Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > GI > Flashcards

GI Flashcards

1
Q

What does GORD stand for?

A

Gastro-oesophageal reflux disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

When does GORD occur?

A
  • prolonged gastric reflux

- causes oesophageal stricture / Barrett’s oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can cause GORD?

A
  • lower oesophageal sphincter hypotension
  • hiatus hernia
  • loss of oesophageal peristaltic function
  • abdominal obesity
  • gastric acid hyper secretion
  • slow gastric emptying
  • overeating / fat / chocolate / coffee
  • smoking / alcohol
  • pregnancy (inc. abdominal pressure)
  • drugs
  • systemic sclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pathophysiology of GORD

A
  • MUCH MORE transient lower oesophageal sphincter relaxations
  • allows gastric acid to flow back into oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why are there more transient LOS relaxations in GORD?

A

LOS has reduced tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When do clinical features of GORD present?

A

When anti-reflux mechanisms fail

- causes prolonged acid contact with lower oesophageal mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What might contribute to transient LOS relaxation?

A
  • increased mucosal sensitivity to gastric acid
  • reduced oesophageal acid clearance
  • delayed gastric emptying after eating
  • delayed nocturnal reflex
  • hiatus hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the oesophageal clinical presentations of GORD

A
  • heartburn
  • belching
  • food/acid/bile regurgitation
  • water brash - increased salivation
  • sinusitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the extra-oesophageal clinical presentations of GORD

A
  • nocturnal asthma
  • chronic cough
  • laryngitis
  • sinusitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What actions can aggravate heartburn?

A
  • bending
  • stooping
  • lying down
    (promote aid exposure)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List the differential diagnoses of GORD

A
  • CHD
  • biliary colic
  • peptic ulcer disease
  • malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the alarm bell signs of GORD?

A
  • weight loss
  • haematemesis
  • dysphagia (swallowing difficulties)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What investigations should you conduct to diagnose GORD if there are alarm bell sings?

A
  • endoscopy
  • barium swallow
  • use LA classification of GORD/ Oesophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When would you conduct an endoscopy?

A
  • alarm bell signs
  • symptoms for more than 4 weeks
  • persistent vomiting
  • GI bleeding
  • palpable mass
  • over 55
  • symptoms despite treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What might a barium swallow show?

A

Hiatus hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the types of hiatus hernia?

A
  1. Sliding hiatus hernia (80%)

2. Rolling / para-oesophageal hiatus (20%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe sliding hiatus hernia

A
  • G-O junction / part of stomach slides up into stomach
  • lies slightly above diaphragm
  • LOS = less competent = acid reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe rolling / para-oesophageal hiatus

A
  • G-O junction remains in abdo
  • fundus prolapses through hiatus
  • reflux is uncommon because junction is intact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the aims of investigating for GORD?

A
  • assess oesophagitis

- document reflux by intraluminal monitoring - 24 hr pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does oesophagitis/Barrett’s confirm?

A

Reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What lifestyle changes can treat GORD?

A
  • weight loss
  • smoking cessation
  • small, regular meals
  • avoid hot drinks, alcohol, citrus fruits
  • don’t eat <3 hours before bed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What pharmacological treatments are used for GORD?

A
  • antacids
  • alginates
  • PPI
  • H2 receptor antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Example of antacid

A

Magnesium trisilicate mixture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How does antacid treat GORD?

A
  • forms gel / foam raft with gastric contents
  • reduces reflux
  • relieves symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is a side effect of magnesium contains antacids?

A

Diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Example of alginates

A

Gaviscon - relieves symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Example of PPI

A

Lansaprazole - reduces gastric acid production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Example of H2 receptor antagonist

A

Cimetidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do H2 receptor antagonists treat GORD?

A
  • blocks histamine receptors on parietal cells

- reduces acid release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the complications of GORD?

A
  1. Peptic stricture

2. Barrett’s oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is peptic stricture?

A
  • inflammation of oesophagus
  • results from gastric acid exposure
  • causes narrowing of oesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does peptic stricture present?

A

Gradually worsening dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do you treat peptic stricture?

A
  • endoscopic dilatation

- long term PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Barrett’s oesophagus?

A

Distal oesophageal epithelium undergoes metaplasia from squamous to columnar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is always present in Barrett’s oesophagus?

A

Hiatus hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the risk of Barrett’s?

A
  • can progress into cancer

- premalignant for adenocarcinoma of oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is a Mallory-Weiss tear?

A
  • linear mucosal tear at the oesophagogastric junction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What produces a Mallory-Weiss tear?

A

By a sudden increase in intra-abdominal pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Epidemiology of Mallory-Weiss tear

A
  • more common in males

- mainly in ages 20-50

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Risk factors of Mallory-Weiss tear

A
  • alcoholism
  • forceful vomiting
  • eating disorders
  • male
  • NSAID abuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the clinical features of Mallory-Weiss tear?

A
  • vomiting
  • haematemesis after vomiting
  • retching
  • postural hypotension
  • dizziness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the differential diagnoses of Mallory-Weiss?

A
  • gastroenteritis
  • peptic ulcer
  • cancer
  • oesophageal varices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How do you diagnose Mallory-Weiss?

A

Endoscopy to confirm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How do you treat Mallory-Weiss?

A
  • most bleeds heal within 24 hours
  • haemorrhage stop spontaneously
  • sometimes surgery to sow the tear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is dyspepsia?

A 
ONE OR MORE OF:
1. Postprandial fullness (after eating)
2. Early satiation 
3. Epigastric pain or burning for >4 weeks 
(essentially indigestion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What % of the population are affected by dyspepsia?

A

25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are dyspeptic symptoms caused by?

A
  • Disorders of the GI tract = most commonly is functional dyspepsia
  • peptic ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Clinical presentation of dyspepsia

A
  • reflux when lying flat
  • heartburn
  • acid taste
  • bloating
  • indigestion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the red flag symptoms of dyspepsia for cancer?

A
  • unexplained weight loss
  • anaemia
  • GI bleeding (melaena / haematemesis)
  • dysphagia
  • upper abdominal mass
  • persistent vomiting
  • over 55
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What could gastric ulcers cause?

A
  • postprandial pain

- pain relieved by milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What could early postprandial pain be due to?

A
  • gastritis
  • GORD
  • gastric carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the differential diagnoses according to history?

A
  • heartburn/ regurgitation / cough = GORD
  • alarm symtpoms/ family history = malignancy
  • onset (acute vs chronic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Management of dyspepsia

A
  • reassurance
  • dietary review
  • antidepressants
  • test for helicobacter pylori
  • endoscopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Name an example of antidepressants that could be given for dyspepsia

A

CITALOPRAM

- type of SSRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why would you give an antidepressant for dyspepsia?

A

Low doses reduce sensitivity of gullet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How can you look for helicobacter pylori in dyspepsia?

A
  • faecal antigen test

- breath test (less common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How many layers does the smooth muscle wall of the stomach have?

A

3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are the 3 layers of the stomach’s smooth muscle wall?

A
  1. Outer longitudinal
  2. Inner circular
  3. Innermost oblique layers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Name the 2 sphincters of the stomach

A
  1. Gastro-oesophageal sphincter

2. Pyloric sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the pyloric sphincter largely made up of?

A
  • thickening of the circular muscle layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How many layers does the duodenum have?

A

2 smooth muscle layers

  1. Outer longitudinal
  2. Inner smooth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What does the mucosa in the upper 2/3 of the stomach contain?

A
  • parietal cells
  • chief cells
  • enterochromaffin-like cells (ECL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What do parietal cells secrete?

A

HCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What do chief cells produce?

A

Pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What do ECL cells release?

A

Histamine (stimulates acid release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What does the astral mucosa of the stomach contain?

A
  • mucus secreting cells
  • G cells
  • D cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What do mucus secreting cells secrete?

A
  • mucin

- bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What do G cells secrete?

A

Gastrin (stimulates acid release)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What do D cells secrete?

A

Somatostatin (suppressant of acid secretion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the mucosal barrier made up of?

A
  • plasma membranes of mucosal cells & mucus layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What does the mucosal barrier do?

A
  • protects gastric epithelium from damage by acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What stimulates mucus secretion?

A

Prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What inhibits synthesis of prostaglandins?

A
  • aspirin
  • NSAIDs
    (inhibit cyclo-oxygenase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What does the duodenal mucosa contain?

A
  • villi

- Brunner’s glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What do Brunner’s glands secrete?

A

Alkaline mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What neutralises acid secretion from stomach in the duodenum?

A
  • alkaline mucus from Brunner’s

- pancreatic & biliary secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Describe peptic ulcer disease (PUD)

A

Consists of a break in the superficial epithelial cells penetrating down to the muscularis mucosa of stomach/duodenum

  • fibrous base
  • increase in inflammatory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Where does a peptic ulcer penetrate down to?

A

Muscularis mucosa of stomach or duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Where are duodenal ulcers most commonly found?

A

In the duodenal cap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Where are gastric ulcers most commonly seen?

A
  • lesser curvature of stomach

- can be anywhere though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What % of the population are affected by duodenal ulcers?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

How many time more common are duodenal ulcers than gastric?

A

2-3 times more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Where are ulcers more common?

A
  • in the elderly

- developing countries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Why are ulcers more common in developing countries?

A

Because of helicobacter pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Describe incidence of PUD in men vs women

A
  • declining in men

- increasing in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Why are ulcers increasing?

A

Due to use of NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What are the main causes of PUD?

A
  • helicobacter pylori
  • drugs (NSAIDs, steroids, SSRIs)
  • smoking
  • increasing gastric acid secretion
  • delayed gastric emptying
  • blood group O
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What do ulcers result in?

A

Gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Why do NSAIDs cause ulcers?

A
  • inhibit cyclo-oxygenase
  • prostaglandin synthesis is inhibited
  • reduced mucosal defence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Where does helicobacter pylori colonise?

A
  • gastric epithelium

- inhibits mucous layer / just beneath it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What does helicobacter pylori cause?

A
  • major destruction to mucin layer that protects mucosa
  • decreases duodenal HCO3-
  • therefore, increases stomach acidity
    (less alkali to buffer acid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What does helicobacter pylori secret and why is this bad?

A
  1. Urease
    - splits urea into CO2 & ammonia
  2. Proteases
  3. Phospholipase
  4. Vacuolating cytotoxin A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Why is urea being split into ammonia bad?

A
  • NH3 + H+ = ammonium
  • ammonium is toxic to gastric mucosa
    = means less mucous produced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What does secretion of proteases/phospholipase/ cytotoxin A result in?

A
  • gastric epithelium is attacked
  • reduces mucous production
    = inflammatory response
    = less mucosal defence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What does helicobacter pylori increase?

A
  • gastrin
  • parietal cell mass
    (MEANS more acid production)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What does helicobacter pylori decrease?

A
  • somatostatin

can’t inhibit acid secretion - so acid increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Overall effects of helicobacter pylori

A
  • inflammation (antral gastritis)
  • gastric cancer
  • peptic ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What is gastric cell ischaemia caused by?

A
  • low BP

- atherosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Why is gastric cell ischaemia bad?

A
  • less mucin produced
  • less protection from acid
  • damages mucosa
    = ulcers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What can cause increased acid production?

A

Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is used to treat increased acid production?

A
  • PPI

- H2 receptor antagonists

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Clinical presentations for PUD

A
  • recurrent burning epigastric pain
  • nausea accompanying pain
  • anorexia / weight loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

When is duodenal ulcer pain typically worse?

A
  • at night

- when patient is hungry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Red flag symptoms of PUD for cancer

A
  • unexplained weight loss
  • anaemia
  • GI bleeding (melaena / haematemesis)
  • dysphagia
  • upper abdominal mass
  • persistent vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Suggest complications of ulcers

A
  • duodenal ulcers can go v deep = hit an artery
  • peritonitis
  • acute pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Which artery would be most commonly hit if duodenal ulcers go too deep? Why is this bad?

A

Gastroduodenal artery

- causes MASSIVE haemorrhage = EMERGENCY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

How can ulcers cause peritonitis?

A
  • acid can leak into peritoneum if ulcers are too deep
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

How would you diagnose peritonitis in PUD?

A

Air can be seen under the diaphragm in an erect X-ray

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What diagnostic tests would you carry out on under 55s for PUD (H. pylori)?

A

NON-INVASIVE TESTING

  • serology
  • C-urea breath test
  • stool antigen testing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What would you do if tests for PUD came back positive?

A

Start eradication immediately

- lansoprazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What do you do if a gastric ulcer is found in an endoscopy?

A

Re-scope 6-8 weeks later

- ensures no malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

When is an endoscopy essential?

A
  • in all alarm patients

- patients over 55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What does a serology test for PUD detect?

A

IgG antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Why does serology testing not confirm current PUD?

A

Because IgG takes 1 year to fall by 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How does the C-urea breath test work?

A
  • measures CO2 in breath after ingestion of C-urea

- monitors infection after eradication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Advantages of C-Urea breath test

A
  • quick
  • reliable test for H. pylori
  • highly sensitive / specific
  • no antibiotics / PPI before test
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Describe the stool antigen test

A

Immunoassay using monoclonal antibodies

  • detects H.pylori
  • monitors efficacy of eradication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

How long should patients be off PPIs for before stool antigen test?

A

2 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What is an endoscopy useful to look at?

A
  • histology

- biopsy urease test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What will histology show in an endoscopy?

A
  • direct visualisation of H.pylori

- reduced if on PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

How will a biopsy urease test show?

A
  • solution will rapidly change from yellow to red

- because of release of ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Why shouldn’t a patient be on PPIs/antibiotics before biopsy urease test?

A

Will give false negatives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Treatment for PUD/ H. pylori

A
  • lifestyle adjustments
  • stop NSAIDs
  • H. pylori eradication (triple therapy)
  • H2 antagonists
  • surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What lifestyle adjustments would you suggest to reduce PUD?

A
  • reduce stress
  • avoid irritating foods
  • reduce smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

How long will H. pylori eradication take?

A

7-14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

What is the triple therapy for H. pylori?

A
  1. PPI

2 & 3 (any 2 of these): Metronidazole / Clarithromycin / Amoxicillin / Tetracycline / bismuth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Which drugs are high resistance?

A
  1. Metronidazole

2. Clarithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Which drugs are low resistance?

A
  1. Amoxicillin

2. Tetracycline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

When are quinolones used to treat PUD?

A

When standard regimens have failed

- as ‘rescue therapy’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Examples of quinolones

A
  • ciprofloxacin
  • furozolidone
  • rifabutin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Example of H2 antagonists to treat PUD

A
  • ranitidine

- cimetidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

When would you conduct surgery for PUD?

A

In case of complications:

- haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What are varices?

A

Dilated veins that are at risk of rupture

In GI system = lead to GI bleeds / haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the normal pressure in the hepatic portal vein?

A

5-8mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What are the classifications of portal hypertension?

A
  1. Pre-hepatic
  2. Intra-hepatic
  3. Post-hepatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What is pre-hepatic obstruction?

A

Blockage of hepatic portal vein BEFORE liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is intra-hepatic obstruction?

A

Distortion of liver architecture (pre or post sinusoidal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is post-hepatic obstruction?

A

Venous blockage OUTSIDE the liver (rare)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

When do varices form?

A
  • portal pressure >10-12mmHg
  • venous system dilates
  • varices formed within systemic venous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Where can varices form?

A
  • G-O junction
  • rectum
  • L renal vein
  • diaphragm
  • anterior abdominal wall via umbilical vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Describe gastro-oesophageal varices

A
  • superficial
  • tend to rupture
  • result in GI bleeding
  • when pressure >12mmHg
142
Q

What % of cirrhosis patients develop G-O varices?

A

90% - over 10 years

only a 1/3 bleed

143
Q

What are main causes of varices?

A
  • alcoholism / viral cirrhosis

- portal hypertension (pre, intra, post hepatic)

144
Q

What can cause pre-hepatic portal hypertension?

A

Thrombosis in portal / splenic vein

145
Q

What can cause intra-hepatic portal hypertension?

A
  • cirrhosis
  • schistosomiasis
  • sarcoid
  • congenital hepatic fibrosis
146
Q

What can cause post-hepatic portal hypertension?

A
  • Budd-Chiari syndrome
  • RH failure
  • constrictive pericarditis
147
Q

What is Budd-Chiari syndrome caused by?

A

Hepatic vein obstruction by tumour / thrombosis

148
Q

What are the risk factors for varices?

A
  • cirrhosis
  • portal HT
  • schistosomiasis
  • alcoholism
149
Q

Pathophysiology cascade of varices

A

Liver injury / fibrogenesis > increased resistance to blood flow > portal HT > splanchnic vasodilation > drop in BP > inc. CO > inc. salt & water retention > hyper-dynamic circulation/increased portal flow > formation of collaterals between portal & systemic systems > GO varices

150
Q

Why does liver injury / fibrogenesis result in increased resistance to blood flow?

A

Because of contraction of the activated myofibroblasts

151
Q

What is contraction of activated myofibroblasts mediated by?

A
  • endothelin
  • nitric oxide
  • prostaglandins
152
Q

Why is there an increased CO in pathophysiology of varices?

A

To compensate for decreased BP

153
Q

Why is there inc. salt & water retention in pathophysiology of varices?

A

To increase blood volume & compensate

154
Q

Clinical presentations if varices has ruptured?

A
  • haematemesis
  • abdo pain
  • shock (if major blood loss)
  • fresh rectal bleeding
  • hypotension / tachycardia
  • pallor
155
Q

When should you suspect varices as cause of GI bleeding?

A
  • alcohol abuse

- cirrhosis

156
Q

Other clinical presentations of varices

A
  • splenomegaly
  • ascites
  • hyponatraemia
157
Q

How do you diagnose varices?

A

Endoscopy

158
Q

How do you treat varices?

A
  • resuscitate until haemodynamically stable
  • blood transfusion if anaemia
  • correct clotting abnormalities
  • vasopressin
  • prophylactic antibiotics
  • varical banding
  • balloon tamponade
  • trans jugular intrahepatic portoclaval shunt (TIPS)
159
Q

What level should Hb aim to be after blood transfusion?

A

80g/L

160
Q

How would you correct clotting abnormalities?

A
  • Vitamin L

- platelet transfusion

161
Q

Example of vasopressin

A

IV terlipressin

162
Q

Why do you administer vasopressin for varices?

A
  • cause vasoconstriction
163
Q

What do you use if terlipressin is contraindicated? (e.g in ischaemic heart disease)

A

IV somatostatin

164
Q

Why do you administer prophylactic antibiotics for varices?

A
  • treat / prevent infection

- reduce re-bleeding and mortality

165
Q

What is variceal banding?

A
  • band put around avarice
  • using endoscope
  • banded varix degenerates after a few days
  • leaves scar
166
Q

How does balloon tamponade work?

A
  • reduces bleeding

- places pressure on avarice if banding fails

167
Q

When is TIPS used to treat varices?

A
  • if bleeding can’t be controlled
  • it is a shunt between systemic & portal systems
  • reduces sinusoidal & portal vein pressure
168
Q

Prevention of varices

A
  • non- selective B blockage
  • variceal banding repeatedly
  • liver transplant
169
Q

What does non-selective B blockage achieve?

A
  • reduces resting pulse rate
  • decrease portal pressure
    e. g PROPRANOLOL
170
Q

Define gastritis

A

Inflammation associated with mucosal injury

171
Q

What does gastropathy indicate?

A

Epithelial cell damage & regeneration without inflammation

172
Q

What are the causes of gastritis?

A
  1. H. pylori
  2. Autoimmune gastritis
  3. Virus (CMV / herpes simplex)
  4. Duodenogastric reflux
  5. Crohn’s
  6. Mucosal ischaemia
  7. Increased acid
  8. Aspirin / NSAIDs / alcohol
173
Q

What parts of the stomach does autoimmune gastritis affect?

A
  1. Fundus

2. Body

174
Q

What does autoimmune gastritis lead to?

A

Atrophic gastritis
- loss of parietal cells
- intrinsic factor deficiency
= causes pernicious anaemia (low RBC due to low B12)

175
Q

Clinical présentation of gastritis

A
  • abdo bloating
  • haematemesis
  • epigastric pain
  • nausea
  • indigestion
  • vomiting
176
Q

Differential diagnoses of gastritis

A
  • PUD
  • GORD
  • non-ulcer dyspepsia
  • gastric lymphoma / carcinoma
177
Q

How to diagnose gastritis?

A
  • endoscopy
  • biopsy
  • H. pylori breath test
  • H. pylori stool antigen test
178
Q

Treatment for gastritis

A
  • remove causative agents
  • reduce stress
  • H. pylori eradication (triple therapy)
  • H2 antagonists
  • PPI
  • antacids
179
Q

Prevention of gastritis

A
  • PPIs + NSAIDs

= prevents bleeding from acute stress ulcers / gastritis

180
Q

Define malabsorption

A

Failure to absorb nutrients because of destruction to epithelium OR problem in the lumen meaning food can’t be digested

181
Q

Examples of small intestine diseases that can result in malabsorption

A
  • Crohn’s
  • Topical sprue
  • Coeliac disease
  • parasite infection
182
Q

What must be ruled out before diagnosing malabsorption?

A

Insufficient intake

183
Q

Causes of malabsorption

A
  1. Defective intraluminal digestion
  2. Insufficient absorptive area
  3. Lack of digestive enzymes
  4. Defective epithelial transport
  5. Lymphatic obstruction
184
Q

Examples of defective intraluminal digestion

A
  1. Pancreatic deficiency
  2. Defective bile secretion
  3. Bacterial overgrowth
185
Q

When might there be pancreatic deficiency?

A
  1. Pancreatitis

2. Cystic fibrosis

186
Q

Why does pancreatitis lead to pancreatic deficiency?

A
  • damages glandular pancreas

- means less/no enzymes are released

187
Q

Why does CF lead to pancreas deficiency?

A
  • blocks pancreatic duct
  • due to excess mucus
  • enzymes fail to be released
188
Q

Why is defective bile secretion bad?

A

There will be a lack of fat solubilisation

189
Q

When might there be defective bile secretion?

A
  1. Biliary obstruction (gall stone)

2. Ileal resection

190
Q

Why does ileal resection lead to defective bile secretion?

A
  • bile salts are reabsorbed in terminal ileum

- if removed = bile salt reuptake is decreased

191
Q

What might cause insufficient absorptive area?

A
  1. Coeliac disease (gluten sensitive enteropathy)
  2. Crohn’s
  3. Giardia lamblia
  4. Surgery
192
Q

Describe coeliac disease

A
  • villous atrophy / short villi
  • crypt hyperplasia
  • lots of lymphocytes in epithelium
193
Q

Describe Crohn’s

A
  • inflammatory damage to lining of bowel
    = cobblestone mucosa
  • significant reduction of absorptive SA
194
Q

Describe how giardia lamblia causes insufficient absorptive area

A
  • extensive surface parasitisation of villi & microvilli
  • parasites coat villi surface
  • food can’t be absorbed
195
Q

Describe how surgery causes insufficient absorptive area

A

Small intestine resection/ bypass

- in small bowel infarction

196
Q

What causes a lack of digestive enzymes?

A
  1. Disaccharidase deficiency (lactose intolerance)

2. Bacterial overgrowth

197
Q

Why does lactose intolerance mean malabsorption?

A
  • lactose can’t be broken down into glucose

- not absorbed

198
Q

What happens to indigested lactose?

A
  • passes into colon
  • eaten by bacteria
  • release CO2
  • leads to wind & diarrhoea
199
Q

What does bacterial overgrowth cause?

A

Brush border damage

200
Q

Examples of defective epithelial transport

A
  1. Abetalipoproteinaemia

2. Primary bile acid malabsorption

201
Q

What is abetalipoproteinaemia?

A

Lack of transporter protein to transport lipoprotein across cell

202
Q

What is primary bile acid malabsorption?

A

Mutations in bile acid transporter protein

203
Q

What can cause lymphatic obstruction?

A
  • lymphoma

- tuberculosis

204
Q

Describe coeliac disease

A

Inflammation of the mucosa of the upper small bowel

- improves when gluten is withdrawn from diet

205
Q

What is describe coeliac disease?

A

T cell mediated autoimmune disease of small bowel in which prolamin intolerance causes villous atrophy & malabsorption

206
Q

What is prolamin?

A

Alcohol- soluble proteins in wheat, barley, rye, oats

prolamin is a component of gluten protein

207
Q

Examples of prolamins

A
  1. Gliadin in wheat
  2. Hordeins in barley
  3. Secalins in rye
208
Q

What % of population are affected by coeliac disease?

A

1%

209
Q

At what age does coeliac disease peak?

A
  • infancy

- 50-60 years

210
Q

What is the risk in relatives for coeliac disease?

A
  • 10% in 1st degree relatives

- 30% in siblings

211
Q

What is gluten found in?

A
  • wheat
  • barley
  • rye
212
Q

What are the risk factors for coeliac disease?

A
  • type 1 diabetes
  • thyroid disease
  • Sjorgen’s
  • IgA deficiency
  • breast feeding
  • rotavirus infection in infancy
213
Q

Why is gluten bad?

A
  • prolamin a-Gliadin is toxic

- it’s resistant to digestion by pepsin & chymotrypsin

214
Q

Why is a-gliadin resistant to digestion?

A

Because of high glutamine & proline content

  • so remain in intestinal lumen
  • triggers immune response
215
Q

What happens to the gliadin peptides?

A
  • pass through epithelium

- deaminated by tissue transglutaminases

216
Q

What are gliadin peptides deaminated by?

A

Transglutaminases

217
Q

What happens to gliadin peptides when they’re deaminated?

A

Increases immunogenicity

218
Q

What happens after deamination of gliadin peptides?

A

They bind to antigen presenting cells (APC)

219
Q

What happens after gliadin peptides bind to APC?

A
  • interact with CD4+ T cells
  • in lamina propria
  • via HLA class II molecules DQ2 or DQ8
220
Q

What do DQ2/DQ8 do?

A

Activate gluten sensitive T cells

221
Q

What do gluten sensitive T cells do when they’re activated?

A

Produce pro-inflammatory cytokines

- initiate inflammatory cascade

222
Q

What does imitation of inflammatory cascade do?

A
  • releases metaloproteinkinases

- releases other mediators

223
Q

What do metaloproteinkinases / other mediators contribute to?

A
  • villous atrophy
  • crypt hyperplasia
  • intraepithelial lymphocytes (result in malabsorption)
224
Q

What does mucosal damage mean?

A
  • B12 / folate / iron can’t be absorbed

- results in anaemia

225
Q

Describe pattern of mucosal damage along length of bowel

A
  • damage DECREASES towards ileum

- gluten digested into non-toxic fragments

226
Q

Clinical presentations of coeliac disease

A
  • stinking/fatty stools
  • diarrhoea
  • abdo pain
  • bloating
  • nausea / vomiting
  • angular stomatitis
  • weight loss
  • fatigue / anaemia
  • dermatitis hepetiformis
227
Q

What proportion of coeliac disease patients are asymptomatic?

A

1/3

228
Q

What is the most important thing to remember when diagnosing coeliac disease?

A

Gluten in diet should be maintained for at least 6 weeks before testing to get true results

229
Q

How would you diagnose coeliac disease?

A
  • FBC
  • duodenal biopsy (GOLD STANDARD)
  • serum antibody testing
230
Q

What will a FBC show if patient has coeliac disease?

A
  • low Hb
  • low ferritin
  • low Hb
231
Q

What will a duodenal biopsy show of coeliac disease?

A
  • villous atrophy
  • crypt hyperplasia
  • increase intraepithelial white cell count
    (reverse on gluten free diet)
232
Q

What do you look at when you carry out a serum antibody test for coeliac disease?

A
  • Endomysial antibody (EMA)
  • tissue transglutaminase antibody (tTG)
    (both are IgA antibodies)
233
Q

Do EMA & tTG correlate with severity of mucosal damage?

A

Yes

- used for dietary monitoring

234
Q

How sensitive is serum antibody testing?

A

95% (unless patient is IgA deficient)

235
Q

How to treat coeliac disease?

A
  • life long gluten free diet
  • correction of mineral/vitamin deficiencies
  • DEXA scan
  • inform 1st degree relatives of risk
236
Q

Why are coeliac disease patients given DEXA scans?

A

Monitor osteoporotic risk (patients are at a higher risk of osteoporosis)

237
Q

What are coeliac disease patients at a higher risk for?

A
  • osteoporosis

- lymphoma malignancy

238
Q

Complications of coeliac disease

A
  • non-responsive coeliac disease (if not diet compliant)
  • anaemia
  • secondary lactose intolerance
  • T-cell lymphoma
  • increased malignancy risk (due to inc. cell turnover)
  • osteoporosis
239
Q

What are the 2 major forms of inflammatory bowel disease (IBD)?

A

BOTH ARE CHRONIC AUTOIMMUNE:

  1. Ulcerative colitis (UC)
  2. Crohn’s disease
240
Q

Which part of the GI tract does ulcerative colitis affect?

A

Only the colon

241
Q

Which part of the GI tract does Crohn’s affect?

A

Any part of the GI - mouth to anus

242
Q

Which ethnic group are more prone to IBD?

A

Jewish

243
Q

When does IBD occur?

A
  • when mucosal immune systems exert inappropriate response
  • to luminal antigens (bacteria)
  • may enter mucosa via leaky epithelium
244
Q

Describe ulcerative colitis (UC)

A

Relapsing and remitting inflammatory disorder of the colonic mucosa

245
Q

What is UC called when it affects just the rectum?

A

Proctitis (50%)

246
Q

What is UC called when it affects rectum & L colon?

A

Left-sided colitis (30%)

247
Q

What is UC called when it affects the entire colon? (up to ileocaecal valve)

A

Pancolitis / extensive colitis (20%)

248
Q

Where is the highest incidence/prevalence of UC?

A
  • Northern Europe
  • UK
  • North America
249
Q

Epidemiology of UC

A
  • males & females affected equally
  • 15-30 years old
  • 3 times more common in non/ex smokers
  • 1 in 6 have first degree relative with UC
250
Q

Risk factors of UC

A
  • family history
  • NSAIDs
  • chronic stress
  • chronic depression
251
Q

Macroscopic pathophysiology of UC

A
  • begins in rectum & extends
  • circumferential & continuous inflammation
  • no skip lesions
  • reddened/inflamed mucosa that bleeds easily
  • ulcers & pseudo-polyps (severe disease)
252
Q

Microscopic pathophysiology of UC

A
  • mucosal inflammation (doesn’t go any deeper)
  • no granulomata
  • depleted goblet cells
  • increased crypt abscesses
253
Q

Clinical presentations of UC

A
  • remissions & exacerbations
  • restricted pain in lower L quadrant
  • episodic/chronic diarrhoea with mucus/blood
  • cramps
  • bowel frequency linked o severity
254
Q

What clinical presentations might there be in acute UC?

A
  • fever
  • tachycardia
  • tender distended abdomen
255
Q

What clinical presentations might there be in an acute attack of UC?

A
  • blood diarrhoea

- diarrhoea at night - urgency & incontinence

256
Q

Extraintestinal signs of UC

A
  • clubbing
  • aphthous oral ulcers
  • erythema nodusum (red round lumps below skins surface)
  • amyloidosis
257
Q

Which parts of the body might suffer from complications of UC?

A
  • liver
  • colon
  • skin
  • joints
  • eyes
258
Q

What complications might the liver have in UC?

A
  • fatty change
  • chronic pericholangitis
  • sclerosing cholangitis
259
Q

What complications might the colon have in UC?

A
  • blood loss
  • perforation
  • toxic dilation
  • colorectal cancer
260
Q

What complications might the skin have in UC?

A
  • erythema nodusum

- pyoderma gangrenous

261
Q

What complications might the joints have in UC?

A
  • ankylosing spondylitis

- arthritis

262
Q

What complications might the eyes have in UC?

A
  • iritis (iris inflammation)
  • uveitis (inflammation of uvea - middle layer of the eye)
  • episcleritis
263
Q

Differential diagnoses of UC

A
  • other causes of diarrhoea

E.G salmonella spp, giardia intestinalis, rotavirus

264
Q

How do you diagnose UC?

A
  1. Blood test
  2. Stool samples
  3. Faecal calprotectin
  4. Colonoscopy with mucosal biopsy (GOLD STANDARD)
  5. Abdo X-ray
265
Q

What will a blood test of UC show?

A
  • raised WBC and platelets
  • iron deficiency anaemia
  • raised ESR & CRP
  • abnormal liver biochem
  • hypoalbuminaemia
  • pANCA may be positive
266
Q

What is pANCA?

A

Anti-neutrophilic cytoplasmic antibody

267
Q

Why do you take stool samples to diagnose UC?

A

To exclude C. diff & campylobacter

268
Q

What does faecal calprotectin test indicate?

A

IBD - but not specific

269
Q

Why do you carry out a colonoscopy in UC diagnosis?

A
  • assess disease activity & extent
  • see inflammatory infiltrate
  • goblet cell depletion
  • crypt abscesses
  • mucosal ulcers
270
Q

Why do you carry out an abdominal x-ray in UC diagnosis?

A
  • to exclude colonic dilatation (in patients suffering acute severe attacks)
271
Q

When is abdominal x-ray useful to diagnose UC?

A

When UC is too severe for colonoscopy

272
Q

How do you treat UC?

A
  • aim to induce remission
  • aminosalicylate
  • maintain remission
  • surgery
273
Q

What is the active component of aminosalicylate?

A

5-aminosalicylic acid (5-ASA)

- absorbed in small intestine

274
Q

What are commonly prescribed 5-ASAs?

A
  • sulfasalazine
  • mesalazine
  • olsalazine
275
Q

How do you treat mild/moderate UC?

A
  • oral 5-ASA (for left sided / extensive UC)
  • rectal 6-ASA (proctitis)
  • glucocorticoid
276
Q

What is an example of glucocorticoid?

A

Oral prednisolone

277
Q

How do you treat severe UC?

A

Oral prednisolone

278
Q

How do you treat severe UC with systemic features?

A
  • hydrocortisone
  • ciclosporin
  • infliximab
279
Q

How do you maintain remission of UC?

A
  • 5-ASA

- azathioprine

280
Q

When do you use azathioprine

A

For patients who relapse despite 5-ASA or ASA intolerant

281
Q

When is surgery for UC indicated?

A

For severe colitis that fails to respond to treatment

282
Q

What surgery is performed for severe colitis?

A

COLECTOMY

  • whole colon removed
  • with ileoanal anastomosis
  • rectum is fused to ileum
  • terminal ileum used to form reservoir pouch (store faeces)
283
Q

What is the terminal ileum used to form in a colectomy?

A

Forms a reservoir pouch

- means patient remains continent

284
Q

What other surgery can be performed for severe UC?

A

Panproctocolectomy and ileostomy

285
Q

What is panproctocolectomy with ileostomy?

A

Whole colon & rectum removed

  • ileum brought out on to abdominal wall
  • as the stoma
286
Q

Define Crohn’s disease? (CD)

A

Chronic inflammatory GI disease characterised by transmural granulomatous inflammation

287
Q

What does transmural mean?

A

Goes deep into mucosa

288
Q

Which part of the GI tract does Crohn’s affect?

A

Any part from the mouth to anus

especially terminal ileum & proximal colon

289
Q

How is Crohn’s unlike UC?

A

There are bits of unaffected bowel between areas of active disease

290
Q

What are unaffected bits of bowel in Crohn’s called?

A

Skip lesions

291
Q

Epidemiology of Crohn’s

A
  • highest incidence/prevalence in N. Europe, UK, N. America
  • less prevalence if Asian
  • females affected more
  • 1 in 5 CD patients have 1st degree relative with disease
292
Q

By how many times does smoking increase risk of Crohn’s by?

A

3 to 4

293
Q

When does Crohn’s usually present?

A

20-40 years

294
Q

Risk factors of Crohn’s

A
  • Smoking
  • Genetic association stronger than UC
  • Family history
  • NSAIDs may exacerbate
  • Chronic stress/depression triggers flares
  • good hygiene
  • appendicectomy
295
Q

What is the genetic mutation in Crohn’s?

A

Mutations on NOD2 gene on chromosome 16 = increases risk

296
Q

Describe macroscopic pathophysiology of Crohn’s

A
  • not continuous (skip lesions)
  • affected bowel is thickened & narrowed
  • cobblestone appearance
  • affects any part of GI tract
297
Q

Why does Crohn’s have a cobblestone appearance?

A

Due to ulcers and fissures

298
Q

Describe microscopic pathophysiology of Crohn’s

A
  • inflammation extends through all layers of bowel
  • increase in chronic inflammatory cells
  • lymphoid hyperplasia
  • granulomas present
  • goblet cells present
  • less crypt abscesses than UC
299
Q

What % of people are granulomas present in?

A

50-60%

- non caseating epithelioid cell aggregates with Langhan’s giant cells

300
Q

Clinical presentation of Crohn’s

A
  • diarrhoea with urgency, bleeding & pain
  • abdo pain
  • weight loss
  • malaise
  • lethargy
  • anorexia
  • abdo tenderness/mass
  • perianal abscess
  • anal strictures
  • extraintenstinal signs
301
Q

Define the urgency for diarrhoea in Crohn’s

A

Need to go 5-6 times in 45 mins

302
Q

What can abdominal pain present as in Crohn’s?

A

Emergency with acute right iliac fossa pain

- pain mimics appendicitis

303
Q

What are some extra-intestinal signs of Crohn’s?

A
  • aphthous oral ulcerations
  • clubbing
  • skin / joint / eye problems
304
Q

Complications of Crohn’s

A
  • perforation & bleeding are MAJOR
  • fistula formation
  • anal: skin tags, fissure, fistula
  • malabsorption
  • small bowel obstruction as grossly dilated
  • toxic dilatation of colon
  • colorectal cancer
  • venous thrombosis
  • amyloidosis (rare)
305
Q

Describe a fistula in Crohn’s?

A

Between loops of bowel

306
Q

Differential diagnosis of Crohn’s

A
  • alternative causes of diarrhoea should be excluded

- chronic diarrhoea

307
Q

How to diagnose Crohn’s

A
  • examination
  • bloods
  • stool sample
  • faecal calprotectin
  • colonoscopy
  • upper GI endoscopy
308
Q

What will examination for Crohn’s show?

A
  • tenderness of R iliac fossa

- anal examination

309
Q

What will blood show for Crohn’s?

A
  • anaemia (due to malabsorption)
  • raised ESR & CRP
  • raised white cell count & platelets
  • hypoalbuminaemia
  • abnormal liver biochem
  • negative pANCA
310
Q

When will hypoalbuminaemia present in Crohn’s?

A
  • severe disease
  • part of acute phase response to inflammation
  • associated with raised CRP
311
Q

Why do you take a stool sample for Crohn’s?

A

To exclude C. difficile & campylobacter

312
Q

What does faecal calprotectin indicate?

A

IBD - not specific

313
Q

Why will you conduct a colonoscopy for Crohn’s?

A
  • confirms spot lesions & granulomatous transmural inflammation
314
Q

What will upper GI endoscopy exclude in Crohn’s test?

A

Oesophageal & gastroduodenal disease

315
Q

Treatment for Crohn’s

A
  • smoking cessation
  • anaemia treated
  • maintain remission
  • surgery
316
Q

How do you treat mild attacks of Crohn’s?

A

Controlled release corticosteroids

- BUDESONIDE

317
Q

How do you treat moderate to severe attacks of Crohn’s?

A

Glucocorticoids

- ORAL PREDNISOLONE (reduce dose every 2-4 weeks if symptoms resolve)

318
Q

How do you treat severe attacks of Crohn’s?

A
  • IV HYDROCORTISONE
  • treat rectal disease - HYDROCORTISONE per rectum
  • antibiotics - IV METRONIDAZOLE
319
Q

What is IV metronidazole used for in Crohn’s?

A

Perianal disease (inflammation at or near anus) & abscesses

320
Q

What treatment would you switch to if severe attacks improve?

A

Oral prednisolone

321
Q

What treatment would you switch to if severe attacks DON’T improve?

A

Anti-TNF antibodies

  • infliximab
  • adalimumab
322
Q

How do anti-TNF antibodies work?

A
  • reduce disease activity by countering neutrophil accumulation & granuloma formation
  • cause cytotoxicity to CD4+ T cells
323
Q

How do you maintain remission of Crohn’s?

A
  • AZATHIOPRINE
  • METHOTREXATE
  • Anti-TNF antibodies
324
Q

Side effects of azathioprine

A
  • bone marrow suppression
  • acute pancreatitis
  • allergic reactions
325
Q

When would you use methotrexate for Crohn’s?

A

If intolerant of azathioprine

326
Q

Why are anti-TNF antibodies used?

A
  • induce remission if resistant to corticosteroids

- immunosuppression then maintains it (infliximab / adalimumab)

327
Q

Define intestinal obstruction (IO)

A

Arrest/blockage of onward propulsion of intestinal contents

328
Q

Classification of intestinal obstruction

A
  1. According to site
  2. Extent of luminal obstruction
  3. According to mechanism
  4. According to pathology
329
Q

Classification of IO: According to site

A

Either:

  • large bowel
  • small bowel
  • gastric
330
Q

Classification of IO: Extent of luminal obstruction

A

Either:

  • partial
  • complete (volvulus = overflow/sickness)
331
Q

Classification of IO: According to mechanism

A

Either:

  • mechanical
  • true (intraluminal/extraluminal)
  • functional
332
Q

Classification of IO: According to pathology

A

Either:

  • simple
  • closed loop
  • strangulation
  • intussusception
333
Q

Describe the functional mechanism classification of IO?

A

Paralytic ileus

  • adynamic bowel
  • due to absence of normal peristaltic contractions
  • caused by abdominal surgery / acute pancreatitis
334
Q

What is intussusception?

A

One hollow structure into its distal hollow structure

- usually in children (bowel is softer)

335
Q

What might obstruction of lumen be due to in IO?

A
  • tumour
  • diaphragm disease
  • meconium ileus
  • gallstone ileus
336
Q

What kind of diseases in the wall of bowel may cause obstruction?

A
  • inflammatory
  • tumour
  • neural
337
Q

Inflammatory disease causing obstruction?

A
  • Crohn’s

- diverticulitis

338
Q

Where does diverticulitis occur?

A

Usually in sigmoid colon

339
Q

Where does diverticular form?

A

At gaps in wall of gut where blood vessels penetrate

340
Q

Describe diverticulitis in low fibre diet

A
  • colon has to push harder
  • pressure increases
  • pushes mucosa through gaps resulting in diverticular / out pouching
  • can get inflamed / burst = results in acute peritonitis / possible death
341
Q

Neural disease causing obstruction in bowel?

A

HIRSCHPRUNG’S DISEASE

- neonates = born without complete innervation of colon/rectum

342
Q

What does Hirschprung’s disease result in?

A
  • gut dilatation
  • filling of faeces that remains
  • no ganglion cells to result in peristalsis & movement of contents = obstruction
343
Q

Outside bowel causes of obstruction

A
  • adhesions
  • volvulus
  • tumour
344
Q

What are adhesions outside of the bowel that cause obstruction?

A
  • abdo structures stick to one another

bowel loops, momentum, other solid organs / abdo wall by fibrous tissue

345
Q

When do adhesions outside of the bowel usually occur?

A

After surgery

- most common cause of obstruction (80%)

346
Q

What can happen at sites of adhesions outside of the bowel?

A
  • intestine twists on itself

- results in obstruction of blood supply / normal movement of intestinal contents

347
Q

What is volvulus?

A

A twist/rotation of bowel segment

  • always occurs at part of the bowel with mesentery
  • type of closed loop bowel obstruction
348
Q

Tumour causing obstruction

A

Peritoneal tumour

- seen in ovarian carcinoma

349
Q

What are most intestinal obstructions due to?

A

Mechanical block

350
Q

What is one of the most common causes of hospital admission?

A

Intestinal obstruction

351
Q

What is typical of obstruction?

A
  • tinkling bowel sounds

- tympanic percussion

Phase 2a (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions