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Clinical sciences > GI > Flashcards

GI Flashcards

1
Q

Patient presents with dyspepsia. In what circumstances would you do an endoscopy?

A
  1. Age over 55
  2. Alarm symptoms - unexplained weight loss, iron deficiency anaemia/ evidence of GI blood loss, dysphagia, upper abdominal mass, persistent vomiting
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2
Q

What is dyspepsia?

A

According to the rome III criteria, it is one or more of the following:

  1. Postprandial fullness
  2. Early satiety
  3. Epigastric pain or burning (over a month)
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3
Q

What is an ulcer?

A

Break in continuity of epithelial surface

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4
Q

What are the main causes of dyspepsia?

A
  1. GORD
  2. Peptic ulcer disease
  3. Gastritis
  4. Drugs (NSAIDs/nitrates/CCB)

There are also other causes such as excess acid production, large volume meals regularly, obesity, smoking and alcohol, and pregnancy

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5
Q

Why are smoking and alcohol risk factors for dyspepsia?

A

Relax lower oesophageal sphincter (GORD)

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6
Q

How do patients with dyspepsia commonly present?

A

Complaining of indigestion, heartburn, acid taste, bloating, reflux (worse lying down) and saying that they have an ulcer

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7
Q

Does PUD present acutely or chronically?

A

Acutely

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8
Q

What are the ‘red flag’ symptoms in a patient presenting with dysphagia?

A
  1. Unexplained weight loss
  2. Iron deficiency anaemia/ evidence of GI blood loss
  3. Upper abdominal mass
  4. Dysphagia
  5. Persistent vomiting
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9
Q

What conditions is early postprandial pain suggestive of?

A

Gastritis, GORD

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10
Q

Patient presents with dyspepsia and claims that milk relieves pain. What is the likely cause of the dyspepsia?

A

Duodenal ulcer

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11
Q

A patient presents complaining of heartburn, regurgitation and a cough. What is the likely cause of their dyspepsia?

A

GORD

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12
Q

A 23 year old patient presents with epigastric pain for the last 6 weeks and early satiety. How would you manage this patient?

A
  1. Lifestyle advice - if fails..
  2. Full dose PPI (e.g. omeprazole) for 1 month
  3. If this fails … Test or treat for h.pylori
  4. If pain persists add histamine 2 antagonist to PPI (e.g. ranitidine)
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13
Q

What change in epithelium is seen in Barrett’s oesophagus?

A

Change from squamous cell to glandular columnar cell epithelium

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14
Q

What investigations can be done in dyspepsia, when a patient refuses endoscopy?

A
  1. Barium swallow
  2. Bravo capsule - measures 24 hr pH of oesophagus
  3. Capsule endoscopy
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15
Q

If patient with functional dyspepsia (non-ulcer) has pain that persists, what drugs could be used on them after normal reassurance and dietary review has taken place?

A

Antidepressants

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16
Q

At what point during the day should patient take their PPI?

A

30 mins before a meal

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17
Q

What score is used in a patient with dysphagia to aid decision making as to whether the patient can be managed as an outpatient?

A

Glasgow-Blatchford score

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18
Q

What score is used to predict mortality of patients after an acute upper GI bleed?

A

Rockall’s score

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19
Q

What score is used in ulcer management to describe endoscopic appearance and therefore the risk of rebleeding?

A

Forrest score

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20
Q

Give the 3 main principles of ulcer management

A
  1. High risk ulcer - IV PPI 72 hours followed by H.pylori test
  2. Low risk ulcer - Oral PPI and discharge after H.pylori test
  3. All gastric ulcers must be re-scoped at 6-8 weeks. Non healing think malignancy
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21
Q

The layer of mucin in the stomach is broken down by 3 actions, what are they?

A
  1. Mucosal ischaemia
  2. Increased acid
  3. Bile reflux
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22
Q

What are the main causes of bile reflux into the stomach?

A

Pyloric valve dysfunction due to:

  1. Gastric surgery
  2. Peptic ulcer blocking valve –> increased pressure
  3. Cholecystectomy - have more bile reflux
  4. Alcohol - relax pyloric sphincter
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23
Q

How do H.pylori cause stomach ulcers?

A

Increase acid secretion as well as secreting chemicals that attract neutrophils and cause inflammation in the stomach

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24
Q

How do NSAIDs cause stomach ulcers?

A

NSAIDs are COX-2 inhibitors, COX is the rate limiting enzyme in prostaglandin synthesis from arachidonic acid.

PG’s eg PGE2 protect the gastric mucosa from inury from pepsin, so with COX inhibited they can no longer do this

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25
Q

What are the potential complications of a gastric ulcer?

A
  1. Erodes into artery
  2. Perforates anteriorly causing peritonitis
  3. Perforates posteriorly causing pancreatitis
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26
Q

What are the 5 main causes of malabsorption?

A
  1. Defective intraluminal digestion
  2. Insufficient absorptive area
  3. Lack of digestive enzymes
  4. Defective epithelial transport
  5. Lymphatic obstruction
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27
Q

What are the two tests for helicobacter pylori?

A
  1. Breath test

2. Stool antigen test

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28
Q

Give 3 examples of defective intraluminal digestion and how they cause malabsorption

A
  1. Pancreatic insufficiency - pancreatitis in past (wiped out glandular function) or CF- pancreatic duct blocked
  2. Defective bile secretion - causing a lack of fat solubilisation. Either due to biliary obstruction or ileal resection (bile salts absorbed here)
  3. Bacterial overgrowth
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29
Q

What is the main disease associated with insufficient absorptive area in malabsorption?

A

Coeliac disease

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30
Q

Describe the appearance of the mucosa in Crohn’s disease

A

‘Cobblestone’ mucosa

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31
Q

Other than coeliac disease, what other conditions or infections can cause malabsorption via insufficient absorptive area?

A
  1. Crohn’s disease - Cobblestone mucosa (due to ulceration as well as thickening of the mucosa in inflammation)
  2. Extensive surface parasitisation e.g. Giardia Lamblia - coats mucosa and restricts absorption
  3. Small intestine resection
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32
Q

Is surgery more commonly performed in Crohn’s disease or Ulcerative Colitis?

A

UC- Crohn’s disease bowel is hardly ever removed because recurrence in another piece of bowel is almost inevitable

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33
Q

What diagnostic test could be done to differentiate between IBD and IBS?

A

Faecal calprotectin

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34
Q

Give an example of malabsorption caused by the lack of disaccharidases

A

Lactose intolerance

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35
Q

Outline the pathology of abetalipoproteinaemia

A

Defective epithelial transport of fat and fat soluble vitamins

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36
Q

What conditions could lead to lymphatic obstruction and consequently malabsorption?

A

Lymphoma, TB

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37
Q

What parts of the digestive tract are affected by a) Crohn’s disease and b) Ulcerative colitis?

A

a) Mouth –> anus (all layers of bowel wall)

b) Rectum–> colon (only mucosa)

38
Q

What type of inflammation is seen in Crohn’s disease?

A

Granulomatous

39
Q

What term is used to describe the whole colon being involved in UC?

A

Pancolitis

40
Q

What are the potential complications of Crohn’s vs complications of UC?

A
  1. Crohns- complications remain in bowel e.g. obstruction, perforation, fistula formation, neoplasia
  2. UC - complications are much more systemic e.g. arthritis in joints, inflammation in layers of eye, erythema nodosum, and sclerosing cholangitis (inflammation and fibrosis of bile ducts) in liver, as well as blood loss of the colon and colorectal cancer
41
Q

What is the estimated prevalence of coeliac disease?

A

1:100

42
Q

Another term for coeliac disease?

A

Gluten sensitive enteropathy

43
Q

Gluten (or more specifically, gliadin) is found in what food?

A

Wheat, rye, barley, oats

44
Q

What is the toxic proportion of gluten known as?

A

Gliadin

45
Q

Outline the pathogenesis of coeliac disease

A
  1. Gliadin transported into lamina propria of the small intestine
  2. Interacts with HLA-DQ2 and DQ8, presenting the gliadin to T helper cells, which stimulate production of B cells and therefore antibodies against gliadin
  3. Sets off inflammatory cascade which causes villous atrophy and crypt hyperplasia
46
Q

What are the symptoms of coeliac disease?

A

Non specific - tiredness/malaise and symptoms of small intestinal disease (diarrhoea, steatorrhoea, abdominal pain, bloating, weight loss) or iron deficiency anaemia or can have no symptoms

47
Q

If patient suspected to have small bowel disease (symptomatic/B12 deficiency/folate deficiency) how would you manage them?

A
  1. Coeliac serology
  2. Small bowel barium follow/MRI
  3. Endoscopic small bowel biopsy
48
Q

What are the 2 most common causes of small bowel disease in developed countries?

A
  1. Coeliac disease

2. Crohn’s disease

49
Q

What is the commonest age for presentation of coeliac disease?

A

4th-6th decade

50
Q

What skin condition is associated with coeliac disease?

A

Dermatitis herpetiformis - small group itchy blisters on extensor surfaces

51
Q

Autoimmune diseases are often seen in clusters. What 5 conditions can be closely associated with Coeliac disease?

A
  1. Type 1 diabetes
  2. Thyrotoxicosis
  3. Addisons
  4. Hypothyroidism
  5. Osteoporosis
52
Q

If coeliac disease is suspected, what investigations should be done?

A
  1. tissue transGlutaminase (tTG) antibodies - have high sensitivity and specificity for coeliac disease
  2. IgA-endomysial antibody (EMA) -less sensitive

if this is +ve or coeliac disease highly suspected…

  1. Endoscopy and duodenal biopsy - definitive diagnosis
53
Q

What would be seen on a histology slide of duodenal biopsy of a patient positive for Coeliac disease?

A
  1. Crypt hyperplasia
  2. Villous atrophy
  3. Intraepithelial lymphocytes
54
Q

Before testing for coeliac disease, what is required of the patient?

A

6 weeks of eating gluten in at least 1 meal every day

55
Q

What is the management of patients with coeliac disease?

A
  1. Gluten free diet
  2. Dietician review
  3. DEXA scan - for osteoporosis
  4. Prescription entitlement
56
Q

Macroscopic signs of coeliac disease?

A
  1. Reduced folds in duodenum
  2. Scalloping of folds
  3. Mosaic sign and visible vessels
57
Q

What two ‘signs’ on abdominal xray suggest sigmoid volvulus?

A
  1. Horse shoe sign

2. Coffee bean sign

58
Q

What is the ‘apple core’ sign on abdominal x ray suggestive of?

A

Colon cancer causing obstruction

59
Q

The ‘birds beak’ or ‘rats tail’ sign is seen in patients with what condition on barium swallow?

A

Achalasia

60
Q

What is achalasia?

A

Oesophageal aperistalsis and failure of relaxation of lower oesophageal sphincter, impairing oesophageal emptying.

61
Q

What is the pathology of achalasia?

A

Decrease in ganglionic cells in the nerve plexus of the oesophageal wall, as well as vagus degeneration

62
Q

What are the clinical features of achalasia?

A

Long history of dysphagia for both solids and liquids which may be assosciated with regurgitation

63
Q

How is achalasia managed, and what is they key complication of treatment?

A
  1. Endoscopic balloon dilatation or surgical division of LOS
  2. In patients that cannot have surgery, medical treatment to relax LOS (botox injection, nitrates)

Key complication = GORD

64
Q

What are the key clinical features in sigmoid volvulus?

A

Abdominal pain, distension, absolute constipation

65
Q

What classification system is used in staging for colorectal cancer?

A

Duke’s criteria

66
Q

Give a brief outline of the stages involved in Duke’s criteria

A

1: Invasion into but not through bowel wall
2: Invasion through bowel wall but not involving lymph nodes
3: Involvement of lymph nodes
4: Widespread metastases

67
Q

Bowel cancer screening is offered to who?

A

All males and females aged 60-74 are sent a home test kit, faecal occult blood test

68
Q

The majority of colorectal cancers occur where?

A

LHS (65% in decending colon, sigmoid colon and rectum)

69
Q

Why do proximal colorectal cancers have a worse prognosis?

A

Present later, larger diameter and often still liquid stool so little obstruction is noticed

70
Q

Name two inherited causes of colorectal cancer?

A

FAP

HNPCC ‘Lynch syndrome’

71
Q

What is the lifetime risk of developing colorectal cancer in FAP and HNPCC?

A

FAP - 100%

HNPCC - 80%

72
Q

How are patients with FAP and HNPCC managed?

A

FAP - prophylactic colectomy before 30

HNPCC - 2 yearly colonoscopy after age 25 and 2 yearly OGD from age 50

73
Q

Granuloma and crypt absesses are seen in what conditions?

A
  1. Granuloma - Crohn’s disease

2. Crypt abscesses - UC

74
Q

What are the 3 main causes of peritonitis?

A
  1. Bacterial - perforated viscus/SBP
  2. Chemical - bile leak post op
  3. Haematological - ectopic pregnancy
75
Q

Innervation of the visceral and parietal peritoneum?

A

Visceral - autonomic innervation

Parietal - somatic innervation

76
Q

Is sensation in the visceral and parietal peritoneum well localised or poorly localised and why?

A

Visceral - poorly localised as is innervated by autonomic nervous system

Parietal- well localised as is innervated by somatic nervous system

77
Q

If visceral peritoneum is irritated in foregut (lower oesophagus to D2) where will this pain be felt?

A

Epigastric

78
Q

If visceral peritoneum is irritated in midgut (D2 to 2/3 across transverse colon) where will this pain be felt?

A

Periumbilical

79
Q

If visceral peritoneum is irritated in hindgut (2/3 across transverse colon to upper rectum) where will this pain be felt?

A

Suprapubic

80
Q

A patient presents with sudden onset pain that is poorly localised and moving to one point. They would rather lie still than move and resting their hand on their abdomen relieves pain. Stated that on the way in over speed bumps excruciatingly painful. They beg you not to examine.

What is the likely cause?

A

Peritonitis (perforation - due to sudden onset)

81
Q

When examining a patient with suspected peritonitis, how do you differentiate between a patient with an inflammatory process of GI tract and one with a ruptured abdominal viscus (eg.duodenal ulcer or appendix)?

A

Inflammatory process = localised pain (point tenderness)

Rupture = generalised pain (rigid abdomen and systemically shocked)

82
Q

What 5 investigations would be done in individual with suspected peritonitis?

A
  1. X ray - may see air underneath the diaphragm (rupture). Abdominal x ray may be done to looked for blocked gut/foreign body
  2. Blood tests - must check serum amylase to exclude acute pancreatitis, increased WBC, platelets and CRP
  3. CT scan of abdomen
  4. B-HCG - exclude ectopic pregnancy
  5. ECG - irregular HB –> clot blocking blood supply to gut
83
Q

Name 6 complications of peritonitis

A
  1. Paralytic ileus
  2. Hypovolaemia
  3. Pulmonary atelectasis/pneumonia
  4. Kidney failure
  5. Portal pyaemia
  6. Systemic sepsis
84
Q

Where will absesses collect if patient is supine?

A

L/R paracolic gutter and suprahepatic/ subphrenic space

85
Q

Where will absess collect if patient is standing?

A

Pelvis

86
Q

What is primary peritonitis and what patients can it occur in?

A

SBP of ascitic fluid, often in immunocompromised during peritoneal dialysis or those with lymphoma

87
Q

25 year old male presents with a one day history of umbilical pain that was poorly localised and going to the right iliac fossa. He is off food with a low grade fever. Raised WCC (15) and o/e rebound tenderness and guarding of RIF. What is most likely diagnosis?

A

Appendicitis

88
Q

23 year old female presents with sudden onset low abdominal pain. She is acutely hypotensive and missed her last period. She was referred to general surgery as query appendicitis. What is most likely diagnosis? and what would be the treatment?

A

Ectopic pregnancy rupture. Remove via keyhole surgery

89
Q

50 year old male presents with sudden onset abdominal pain, rated 10/10. He is a smoker and is diabetic. Pain is not settling with morphine. What is the most likely diagnosis?

A

Ischaemic bowel

90
Q

75 year old smoker presents with sudden onset epigastric pain and a board like abdomen. Acid reflux and uses ibuprofen for arthritis. Previous MI. What is the most likely diagnosis?

A

Perforated duodenal ulcer

91
Q

What two scores can be used to assess the fitness of the patient pre surgery - e.g. in perforated viscera in peritonitis?

A

P-POSSUM

ASA

92
Q

If patient has pale mucous membranes and appears pale, blood test has increased urea, and black stool what is likely diagnosis?

A

GI bleed high up - has digested blood which is why there is an increase in urea

Clinical sciences (10 decks)

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