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Y6 > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

What are mallory bodies?

A

Seen in injured hepatocytes (specifically alcohol hepatitis) and they show intracytoplasmic eosinophilic inclusions

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2
Q

Which embryonic structure do mallory bodies originate from?

A

Endoderm - this is where hepatocytes originate from

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3
Q

Risk factors for peptic ulcers

A
  • S Smoking/Spicy foods
  • H Helicobacter pylori/Hypercalcaemia
  • A Aspirin/Alcohol
  • Z Zollinger–Ellison syndrome
  • A Acidity
  • N Non-steroidal anti-inflammatory drug use (NSAID) use
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4
Q

What is the first line diuretic for treating ascites in cirrhosis?

A

Spirinolactone - aldosterone antagonist

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5
Q

Reduction of what mediator leads to oesophageal achalasia?

A

Nitric oxide - normally it increases smooth muscle relaxation and relaxes the tone of the lower oesophageal sphincter

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6
Q

What are the classical features of pellagra?

A

Diarrhoea, dermatitis and dementia

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7
Q

What are the three types of autoimmune hepatitis?

A

Type 1- Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (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

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8
Q

What is the treatment for C. difficile infection?

A

First-line therapy: oral vancomycin for 10 days

Second-line therapy: oral fidaxomicin

Third-line therapy: oral vancomycin ± IV metronidazole

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9
Q

What is Peutz-Jegher’s syndrome?

A

Autosomal dominant condition with hamartomatous polyps in the gastrointestinal tract (mainly small bowel) –> small bowel obstruction is a common presenting complaint, often due to intussusception + gastrointestinal bleeding

There are also pigmented lesions on lips, oral mucosa, face, palms and soles

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10
Q

What type of diet is useful in IBS?

A

Fermentable Oligo-Di-Monosaccharides and Polyols (FODMAP) diet

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11
Q

What two blood tests are used to monitor haemochromatosis?

A

Ferritin and transferrin

Transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/L.

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12
Q

What sign can you see on imaging of pancreatic cancer?

A

Double duct sign - the presence of dilatation of both the pancreatic and common bile ducts

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13
Q

What is alcohol ketoacidosis?

A

The presence of acidosis, raised ketones and normal/low blood glucose. This occurs in chronic alcoholics following an episode of reduced intake of food.

Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones.

Mx: Need to rehydrate with saline and give thiamine to prevent Wernicke’s encephalopathy

*If glucose is low, you should never replace it without providing thiamine first as glucose promotes metabolism, in which thiamine acts as a co-factor –> accelerates the depletion of thiamine and increases the risk of Wernicke’s.

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14
Q

How can you categorise ascites?

A

Based on serum-ascites albumin gradient (SAAG)

SAAG > 11g/L (indicates portal hypertension):
* cirrhosis/alcoholic liver disease
* acute liver failure
* liver metastases
* Cardiac: right heart failure, constrictive pericarditis

SAAG < 11g/L:
* Hypoalbuminaemia:nephrotic syndrome, severe malnutrition (e.g. Kwashiorkor)
* Malignancy: peritoneal carcinomatosis
* Infections: tuberculous peritonitis

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15
Q

Why should you avoid metoclopramide in bowel obstruction?

A

Despite metoclopramide having prokinetic properties where it stimulates peristalsis, in a complete bowel obstruction picture, stimulation of bowel movement can precipitate perforation

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16
Q

How does urea levels differ in an upper vs lower GI bleed?

A

Upper = raised
Lower = normal

The raised urea is caused by the large protein ‘meal’ of blood in the upper GI tract, which is digested.

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17
Q

What are the features of Budd Chiari Syndrome?

A

Triad of sudden onset abdominal pain, ascites, and tender hepatomegaly

It is usually caused by haemotological diseases and procoagulant conditions such as:
* 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

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18
Q

Whar scoring systems are used in upper GI bleeds?

A

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

Rockall score is used after endoscopy
* provides a percentage risk of rebleeding and mortality
* includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

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19
Q

What is the acute treatment of variceal haemorrhage?

A
  1. ABC resusctitation + consider blood products
  2. Vasoactive drugs: terlipressin, octreotide
  3. Prophylactic IV Abx
  4. Endoscopy –> variceal band ligation
  5. Sengstaken-Blakemore tube if uncontrolled haemorrhage
  6. Transjugular Intrahepatic Portosystemic Shunt (TIPSS) where hepatic vein is connected to portal vein if above measures fail (however risks hepatic encephalopathy)
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20
Q

What is the prophylactic management of variceal haemorrhage?

A

Propanolol

Non-cardioselective beta-blockers will cause vasodilation in these engorged vessels and reduced heart rate which lowers the blood pressure in the variceal veins and reduces the risk of rupture.

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21
Q

What is the management of UC remission?

A

Aminosalicylate (oral or topical/rectal, or a combination of both)

If patients experience a severe relapse or >=2 exacerbations in the past year: consider oral azathioprine or oral mercaptopurine

*Methotrexate is not licensed for UC management unlike in Crohn’s

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22
Q

What causes achalasia and what are its features?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus

Features:
* dysphagia of BOTH liquids and solids
* typically variation in severity of symptoms
* heartburn
* regurgitation of food
* may lead to cough, aspiration pneumonia etc
* malignant change in small number of patients

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23
Q

What investigations can you do in achalasia and what would the findings be?

A

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

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24
Q

What is the first-line treatment of achalasia?

A

Pneumatic (balloon) dilation is increasingly the preferred first-line option
* less invasive and quicker recovery time than surgery
* patients should be a low surgical risk as surgery may be required if complications occur

If doesn’t work: Heller cardiomyotomy surgical intervention OR intra-sphincteric injection of botulinum toxin OR drug therapy (e.g. nitrates, calcium channel blockers)

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25
Q

What is required before performing a large-volume paracentesis for ascites treatment?

A

Albumin cover with IV human albumin solution (HAS) to avoid paracentesis-induced circulatory dysfunction (PICD). PICD leads to faster accumulation of ascites, hyponatraemia, and renal impairment.

It can affect as many as 80% of patients who have large-volume paracentesis without any additional therapeutic management (with volume expanders such as HAS).

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26
Q

What is the first-line medication for constipation in IBS?

A

Bulk-forming laxative such as isphagula husk

You should avoid lactulose.

If constipation is not not responding to conventional laxatives, consider linaclotide

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27
Q

What PPIs are not advised for someone taking clopidogrel?

A

Omeprazole and esomeprazole: they decrease the efficacy of clopidogrel due to its inhibition of the CYP2C19 enzyme, which is needed to convert clopidogrel into its active metabolite

Consider lansoprazole instead which does not exhibit these effects

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28
Q

What is the best measure of acute liver failure?

A

INR/prothrombin time is better than albumin as it has a lower half-life.

These two measures are better than the other conventional “liver function tests” such as ALT, AST.

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29
Q

What pH and electrolye imbalance would be seen in prolonged vomiting?

A

Hypokalaemic, hypochloraemic metabolic alkalosis

Large amounts of hydrochloric acid are lost, causing loss of H+ ions, along with fluid loss. This leads to activation of RAAS due to reduced renal perfusion leading to increased aldosterone secretion. Aldosterone promotes the reabsorption of Na+ in exchange for H+ and K+ in the distal convoluted tubules of the kidneys. In general, where Na+ goes, water follows, meaning the blood volume is increased, however, more potassium and H+ are lost, leading to hypokalaemic metabolic alkalosis.

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30
Q

What is the management of haemochromatosis?

A

Regular venesection to keep transferrin saturation below 50% and serum ferritin concentration below 50 ug/l.

2nd line: desferrioxamine

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31
Q

Which tuberculosis medication has a side effect of peripheral neuropathy (B6 deficiency)?

A

Isoniazid

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32
Q

What are consequences of B6 deficiency?

A

Peripheral neuropathy
Sideroblastic anemia

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33
Q

What is carcinoid syndrome?

A

Group of slow-growing neuroendocrine tumours that release serotonin into the systemic circulation.

Usually occurs when metastases are present in the liver and release serotonin into the systemic circulation. May also occur with lung carcinoid as mediators are not ‘cleared’ by the liver

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34
Q

What are the features of carcinoid syndrome?

A
  • flushing (often the earliest symptom)
  • diarrhoea
  • bronchospasm
  • hypotension
  • right heart valvular stenosis (left heart can be affected in bronchial carcinoid) - pulmonary stenosis & tricuspid regurgitation
  • other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
  • pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
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35
Q

What are the investigations and management options in carcinoid syndrome?

A

Investigation:
* urinary 5-HIAA
* plasma chromogranin A y

Management:
* somatostatin analogues e.g. octreotide
* diarrhoea: cyproheptadine may help

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36
Q

What is a Sister Mary Joseph nodule?

A

It is a sign of metastasis to periumbilical lymph nodes, classically from gastric cancer primary

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37
Q

What is the management of 1st episode C. diff infection?

A
  • First-line therapy is oral vancomycin for 10 days
  • Second-line therapy: oral fidaxomicin
  • Third-line therapy: oral vancomycin ± IV metronidazole
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38
Q

What is the management of recurrent episode C. diff infection?

A
  • Within 12 weeks of symptom resolution: oral fidaxomicin
  • After 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
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39
Q

What is the management of life-threatening C. diff infection?

A

Oral vancomycin + IV metronidazole

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40
Q

What are predisposing factors that can cause bowel ischaemia (acute mesenteric ischaemia, chronic mesenteric ischaemia, ischaemic colitis)?

A
  • increasing age
  • atrial fibrillation - particularly for mesenteric ischaemia
  • other causes of emboli: endocarditis, malignancy
  • cardiovascular disease risk factors: smoking, hypertension, diabetes
  • cocaine: ischaemic colitis is sometimes seen in young patients following cocaine use
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41
Q

What is the guidance for men and women for alcohol consumption?

A

Men and women should drink no more than 14 units of alcohol per week

If you do drink as much as 14 units per week, it is best to spread this evenly over 3 days or more

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42
Q

What is Plummer-Vinson syndrome?

A

Triad of iron deficiency anaemia, atrophic glossitis and oesophageal webs or strictures. Oesophageal webs are mostly located in the upper oesophagus and consist of multiple concentric narrowings.

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43
Q

What is the most common oesophageal cancer?

A

Adenocarcinoma

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44
Q

How do adenocarcinomas and squamous cell carcinomas in the oesophagus differ?

A

Adeno:
* Most common type in the UK/US
* Lower 1/3 of oesophagus
* Associated with GORD, Barrett’s, smoking, obesity

SCC:
* Most common in world
* Upper 2/3 of oesophagus
* Associated with smoking, alcohol, achalasia, Plummer-Vinson syndrome, diets rich in nitrosamines

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45
Q

What is the management of non-variceal bleeding (i.e. ulcers)?

A

Endocsocpy

Do not prescribe PPI before endoscopy. Can be prescribed to patients post-endoscopy if there is evidence of recent non-variceal haemorrhage.

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46
Q

What is the management of first-presentation dyspepsia?

A

Offer one of the following strategies depending on clinical judgement:
* Prescribe a full-dose PPI for 1 month
* Test for Helicobacter pylori infection if the person’s status is not known or uncertain. If positive, prescribe first-line eradication therapy.

If symptoms persist or recur following initial management, switch to the alternative strategy (for example, offer a full-dose PPI for 1 month if the person has been tested for H. pylori infection and vice versa).

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47
Q

What scoring system is used to assess the severity of liver cirrhosis?

A

Child-Pugh classification

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48
Q

In which conditions can you see apple core lesions on CT imaging?

A

Colorectal carcinoma

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49
Q

What should be given to patients before an endoscopy for suspected variceal bleed?

A

Terlipressin (potent vasoconstrictor, which increases systemic vascular resistance, reduces cardiac output and reduces portal pressure by about 20%)

Antibiotics (reduce the rate of bacterial infection, treatment failure, rebleeding and mortality)

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50
Q

What do the following hepatitis B results suggest?

anti-HBs positive, all others negative
anti-HBc positive, HBsAg negative
anti-HBc positive, HBsAg positive

A

anti-HBs positive, all others negative: previous immunisation
anti-HBc positive, HBsAg negative: previous infection (>6months), not a carrier
anti-HBc positive, HBsAg positive: previous infection, now a carrier

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51
Q

What are adverse effects of PPIs?

A
  • hyponatraemia, hypomagnasaemia
  • osteoporosis → increased risk of fractures
  • microscopic colitis
  • increased risk of C. difficile infections
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52
Q

What is the medical management of Wilson’s disease?

A

Penicillamine (chelates copper)

Tridentine hydrochloride is also becoming more popular.

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53
Q

What is the first-line pharmacological treatment of the following IBS symptoms?

Pain
Consipation
Diarrhoea

A

Pain: antispasmodic agents

Constipation: laxatives but avoid lactulose

Diarrhoea: loperamide

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54
Q

What route of aminosalicylate administration is preferred in mild/moderate flare up of distal UC (proctitis or proctosigmoiditis)?

A

Topical (rectal) suppositories of aminosalicylates

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55
Q

How does dysphagia present differently in oesophageal malignancy and achalasia?

A

Oesophageal malignancy: dysphagia symptoms initially with solids and then progressively moving onto liquids (progressive)

Achalasia: inability to swallow both liquids and solids from onset

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56
Q

What diet do suspected coeliac patients need to be on prior to serology testing and biopsy?

A

Patients need to be on gluten-containing diet for 6 weeks prior to serology testing and biopsy.

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57
Q

What is the management of primary biliary cirrhosis?

A

First-line: ursodeoxycholic acid (slows disease progression and improves symptoms)

Pruritis: cholestyramine

Fat-soluble vitamin supplementation

Liver transplantation

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58
Q

What conditions are associated with primary biliary cirrhosis?

A

Sjögren’s syndrome (seen in 80% of patients)
Rheumatoid arthritis
Systemic sclerosis
Thyroid disease

59
Q

What is a pharyngeal pouch and what are its features?

A

aka Zenker’s diverticulum, commonly seen in older patients and 5x more common in men.

Features: dysphagia, regurgitation, aspiration, neck swelling which gurgles on palpation, halitosis

60
Q

What is melanosis coli?

A

Abnormal pigmentation of the large bowel due to the presence of pigment-laden macrophages. It is most commonly due to laxative abuse

61
Q

What is the classical presentation of hepatitis A infection?

A

Incubation period do 2-4 weeks. There is a flu-like prodrome which is followed by nauseousness and arthralgia. It can also cause hepatosplenomegaly and jaundice.

62
Q

What is the most common organism causing pyogenic liver abscesses?

A

Staph aureus in children
E. coli in adults

63
Q

What is the management of liver abscesses?

A

Drainage (usually image-guided percutaneous) and antibiotics (amoxicillin + ciprofloxacin + metronidazole)
If penicillin allergic: ciprofloxacin + clindamycin

64
Q

What are risk factors for liver decompensation?

A

ABCDI
Alcohol
Bleeding
Constipation
Dehydration/drugs
Infection

65
Q

What are causes of liver cirrhosis?

A

Alcohol
NAFLD
Hepatitis B and C

66
Q

How do you manage alcoholic hepatitis?

A

Glucocorticoids (e.g. prednisolone)
Pentoxyphylline is also sometimes used

67
Q

What are common LFT findings in alcoholic liver disease?

A

AST:ALT ratio >2
Gamma-GT is raised

68
Q

In which conditions is metoclopramide contraindicated?

A

Parkinson’s and those with PD symptoms such as extrapyramidal effects

69
Q

What is transient elastography?

A

aka fibroscan, it is used for diagnosis and monitoring the severity of liver cirrhosis.

It is an USS that measures the ‘stiffness’ of the liver which is a proxy for fibrosis.

70
Q

What medication is first-line to maintain remission in patients with Crohn’s?

A

Azathiopurine or mercaptopurine

71
Q

When should PPIs be stopped before an upper GI endoscopy?

A

2 weeks

72
Q

When should the following medications be stopped before an endoscopy?
Gaviscon
PPIs
Ranitidine
Abx

A

1234
1 day = gaviscon
2 weeks = PPIS
3 days = ranitidine
4 weeks = abx

73
Q

What are indications for upper GI endoscopy?

A

Age >55yrs
Symptoms >4weeks or persistent treatment despite treatment
Dysphagia
Relapsing symptoms
Weight loss

74
Q

What can you do if endoscopy is negative and you are still suspecting GORD?

A

24-hr oesophageal pH monitoring (the gold standard test for diagnosis)

75
Q

What is the ideal management of haemochromatosis?

A

Venesection is first-line: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l

Desferrioxamine can be used 2nd-line. It is an iron chelator

76
Q

Is C. diff toxin or antigen used for diagnosis of C. difficile infection?

A

Diagnosis is made by detecting C. difficile toxin (CDT) in the stool. If the toxin is positive, it means the bacteria is actively replicating and is likely the cause of the diarrhoea.

C. difficile antigen positivity only shows exposure to the bacteria, rather than current infection

77
Q

What is the difference in presentation of a bleeding peptic ulcer and perforated peptic ulcer?

A

Bleeding: melaena, hypotension ± syncope

Perforated: peritonitis - diffuse abdominal pain, abdominal distension, rigidity and guarding

78
Q

Which antibiotic treatment is given in spontaneous bacterial peritonitis?

A

IV cefotaxime

79
Q

What are the features of spontaneous bacterial peritonitis?

A

Form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.
Features: ascites, abdominal pain and fever
*Alcohol liver disease is a poor prognostic marker of SBP

80
Q

How do you diagnose spontaneous bacterial peritonitis?

A

Paracentesis: neutrophil count > 250 cells/ul

81
Q

What sign is usually seen in pancreatic cancer on CT?

A

Double duct sign

82
Q

What is Rigler’s sign?

A

a.k.a. the double wall sign. This means that you can see both sides of the bowel wall. It is indicative of gas in the peritoneal cavity - usually appearing after 1L of gas (a lot). Causes include perforation or recent surgery.

83
Q

Which H. pylori test is used to check for eradication?

A

Only the urea breath test
The other tests still remain positive after eradication

84
Q

What are the causes of extremely raised ALT (exceeding 1000 international unit/L or 50 times the upper limit of normal)?

A

Toxic hepatitis
Ischaemic hepatitis
Viral hepatitis

85
Q

What scoring system is used to assess the severity of UC in adults.

A

True love and Witt’s severity index

86
Q

What do you seen on AXR in a gallstone ileus?

A

Small bowel obstruction (multiple dilated loops of bowel) and air in the biliary tree (pneumobilia).

87
Q

What is Mirizzi’s syndrome?

A

Where a gallstone within the gallbladder compresses the bile duct causing an obstructive jaundice

88
Q

What cancer is associated with pernicious anaemia?

A

Gastric carcinoma - thought due to be from hypochlorhydria and chronic inflammation.

89
Q

What is the pathophysiology of pernicious anaemia?

A

Intrinsic factor antibodies → bind to intrinsic factor blocking the vitamin B12 binding site

Gastric parietal cell antibodies → reduced acid production and atrophic gastritis. Reduced intrinsic factor production → reduced vitamin B12 absorption

90
Q

What is small bowel bacterial overgrowth syndrome?

A

Small bowel bacterial overgrowth syndrome (SBBOS) is a disorder characterised by excessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms.
Features (of which many overlap with IBS): chronic diarrhoea, bloating, flatulence, abdominal pain.

91
Q

What are risk factors for small bowel bacterial overgrowth syndrome?

A

Neonates with congenital gastrointestinal abnormalities
Scleroderma
Diabetes mellitus

92
Q

What is the diagnosis and management of small bowel bacterial overgrowth syndrome?

A

Diagnosis:
* Hydrogen breath test
* Small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
* Clinicians may sometimes give a course of antibiotics as a diagnostic trial

Management:
* Correction of the underlying disorder
* Antibiotic therapy: rifaximin is now the treatment of choice due to relatively low resistance. Co-amoxiclav or metronidazole are also effective in the majority of patients.

93
Q

What is the minimum amount of time a C diff patient needs to isolate for?

A

Patients diagnosed with C. difficile should be isolated until they have experienced no diarrhoea (types 5-7 on the Bristol Stool Chart) for a minimum of 48 hours.

94
Q

What vaccine should coeliac patients receive?

A

Pneumococcal vaccination (with a booster every 5 years) as they are prone to a degree of functional hyposplenism

95
Q

What extra investigation should be done in a flare-up of ulcerative colitis?

A

AXR to exclude toxic megacolon (transverse colon being > 6 cm in diameter in combination with signs of systemic upset)

96
Q

What is hepatorenal syndrome?

A

Triad of: Cirrhosis, Ascites, AKI not attributable to any other cause

Pathophysiology: vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This 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.

97
Q

What are the types of hepatorenal syndrome?

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

98
Q

What are the management options for hepatorenal syndrome?

A
  • Vasopressin analogues, for example terlipressin - cause vasoconstriction of the splanchnic circulation
  • Volume expansion with 20% albumin
  • Transjugular intrahepatic portosystemic shunt
99
Q

What is the first-line medical management of the following causes of nausea and vomiting:

  • Reduced gastric motility
  • Chemically-related (2º to hypercalcaemia, opioids, or chemotherapy)
  • Visceral/serosal (constipation)
  • Raised ICP
  • Vestibular
  • Cortical
A
  • Reduced gastric motility: metoclopramide and domperidone
  • Chemically-related (2º to hypercalcaemia, opioids, or chemotherapy): ondansetron
  • Visceral/serosal (constipation): Cyclizine and levomepromazine
  • Raised ICP: cyclizine ± dexamethasone
  • Vestibular: cyclizine
  • Cortical: short acting benzodiazepine e.g. lorazepam
100
Q

What is seen on light microscopy in a chronic hepatitis B infection?

A

Ground-glass hepatocytes

101
Q

What is the most common organism found on ascitic fluid culture?

A

E. coli

102
Q

What is a common histology of an ulcer?

A

Granulation tissue with necrotic debris

*This is common in chronic ulcers of the body (such as reflux) as opposed to accute ones (like a simple mouth ulcer)

103
Q

What are some features of iron deficiency anaemia?

A
  • Fatigue
  • Koilonychia
  • Atrophic glossitis
  • Angular cheilosis
  • Plummer-vinson syndrome
104
Q

What are the different degrees of haemorrhoids?

A
  • 1st Degree - haemorrhoids that do NOT prolapse
  • 2nd Degree - prolapse with defecation but reduce spontaneously
  • 3rd Degree - prolapse and require manual reduction
  • 4th Degree - prolapse that CANNOT be reduced
105
Q

What are conservative measures for haemorrhoids?

A
  • High-fibre diet
  • Increase fluid intake
  • Bulk laxatives (lactulose) + stool softeners (docusate)
  • Topical creams (e.g. local anaesthetics)
106
Q

What is the mechanism of action of orlistat?

A

Inhibits gastric and pancreatic lipase to reduce the digestion of fat

107
Q

What medications cause c diff infections?

A

Clindamycin
2nd and 3rd generation cephalosporins (e.g. cefuroxime, cefoxatime)
PPIs

108
Q

What is the triad of Boerhaaves syndrome?

A

Vomiting, thoracic pain, subcutaneous emphysema

109
Q

What is used to diagnose and treat Boerhaaves syndrome?

A

Diagnosis: CT contrast swallow

Treatment: thoractomy and lavage - primary repair if within 12 hours

110
Q

What are symptoms of postoperative ileus?

A

aka paralytic ileus:
* Abdominal pain
* Bloating
* Nausea/vomiting
* Inability to pass flatus
* Inability to tolerate oral diet

*You can also get deranged electrolytes

111
Q

Risk factors for biliary colic

A

4Fs:
* Fat
* Female
* Fertile
* Forty

112
Q

Definition of acute vs chronic anal fissure

A

Acute: under 6 weeks, usually 1-2 weeks

Chronic: over 6 weeks

113
Q

Treatment of anal fissures

A

Acute:
* soften stool: increase fibre intake ± bulk-forming laxatives
* lubricants such as petroleum jelly may be tried before defecation
* topical anaesthetics
* analgesia

Chronic:
* same as above
* topical GTN - if not effective after 8 weeks, then refer for sphincterotomy or botulim toxin

114
Q

What is the management of acutely thrombosed external haemorrhoids?

A
  • Typically present with significant pain
  • Examination reveals a purplish, oedematous, tender subcutaneous perianal mass
  • If patient presents within 72 hours then referral should be considered for excision.
  • Otherwise patients can usually be managed with stool softeners, ice packs and analgesia. Symptoms usually settle within 10 days
115
Q

Why are biliary stones common in Crohn’s disease?

A

Bile salts are absorbed in the terminal ileum. When this process is impaired as in Crohns the patient may develop gallstones

116
Q

What is the most common organism to cause cholangitis?

A

E. coli

117
Q

What is the most common type of volvulus?

A

Sigmoid volvulus (80% of cases)

20% of cases are caecal volvulus

118
Q

What do you see on AXR of a volvulus?

A

Sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign

Caecal volvulus: small bowel obstruction may be seen (bowel will be more central)

119
Q

What is the management of a volvulus?

A

Sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion

Caecal volvulus: management is usually operative. Right hemicolectomy is often needed

120
Q

What is the investigation of choice for a pharyngeal pouch?

A

Barium swallow combined with dynamic video fluoroscopy

121
Q

What is a key first-step management of acute pancreatitis?

A

Aggressive fluid resuscitation - correct the third space losses and increase tissue perfusion with the aim of preventing severe inflammatory response syndrome which can lead to pancreatic necrosis

122
Q

Should you offer to make a patient nil-by-mouth in acute pancreatitis?

A

Not unless there is a clear reason e.g. the patient is vomiting - patients actually have increased caloric demands during infection

Enteral nutrition should be offered to anyone with moderately severe or severe acute pancreatitis within 72 hours of presentation

123
Q

What investigations can you do in chronic pancreatitis?

A

AXR or CT - shows calcifications
Faecal elastase

124
Q

What are features of chronic pancreatitis?

A
  • Pain is typically worse 15 to 30 minutes following a meal
  • Steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
  • Diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin
125
Q

What are common differences in ileostomy vs colostomy?

A

Ileostomy:
* Location: Right iliac fossa
* Appearance: Spouted
* Output: Liquid

Colostomy:
* Location: more likely on the left side of the abdomen
* Appearance: Flushed
* Output: Solid

126
Q

What is a common way to anatomically distinguish femoral and inguinal hernias?

A

Femoral = inferior and lateral to pubic tubercle
Inguinal = superior and medial to pubic tubercle

127
Q

Which part of the colon is diverticular disease more common in?

A

Left side, particularly sigmoid colon

128
Q

What is the management of small bowel obstruction?

A

“Drip and suck”
NBM
IV fluids
NG tube with free drainage

129
Q

Symptoms of small bowel obstruction vs large bowel obstruction

A

SBO:
* Abdominal pain higher up
* Vomiting, which can be bilious
* Hyperactive bowel sounds
* Rapid abmonial distension

LBO:
* Abominal pain lower down
* Constipation
* Hypoactive bowel sounds
* Gradual abdominal distension

130
Q

What are the types of hiatus hernia?

A

Sliding (95%): the gastroesophageal junction moves above the diaphragm

Rolling (paraoesophageal): the gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus

131
Q

What is the ideal investigation and management of a hiatus hernia?

A

Barium swallow is the most sensitive test - but many patients have incidental findings on endoscopy

Management:
* All patients benefit from conservative management e.g. weight loss
* Medical: proton pump inhibitor therapy
* Surgical: only really has a role in symptomatic paraesophageal hernias

132
Q

What are reasons for endoscopy following ingestion of corrosive substances?

A

Symptomatic ingestion (drooling, vomiting, dysphagia, odynophagia, chest pain) requires urgent assessment with upper GI endoscopy to assess the degree of ulceration (Zargar classification).

Extensive injury on endoscopy should prompt consideration of urgent surgical exploration

133
Q

What are complications of ingestion of corrosive substances?

A

Acute:
* Upper GI ulceration, perforation
* Upper airway injury and compromise
* Aspiration pneumonitis
* Infection
* Electrolyte disturbance (e.g. hypocalcaemia in hydrofluoric acid ingestion)

Chronic:
* Strictures, fistulae, gastric outlet obstruction
* Upper GI carcinoma (estimated 1000-3000 fold increased risk)

134
Q

What is the most common type of anal cancer and what causes it?

A

Squamous cell carcinoma - linked to HPV infection

*High incidence in anal intercourse and MSM

135
Q

What is the second most common cancer associated with hereditary non-polyposis colorectal cancer (Lynch syndrome)?

A

Endometrial cancer

136
Q

What is globus pharyngis?

A

Globus pharyngis (also known as globus hystericus) is the persistent sensation of having a ‘lump in the throat’, when there is none. Symptoms are often intermittent and relieved by swallowing food or drink. Swallowing of saliva is often more difficult.

137
Q

What blood test abnormalities can you spot in acute pancreatitis?

A

Raised amyslase
Raised lipase
Hypocalcaemia - poor prognostic indicator

138
Q

What investigation do you do when you initially suspect Budd-Chiari syndrome?

A

Ultrasound with Doppler flow studies

139
Q

What are the components of the Child-Pugh score?

A

ABCDE:
Albumin
Bilirubin
Clotting (prothrombin)
Diffuse ascites
Encephalopathy

140
Q

What are two common risk factors of oesophageal candidiasis?

A

HIV
Steroid inhalers

141
Q

What investigations are required before undergoing fundoplication surgery in treatment resistant gord?

A

Oesophageal pH
Manometry studies

142
Q

What surveillance criteria exists for Barrett’s oesophagus?

A

Endoscopy with biopsies:

Every 2 to 3 years to people with long-segment (3 cm or longer) Barrett’s oesophagus

Every 3 to 5 years to people with short-segment (less than 3 cm) Barrett’s oesophagus with intestinal metaplasia

143
Q

How do you manage Barrett’s oesophagus with dysplasia?

A

High grade dysplasia: endoscopic resection of visible lesions, followed by endoscopic ablation

Low grade dysplasia: radiofrequency ablation

144
Q

How do you manage stage 1 oesophageal adenocarcinoma?

A

T1a (mucosa): endoscopic resection ± endoscopic ablation

T1b (submucosa): oesophagectomy or radiotherapy (if not fit for surgery)

Y6 (24 decks)

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