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Y3 Medicine > Gastroenterology > Flashcards

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
Q

How is disease progression monitored in Crohn’s and how is it managed?

A

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

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26
Q

Management of ‘undiagnosed’ dyspepsia?

A

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

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27
Q

When is urgent referral required for dyspepsia?

A

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

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28
Q

What tests are needed in a pt with GORD being considered for surgery?

A

oesophageal pH and manometry studies- measures pressure in oesophageal sphincter to confirm diagnosis

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29
Q

Sign on biopsy in gastric cancer?

A

Signet ring cells - more = worse prognosis

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30
Q

What is Gilbert’s syndrome and how does it present?

A

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

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31
Q

Describe presentation, investigation and management of hereditary haemochromatosis

A

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

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32
Q

Describe presentation and tx of hepatic encephalopathy

A

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

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33
Q

What is indicated by:
1. HBsAG
2. Anti-HBc
3. Anti-HBc IgM
4. Anti-HBc IgG
5. Anti-HBs
6. HbeAg

A
  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
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34
Q

What is the Sister Mary Joseph node?

A

a palpable nodule in the umbilicus due to metastasis of malignant cancer within the pelvis or abdomen

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35
Q

Describe the nature of hepatomegaly in:
Early cirrhosis
Malignancy
RHF

A

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

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36
Q

Most common disease pattern in UC and Crohn’s?

A

UC- proctitis
Crohn’s- ileitis

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37
Q

Tx of IBS?

A

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

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38
Q

Features and test for acute mesenteric ischaemia (occlusion of blood flow to small bowel)

A

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

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39
Q

What is ischemic colitis? Sign on Xray?

A

Transient compromise in blood flow to large bowel

Often occurs in watershed areas like splenic flexure

Thumb-printing seen on xray

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40
Q

Give 3 causes of liver cirrhosis. Investigation of choice?

A

Causes:
alcohol
non-alcoholic fatty liver disease (NAFLD)
viral hepatitis (B and C)

Transient elastography is now the investigation of choice

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41
Q

What is Melanosis coli?

A

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

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42
Q

Briefly differentiate between Mallory Weiss, Plummer Vinson Syndrome and Boerhaave Syndrome

A

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

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43
Q

key investigation for a suspected perforated peptic ulcer?

A

Erect CXR to look for pneumoperitoneum

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44
Q

Difference between duodenal and gastric ulcers?

A

Duodenal ulcers characteristically cause pain when hungry, and are relieved by eating

Gastric ulcers are worse with food

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45
Q

Outline presentation and tx of pernicious anaemia

A

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).

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46
Q

What is Peutz Jehgers syndrome?

A

Aut. dom condition
Hamartomatous polyps in GI tract (often presents with small bowel obstruction)
Pigmented freckles on lips, palms and soles

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47
Q

Dysphagia, aspiration pneumonia, halitosis (bad breath) →

A

pharyngeal pouch
Investigate with barium swallow

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48
Q

Outline presentation and management of primary biliary cholangitis

A

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

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49
Q

What is SBBO? Give risk factors, diagnostic test and tx.

A

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

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50
Q

For SBP, give the presentation, diagnostic test and tx.

A

Features:
ascites, abdominal pain, fever

Diagnosis is by paracentesis. Confirmed by neutrophil count >250 cells/ul

Managed with IV cefotaxime (E.coli infection)

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51
Q

what should you do when there is evidence of systemic disturbance and increase in bloody stool in patient with UC?

A

abdo xray to look for toxic megacolon

52
Q

Outline tx of flares in UC

A

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
Q

Give tx for:

  1. prophylaxis of variceal bleeding
  2. acute variceal bleeding
  3. uncontrolled variceal haemorrhage
A
  1. non selective BB e.g. propanolol
  2. terlipressin
  3. A Sengstaken-Blakemore tube
54
Q

What supplement is routinely recommended in alcoholism?

A

Thiamine

55
Q

Give the 4 Ds of pellagra (Vit B deficiency )

A

Dermatitis (sunburn like), diarrhoea, dementia/delusions, leading to death

56
Q

Describe presentation and tx of Wilson’s disease

A

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
Q

What is Zollinger-Ellison syndrome? Give features and screening test

A

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
Q

What can you do to reduce mortality when doing a high vol ascitic drain?

A

give IV human albumin solution

59
Q

What is the M rule for primary biliary cholangitis?

A

Primary biliary cholangitis - the M rule
IgM raised
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

60
Q

Causes of drug-induced cholestasis?

A

COCP
antibiotics
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas and fibrates

61
Q

What do hypersegmented polymorphs show?

A

Early sign of megaloblastic anaemia

62
Q

Most common cause of hepatocellular carcinoma?
How does it present?

A

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
Q

Investigation of choice in pancreatic cancer?

A

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
Q

What is seen on histology in Crohn’s?

A

Inflammation in all layers from mucosa to serosa
increased goblet cells
granulomas

65
Q

What is seen on histology in UC?

A

No inflammation beyond submucosa
crypt abscesses
depletion of goblet cells and mucin

66
Q

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?

A

Acute pancreatitis- Pancreatitis may develop following an ERCP.

67
Q

Acute cholecystitis→ abdo pain, distension and vomiting=

A

Gallstone ileus- small bowel obstruction secondary to an impacted gallstone

68
Q

How are perianal fistulae managed in Crohn’s disease?

A

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
Q

Ulcerative colitis + cholestatis (e.g. jaundice, raised ALP) →

A

? primary sclerosing cholangitis

70
Q

What is the gold standard for diagnosis of coeliac disease?

A

Endoscopic intestinal biopsy- e.g. jejunal biopsy

71
Q

What are the associations of primary sclerosing cholangitis (PSC) ? How does it present?

A

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
Q

How is PSC diagnosed?

A

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
Q

What are the complications of Primary Sclerosing Cholangitis?

A

cholangiocarcinoma (in 10%)
increased risk of colorectal cancer

74
Q

What are the complications of Primary Biliary Cholangitis?

A

cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)

75
Q

What should be given before endoscopy in patients with suspected variceal haemorrhage?

A

terlipressin and antibiotics

76
Q

What is the TIPSS procedure? Common complication?

A

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
Q

Right-sided tenderness on PR exam→

A

appendicitis

78
Q

triad of CVD, high lactate and soft but tender abdomen =

A

mesenteric ischaemia

79
Q

If NAFLD is found incidentally, what blood test should be performed to look for more severe disease? How should it be managed?

A

enhanced liver fibrosis (ELF) testing is recommended to aid diagnosis of liver fibrosis

Weight loss is the best first line management

80
Q

How do you differentiate between iron deficiency anaemia and anaemia of chronic disease on bloods?

A

Total Iron Binding Capacity is high in IDA, and low/normal in anaemia of chronic disease

81
Q

What is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease?

A

Thrombocytopenia (platelet count <150,000 mm^3)

82
Q

What are the primary care investigations for IBS?

A

full blood count
ESR/CRP
coeliac disease screen (tissue transglutaminase antibodies)

83
Q

Give some symptoms and signs of iron deficiency anaemia

A

Symptoms:
Fatigue
SOB on exertion
Palpitations

Signs:
Pallor
Hair loss
Koilonychia
Angular stomatitis and glossitis
Tachycardia/systolic murmur - compensation

84
Q

What are the main causes of iron deficiency anaemia?

A

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
Q

Investigations in iron deficiency anaemia?
Who should be referred to a gastroenterologist within 2 weeks?

A

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
Q

How should iron deficiency anaemia be managed?

A

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
Q

What are the commonest causes of pyogenic liver abscesses? How should they be managed?

A

Staphylococcus aureus in children and Escherichia coli in adults.

Management
drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin

88
Q

What can be seen on small bowel enema in Crohn’s?

A

strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

89
Q

Outline the management of ascites

A

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
Q

Classical patient presentation:

Colicky abdominal pain, worse postprandially, worse after fatty foods

Give the diagnosis and management

A

Biliary colic

Do abdo USS and LFTs

If imaging shows gallstones and history compatible then laparoscopic cholecystectomy

91
Q

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

A

Acute cholecystitis

Imaging (USS) and cholecystectomy (ideally within 48 hours of presentation)

92
Q

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

A

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
Q

Classical patient presentation:

Patient severely septic and unwell
Jaundice
Right upper quadrant pain

Give the diagnosis and management

A

Cholangitis

Fluid resuscitation
Broad-spectrum intravenous antibiotics
Correct any coagulopathy
Early ERCP

94
Q

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

A

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
Q

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

A

Acalculous cholecystitis

If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy

96
Q

Give the key causes of Budd Chiari syndrome (hepatic vein thrombosis)

A

polycythaemia rubra vera
thrombophilia
pregnancy
COCP: accounts for around 20% of cases

97
Q

What is seen on histology in Coeliac disease?

A

villous atrophy, raised intra-epithelial lymphocytes, and crypt hyperplasia

98
Q

A triad of severe, colicky post-prandial abdominal pain, weight loss, and an abdominal bruit points towards…?

A

Intestinal angina (or chronic mesenteric ischaemia)

99
Q

What can be seen on barium enema in UC?

A

loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

100
Q

Classical presentation of UC?

A

Bloody diarrhoea more common
Abdominal pain in the left lower quadrant
Tenesmus

101
Q

Classical presentation of Crohn’s?

A

Diarrhoea usually non-bloody
Weight loss more prominent
Upper gastrointestinal symptoms, mouth ulcers, perianal disease
Abdominal mass palpable in the right iliac fossa

102
Q

Which artery is at risk of damage in duodenal ulceration?

A

Gastroduodenal artery is at risk with duodenal ulcers on the posterior wall

103
Q

Give some oesophageal causes of acute upper GI bleeding and how they present

A

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
Q

Give some gastric causes of acute upper GI bleeding and how they present

A

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
Q

Give 2 duodenal causes of acute upper GI bleeding and how they present

A

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
Q

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

A

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
Q

How is hepatorenal syndrome managed?

A

vasopressin analogues, for example terlipressin (they work by causing vasoconstriction of the splanchnic circulation)

volume expansion with 20% albumin

transjugular intrahepatic portosystemic shunt

108
Q

How is remission maintained in UC after a severe relapse?

A

Following a severe relapse or 2 exacerbations in the past year : tx is oral azathioprine or oral mercaptopurine

109
Q

What key investigation is done to diagnose UC?

A

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
Q

Define malnutrition

A

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
Q

How should malnutrition be managed?

A

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
Q

Which patients are at an increased risk of developing hepatotoxicity after paracetamol overdose?

A

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
Q

How should paracetamol overdose be managed?

A

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
Q

What is the major potential adverse affect of acetylcysteine and how is this mitigated?

A

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
Q

What are the criteria for liver transplant following paracetamol overdose?

A

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
Q

How can you quickly screen for alcohol abuse in a history?

A

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
Q

Key investigations to order in acute liver failure?

A

liver function tests
prothrombin time/INR
basic metabolic panel
FBC

118
Q

What is the Mackler triad for Boerhaave syndrome?

A

vomiting, thoracic pain, subcutaneous emphysema

119
Q

What do ALT and ALP show?

A

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
Q

Give some causes of an isolated rise in ALP

A

Bony metastases or primary bone tumours (e.g. sarcoma)
Recent bone fractures
Vitamin D deficiency
Renal osteodystrophy

121
Q

Causes of an isolated rise in bilirubin?

A

Gilbert’s syndrome: the most common cause.
Haemolysis: check a blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.

122
Q

How can you investigate the liver’s synthetic function?

A

Serum bilirubin
Serum albumin
Prothrombin time (PT)
Serum blood glucose

123
Q

What can cause albumin levels to fall?

A
  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
Q

most common inheritable form of colorectal cancer?

A

HNPCC (Lynch syndrome)

125
Q

What therapy is used for H.pylori eradication?

A

PPI + amoxicillin + clarithromycin, or
PPI + metronidazole + clarithromycin

126
Q

Sign on barium swallow in oesophageal cancer?

A

‘apple core sign’

Y3 Medicine (9 decks)

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