended if the sodium is < 125 mmol/L aldosterone antagonists: e.g. spironolactone drainage if tense ascites (therapeutic abdominal paracentesis) prophylactic antibiotics to reduce the risk of SBP - oral ciprofloxacin or norfloxacin with an ascitic protein of 15 g/litre or less a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients
90
Classical patient presentation: Colicky abdominal pain, worse postprandially, worse after fatty foods Give the diagnosis and management
Biliary colic Do abdo USS and LFTs If imaging shows gallstones and history compatible then laparoscopic cholecystectomy
91
Classical patient presentation: Right upper quadrant pain Murphys sign on examination (pain on inspiration while palpating RUQ) Fever Occasionally mildly deranged LFT's (especially if Mirizzi syndrome) Give the diagnosis and management
Acute cholecystitis Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)
92
Classical patient presentation: Usually prodromal illness and right upper quadrant pain Swinging pyrexia Patient may be systemically unwell Generalised peritonism not present Give the diagnosis and management
Gallbladder abscess Imaging with USS +/- CT Scanning Ideally surgery (although subtotal cholecystectomy may be needed if Calot's triangle is hostile) In unfit patients, percutaneous drainage may be considered
93
Classical patient presentation: Patient severely septic and unwell Jaundice Right upper quadrant pain Give the diagnosis and management
Cholangitis Fluid resuscitation Broad-spectrum intravenous antibiotics Correct any coagulopathy Early ERCP
94
Classical patient presentation: Small bowel obstruction (may be intermittent) Patients may have a history of previous cholecystitis and known gallstones Give the diagnosis and management
Gallstone ileus Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.
95
Classical patient presentation: Gallbladder inflammation in absence of stones Systemically unwell with high fever Patients with intercurrent illness (e.g. diabetes, organ failure) Give the diagnosis and management
Acalculous cholecystitis If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy
96
Give the key causes of Budd Chiari syndrome (hepatic vein thrombosis)
polycythaemia rubra vera thrombophilia pregnancy COCP: accounts for around 20% of cases
97
What is seen on histology in Coeliac disease?
villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia
98
A triad of severe, colicky post-prandial abdominal pain, weight loss, and an abdominal bruit points towards...?
Intestinal angina (or chronic mesenteric ischaemia)
99
What can be seen on barium enema in UC?
loss of haustrations superficial ulceration, 'pseudopolyps' long standing disease: colon is narrow and short -'drainpipe colon'
100
Classical presentation of UC?
Bloody diarrhoea more common Abdominal pain in the left lower quadrant Tenesmus
101
Classical presentation of Crohn's?
Diarrhoea usually non-bloody Weight loss more prominent Upper gastrointestinal symptoms, mouth ulcers, perianal disease Abdominal mass palpable in the right iliac fossa
102
Which artery is at risk of damage in duodenal ulceration?
Gastroduodenal artery is at risk with duodenal ulcers on the posterior wall
103
Give some oesophageal causes of acute upper GI bleeding and how they present
Oesophageal varices - Large volume of fresh blood. Sometimes malena due to swallowed blood. Often associated with haemodynamic compromise. Oesophagitis - Small volume of fresh blood, often streaking vomit. Malena rare. Usually history of GORD type symptoms. Cancer - Usually small volume of blood, except as a preterminal event with erosion of major vessels. Often dysphagia and constitutional symptoms such as weight loss. Mallory Weiss tear - brisk bright red blood following a bout of repeated vomiting. Malena rare.
104
Give some gastric causes of acute upper GI bleeding and how they present
Gastric ulcer- tends to present as iron deficiency anaemia due to repeated small bleeds. Erosion into a significant vessel may produce considerable haematemesis. Gastric cancer - frank haematemesis or altered blood mixed with vomit. Usually dyspepsia and may have constitutional symptoms. Dieulafoy lesion (AV malformation)- Often no prodromal features prior to haematemesis and melena. May produce considerable haemorrhage and may be difficult to detect endoscopically Diffuse erosive gastritis - Usually haematemesis and epigastric discomfort. Usually underlying cause such as NSAID usage. Large volume haemorrhage may occur with considerable haemodynamic compromise
105
Give 2 duodenal causes of acute upper GI bleeding and how they present
Duodenal ulcer- haematemesis, melena and epigastric discomfort. Aorto-enteric fistula - In patients with previous AAA surgery, can cause major haemorrhage associated with high mortality.
106
Hepatorenal syndrome is thought to come about when vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance and causes underfilling of the kidneys. Describe the 2 types
Type 1 HRS Rapidly progressive Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks Very poor prognosis Type 2 HRS Slowly progressive Prognosis poor, but patients may live for longer
107
How is hepatorenal syndrome managed?
vasopressin analogues, for example terlipressin (they work by causing vasoconstriction of the splanchnic circulation) volume expansion with 20% albumin transjugular intrahepatic portosystemic shunt
108
How is remission maintained in UC after a severe relapse?
Following a severe relapse or 2 exacerbations in the past year : tx is oral azathioprine or oral mercaptopurine
109
What key investigation is done to diagnose UC?
colonoscopy + biopsy is generally done for UC diagnosis however in patients with severe colitis colonoscopy should be avoided due to the risk of perforation - a flexible sigmoidoscopy is preferred
110
Define malnutrition
a Body Mass Index (BMI) of less than 18.5; or unintentional weight loss greater than 10% within the last 3-6 months; or a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
111
How should malnutrition be managed?
Stratify risk using the MUST score dietician support if the patient is high-risk a 'food-first' approach with clear instructions (e.g. 'add full-fat cream to mashed potato'), rather than just prescribing oral nutritional supplements (ONS) such as Ensure if ONS are used they should be taken between meals, rather than instead of meals
112
Which patients are at an increased risk of developing hepatotoxicity after paracetamol overdose?
patients taking liver enzyme-inducing drugs (rifampicin, phenytoin, carbamazepine, chronic alcohol excess, St John's Wort) malnourished patients (e.g. anorexia nervosa) or patients who have not eaten for a few days Acute alcohol intake is not associated with an increased risk of developing hepatotoxicity and may actually be protective.
113
How should paracetamol overdose be managed?
Activated charcoal if presents within 1 hour Acetylcysteine should be given if: there is a staggered overdose or there is doubt over the time of paracetamol ingestion, regardless of the plasma paracetamol concentration; or the plasma concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
114
What is the major potential adverse affect of acetylcysteine and how is this mitigated?
Acetylcysteine commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release). Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate. Acetylcysteine is now infused over 1 hour (rather than the previous 15 minutes) to reduce the number of adverse effects.
115
What are the criteria for liver transplant following paracetamol overdose?
Arterial pH < 7.3, 24 hours after ingestion or all of the following: prothrombin time > 100 seconds creatinine > 300 µmol/l grade III or IV encephalopathy
116
How can you quickly screen for alcohol abuse in a history?
CAGE Cut down - ever thought you should? Annoyed- do you get annoyed at others commenting on your drinking? Guilty- do you ever feel guilty about drinking? Eye opener- ever drink in the morning to help your hangover or nerves?
117
Key investigations to order in acute liver failure?
liver function tests prothrombin time/INR basic metabolic panel FBC
118
What is the Mackler triad for Boerhaave syndrome?
vomiting, thoracic pain, subcutaneous emphysema
119
What do ALT and ALP show?
ALT is found in high concentrations within hepatocytes and enters the blood following hepatocellular injury. It is, therefore, a useful marker of hepatocellular injury. ALP is particularly concentrated in the liver, bile duct and bone tissues. ALP is often raised in liver pathology due to increased synthesis in response to cholestasis. As a result, ALP is a useful indirect marker of cholestasis.
120
Give some causes of an isolated rise in ALP
Bony metastases or primary bone tumours (e.g. sarcoma) Recent bone fractures Vitamin D deficiency Renal osteodystrophy
121
Causes of an isolated rise in bilirubin?
Gilbert’s syndrome: the most common cause. Haemolysis: check a blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.
122
How can you investigate the liver's synthetic function?
Serum bilirubin Serum albumin Prothrombin time (PT) Serum blood glucose
123
What can cause albumin levels to fall?
1. Liver disease resulting in a decreased production of albumin (e.g. cirrhosis). 2. Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin. 3. Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome.
124
most common inheritable form of colorectal cancer?
HNPCC (Lynch syndrome)
125
What therapy is used for H.pylori eradication?
PPI + amoxicillin + clarithromycin, or PPI + metronidazole + clarithromycin
126
Sign on barium swallow in oesophageal cancer?
'apple core sign'