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Medicine > Upper and Lower GI tract > Flashcards

Upper and Lower GI tract Flashcards

1
Q

Name 3 causes of dysphagia. (3)

A

Mouth: acute pharyngitis
Neuromuscular: Bulbar palsy, myasthenia gravis
Oesophageal motility:
Primary : achalasia, eosinophilic oesophagitis
Systemic : diabetes, scleroderma
Extrinsic pressure: mediastinal glands, goitre, large L atrium
Intrinsic pressure: benign stricture, malignant stricture, oesophageal ring, foreign body, oesophageal pouch

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2
Q

What symptom would suggest vomiting is a GI cause? (1)

A

Pain with vomiting suggestive of GI cause.

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3
Q

Vomiting without pain suggests a non GI cause.

Name 3 non-GI causes of vomiting. (3)

A

CNS: raised ICP, migraine
Drugs: chemotherapy, excess alcohol
Metabolic: uraemia, DKA, pregnancy

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4
Q

Name 3 causes of steatorrhoea. (3)

A

Fat malabsorption as a result of;

  • small bowel
  • pancreatic disease (lipase deficiency)
  • cholestatic liver/biliary disease (intestinal bile salt deficiency)
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5
Q

What is leukoplakia? (2)

A

Oral white plaques or patches for which there is no local cause (diagnosis of exclusion).
They should be biopsied as they may be pre-alignant.

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6
Q

What is atrophic glossitis? (1)

Name 2 conditions associated with it. (2)

A

Smooth, sore tongue with loss of filiform papillae.

Iron, B12 or folate deficiency.

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7
Q

What is geographical tongue? (2)

A

Affects 1-2% of the population and described discrete areas of depapillation on the dorsum of the tongue.
The aetiology is unknown and there is no specific treatment.

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8
Q

What is xerostomia? (1)

Name 2 causes. (2)

A

Dry mouth.

Anxiety, Sjogren’s, dehydration, tricyclic antidepressants.

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9
Q

Roy is a 69 yea old man presenting with dysphagia.
What history would suggest an initial investigation of urgent OGD and what history would suggest a barium swallow as initial investigation? (2)

A

Urgent OGD: short history of progressive dysphagia initially for solids and then for liquids is suggestive of mechanical stricture.
Barium: Slow onset of dysphagia for both solids and liquids is suggestive of a motility disorder e.g. achalasia.

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10
Q

What 2 investigations may help to diagnose achalasia? (2)

A

Barium swallow

Oesophageal manometry

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11
Q

What is regurgitation? (1)

A

Effortless reflux of oesophageal contents into the mouth and pharynx.
Occurs in reflux disease and oesophageal strictures.

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12
Q

What is odynophagia? (1)

A

Pain during swallowing particularly with alcohol and hot liquids.
Suggestive of oesophagitis due to GORD, infection of oesophagus or drugs.

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13
Q

Describe the pathophysiology of GORD. (3)

A

Lower oesophageal sphincter tone is reduced causing frequent, transient LOS relaxations.
Increased mucosal sensitivity to gastric acid and reduced oesophageal clearance of acid.
Delayed gastric emptying, post-prnadial and nocturnal reflux may also contribute.

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14
Q

Name 3 risk factors for developing GORD. (3)

A 
Hiatus hernia
Pregnancy
Obesity
Systemic sclerosis
Medications (nitrates, tricyclics, etc)
Smoking
Excessive alcohol
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15
Q

What are the ALARM symptoms? (6)

A 
Anaemia (iron deficient)
Loss of weight
Anorexia
Recent onset
Malaena/haematemesis
Swallowing difficulties

Indicate need for urgent OGD to exclude upper GI malignancy.

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16
Q

What is the management of uncomplicated GORD? (3)

A

Conservative: weight loss, smoking cessation, avoidance of excess alcohol, avoidance of aggravating foods.
Medical: simple antacids for mild; PPI for severe or with proven pathology e.g. oesophagitis.

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17
Q

What surgical option is available for severe unremitting GORD? (1)

A

Laproscopic Nissen fundoplication.

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18
Q

Describe the mechanism of PPI’s. (2)

A

Inhibition of the gastric hydrogen-potassium pump, inhibiting the release of gastric acid.

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19
Q

What are the 2 main complications of GORD? (2)

A

Oesophageal stricture formation: gradually worsening dysphagia.
Barrett’s oesophagus: metaplasia of squamous to columnar epithelium in the distal oesophagus; pre-malignant for oesophageal adenocarcinoma.

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20
Q

Fred has Barrett’s oesophagus diagnosed by epithelial appearance on OGD.
What is the next management step? (2)

A

Treatment with PPI

Endoscopic surveillance every 2 years, with biopsies for dysplasia and carcinoma.

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21
Q

What is achalasia? (1)

A

Unknown aetiology.

Oesophageal aperistalsis and failure of relaxation of the lower oesophageal sphincter impairs oesophageal emptying.

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22
Q

Gerry has had a long history of dysphagia of both solids and liquids. You suspect achalasia.
Name 3 investigations that may help with the diagnosis. (3)

A
  • Barium swallow: Initial investigations showing dilated oesophagus with gradually tapering lower end.
  • Oesophageal manometry: (diagnostic) demonstrates aperistalsis and failure of LOS relaxation on swallowing.
  • OGD: may be needed to exclude carcinoma.
  • X-ray: may show dilated oesophagus with fluid level behind the heart. Loss of fundal gas shadow.
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23
Q

What carcinoma is achalasia a risk factor for? (1)

A

Squamous cell oesophageal carcinoma.

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24
Q

Name 2 treatment options for achalasia. (2)

What is the most common complication of all treatment options? (1)

A

Medical: oral nitrates or nifedipine, endoscopic injection of botulinium to relax sphincter in elderly (efficacy is limited)
Surgical: endoscopic balloon dilatation or surgical division of the LOS.

GORD

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25
Q

In diffuse oesophageal spasms what sign can be seen on barium swallow? (1)

A

Corkscrew appearance.

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26
Q

What is a hiatus hernia? (2)

Name the 2 types. (2)

A

Part of the stomach herniates through the oesophageal hiatus of the diaphragm.
Sliding (95%) and Para-oesophageal hernias.

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27
Q

Describe a sliding hiatus hernia. (2)

A

Gastro-oesophageal junction slides through the hiatus and lies above the diaphragm. Does not cause symptoms unless there is associated reflux.

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28
Q

Describe a para-oesophageal hernia. (2)

A

Gastric fundus rolls up through the hiatus alongside the oesophagus, the gastro-oesophageal junction remains below the diaphragm.
There is a risk of gastric volvulus, bleeding and respiratory complications and should be treated surgically.

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29
Q

Name 2 causes of oesophageal perforation. (2)

A 
Iatrogenic: endoscopic dilatation of strictures, management of achalasia, passage of NG tube
Blunt chest trauma
Forceful vomiting (Boerhaave's syndrome)
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30
Q

What is Boerhaave’s syndrome? (1)

A

Perforation of the oesophagus caused by forceful vomiting.

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31
Q

What are the two types of oesophageal tumours and where do they most commonly occur? (2)

A

Adenocarcinoma in lower 1/3

Squamous cell carcinoma in middle 1/3

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32
Q

Name 3 risk factors for developing squamous cell carcinoma of the oesophagus. (3)

A 
Smoking
Alcohol
Ingestion of very hot food and drinks
Achalasia
Coeliac disease
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33
Q

Why is oGD preferred to a barium swallow when trying to diagnose carcinoma of the oesophagus? (1)

A

Barium swallow may show stricture but cannot be used to take biopsies to confirm diagnosis.

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34
Q

Name 3 functions of the stomach. (3)

A
  • Emulsification of fats and mechanical break up of food
  • Reservoir for food
  • Secretion of intrinsic factor and gastric acid
  • Secretion of mucus and pepsinogen from chief cells (converted to pepsin by gastric acid)
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35
Q

What increases acid secretion from the stomach? (2)

A

Vagal nerve stimulation
Histamine
Gastrin

Reduced by somatostatin from antral D cells.

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36
Q

What is H. pylori? (2)

Where is it found in the GI tract? (2)

A

Gram negative urease producing spiral shaped bacterium found predominantly in the antrum and areas of gastric metaplasia in the duodenum.

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37
Q

Name 2 conditions associated with H. pylori infection. (2)

A

Chronic active gastritis
Peptic ulcer disease
Gastric cancer
gastric B cell lymphoma

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38
Q

What is triple therapy? (3)

A

7 day regimens for eradicating H pylori

eg Omeprazole 20mg +Amoxicillin 1g + Clarithromycin 500mg

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39
Q

Name 3 tests for diagnosing H pylori. (3)

A 
C13-urea breath test
Stool antigen test
Serology
Rapid urease (CLO) test (invasive)
Histology (invasive)
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40
Q

Define peptic ulcer. (2)

A

Break in the mucosa in or adjacent to an acid-bearing area. (most in stomach or proximal duodenum)

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41
Q

Which kind of peptic ulcer is most common? (1)

A

Duodenal ulcer (2-3x more common)

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42
Q

What is Zollinger-Ellison syndrome? (1)

A

Gastrinoma

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43
Q

Clinically how can a gastric ulcer and duodenal ulcer be differentiated? (2)

A

Duodenal: pain when patient is hungry or at night.
Gastric: pain after eating

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44
Q

Gary is suspected of having a gastric ulcer.
What test should he have initially if;
a) is under 55 years old
b) is over 55 years old? (2)

A

a) non invasive H pylori testing

b) OGD with multiple biopsies from centre and edges of ulcer.

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45
Q

Name 2 complications of peptic ulcers. (2)

A

Perforation (DU>GU)
Gastric outlet obstruction (surrounding oedema or scarring)
Haemorrhage

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46
Q

How do NSAIDs cause gastropathy? (2)

A

Inhibition of cycle-oxygenase 1 causes depletion of mucosal prostaglandins, leading to mucosal damage.

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47
Q

How does acute and chronic gastritis differ histologically? (2)

A

Acute: neutrophilic infiltration
Chronic: mononuclear cells (mainly lymphocytes, also plasma cells and macrophages)

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48
Q

Where in the stomach are gastric cancers most likely to be found? (1)
What type of cancer is it usually? (1)

A

Antrum

Adenocarcinoma

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49
Q

Name 4 clinical features associated with gastric cancer. (4)

Which area would you pay careful attention to? (1)

A

Burning, epigastric pain, worsened by eating.
Nausea, anorexia, weight loss.
Palpable epigastric mass (50%)
Skin: dermatomyositis, acanthosis nigricans

Nr pylorus: gastric outlet obstruction, vomiting
In cardia: dysphagia

Mets in peritoneum and liver: ascites, hepatomegaly

50
Q

What is a GIST? (2)

A

most common type of stromal or mesenchymal tumour of the GI tract occurring most commonly in the stomach or proximal small intestine.
Usually asymptomatic but have malignant potential.
Resect surgically.

51
Q

What is a MALToma? (2)

A

Mucosa-associated lymphoid tissue tumour (gastric lymphoma)

52
Q

Harry has been passing black, tarry stools.

Where is his GI bleeding likely to be? (1)

A

Proximal to the jejunum.

53
Q

Name a scoring system that helps to identify those patients with a GI bleed who are at high risk of recurrent or life threatening haemorrhage. (1)

A

Rockall score

54
Q

Harry has a upper GI bleed. You wish to perform endoscopy.

Which anti-coagulants/anti-platelets should be stopped? (2)

A

Stop: warfarin, aspirin, NSAIDs.

Consult cardiology before stopping aspirin and clopidogrel in patients with low risk bleeds.

55
Q

Name 3 causes of upper GI bleed. (3)

A 
Reflux oesophagitis
PUD
Mallory-Weiss tear
Varices
Gastric carcinoma
Blood dyscrasias
56
Q

You have assessed Harry using the Rockall score which is 4 (high risk) and have stopped and reversed his warfarin.
What is the next step in management? (1)
What if you suspected variceal bleeding? (1)

A

Endoscopy.
If not possible immediately, give PPI IV.

Antibiotics and consider terlipressin.

57
Q

What two non-invasive tests can be used to ensure eradication of H. pylori? (2)

A

Urea breath test or stool antigen test.

58
Q

What is the Rockall score? (2)

What parameters does the Rockall score use? (2)

A

A scoring tool used pre-endoscopy to determine risk of significant haemorrhage and post-endoscopy to determine risk of re-bleed or death.

Pre: Age, Signs of shock, Co-morbidities
Post: as above + Endoscopic stigmata and Diagnosis

59
Q

Quinn has presented to the GP with small amounts of bright red bleeding per rectum.
Whereabouts would this suggest the bleed has originated? (1)
What is the most appropriate imaging for this bleed? (1)

A

Distal to the splenic flexure.

Flexible sigmoidoscopy.

60
Q

What is a proctoscope used for? (1)

A

Looks for ano-rectal disease.

61
Q

Name 3 causes of lower GI bleeding. (3)

A 
Colon:
haemorrhoids
anal fissure
neoplasms (benign and malignant)
colitis (UC, crohn's, infective, ischaemic)
angiodysplasia
diverticular disease
Small intestine:
neoplasms
ulcerative disease (crohn's, vasculitis, NSAIDs)
angiodysplasia
Meckel's diverticulum.
62
Q

Apart from chronic bleeding. Name 2 causes of iron deficient anaemia. (2)

A

Menstruation
Malabsorption (coeliac)
Previous gastrectomy
Poor dietary intake

63
Q

Which patients with iron deficient anaemia require OGD and colonoscopy to look for malignancy? (2)

A

Any men
Non menstruating women
Menstruating women over 50
Menstruating women under 50 with GI symptoms

64
Q

Which nutrients have specific receptors in the terminal ileum for their absorption? (2)

A

B12

Bile salts

65
Q

Name 3 disorders of the small bowel that causes malabsorption. (3)

A 
Coeliac
Crohn's
Dermatitis herpetiformis
Tropical sprue
Bacterial overgrowth
Intestinal resection
Whipple's disease
Radiation enteritis
66
Q

Bill presents to his GP with steatorrhoea, abdominal pain and anorexia. His FBC shows B12 deficiency.
Where in the GI tract do you suspect the lesion is? (1)

What investigations would you do? (2)

A

Small bowel

Coeliac serology
Small bowel barium follow
Endoscopic small bowel biopsy

67
Q

Which HLA molecules are associated with coeliac disease? (2)

A

HLA-DQ2

HLA-DQ8

68
Q

What is the best serological test for coeliac disease? (1)
What scenario would cause this to be falsely negative? (1)
Which antibodies should be looked for in the above scenario? (1)
Name one other less sensitive serological test for coeliac disease. (1)

A

IgA tissue transglutaminase antibodies
IgA deficiency (2% of coeliacs)
IgG tTG antibodies.

IgA endomysial antibodies

69
Q

What is the diagnostic test for coeliac disease? (2)

Describe the histological changes. (2)

A

Endoscopic distal duodenal biopsy
Increase in number of intra-epithelial lymphocytes, crypt hyperplasia with chronic inflammatory cells in the lamina propria and villious atrophy.

70
Q

Name 3 prior diagnoses that should be offered serological testing for coeliac disease. (3)

A 
AI: T1DM, thyroid, Addison's
IBS
Unexplained osteoporosis
1st degree relative with coeliac
Down's
Turner's
Infertility/recurrent miscarriages
71
Q

Why is the pneumococcal vaccine given to those with coeliac disease? (1)

A

Coeliac is associated with hyposplenism.

72
Q

Which malignancies are coeliacs at increased risk of developing? (2)

A

Intestinal T cell lymphoma, small bowel and oesophageal cancer

73
Q

What is dermatitis herpetiformis? (2)

A

Itchy, symmetrical eruption of vesicles over extensor surfaces of the body. There is deposition of IgA at the dermo-epidermal junction. Patients also have an asymptomatic gluten-sensitive enteropathy.

74
Q

What is tropical sprue? (2)

A

Progressive small bowel disorder presenting with diarrhoea, steatorrhoea and megaloblastic anaemia. The small bowel biopsy will show a similar picture to untreated coeliac disease.

75
Q

What causes bacterial overgrowth of the small bowel? (2)

A

Usually almost sterile.

bacterial overgrowth is caused by abnormal motility or structural abnormality.

76
Q

name 2 complications of resection of the terminal ileum. (2)

A

Decreased absorption of B12 = megaloblastic anaemia
Decreased absorption of bile salts = diarrhoea (increases water secretion) and oxalate stones (increased absorption of oxalate).

77
Q

After bowel resection, what length of remaining small bowel can cause short bowel syndrome? (1)

A

<1m

78
Q

Which small bowel disease is associated with periodic acid-Schiff (PAS)-positive macrophages on electron microscopy? (1)

A

Whipple’s disease (cased by bacteria Tropheryma whipplei.

79
Q

Which part of the small bowel is most likely to be affected by TB? (1)

A

Ileo-caecal junction

can mimic crohn’s

80
Q

Name 2 enteropathies that can lead to oedema and hypoalbuminaemia? (2)

A

Crohn’s disease
Coeliac disease
Lymphatic disorders

81
Q

Name 3 causes of intestinal ischaemia. (3)

A

Thrombosis
Emboli
Vasculitis
Profound and prolonged shock

82
Q

What is Peutz-Jeghers syndrome? (2)

A

Autosomal dominant condition that has mucocutaneous pigmentation and hamartomatous gastrointestinal polyps.
Usually polyps are in small bowel and can cause intussusception, bleeding or malignant change.

83
Q

What is a carcinoid tumour? (3)

A

Originates from entero-chromaffin cells (serotonin producing). Liver mets causes carcinoid syndrome.

84
Q

Name the 3 co-factors for the aetiology of IBD. (3)

A

Genetics
Environment
Host immune response

85
Q

How does smoking affect IBD? (2)

A

Crohn’s: smoking increases risk

UC: smoking decreases risk

86
Q

How can Crohn’s disease and UC be distinguished clinically? (3)

A

UC: diarrhoea often containing blood and mucus.
-also may have extra-intestinal manifestations
Cr: varied depending on site affected:
-small bowel: abdo pain and weight loss
-terminal ileum: acute abdomen with RIF pain
-colon: diarrhoea, blood and pain related to defecation
-perianal: anal tags, fissures, fistulae and abscess.

87
Q

Describe the macroscopic differences between UC and Crohn’s. (4)

A

Location: C is anywhere in GI tract; UC is rectum proximally
Lesions: C is skip lesions; UC in continuous
Endoscopy: C is deep ulcers and fissures, Cobblestone appearance; UC is red mucosa, bleeds easily, ulcers and pseudo polyps.

88
Q

Describe the microscopic differences between UC and Crohn’s. (2)

A

C: transmural inflammation, granulomas present in 50%
UC: mucosal inflammation, no granulomata, goblet cell depletion and crypt abscesses.

89
Q

The ulcerative colitis severity index.

Name 3 features used to distinguish between mild and severe UC. (3)

A 
Bloody diarrhoea: Mild 6 /day
Fever: Mild none; Severe >37.5 'C
Tachycardia: Mild none; Severe >90 bpm
ESR: Mild: 30
Anaemia: Mild none; Severe Hb <30g/L

Severe is bloody diarrhoea plus any one other systemic.

90
Q

What anaemia would you expect in IBD? (2)

A

Chronic disease: normocytic normochromic
Iron deficient
Vitamin B12 or floate deficiency

91
Q

Name 5 extra-intestinal manifestations of IBD. (5)

A

Eyes: episcleritis, uveitis, conjunctivitis
Joints: arthalgia, small joint arthritis, ankylosing spondylitis, inflammatory back pain
Skin: erythema nodosum, pyoderma gangrenosum
Hepatobiliary: fatty liver, sclerosing cholangitis, chronic hepatitis, cirrhosis, gallstones*
Renal: Oxalate stones
Venous thrombosis

92
Q

Name 4 treatments that may be used in the management of CD. (4)

A

Oral 5-ASA eg mesalazine in mild disease only
Steroids eg prednisolone in mod/severe disease
Liquid enteral nutrition can induce remission in CD
Azathioprine or 6-MP to maintain remission
Metronidazole for perianal CD
Methotrexate if resistant to steroids or intolerant to azathioprine
Anti-TNF antibodies eg infliximab to induce remission in resistant cases.

93
Q

When is surgery considered an option for IBD? (2)

A

Failure of medical therapy with symptoms producing ill health
Complications
Failure to grow despite medical treatment

94
Q

What is the surgical management of CD and UC? (2)

A

CD: resection is minimal due to frequent recurrence
UC:
-Colectomy with ileo-anal anastomosis (terminal ileum used to make pouch to act as rectum)
-Panproctocolectomy with ileostomy (whole colon and rectum removed)

95
Q

Name 4 medical treatments of UC. (4)

A

Mild/mod: oral or rectal 5-ASA; oral prednisolone 2nd
Severe: oral prednisolone
Severe with systemic: hydrocortisone, ciclosporin, infliximab
Maintain remission: 5-ASA or azathioprine/6-MP

96
Q

Name 3 complications of IBD. (3)

A 
Toxic megacolon + perforation
Stricture formation
Abscess formation (CD)
Fistulae and fissures (CD)
Colon cancer
97
Q

Give 4 differentials (causes) of constipation. (4)

A

General: pregnancy, diet, immobility
Endocrine: DM, hypothyroidism, hypercalcaemia
Functional: IBS
Drugs: opiates, calcium channel blockers, anti-muscarinics
Neuro: Parkinson’s, spinal cord lesions
Psych: depression, anorexia
GI: obstruction, painful anal conditions, Hirschsprung’s
Defecatory: Rectal prolapse, pelvic floor dyssynergia, large rectocoele, megarectum

98
Q

Give 3 factors that are required for faecal continence. (3)

A 
Mental function
Stool volume and consistency
Structural and functional integrity of anal sphincters
Pubo-rectalis
Pudendal nerve function
Rectal distensibility
Anorectal sensation
99
Q

What is diverticulosis? (2)

A

Out-pouchings of colonic mucosa and submucosa through the muscular wall of the large bowel.

100
Q

Why is the splenic flexure described as a “watershed area”? (2)

A

It is the part of the colon that is supplied by the distal branches of the superior and inferior mesenteric arteries and so is more prone to ischaemia.

101
Q

What is a polyp? (1)

A

Abnormal growth of tissue projecting into intestinal lumen from normally flat mucosal surface. Most are adenomas.

102
Q

What is an adenomatous polyp? (2)

A

Tumours of benign neoplastic epithelium, more common with increasing age.
Usually asymptomatic but can bleed and cause anaemia or large villous adenoma can cause diarrhoea and hypokalaemia.

103
Q

Name 2 factors that increase the risk of malignancy in an adenomatous polyp. (2)

A 
Size >1cm
Sessile polyps > pedunculated polyps
Severe dysplasia > Mild dysplasia
Villous histology
Multiple polyps
104
Q

Name 3 risk factors for developing colorectal cancer. (3)

A

Increasing age
Family history
FAP/HNPCC
Low fibre diet

105
Q

What is HNPCC? (3)

A

Hereditary non-polyposis colorectal cancer
Causes accelerated progression from adenoma to CRC. Lifetime risk of CRC is 50%. Also increased risk of endometrial cancer.

106
Q

What is FAP? (2)

A

Familial adenomatous polyposis is a mutation of the APC gene causing numerous colorectal polyps (>100) to develop in teenage years. The lifetime cancer risk of FAP is 100%.

107
Q

Name 3 of the two week wait criteria. (3)

A
  • Pt >40 with looser stools and rectal bleeding for >6 weeks
  • Pt >60 with rectal bleeding for >6 weeks
  • Pt >60 with looser stools for >6 weeks
  • Men of any age with Hb <100g/L
  • Mass in RIF
  • Palpable rectal mass
108
Q

What biomarker can be use din the follow up of colorectal cancer? (1)

A

CEA - carcinoembryonic antigen

109
Q

What is the gold standard investigations for colorectal cancer? (2)

A

Colonoscopy and biopsy

110
Q

Name 2 tests to help stage colorectal cancer. (2)

A

LFTs for liver mets
CT chest, abdo, pelvis for lung and other mets
PET scan can investigate suspicious CT lesions.

111
Q

What is the screening in the UK for colorectal cancer? (2)

A

If FH: screening colonoscopy

All age 60-69 years, biannual faecal occult blood.

112
Q

After what time frame does acute diarrhoea become chronic diarrhoea? (1)

A

14 days

113
Q

What is guarding? (2)

A

Involuntary contraction of the abdominal muscles when the abdomen is palpated

114
Q

Name 4 differentials for acute lower abdominal pain. (4)

A 
Aortic aneurysm
Ectopic pregnancy
rupture of ovarian cyst
Ovarian torsion
Testicular torsion
Renal obstruction
Mesenteric ischaemia
Mesenteric adenitis
Appendicitis
Acute pancreatitis
Small bowel obstruction
Large bowel obstruction
IBD
Diverticulitis
Meckel's diverticulum
115
Q

What is the difference between localised and generalised peritonitis? (2)

A

Localised: occurs in all acute inflammatory conditions of the GI tract.
Generalised: as a result of rupture of abdominal viscus. Sudden onset of abdominal pain, patient is shocked and lies still as movement aggravates the pain.

116
Q

What are the two types of intestinal obstruction? (2)

How can they be distinguished? (2)

A

Mechanical and functional

Mechanical is painful, colicky, imaging shows dilation above the obstruction, with increased secretion of fluid into the lumen. Associated with vomiting and absolute constipation. O/E there is distension and tinkling BS.
Functional eg paralytic ileus post-surgery. Often pain is not present and bowel sounds may be decreased. Gas can be seen throughout the bowel on plain x-ray.

117
Q

What cells line the peritoneal cavity? (1)

A

Mesothelium (simple squamous, same as pleura)

118
Q

Name 2 conditions that affect the peritoneum. (2)

A

Infective (peritonitis): secondary to gut disease, chronic peritoneal dialysis, TB, spontaneous.
Neoplasia: Secondary deposits e.g. from ovary, primary mesothelioma.
Vasculitis: Connective tissue disease.

119
Q

What is refeeding syndrome? (3)

A

Occurs within first few days of feeding.
Shift from use of fat as energy source (during starvation) to carbohydrate (during refeeding).
Increased insulin release, and intracellular movement of phosphate, potassium and magnesium.
Low serum levels of K, Mg and PO4 cause widespread organ dysfunction.

120
Q

What test that if negative can rule out IBD? (1)

A

Faecal calprotectin

Medicine (14 decks)

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