GI Flashcards

Question 1

Q

what is the clinical presentation of GORD?

Answer

A

heartburn
belching
food/acid brash (food, acid or bile regurgitation)
water brash (increased salivation)
odynophagia (painful swallowing)

Question 2

Q

what is heartburn? what are some features of it?

Answer

A

burning chest pain that is aggravated by bending, stooping and lying down which promotes acid exposure and may be relieved by antacids
worse with hot drinks or alcohol
seldom radiates to the arms

Question 3

Q

what is odynophagia?

Answer

A

painful swallowing

Question 4

Q

what are extra-oesophageal clinical presentations of GORD?

Answer

A

nocturnal asthma
chronic cough
laryngitis (hoarseness and throat clearing)
sinusitis

Question 5

Q

what are differential diagnoses of GORD?

Answer

A

ACS
Stable angina
peptic ulcer disease
malignancy

Question 6

Q

when can GORD be diagnosed without investigation?

Answer

A

when there are no alarm bell signs, e.g. weight loss, haematemesis, dysphagia >55
patients under 55 can safely be treated initially without investigation

Question 7

Q

what is used to investigate and diagnose GORD?

Answer

A

endoscopy

- barium swallow may show hiatus hernia

Question 8

Q

what are the aims of investigations of GORD?

Answer

A

assess oesophagitis (inflammation of oesophagus) and hiatal hernia by endoscopy:
- if there is oesophagitis or Barrett’s oesophagus then reflux is confirmed

document reflux by intraluminal monitoring:

24hr oesophageal pH monitoring is helpful in diagnosing GORD when endoscopy is normal or just prior to surgery to confirm reflux
also helpful if there is no response to proton-pump inhibitors

Question 9

Q

what classification is used to assess GORD?

Answer

A

use Los Angeles classification of GORD/Oesophagitis when doing endoscopy to gauge extent of damage

Question 10

Q

what lifestyle changes can be used to treat GORD?

Answer

A

encourage weight loss
smoking cessation
small, regular meals
avoid; hot drinks, alcohol, citrus fruits and eating less than 3 hours before bed

Question 11

Q

what drugs are used to treat GORD? how do they work?

Answer

A

antacids e.g. magnesium triscilicate mixture: relieves symptoms by forming a gel or ‘foam raft’ with gastric contents to reduce reflux, note: side effect of magnesium containing antacids is diarrhoea
alginates e.g. gaviscon; relieves symptoms
proton pump inhibitor (PPI) e.g. lanzoprazole to reduce gastric acid production
H2 receptor antagonists e.g. cimetidine

Question 12

Q

what surgery can be used to treat GORD? when is it used?

Answer

A

nissen fundoplication; aims to laparoscopically increase the resting LOS pressure

only in severe GORD
use when not responding to therapy
complications include dysphagia and bloating

Question 13

Q

what are complications of GORD?

Answer

A

peptic stricture and Barrett’s oesophagus

Question 14

Q

what is peptic stricture? what is its clinical presentation and treatment?

Answer

A

oesophagitis resulting from gastric (peptic) acid exposure resulting in the narrowing and stricture of the oesophagus
usually occurs in patients over 60
presents as gradually worsening dysphagia
treat with endoscopic dilatation and long term PPI therapy

Question 15

Q

what is barrett’s oesophagus? what is its clinical presentation?

Answer

A

GORD may induce barrett’s oesophagus
distal oesophageal epithelium undergoes metaplasia from squamous to columnar epithelium
always a hiatus hernia present
risk of progressing to oesophageal cancer; is premalignant for adenocarcinoma of the oesophagus

Question 16

Q

what is a Mallory-Weiss tear? what is its epidemiology?

Answer

A

this is a linear mucosal tear occurring at the oesophagogastric junction and is produced by a sudden increase in intra-abdominal pressure
often follows a bout of coughing or retching and is classically seen after alcoholic ‘dry heaves’
most common in males
seen mainly in age 20-50

Question 17

Q

what are risk factors for Mallory-Weiss tears?

Answer

A

alcoholism
forceful vomiting
eating disorders
male
NSAID abuse

Question 18

Q

what are clinical features of Mallory-Weiss tears?

Answer

A

vomiting
haematemesis after vomiting
retching
postural hypotension
dizziness

Question 19

Q

what are differential diagnoses of Mallory-Weiss tears?

Answer

A

gastroenteritis
peptic ulcer
cancer
oesophageal varices

Question 20

Q

what is used to diagnose Mallory-Weiss tears?

Answer

A

endoscopy to confirm

Question 21

Q

what is the treatment of Mallory-Weiss tears?

Answer

A

most bleeds are minor and heal in 24 hours
haemorrhage may be large but tends to stop spontaneously
if surgery is required then it involves the oversewing of the tear but this is rarely needed

Question 22

Q

what is dyspepsia?

Answer

A

one or more of the following:

postprandial fullness
early satiation
epigastric pain or burning for more than 4 weeks

an inexact term used to describe a number of upper abdominal symptoms such as heartburn, acidity, epigastric pain or discomfort, fullness or belching

Question 23

Q

what is the epidemiology of dyspepsia?

Answer

A

dyspepsia is a common complaint affecting up to 25% of the population each year
patients may say it’s indigestion

Question 24

Q

what are causes of dyspepsia?

Answer

A

disorders of the GI tract - the most common is functional dyspepsia that affects around 75% with no known cause
other causes are peptic ulcers

Question 25

Q

what is the clinical presentation of dyspepsia?

Answer

A

reflux when lying flat
heartburn
acid taste due to reflux
bloating
indigestion

Question 26

Q

what are red flag alarm symptoms in dyspepsia for cancer?

Answer

A

unexplained weight loss
anaemia
evidence of GI bleeding e.g. melaena (dark tar like black stools) or haematemesis
dysphagia
upper abdominal mass
persistent vomiting

Question 27

Q

what is the history/differentials of dyspepsia?

Answer

A

heartburn/regurgitation/cough: possibly GORD
alarm symptoms or family history can be an indicator of possible malignancy
onset; acute vs. chronic
age; over 55 is a red flag and thus means increased risk of cancer
relationship to food

Question 28

Q

what is the relationship to food of dyspepsia?

Answer

A

early postprandial pain - could be due to gastritis, GORD or gastric carcinoma
postprandial pain could be due to a gastric ulcer
pain that is relieved by milk could also be a sign of gastric ulcer

Question 29

Q

what is the management of dyspepsia?

Answer

A

reassurance
dietary review
antidepressants e.g. SSRIs
look for Helicobacter pylori using faecal antigen testing or breath test
endoscopy

Question 30

Q

what is the structure of the mucosal lining of the stomach?

Answer

A

can stretch in size with feeding
the greater curvature of the undistended stomach has thick folds called rugae
the mucosa of the upper two thirds of the stomach contain:
• parietal cells - secrete HCl
• chief cells - produce pepsinogen and thus initiate proteolysis - the digestion of proteins
• enterochromaffin-like (ECL) cells - releases histamine (stimulates acid release)

Question 31

Q

what cells does the antral mucosa of the stomach contain?

Answer

A

mucus secreting cells - secrete mucin (protects gastric mucosa) and bicarbonate
G cells - secrete gastrin which stimulates acid release
D cells - secrete somatostatin which suppresses acid secretion

Question 32

Q

what is the mucosal barrier of the stomach? what is its structure and function?

Answer

A

is made up of the plasma membranes of the mucosal cells and the mucus layer (made up of mucin), protects the gastric epithelium from damage by acid and, for example, alcohol, aspirin, NSAIDs and bile salts
prostaglandins stimulate the secretion of mucus and their synthesis is inhhibited by aspirin and NSAIDs, which inhibit cyclo-oxygenase

Question 33

Q

what is the structure/function of the duodenal mucosa?

Answer

A

has villi like the rest of the small bowel and also contains Brunner’s glands which secrete alkaline mucus
this, along with the pancreatic and biliary secretions, helps to neutralise the acid secretion from the stomach when it reaches the duodenum

Question 34

Q

what is a peptic ulcer?

Answer

A

consists of a break in the superficial epithelial cells which penetrates down to the muscularis mucosa of either the stomach or the duodenum; there is a
fibrous base and an increase in inflammatory cells

Question 35

Q

where are duodenal and gastric peptic ulcers often seen?

Answer

A

duodenal ulcers most commonly seen in duodenal cap

- gastric ulcers most commonly found on the lesser curve of the stomach but can be found anywhere in the stomach

Question 36

Q

what is the epidemiology of peptic ulcer disease?

Answer

A

duodenal ulcers affect around 10% of the adult population and are 2-3 times more common than gastric ulcers
more common in the elderly
more common in developing countries due to Helicobacter pylori
ulcers due to NSAID use is increasing
decline in incidence in men and increasing in women

Question 37

Q

what are the main causes of peptic ulcer disease?

Answer

A

Helicobacter pylori infection
drugs e.g. NSAIDs (including aspirin), steroids and SSRIs
increased gastric acid secretion (minor)
smoking (minor)
delayed gastric emptying
blood group O

Question 38

Q

what is the pathophysiology of peptic ulcer disease?

Answer

A

ulcers result in gastritis
usually the gastric mucosa is protected by a layer of mucin that is produced by gastric cells
NSAIDs e.g. naproxen and aspirin
Helicobacter pylori
ischaemia of the gastric cells
too much acid production
alcohol has a direct toxic effect on gastric cells in high concentrations

Question 39

Q

how can NSAIDs lead to peptic ulcer disease?

Answer

A

e.g. naproxen and aspirin
• mucous secretion is stimulated by prostaglandins (in inflamed tissue, prostaglandin triggers inflammatory response thus inhibition = less inflammation)
• cyclo-oxygenase 1 is needed for prostaglandin synthesis
• NSAIDs inhibit cylclo-oxygenase 1
• thus reduced mucosal defence

Question 40

Q

how can Helicobacter pylori lead to peptic ulcer disease?

Answer

A

highly adapted to the stomach environment and exclusively colonises gastric epithelium and inhabits the mucous layer/just beneath it
causes major destruction to the protective mucin layer
causes decrease in duodenal HCO3- thereby increasing the acidity of the stomach as there will be less alkali to buffer the acid
secretes urease, splitting urea into CO2 and ammonia
ammonia + H+ = ammonium
ammonium is toxic to gastric mucosa resulting in less mucous produced
secreted proteases, phospholipase and vacuolating cytotoxin A can then begin attacking the gastric epithelium further reducing mucous production
results in an inflammatory response and less mucosal defence
also increases gastrin release, causing more acid secretion from parietal cells and also triggering the release of histamine which further increases acid secretion
also increases parietal cell mass meaning more acid production
also decreases somatostatin release (which reduces acid secretion) resulting in increased acid release
increased acidity overwhelms the protective mucin layer resulting in mucosal damage and ulceration

Question 41

Q

what are the overall effects of H. pylori?

Answer

A

inflammation e.g. antral gastritis
gastric cancer
peptic ulcers

Question 42

Q

how can ischaemia of the gastric cells lead to peptic ulcer disease?

Answer

A

causes gastric cells to produce less mucin resulting in less protection from acid, meaning acid is able to damage mucosa and cause an ulcer
caused by low blood pressure or atherosclerosis

Question 43

Q

how can too much acid production lead to peptic ulcer disease?

Answer

A

too much acid overwhelms mucin and results in ulceration
stress can result in increased acid production
PPIs and H2 blockers used to treat this

Question 44

Q

what is the clinical presentation of peptic ulcer disease?

Answer

A

recurrent burning epigastric pain
nausea may accompany the pain
anorexia and weight loss, particularly with gastric ulcers

Question 45

Q

what are features of recurrent burning epigastric pain in peptic ulcer pain?

Answer

A

if patient points with a single finger to the epigastrium as the site of pain, then this is strongly suggestive of peptic ulcer disease
pain of duodenal ulcers classically occurs at night (as well as during the day) and is worse when the patient is hungry
pain in both gastric and duodenal ulcers can be relieved by antacids

Question 46

Q

what are complications of peptic ulcers?

Answer

A

in duodenal ulcers, the ulcer can get deeper and deeper until it hits an artery, most commonly the gastroduodenal artery, which can result in massive haemorrhage, presents as an emergency
can result in peritonitis as acid enters peritoneum; will see air under diaphragm on erect X-ray
can result in acute pancreatitis if the ulcer hits the pancreas

Question 47

Q

what is the diagnosis of peptic ulcer disease?

Answer

A

if patients is under 55 then carry out non-invasive testing e.g. serological test, breath test or stool antigen testing, if test is positive then start eradication immediately
usually an endoscopy is not necessary, but if found to have a gastric ulcer then re-scope 6-8 weeks later to ensure there is no malignancy
endoscopy is essential is all red flag patients and those who are over 55
non-invasive H. pylori testing (serology, C-urea breath test, stool antigen test)

Question 48

Q

how is serology used as a non-invasive H. pylori test for peptic ulcer disease?

Answer

A

detects IgG antibodies - not useful for confirming eradication or presence of current infection since IgG takes 1 year to fall by 50%

Question 49

Q

how is a C-urea breath test used as a non-invasive H. pylori test for peptic ulcer disease?

Answer

A

quick and reliable test for H.pylori
measures CO2 in breath after the ingestion of C-Urea
used to monitor infection after eradication
highly sensitive and specific
no antibiotics or proton-pump inhibitors (PPIs) before test

Question 50

Q

how is a stool antigen used as a non-invasive H. pylori test for peptic ulcer disease?

Answer

A

immunoassay using monoclonal antibodies for detection of H. pylori
monitors the efficacy of eradication therapy
patients should be off PPIs for 2 weeks before

Question 51

Q

how is biopsy used as an invasive H. pylori test for peptic ulcer disease?

Answer

A

• histology - direct visualisation of H.pylori, reduced if on PPIs
• biopsy urease test:
- H. pylori produces urease
- splits urea to release ammonia which will raise pH of the solution and causes a rapid colour change of yellow to red
- no PPIs or antibiotics should be used before since this will give false negatives

Question 52

Q

what is the treatment of peptic ulcer disease?

Answer

A

lifestyle adjustments (reduce stress, avoid irritating foods, reduce smoking)
stop NSAIDs
H.pylori eradication (7-14 days)
H2 antagonists to reduce acid release
surgery if complications arise such as haemorrhage

Question 53

Q

how is H. pylori eradication confirmed? how long does it take?

Answer

A

7-14 days

- confirmed by urea breath or faecal antigen test

Question 54

Q

what is used for H. pylori eradication?

Answer

A

triple therapy

PPI for acid suppression e.g. lansoprazole or omeprazoel
plus 2 of: metronidazole, clarithromycin, amoxicillin, tetracycline, bismuth
note: amoxicillin and tetracycline have low resistance, and clarithromycin has high resistance
quinolones e.g. ciprofloxacin, furozolidone and rifabutin are used when standard regimens have failed as rescue therapy

Question 55

Q

what is a varice?

Answer

A

dilated vein which is at risk of rupture resulting in haemorrhage and can result in GI bleeding

Question 56

Q

what is the function of the hepatic portal vein?

Answer

A

carries nutrient rich blood from the GI tract, gallbladder, pancreas and spleen to the liver
rich in nutrients that have been extracted from food and the liver processes these nutrients; it also filters toxins that may have been ingested alongside the food
the blood leaves the liver to the heart in the hepatic veins via the IVC

Question 57

Q

what is the normal pressure of the hepatic portal vein?

Question 58

Q

how is portal hypertension classified? what are the classifications?

Answer

A

according to the site of obstruction

pre-hepatic; blockage of the hepatic portal vein before the liver
intra-hepatic; distortion of the liver architecture, either pre-sinusoidal (e.g. schistosomiasis) or post-sinusoidal (e.g. cirrhosis)
post-hepatic; venous blockage outside the liver (rare)

Question 59

Q

how are varices formed within the systemic venous system?

Answer

A

as portal pressure rises above 10-12mmHg, the compliant venous system dilates and varices form within the systemic venous system
these can form at the gastro-oesophageal junction, rectum, left renal vein, diaphragm and the anterior abdominal wall via the umbilical vein
gastro-oesophageal varices are superficial and tend to rupture, resulting in GI bleeding, usually when pressure exceeds 12mmHg

Question 60

Q

what is the epidemiology of gastro-oesophageal varices? where do they tend to develop?

Answer

A

around 90% of patients with cirrhosis will develop gastro-oesophageal varices over 10 years, but only a third of these will bleed
bleeding is likely to occur with large varices, or those with red flag signs at endoscopy and in severe liver disease
varices tend to develop in the lower oesophagus and gastric cardia

Question 61

Q

what are the main causes of gastro-oesophageal varices?

Answer

A

alcohol and viral cirrhosis

- portal hypertension

Question 62

Q

what are causes of pre-hepatic portal hypertension?

Answer

A

thrombosis in portal or splenic vein

Question 63

Q

what are causes of intra-hepatic portal hypertension?

Answer

A

cirrhosis (commonest cause in UK)
schistosomiasis (commonest cause worldwide)
sarcoid
congenital hepatic fibrosis

Question 64

Q

what are causes of post-hepatic portal hypertension?

Answer

A

Budd-Chiari syndrome (hepatic vein obstruction by tumour or thrombosis)
right heart failure
constrictive pericarditis

Answer 64

A

hepatic vein obstruction by tumour or thrombosis

- causes post-hepatic portal hypertension

Answer 65

A

cirrhosis
portal hypertension
schistosomiasis infection
alcoholism

Answer 66

A

following liver injury and fibrogenesis, the contraction of activated myofibroblasts (mediated by endothelin, nitric oxide and prostaglandins) contributes to increased resistance to blood flow
this leads to portal hypertension → splanchnic vasodilation → drop in BP → increased cardiac output to compensate for BP drop → salt and water retention to increase blood volume and compensation → hyperdynamic circulation → formation of collaterals between the portal and systemic systems → gastro-oesophageal varices develop once portal pressure is above 10mmHg - can occur rapidly and result in major haemorrhage

Answer 67

A

haematemesis
abdominal pain
shock - if major blood loss
fresh rectal bleeding - associated with shock in acute massive GI bleed
hypotension and tachycardia
pallor
suspect varices as the cause of GI bleeding if there is alcohol abuse or cirrhosis

Answer 68

A

signs of rupture
signs of chronic liver damage e.g. jaundice, increased bruising and ascites
splenomegaly
ascites
hyponatraemia

Answer 69

A

endoscopy to find bleeding source

Answer 70

A

resuscitate until haemodynamically stable
if anaemic then do blood transfusion aiming to get Hb to 80g/L
correct clotting abnormalities with vitamin K and platelet transfusion
vasopressin e.g. IV terlipressin or somatostatin
prophylactic antibiotics
variceal banding
balloon tamponade to reduce bleeding
transjugular intrahepatic portoclaval shunt (TIPS); a shunt between the systemic and portal systems which reduces sinusoidal and portal vein pressure

Answer 71

A

transjugular intrahepatic portoclaval shunt

artificial channel within the liver that establishes communication between the inflow portal vein and the outflow hepatic vein
uses endoscope
jugular vein is usual entry site
used to treat varices

Answer 72

A

non-selective beta-blockade to reduce resting pulse rate to decrease portal pressure
variceal banding repeatedly
liver transplant

Answer 73

A

characterised by oesophageal aperistalsis and impaired relaxation of the lower oesophageal sphincter
the lower oesophageal pressure is elevated in more than half of patients
incidence is 1 in 100,000 and is equal in both males and females
occurs at all ages but rare in childhood
patients usually have a long history of intermittent dysphagia characteristically for both liquids and solids from the onset
cause is unknown

Answer 74

A

failure of smooth muscle fibres in the oesophagus to relax, which can cause the LOS to remain closed

Answer 75

A

the LOS fails to relax due to degeneration of the

mesenteric plexus of the oesophagus, with reduction of ganglion cell numbers

Answer 76

A

dysphagia for fluids and solids
regurgitation of food particularly at night and aspiration pneumonia is a complication
substernal cramps
weight loss (usually minimal)
spontaneous chest pain occurs due to oesophageal ‘spasm’; may be misdiagnosed as cardiac pain

Answer 77

A

CXR
• dilated oesophagus
• may be fluid level behind/above the heart

barium swallow
• shows lack of peristalsis
• lower end shows a ‘birds beak’ due to failure of sphincter to relax

manometry
• confirms diagnosis
• shows aperistalsis of the oesophagus and failure of relaxation of the LOS

CT and oesophagoscopy used to rule out carcinoma at the lower end of the oesophagus which can produce a similar x-ray appearance

Answer 78

A

relief of symptoms
medical treatment to relax the LOS e.g. nifepidine,
nitrates or sildenafil
surgery

Answer 79

A

endoscopic balloon dilation to open sphincter
Heller’s cardiomyotomy - the surgical division of the lower oesophageal sphincter and then PPIs
botox injection into sphincter to relax it (effects wear off)

Answer 80

A

there is a slight increase in the incidence of squamous carcinoma of the oesophagus in both treated and untreated cases

Answer 81

A

group of autoimmune disease that may result in changes to skin, blood vessels, muscles, and internal organs
increased synthesis of collagen, damage to small blood vessels, activation of T lymphocytes and production of altered connective tissues
multi-system disease

Answer 82

A

more common in females than males
peak incidence is between 30 and 50
rare in children
there is oesophageal involvement in almost all patients with this disease

Answer 83

A

vinyl chloride

- silica dust

Answer 84

A

diminished peristalsis and oesophageal clearance due to the replacement of the smooth muscle by fibrous tissue
LOS pressure is decreased thereby allowing GORD with consequent mucosal damage
strictures may develop

Answer 85

A

initially there are no symptoms
dysphagia and heartburn occur as the oesophagus becomes more severely
involved

Answer 86

A

barium swallow
CXR
manometry

Answer 87

A

same as for GORD. e.g. PPIs

Answer 88

A

inflammation of the lining of the stomach
may occur as a short episode or have long duration
inflammation that is associated with mucosal injury
gastropathy indicates epithelial cell damage and regeneration without inflammation; commonest cause is mucosal damage associated with aspirin/NSAIDs

Answer 89

A

Helicobacter pylori infection
autoimmune gastritis
viruses e.g. cytomegalovirus and herpes simplex
duodenogastric reflux, where bile salts enter stomach and damage mucin protection, resulting in gastritis
specific causes e.g. Crohn’s (more common in children than adults)
mucosal ischaemia; reduced blood supply to mucosal cells can mean less mucin produced so acid can induce gastritis
increased acid; can overwhelm mucin resulting in gastritis, stress can increase acid production
aspirin and NSAIDs
alcohol

Answer 90

A

most common cause
causes severe inflammatory response
gastric mucus degradation and increased mucosal permeability, which is directly cytotoxic to the gastric epithelium

Answer 91

A

affects the fundus and body of the stomach leading to

atrophic gastritis and loss of parietal cells with intrinsic factor deficiency resulting in pernicious anaemia

Answer 92

A

NSAIDs will inhibit prostaglandins (which stimulate mucus production) via the inhibition of cyclo-oxygenase resulting in less mucus production and thus gastritis

Answer 93

A

nausea or recurrent upset stomach
abdominal bloating
epigastric pain
vomiting
indigestion
haematemesis

Answer 94

A

peptic ulcer disease (PUD)
GORD
non-ulcer dyspepsia
gastric lymphoma
gastric carcinoma

Answer 95

A

endoscopy
biopsy
H.pylori urea breath test
H.pylori stool antigen test

Answer 96

A

remove causative agents
reduce stress
H. pylori eradication (7-14 days)
H2 antagonists and PPIs to reduce acid release
antacids

Answer 97

A

the failure to fully absorb nutrients due to the destruction of epithelium or due to a problem in the lumen meaning food cannot be digested

Answer 98

A

coeliac disease
tropical sprue
Crohn’s
parasite infection

Answer 99

A

defective intraluminal digestion
insufficient absorptive area
lack of digestive enzymes
defective epithelial transport
lymphatic obstruction

Answer 100

A

pancreatic insufficiency
defective bile secretion
bacterial overgrowth

Answer 101

A

pancreas produce majority of digestive enzymes such as amylase
pancreatitis causes damage to most of the glandular pancreas meaning less or no enzymes are released
cystic fibrosis results in the blockage of the pancreatic duct due to excess mucus, meaning enzymes are not released

Answer 102

A

lack of fat solubilisation
biliary obstruction
ileal resection (bile salts are reabsorbed in the terminal ileum so if removed then bile salt reuptake will be decreased)

Answer 103

A

essentially anything that damages microvilli and villi thereby reducing absorptive surface area and thus absorption potential
Coeliac disease
Crohn’s
giardia lamblia
surgery for small bowel infarction

Answer 104

A

extensive surface parasitisation of the villi and microvilli
parasites coat the surface of the villi thus food cannot be absorbed

Answer 105

A

disaccharidase deficiency (lactose intolerance) - cannot break down the lactose in milk into glucose which can then be absorbed. the undigested lactose passes into the colon where it is then eaten up by bacteria and CO2 is released leading to wind and diarrhoea
bacterial overgrowth resulting in brush border damage

Answer 106

A

abetalipoproteinaemia - lack of transporter protein to transport lipoprotein across cell
primary bile acid malabsorption - mutations in bile acid transporter protein

Answer 107

A

lymphoma

- TB

Answer 108

A

• condition in where there is inflammation of the mucosa of the upper small bowel that improves when gluten is withdrawn from the diet and relapses when gluten is reintroduced
• T-cell mediated autoimmune disease of the small bowel in which prolamin (alcohol-soluble proteins in wheat, barley, rye and oats) intolerance causes villous
atrophy and malabsorption

Answer 109

A

gliadin in wheat, hordeins in barley and secalins in rye

Answer 110

A

around 1% of population affected
occurs at any age but peaks in infancy and 50-60yrs
affects males and females equally
10% risk in 1st degree relatives and 30% risk in siblings

Answer 111

A

other autoimmune diseases: type 1 diabetes, thyroid disease, Sjorgrens
IgA deficiency
breast feeding
age of introduction to gluten into diet
rotavirus infection in infancy increases risk

Answer 112

A

in wheat and in gluten the prolamin a-gliadin is toxic and resistant to digestion by pepsin and chymotrypsin because of their high glutamine and proline content, and it remains in the intestinal lumen thereby triggering
immune responses
the gliadin peptides pass through the epithelium and are deaminated by tissue transglutaminase, which increases their immunogenicity
the gliadin peptides bind to antigen-presenting cells which interact with CD4+ T cells in the lamina propria via HLA class II DQ2 or DQ8
these two HLA class II molecules DQ2 (95%) or DQ8 (5%) activate the gluten-sensitive T cells
these T cells produce pro-inflammatory cytokines and initiate an inflammatory cascade
the cascade releases metalloproteinkinases and other mediators, which contribute to the villous atrophy, crypt hyperplasia and intraepithelial lymphocytes that are typical of the disease and result in malabsorption
proximal small bowel mucosa is predominantly affected
this mucosal damage means that B12, folate and iron cannot be absorbed resulting in anaemia
mucosal damage decreases in severity towards the ileum as gluten is digested into small ‘non-toxic’ fragments

Answer 113

A

HLA class II molecules DQ2 or DQ8
these two HLA class II molecules DQ2 (95%) or DQ8 (5%) activate the gluten-sensitive T cells
these T cells produce pro-inflammatory cytokines and initiate an inflammatory cascade

Answer 114

A

1/3 are asymptomatic and only detected on routine blood tests (raised MCV)
stinking stools/fatty stools (steatorrhoea)
diarrhoea
abdominal pain
bloating
nausea and vomiting
angular stomatitis
weight loss
fatigue
anaemia
osteomalacia; softening of bones due to impaired bone metabolism due to lack of phosphate, calcium and vitamin D leading to osteoporosis (40-60% risk
in untreated patients leading to fracture risk)
dermatitis hepetiformis; red raised patches, often with blisters that burst on scratching, commonly seen on elbows, knees and buttocks

Answer 115

A

chronic autoimmune blistering skin condition
characterised by blisters filled with watery fluid
itchy
cutaneous manifestation of Coeliac disease
red raised patches
commonly seen on elbows, knees and buttocks

Answer 116

A

should maintain gluten for at least 6 weeks before testing to get true results
duodenal biopsy is gold standard for diagnosis
serum antibody testing

Answer 117

A

low Hb
low B12
low ferritin

Answer 118

A

see villous atrophy, crypt hyperplasia and increased intraepithelial WCC
all reverse on gluten free diet

Answer 119

A

persistent diarrhoea
folate or iron deficiency
family history of Coeliac disease or associated autoimmune disease

Answer 120

A

95% sensitive unless patient is IgA deficient
endomysial antibody (EMA)
tissue transglutaminase antibody (tTG)
both are IgA antibodies
these correlate with the severity of mucosal damage and can thus be used for dietary monitoring

Answer 121

A

lifelong gluten free diet; use serum antibody testing for monitoring
correction of vitamin and mineral deficiencies e.g. B12, folate, iron, calcium and vitamin D
DEXA scan to monitor osteoporotic risk

Answer 122

A

eliminate wheat, barley and rye; see results in days/weeks
poor compliance is main reason for recurrent issues
oats usually tolerated unless contaminated with flour during production
meat, dairy product, fruits and vegetables are all gluten-free

Answer 123

A

a few patients do not improve on a strict diet and are said to have non-responsive coeliac disease
anaemia
secondary lactose intolerance
T-cell lymphoma
increased risk of malignancy (gastric, oesophageal, bladder, breast and brain) due to increased cell turnover
osteoporosis

Answer 124

A

malabsorption disease commonly found in tropical regions, marked with abnormal flattening of the villi and inflammation of the lining of the small intestine
severe malabsorption of two or more substances accompanied by diarrhoea and malnutrition

Answer 125

A

the term tropical sprue is reserved for severe malabsorption (of two or more substances) accompanied by diarrhoea and malnutrition
occurs in residents or visitors to tropical areas where the disease is endemic; most of Asia, some Caribbean islands, Puerto Rico and parts of South America
cause is unknown but is likely to be infective because the disease occurs in epidemics and patients improve on antibiotics

Answer 126

A

villous atrophy with malabsorption
onset is acute and occurs either a few days or many years after being in the tropics
epidemics can break out in villages, affecting thousands of people at the same time

Answer 127

A

diarrhoea
anorexia
severe malabsorption
weight loss
abdominal distension
the onset can also be insidious with chronic diarrhoea and evidence of nutritional deficiency

Answer 128

A

exclude acute infective causes of diarrhoea e.g. Giardia intestinalis, which can produce similar symptoms
bloods: anaemia due to malabsorption of B12, folate and iron
jejunal biopsy: jejunal mucosa is abnormal showing partial villous atrophy

Answer 129

A

leave area
folic acid daily and antibiotics for up to 6 months
severe cases require resuscitation with fluids and electrolytes for dehydration and nutritional deficiencies should be corrected and B12 given
excellent prognosis
mortality is only associated with water and electrolyte depletion particularly in epidemics

Answer 130

A

both autoimmune conditions:

ulcerative colitis (UC), which affects only the colon
crohn’s disease (CD), can affect any part of the GI tract (mouth to anus)

Answer 131

A

jewish people are more prone to IBD than any other ethnic group

Answer 132

A

IBD occurs when the mucosal immune system exerts an inappropriate response to luminal antigens, such as bacteria, which may enter the mucosa via a leaky epithelium

Answer 133

A

• relapsing and remitting inflammatory disorder of the colonic mucosa
• it may affect just the rectum; proctitis (50%)
• it may affect the rectum and left colon; left-sided colitis (30%)
• it may affect the entire colon (entire large bowel) up to
the ileocaecal valve; pancolitis/extensive colitis
• it never affects proximal to the ileocaecal valve

Answer 134

A

highest incidence and prevalence in Northern Europe, UK and North America
higher incidence than Crohn’s per year
affects males and females equally
presentation mostly at 15-30 years
is 3 times more common in non/ex-smokers; symptoms may relapse on cessation
cause is unknown
1 in 6 will have a first degree relative with UC
an appendicectomy appears to be protective against the development of UC, especially if performed for appendicitis before 20yrs. It also leads to a lower incidence of colectomy and reduced need for immunosuppressive therapy

Answer 135

A

family history
NSAIDs
chronic stress and depression triggers flares

Answer 136

A

affects only the colon up to the ileocaecal valve
begins in the rectum and extends
circumferential and continuous inflammation - no skip lesions
mucosa looks reddened and inflamed and bleeds easily (friability)
ulcers and pseudo-polyps (regenerating mucosa) in severe disease

Answer 137

A

mucosal inflammation; inflammation does not go deeper e.g. transmural
no granulomata (rare)
depleted goblet cells
increased crypt abscesses

Answer 138

A

remissions and exacerbations
restricted pain usually in lower left quadrant
episodic or chronic diarrhoea with blood and mucus
cramps
bowel frequency linked to severity
in acute UC there may be fever, tachycardia and tender distended abdomen
in acute attack patients have bloody diarrhoea (passing 10-20 liquid stools per day), diarrhoea also occurs at night, with urgency and incontinence that is
severely disabling
extraintestinal signs; clubbing, aphthous oral ulcers, erythema nodusum and amyloidosis

Answer 139

A

clubbing
aphthous oral ulcers
erythema nododum
amyloidosis

Answer 140

A

fatty change
chronic pericholangitis
sclerosing cholangitis

Answer 141

A

blood loss
perforation
toxic dilatation
colorectal cancer

Answer 142

A

erythema nodosum

- pyoderma gangrenosum

Answer 143

A

ankylosing spondylitis

- arthritis

Answer 144

A

iritis
uveitis
episcleritis

Answer 145

A

blood tests
stool samples to exclude C. diff and Campylobacter etc
faecal calprotectin; indicates IBD but not specific
colonoscopy with mucosal biopsy
abdominal X-ray

Answer 146

A

WCC and platelets raised in moderate/severe attacks
iron deficiency anaemia
ESR and CRP raised
liver biochemistry may be abnormal
hypoalbuminaemia is severe disease
pANCA may be positive (in Crohn’s it’s negative)

Answer 147

A

gold standard for diagnosis
allows for assessment of disease activity and extent
can see inflammatory infiltrate, goblet cell depletion, crypt abscesses and mucosal ulcers

Answer 148

A

done in all patients suffering acute severe attacks to exclude colonic dilatation
useful when UC too severe for colonoscopy

Answer 149

A

aim is to induce remission
aminosalicylate which acts topically in the colonic lumen
the active component of these drugs is 5-aminosalicylic acid (5-ASA) which is absorbed in the small intestine
the aminosalicylate preparations are designed to deliver the active 5-ASA to the colon by binding to something else
commonly prescribed 5-ASA aminosalicylates are sulfalazine, mesalazine or olsalazine

Answer 150

A

sulfalazine
mesalazine
olsalazine

Answer 151

A

oral 5-ASA; first line for left sided/extensive
rectal 5-ASA for proctitis
glucocorticoid if no response to 5-ASA

Answer 152

A

glucocorticoids

Answer 153

A

hydrocortisone
ciclosporin
infliximab

Answer 154

A

5-ASA

* azathioprine, for patients who relapse despite 5-ASA treatment or are ASA intolerant

Answer 155

A

• indicated for severe colitis that fails to respond to treatment
• colectomy with ileoanal anastomosis:
- whole colon removed and rectum fused to ileum
- terminal ileum is used to form a reservoir ‘pouch’ to store faeces and patients remain continent
• panproctocolectomy with ileostomy:
- whole colon and rectum are removed and the ileum brought out on to the abdominal wall as a stoma

Answer 156

A

a chronic inflammatory GI disease characterised by transmural (goes deep into mucosa) granulomatous inflammation affecting any part of the gut from mouth to anus (especially in the terminal colon and the proximal colon)
unlike in UC, there is unaffected bowel between areas of active disease; these are skip lesions

Answer 157

A

occur in Crohn’s disease and not in UC

- unaffected bowel between areas of active disease

Answer 158

A

highest incidence and prevalence in Northern Europe, UK and North America
lower incidence than UC per year
prevalence is less if asian
affects females more than males
cause is unknown
smoking increases risk by 3-4 x
1 in 5 patients with Crohn’s have a first-degree relative with the disease
presentation mostly at 20-40 yrs

Answer 159

A

genetic association is stronger in CD than in UC:
• mutations on NOD2 (CARD 15) gene on chromosome 16 increases risk
smoking
NSAIDs may exacerbate disease
family history
chronic stress and depression triggers flares
good hygiene - those who live in poor hygiene families have a lower risk of developing CD
appendicectomy may increase the risk of CD development

Answer 160

A

mutations on NOD2 (CARD 15) gene on chromosome 16 increases risk

Answer 161

A

transmural granulomatous inflammation affecting any part of gut from mouth to anus
in particular the terminal ileum and proximal colon is affected

Answer 162

A

• not continuous i.e. there are skip lesions/patchy areas where there is a gap between affected and unaffected mucosa
• involved bowel is usually thickened and is often
narrowed
• cobblestone appearance due to ulcers and fissures in mucosa
• affects any part of GI tract

Answer 163

A

inflammation extends through all layers of the bowel
increase in chronic inflammatory cells and there is lymphoid hyperplasia
granulomas present in 50-60% - these are non-caseating epithelioid cell aggregates with Langerhans’s giant cells
goblet cells are present
less crypt abscesses than UC

Answer 164

A

diarrhoea with urgency (need to go 5-6 times in 45 mins), bleeding and pain due to deification
abdominal pain can present as an emergency with acute right iliac fossa pain mimicking appendicitis
weight loss
malaise
lethargy
anorexia
abdominal tenderness/mass
perianal abscess
anal strictures
extraintestinal signs; aphthous oral ulcerations, clubbing, skin, joint and eye problems

Answer 165

A

aphthous oral ulcerations
clubbing
skin
joint and eye problems

Answer 166

A

perforation and bleeding are major
fistula formation
anal; skin tags, fissure, fistula (between loops of bowel)
malabsorption
small bowel obstruction as grossly dilated
toxic dilatation of colon
colorectal cancer
venous thrombosis
amyloidosis

Answer 167

A

alternative causes of diarrhoea should be excluded e.g. Salmonella spp, Giardia intestinalis and rotavirus
chronic diarrhoea

Answer 168

A

tenderness of right iliac fossa

* anal examination

Answer 169

A

anaemia is common due to malabsorption and thus deficiency of iron and folate
however, despite terminal ileal involvement, B12 anaemia is not unusual
raised ESR and CRP
raised white cell count and platelets
hypoalbuminaemia present in severe disease as part of an acute phase response to inflammation associated with a raised CRP
liver biochemistry may be abnormal
negative pANCA

Answer 170

A

biopsy to confirm; will see skip lesions and granulomatous transmural inflammation

Answer 171

A

examination
bloods
stool sample to exclude C.difficile and Campylobacter
faecal calprotectin; indicates IBD but not specific
colonoscopy: biopsy to confirm will see spot lesions and granulomatous transmural inflammation
upper GI endoscopy: to exclude oesophageal and gastroduodenal disease

Answer 172

A

smoking cessation

- anaemia due to iron, B12 or folate should be treated with replacement

Answer 173

A

controlled release corticosteroids e.g. budesonide

Answer 174

A

glucocorticoids; reduce dose every 2-4 weeks if symptoms resolve

Answer 175

A

IV hydrocortisone
treat rectal disease using hydrocortisone per rectum
antibiotics e.g. IV metronidazole for perianal disease (inflammation at or near the anus) and abscesses
if there is improvement then transfer to oral prednisolone

Answer 176

A

if no improvement then switch to anti-TNF antibodies e.g. infliximab or adalimumab:
- can reduce disease activity by countering neutrophil
accumulation and granuloma formation, and activating
complement
- also causes cytotoxicity to CD4+ T cells thereby clearing cells which drive the immune response

Answer 177

A

azathioprine - side effects; bone marrow suppression, acute pancreatitis and allergic reactions
methotrexate if intolerant of azathioprine
anti-TNF antibodies to induce remission if resistant to corticosteroids, immunosuppression then maintains it e.g. infliximab or adalimumab

Answer 178

A

80% require surgery at some point
avoided and only minimal resection
indicated in medical therapy failure, failure to thrive (in children) and perianal sepsis
temporary ileostomy to allow time for affected areas to rest
resection at worst areas, but can result in short bowel syndrome (leading to diarrhoea and malabsorption)

Answer 179

A

Coeliac: duodenum
UC: colon; starts at rectum and goes up, stops at ileocaecal valve
Crohn’s: whole GI tract: mouth to anus, affects other places more often than UC

Answer 180

A

Coeliac: jejunal biopsy via endoscopy; flattened villi and deeper crypts
UC: no skip lesions, circumferential and continuous inflammation, not transmural
Crohn’s: cobblestoning of mucosa, skip lesions, scattered inflammation, transmural

Answer 181

A

arrest/blockage of onward propulsion of intestinal contents

Answer 182

A

according to site
extent of luminal obstruction (partial or complete)
according to mechanism (mechanical, true or functional)
according to pathology

Answer 183

A

simple
closed loop
strangulation
intussusception

Answer 184

A

tumour: carcinoma or lymphoma
diaphragm disease
meconium ileus - in neonates, content of bowel is sticky = blockage
gallstone ileus; gallstone within lumen of small bowel

Answer 185

A

Crohn’s disease

- diverticulitis

Answer 186

A

usually occurs in the sigmoid colon
diverticula forms at gaps in the wall of the gut where blood vessels penetrate
in a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases
this pressure increases, pushes the mucosa through the gaps which results in a diverticula or outpouching
this can get inflamed or burst resulting in acute peritonitis and possible death

Answer 187

A

birth defect in which nerves are missing from parts of the intestine
• neonates are born without complete innervation of
colon to rectum
• results in gut dilatation and the filling of faeces which remains since there are no ganglion cells to result in peristalsis and movement of contents; results in obstruction

Answer 188

A

sticking together of abdominal structures to one another, bowel loops, omentum, other solid organs or the abdominal wall by fibrous tissue
commonly occurs after surgery
in the intestines, the loops of the small and large intestines can normally move around freely within the abdominal cavity
when adhesions form, the intestines are no longer able to move around freely because they become tethered to each other, the abdominal wall or to other abdominal organs
at the sites where the adhesions occur, the intestine can twist on itself, resulting in the obstruction of blood supply or the normal movement of the contents of the intestines, the small intestine in particular

Answer 189

A

adhesions (80%)

Answer 190

A

a twist/rotation of segment of bowel which is on a long mesentery can twist on itself, resulting in obstruction
always occurs at the part of bowel with a mesentery
type of closed loop bowel obstruction

Answer 191

A

most intestinal obstruction is due to a mechanical block
intestinal obstruction is one of the most common causes of hospital admission
tinkling bowel sounds and tympanic percussion is typical of obstruction

Answer 192

A

accounts for 60-75% of intestinal obstruction
majority is caused by previous surgery (60%)
Crohn’s disease is also a significant cause (25%)

Answer 193

A

• adhesions (60%):
- usually secondary to previous abdominal surgery
- increased incidence in; pelvic, gynaecology and colorectal surgery
• hernia:
- abnormal protrusion of an organ or tissue out of the body cavity in which it normally lies
- particularly in the developing world
- untreated can result in strangulation
• malignancy
• Crohn’s disease

Answer 194

A

mechanical obstruction is most common e.g. adhesions, hernia and Crohn’s
obstruction of the bowel leads to bowel distension above the block with increased secretion of fluid into the distended bowel
also leads to proximal dilatation above the block

Answer 195

A

increased secretions and swallowed air in the small bowel
more dilatation results decreased absorption and mucosal wall oedema
increased pressure with the intramural vessels becoming compressed resulting in ischaemia and or perforation

Answer 196

A

ischaemia
necrosis
perforation

Answer 197

A

pain; initially colicky (starts and stops abruptly) then diffuse, pain is higher in the abdomen than in LBO
profuse vomiting that follows pain; vomiting occurs earlier in SBO compared to LBO
less distension compared to LBO (since the more distal the obstruction, the greater the distension)
nausea and anorexia
tenderness suggests strangulation and urgent surgery is required
constipation with no passage of wind occurs late in SBO
increased bowel sounds

Answer 198

A

abdominal X-ray:
• shows central gas shadows that completely cross the lumen and no gas in the large bowel
• distended loops of bowel proximal to obstruction
• fluid levels seen
examination of hernia orifices and rectum
FBC
CT: gold standard to localise lesion accurately

Answer 199

A

aggressive fluid resuscitation
bowel decompression
analgesia and antiemetics
antibiotics
surgery to remove obstruction done by laparotomy

Answer 200

A

less common, accounting for only 25% of all intestinal obstruction

Answer 201

A

large bowel has a larger lumen as well as circular and longitudinal muscles thus the ability of the large bowel to distend is much greater thus symptoms present slower and later than in SBO
about 5 days of symptoms

Answer 202

A

90% due to colorectal malignancy in US/Europe

* in African countries the cause is more likely to be volvulus

Answer 203

A

the colon dilates proximal to the obstruction
there is increased colonic pressure and decreased mesenteric blood flow resulting in mucosal oedema; transudation of fluid and electrolytes from the lumen
this can compromise the arterial blood supply and also cause mucosal ulceration resulting in full thickness necrosis as well as perforation
bacterial translocation can also occur resulting in sepsis

Answer 204

A

there is axis rotation off of mesentery and a 360 degree twist results in a closed loop obstruction
fluid and electrolytes shift into the closed loop
this results in increased pressure and tension in the loop causing impaired colonic blood flow
ischaemia, necrosis and perforation of the loop of the bowel soon follows if untreated

Answer 205

A

abdominal pain that is more constant than in SBO
abdominal distension
bowel sounds normal then increased then quiet later
palpable mass e.g. hernia, distended bowel loop or caecum
late vomiting which is more faecal like; suggestive of LBO
vomiting may be absent
constipation
fullness/bloating/nausea

Answer 206

A

digital rectal exam
FBC essential: see low Hb as a sign of chronic occult blood loss
abdominal X-ray
CT

Answer 207

A

empty rectum, hard stools, blood

Answer 208

A

peripheral gas shadows proximal to the blockage e.g. in caecum but not in the rectum, unless PR examination done (this is always essential)
caecum and ascending colon distended

Answer 209

A

aggressive fluid resuscitation
bowel decompression
analgesia and antiemetics
antibiotics
surgery to remove obstruction is done by laparotomy
• obstruction due to malignancy requires colorectal stents followed by elective surgery

Answer 210

A

clinical picture mimicking obstruction but with no mechanical cause

Answer 211

A

intra-abdominal trauma
pelvic, spinal and femoral fractures
postoperative states e.g. abdominal, pelvic, cardiothoracic, orthopaedic and neuro
intra-abdominal sepsis
pneumonia
drugs e.g. opiates, antidepressants
metabolic disorders e.g. electrolyte disturbances, malnutrition, diabetes mellitus and Parkinson’s disease

Answer 212

A

patients present with rapid and progressive abdominal distension and pain

Answer 213

A

X-ray shows a gas-filled large bowel

Answer 214

A

treat underlying problem e.g. withdrawal of opiate analgesia
IV neostigmine

Answer 215

A

acute mesenteric ischaemia
chronic mesenteric ischaemia
ischaemic colitis (aka chronic colonic ischaemia)

Answer 216

A

usually seen in those over 50

- almost always involves the small bowel

Answer 217

A

superior mesenteric artery (SMA) thrombosis; commonest cause
superior mesenteric artery (SMA) embolism (e.g. due to AF); rarer now
mesenteric vein thrombosis; common in younger patients with hypercoagulable states and tends to affect small lengths of bowel
non-occlusive disease; occurs in low flow states and reflects poor cardiac output

Answer 218

A

acute severe abdominal pain; tends to be constant, central or around the right iliac fossa
no abdominal signs
rapid hypovolaemia resulting in shock; pale skin, weak rapid pulse, reduced urine output, confusion
note: the degree of illness is often far out of proportion with clinical signs

Answer 219

A

raised Hb due to plasma loss
raised WCC
persistent metabolic acidosis

Answer 220

A

used to rule out other pathology

* see gasless abdomen

Answer 221

A

laparotomy:
• to make diagnosis
• may see necrotic bowel if not treated quickly
CT/MRI angiography:
• provides non-invasive alternative to simple arteriography

Answer 222

A

fluid resuscitation
antibiotics e.g. IV gentamicin and IV metronidazole
IV heparin to reduce clotting
surgery to remove dead bowel

Answer 223

A

septic peritonitis
systemic inflammatory response syndrome (SIRS) progressing into a multi-organ dysfunction syndrome, mediated by bacteria translocation across the dying gut wall

Answer 224

A

medical condition in which inflammation and injury of the large intestine result from inadequate blood supply
usually follows low flow in the inferior mesenteric artery (IMA) territory and ranges from mild ischaemia to gangrenous colitis

Answer 225

A

older age group usually
related to underlying atherosclerosis and vessel occlusion
in young population is associated with women taking contraceptive pill, thrombophilia and vasculitis

Answer 226

A

thrombosis
emboli
decreased cardiac output and arrhythmias
drugs e.g. oestrogen, antihypertensives, vasopressin
surgery e.g. cardiac bypass, aortic dissection and repair, aortoiliac reconstruction
vasculitis e.g. SLE, sickle cell disease and polyarthritis nodosa (hep B and C)
coagulation disorders
idiopathic

Answer 227

A

contraceptive pill
nicorandil drug
thrombophilia
vasculitis

Answer 228

A

occlusion of branched of the superior mesenteric artery (SMA) or inferior mesenteric artery (IMA), often in the older age group
the anatomy of the vascular supply to the colon results in a watershed area at the splenic flexure, which is thus the most common site affected

Answer 229

A

sudden onset lower left side abdominal pain
passage of bright red blood with/without diarrhoea
may be signs of shock (pale skin, weak rapid pulse, reduce urine output, confusion) and evidence of underlying cardiovascular disease

Answer 230

A

other causes of acute colitis, e.g. IBD

Answer 231

A

urgent CT scan to exclude perforation
flexible sigmoidoscopy: biopsy shows epithelial cell apoptosis
colonoscopy and biopsy - gold standard:
• only done after patient has fully recovered to exclude stricture formation at the site of disease and confirm mucosal healing
barium enema: thumb printing of submucosal swelling at splenic flexure

Answer 232

A

most patients settle on symptomatic treatment
fluid replacement
antibiotics to reduce infection risks due to translocation of bacteria across possibly dying gut wall
most recover but strictures are common

Answer 233

A

presenting with peritonitis and hypovolaemic shock
requires prompt resuscitation followed by surgical resection of the affected bowel and stoma formation
high mortality

Answer 234

A

disrupted and dilated anal cushions masses of spongy vascular tissue due to swollen veins around the anus
- the anus is lined by discontinuous masses of spongy vascular tissue (the anal cushions) which contribute to anal closure

Answer 235

A

prevalence increases with age with a peak in 45-65 year olds
equally common in both males and females

Answer 236

A

constipation with prolonged straining is a key factor
diarrhoea
effects of gravity due to posture
congestion from a pelvic tumour, pregnancy, portal hypertension
anal intercourse

Answer 237

A

the normal/healthy anus is lined by discontinuous masses of spongy vascular tissue (anal cushions), which contribute to anal closure
they are attached by smooth muscle and elastic tissue but are prone to displacement and disruption, either singly or together
the effects of gravity (erect posture), increased anal tone (possibly due to stress) and the effects of straining when defecating may make them become both bulky and loose, and protrude to form piles
they are vulnerable to trauma (e.g. from hard stools) and bleed readily from the capillaries of the underlying lamina propria
since blood loss is from capillaries, it is bright red
since there are no sensory fibres above the dentate line (squamomucosal junction), piles are not painful unless they thrombose when they protrude and are gripped by the anal sphincter, blocking venous return
there is a vicious circle; the vascular cushions protrude through a tight anus → become more congested and hypertrophy → protrude again more readily
these protrusions may then strangulate

Answer 238

A

effects of gravity (erect posture)
increased anal tone (possibly due to stress)
effects of straining when defecating

Answer 239

A

origin above the dentate line (internal rectal plexus)

Answer 240

A

1st: remain in rectum
2nd: prolapse through the anus on defecation but spontaneously reduce
3rd: prolapse but can be reduced manually
4th: remain persistently prolapsed

Answer 241

A

originate below the dentate line (internal rectal plexus)
may be visible externally
extremely painful since there is sensory nerve supply below the dentate line

Answer 242

A

bright red rectal bleeding (since there is blood from the capillaries) that often coats stools, seen on tissue or drips into toilet
mucus discharge and pruritus ani (itchy bottom)
severe anaemia may occur
weight loss and change in bowel habit should prompt thoughts of pathology

Answer 243

A

perianal haematoma
anal fissure
abscess
tumour

Answer 244

A

abdominal examination to rule out other disease
PR (per rectum) exam:
• prolapsing piles are obvious
• internal haemorrhoids are not palpable
proctoscopy to see internal haemorrhoids
sigmoidoscopy to see rectal pathology higher up

Answer 245

A

increase fluid and fibre

* topical analgesic and stool softener

Answer 246

A

rubber band ligation: cheap, produces an ulcer to anchor the mucosa (side effects are bleeding, infection and pain)
infra-red coagulation: locally coagulates vessels and tethers mucosa to subcutaneous tissue

Answer 247

A

excisional haemorrhoidectomy

- stapled haemorrhoidopexy

Answer 248

A

treated with analgesia, ice packs and stool softeners

* pain usually resolved in 2-3 weeks

Answer 249

A

chronic abnormal communication between the epithelialised surface of the anal canal and usually the perianal skin
narrow tunnel with its internal opening in the anal canal and its external opening in the skin near the anus
blockage of deep intramuscular gland ducts is thought to predispose to the formation of accesses, which discharge to form the fistula

Answer 250

A

perianal sepsis
abscesses
Crohn’s
TB
diverticular disease
rectal carcinoma

Answer 251

A

pain
discharge (blood or mucus)
pruritus ani
systemic abscess if it becomes infected

Answer 252

A

MRI:
• to exclude sepsis
• to detect associated conditions e.g. Crohn’s or TB

endoanal ultrasound:
• to determine track location and underlying causes

Answer 253

A

fistulotomy and excision

- drain abscess with antibiotics if infected

Answer 254

A

a break or tear in the skin of the anal canal

- painful tear in the sensitive skin-lined lower anal canal, distal to the dentate line resulting in pain on defecation

Answer 255

A

90% are posterior
anterior ones follow childbirth
females affected more than males
can be an isolated primary problem in young middle-aged adults or can occur in associated with Crohn’s or ulcerative colitis

Answer 256

A

hard faeces
spasm may constrict the inferior rectal artery resulting in ischaemia which makes healing difficult and exacerbates the problem

Answer 257

A

syphilis
herpes
trauma
Crohn’s
anal cancer

Answer 258

A

extreme pain especially on defecation

- bleeding

Answer 259

A

can usually be made on history alone
confirmed on perianal inspection
rectal examination is often not possible due to pain and sphincter spasm

Answer 260

A

increase dietary fibre and fluids to make stools softer
lidocaine ointment + GTN ointment or topical diltiazem
botulinum toxin injection (2nd line)
surgery if medication fails

Answer 261

A

abscess (collection of pus that has built up within the body) adjacent to the anus

Answer 262

A

2/3 times more common in gay sex and in those who have anal sex

Answer 263

A

painful swellings
tender
discharge

Answer 264

A

MRI

- endoanal ultrasound

Answer 265

A

surgical excision

- drainage with antibiotics

Answer 266

A

hair follicles get stuck under the skin in the natal cleft resulting in irritation and inflammation leading to small tracts which can become infected (abscess)

Answer 267

A

much more common in males than females

- commonly presents between 20-30 yrs

Answer 268

A

obese caucasians and those from Asia, Middle East and Mediterranean are at increased risk
large amount of body hair
sedentary job
occupation involving sitting or driving
family history

Answer 269

A

the ingrowing of hair triggers a foreign body reaction and may cause secondary tracks to open laterally with or without abscesses, with foul-smelling discharge

Answer 270

A

painful swelling over days
pus filled with foul smell from abscess
systemic signs of infection

Answer 271

A

4 in 10 have repeated recurrent pilonidal sinus

* infection never clears completely

Answer 272

A

detected on clinical examination

Answer 273

A

surgery:
• excision of the sinus tract and primary closure and pus drainage
• pre-op antibiotics
hygiene and hair removal advice (near sinus)

Answer 274

A

a mixed group of abdominal symptoms without any evidence of underlying damage/organic cause

Answer 275

A

age of onset is under 40
more common in females than males
common, in western world around 1 in 5 report symptoms consistent with IBS
symptoms are exacerbated by stress, food, gastroenteritis or menstruation

Answer 276

A

depression, anxiety
psychological stress and trauma
GI infection
sexual, physical or verbal abuse
eating disorders

Answer 277

A

IBS-D: diarrhoea
IBD-C: constipation
IBS-M: diarrhoea and constipation
IBS-U: neither diarrhoea nor constipation are common

Answer 278

A

female
previous severe and long diarrhoea
high hypochondrial anxiety and neurotic score at time of initial illness

Answer 279

A

altered gut microbiota
abnormal gut motility
autonomic nervous dysfunction
visceral hypersensitivity
genetic factors
mood/stress/psychological morbidity
dysfunction in the brain-gut axis results in disorder of intestinal motility and/or visceral hypersensitivity

Answer 280

A

painful period
urinary frequency, urgency, nocturia and incomplete emptying of bladder
back pain
joint hypermobility
fatigue

Answer 281

A

A: abdominal pain or discomfort
B: bloating
C: change in bowel habit

Answer 282

A

• abdominal pain that is either relieved by defecation or is associated with altered stool form or bowel frequency (constipation and diarrhoea
may alternate) AND:
• there are 2 or more of:
- urgency
- incomplete evacuation
- abdominal bloating/distension
- mucous in stool
- worsening symptoms after food
• other symptoms: nausea, bladder symptoms and backache
• symptoms are chronic (more than 6 months) and exacerbated by stress, menstruation or gastroenteritis (post-infection IBS)
• general abdominal tenderness

Answer 283

A

unexplained weight loss
PR bleed/blood in stool
family history of bowel or ovarian cancer
change in bowel habit and aged over 50
nocturnal symptoms
rectal or abdominal mass
anaemia
raised inflammatory markers
if any found then refer to secondary care for further investigations

Answer 284

A

coeliac disease (5% of IBS patients)
lactose intolerance (esp. in IBS-D)
bile acid malabsorption
IBD
colorectal cancer

Answer 285

A

• FBC to look for anaemia
• ESR and CRP to look for inflammation
• coeliac serology testing for endomysial antibody (EMA) and tissue transglutaminase antibody (tTG)
- if either positive then there is a high chance of coeliac disease

Answer 286

A

since there is nothing physical to be found, diagnosis is made by ruling out the differentials
bloods
faecal calprotectin is raised in IBD
colonoscopy to rule out IBD or colorectal cancer
Rome III diagnostic criteria

Answer 287

A

recurrent abdominal pain or discomfort at least 3 days a month in the past 3 months, associated with two or more of the following:

improvement with defecation
onset associated with a change in frequency of stool
onset associated with a change in form (appearance) of stool

Answer 288

A

education
reassurance
dietary modification

Answer 289

A

pharmacotherapy

* psychological treatment

Answer 290

A

referral to pain treatment centre

Answer 291

A

• regular or small frequent meals
• plenty of fluids (8 cups/day)
• reduce/avoid caffeinated drinks, alcohol and fizzy drinks
• for IBS-D and bloating, reduce/avoid:
- insoluble fibre intake
- fruit intake to 3 portions/day
• for wind and bloating, increase soluble fibre intake
• fibre

Answer 292

A

good for constipation (IBS-C)
dissolves in water and is broken down by bacteria
softens stool
slows down sugar release
e.g. barley, oats, beans, prunes, figs

Answer 293

A

makes IBS-D worse so should be cut down
not dissolved in water
passes through the gut mostly unchanged
absorbs water and bulks up faeces
increases gut motility
e.g. cereals, whole-wheat bread, lentils, apple, avocado

Answer 294

A

fermentable
oligosaccharides
disaccharides
monosaccharides
and
polyols
all produce a lot of gas, bloating, diarrhoea and pain
e.g. apple, artichoke, cottage cheese, baked beans, cow milk

Answer 295

A

antispasmodics e.g. Mebeverine or Buscopan

Answer 296

A

laxative e.g. mavicol, sodiumdocusate or senna
linaclotide only used for constipation lasting for more than 12 months and not relieved by 2 different classes of max dose laxatives
can also use 5-HT4 receptor agonist e.g. prucalopride

Answer 297

A

anti-motility agents e.g. loperamide

Answer 298

A

tricyclic antidepressants e.g. amitriptyline or nortriptyline
but warn about drowsiness
need to take it for 4-6 weeks to take effect
not to treat depression but to dampen down gut sensitivity
if not tolerated then move to SSRI
can also use psychological therapy in conjunction

Answer 299

A

IBS:

normal investigation results
persistant/fluctuating symptoms
wouldn’t really get fever
no symptoms outside GI tract
no blood in stool
no melaenea
food triggers
no weight loss
no mouth ulcers
constipation more common
exacerbated by stress
bloating

IBD

abnormal investigation results
persistent/fluctuating symptoms
more likely to get fever
symptoms outside GI tract
blood in stools
melaena (black stool)
food triggers
weight loss
mouth ulcers
constipation but less common than in IBS
can be exacerbated by stress
bloating much less common than in IBS

Answer 300

A

a GI diverticulum is an outpouching of the gut wall, usually at sites of entry of perforating arteries

Answer 301

A

presence of diverticula

Answer 302

A

caused by diverticula that are symptomatic

Answer 303

A

inflammation of a diverticulum

Answer 304

A

frequently found in the colon and occur in 50% of patients over the age of 50 yrs
they are most frequent in the sigmoid colon, but can be present throughout the whole colon
diverticula can be acquired or congenital and may occur elsewhere but the most important are acquired colonic diverticula
rare in the young
95% are asymptomatic

Answer 305

A

• low fibre diet:
- commonly eaten in developed countries
- rare in rural Africa
• obesity
• smoking
• NSAIDs

Answer 306

A

low-fibre diet

- over age of 50

Answer 307

A

diverticula form at gaps in the wall of the gut where blood vessels penetrate
in a low fibre diet, the colon must push harder to move things along (fibre helps gut motility) so pressure increases
this pressure increase results in pouches of mucosa being extruded through the muscular wall through weakened areas near blood vessels leading to diverticula formation
there is also thickening of the muscle layer

Answer 308

A

occurs when faeces obstruct the neck of the diverticulum, causing stagnation and allowing bacteria to multiply and produce inflammation
this can then lead to bowel perforation (peridiverticulitis), abscess formation, fistulae into adjacent organs, haemorrhage and generalised acute peritonitis and possibly death

Answer 309

A

• asymptomatic in 95% of cases and is usually detected incidentally on colonoscopy or barium enema examination
• in symptomatic cases:
- intermittent left iliac fossa pain
- erratic bowel habit
• in severe cases:
- severe pain and constipation due to luminal narrowing

Answer 310

A

most commonly affects diverticula in the sigmoid colon
severe pain in the left iliac fossa
fever and constipation
symptoms are similar to those of appendicitis but are located on the left side

Answer 311

A

febrile
tachycardia
abdominal examination:
• tenderness, guarding and rigidity on the left side of the abdomen
• a palpable tender mass is sometimes felt in the left iliac fossa

Answer 312

A

perforation
fistula formation
intestinal obstruction
bleeding
mucosal inflammation

Answer 313

A

usually occurs in association with acute diverticulitis
can lead to paracolic or pelvic abscess or generalised peritonitis
rurgery may be required

Answer 314

A

fistula formation into:

the bladder resulting in dysuria or pneumaturia (gas or air in urine resulting in bubbles)
the vagina resulting in discharge

Answer 315

A

usually after repeated episodes of acute diverticulitis

Answer 316

A

sometimes this is massive
in most cases the bleeding stops and the cause is established by colonoscopy and sometimes angiography
in some cases emergency segment colectomy is required

Answer 317

A

occurs in areas of diverticula, giving the appearance of Crohn’s on endoscopy

Answer 318

A

in the absence of clinical signs of acute diverticulitis (i.e. excluding this) then colonoscopy is best option

Answer 319

A

polymorphonuclear leucocytosis

- ESR and CRP raised

Answer 320

A

best for diagnosis
will show colonic wall thickening and diverticula
also pericolic collections and abscesses
findings above are diagnostic for acute diverticulitis and differ from those of malignant disease
sigmoidoscopy or colonoscopy are not performed during an acute attack

Answer 321

A

may identify obstruction or free air (indicative of perforation)

Answer 322

A

can clarify diagnosis in patients with abdominal pain and altered bowel habit

Answer 323

A

in uncomplicated symptomatic disease a well-balanced high fibre diet with smooth muscle relaxants i.e. antispasmodics e.g. mebeverine is recommended

Answer 324

A

mild attacks can be treated with oral antibiotics e.g. ciprofloxacin and metronidazole
those with signs of systemic upset (fevers, tachycardia) and significant abdominal pain require bowel rest, IV fluids and IV antibiotics
surgical resection is occasionally required

Answer 325

A

true congenital diverticulum
slight bulge in the small intestine present at birth
vestigial remnant of the omphalomesenteric duct

Answer 326

A

affects 2-3% population

Answer 327

A

usually symptomless
in 50% of cases, the distal ileum contains gastric mucosa that secretes HCL, meaning peptic ulcers can occur which may bleed or perforate; causes GI pain
acute inflammation of the diverticulum also occurs and is clinically indistinguishable from acute appendicitis
treatment is surgical removal of diverticula, often laparoscopically

Answer 328

A

acute inflammation of the appendix
should be considered for all right sided pain if appendix is present in patient
located at McBurney’s point which lies 2/3 of the way from the umbilicus to the anterior superior iliac spine

Answer 329

A

lies 2/3s of the way from the umbilicus to the anterior superior iliac spine

Answer 330

A

most common surgical emergency
more common in males than females
can occur at any age although highest incidence is
between 10-20 yrs
rare before age of 2 since appendix is cone shaped with a larger lumen

Answer 331

A

faecolith
lymphoid hyperplasia
filarial worms

Answer 332

A

occurs when the lumen of the appendix becomes obstructed by lymphoid hyperplasia, filarial worms or a faecolith (most common) resulting in the invasion of gut organisms into the appendix wall
this leads to oedema, ischaemia, necrosis and perforation as well as inflammation
if the appendix ruptures then infected and faecal matter will enter the peritoneum resulting in life threatening peritonitis

Answer 333

A

pain in the umbilical region that migrates to the right iliac fossa, specifically McBurney’s point after a few hours
anorexia is important
nausea and vomiting and occasionally diarrhoea can occur
constipation is usual
examination of abdomen reveals tenderness in the right iliac fossa with guarding due to localised peritonitis
may be a tender mass in the right iliac fossa
patient is pyrexic

Answer 334

A

this is because the internal organs and the visceral peritoneum have no somatic innvervation, so the brain attributes the visceral signals to a physical location whose dermatome corresponds to the same entry level in the spinal cord; importantly, there is no laterality to the visceral unmyelinated C-fibre pain signals, which enter the cord bilaterally and at multiple levels
early inflammation irritates the structure and walls of the appendix, so a colicky pain is referred to the mid-abdomen around the umbilical area known as periumbilical pain
as the inflammation progresses and irritates the parietal peritoneum (especially on examination and palpation) the somatic, lateralised pain settles at McBurney’s point

Answer 335

A

acute terminal ileitis due to Crohn’s
ectopic pregnancy
UTI
diverticulitis
perforated ulcer
food poisoning

Answer 336

A

raised white cell count with neutrophil leucocytosis

* elevated CRP and ESR

Answer 337

A

can detect inflamed appendix and can also indicate an appendix mass or other localised lesion

Answer 338

A

highly sensitive and specific - gold standard for diagnosis
reduces risk of removal of a healthy appendix

Answer 339

A

pregnancy test

- urinalysis to exclude UTI

Answer 340

A

laparascopic appendicectomy
IV antibiotic pre-op to reduce wound infections e.g. IV metronidazole and IV cefuroxime
if appendix mass is present, the patient is usually treated with IV fluids and antibiotics until mass disappears over a few weeks; appendicectomy is recommended later to prevent further acute episodes

Answer 341

A

• perforation: commoner if faecolith present and in young children
• appendix mass:
- when an inflamed appendix becomes covered in omentum (thus forming a mass); ultrasound or CT can help diagnose
- treat with antibiotics and then surgery to remove appendix later to prevent further event
• appendix abscess:
- results if appendix mass fails to resolve but instead enlarges and the patient gets more unwell
- treat by draining appendix
- antibiotics

Answer 342

A

no ducts, secreted directly at site of action, secrete enzyme, short term activity
functional unit of the exocrine pancreas comprises of an acinus and its draining ductule
a ductule from the acinus drains into interlobar (intercalated) ducts, which in turn drain into the main pancreatic ductal system
the main pancreatic duct itself joins the common bile duct to enter the duodenum as a short single duct at the ampulla of Vater

Answer 343

A

acinar cells are responsible for the production of digestive enzymes e.g. amylase, lipase, colipase, phospholipase and the proteases (trypsinogen
and chymotrypsinogen)
these enzymes are released by acinar cells and are then transported into the duodenum via pancreatic secretions

Answer 344

A

ductless, released directly into blood, secrete hormones, long term activity
endocrine component is scattered through the gland in the form of pancreatic islets of Langerhans

Answer 345

A

alpha cell: glucagon production
beta cells: insulin production
D cells: somatostatin (inhibits acinar enzyme secretion) production
PP cells: pancreatic polypeptide (inhibits acinar enzyme secretion)
enterochrommaffin cells: serotonin production

Answer 346

A

process that occurs on the background of a previously normal pancreas and can return to normal after resolution of the episode
sudden inflammation of the pancreas

Answer 347

A

syndrome of inflammation of the pancreatic gland initiated by any acute injury
recurrent episodes if untreated
in most severe form (10% of all cases) mortality is 40% - 80%:
• extensive pancreatic and peripancreatic necrosis
• haemorrhage
difficult to differentiate between chronic and acute

Answer 348

A

I GET SMASHED

Idiopathic
Gallstones (majority - 60%)
Ethanol (30%)
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hyperlipidaemia
ERCP (endoscopic retrograde cholangiopancreatography)
Drugs e.g. azathioprine, furosemide (diuretics), corticosteroids, NSAIDs, ACE inhibitors
also pregnancy and neoplasia

Answer 349

A

acute pancreatitis is caused by the destructive effect of premature activation of pancreatic enzymes which causes self-perpetuating pancreatic inflammation by enzyme-mediated autodigestion
there are many mechanisms by which this can occur, with the majority being caused by gallstones and alcohol

Answer 350

A

accumulation of enzyme-rich fluid within the pancreas due to obstruction of the pancreatic duct by gallstones
intracellular Ca2+ increases and causes the early activation of trypsinogen
in this situation, trypsinogen is cleaved (by cathepsin B) to trypsin, and trypsin degradation (by chymotrypsin C) is impaired and overwhelmed leading to a buildup of trypsin and thus increased enzymatic digestion of the pancreas and inflammation leading to extensive acinar damage

Answer 351

A

alcohol is shown to interfere with Ca2+ homeostasis in increased stimulation of enzyme secretion and obstruction of the duct due to contraction of the ampulla of Vater

Answer 352

A

the prematurely activated enzymes also cause leaky vessels by digesting vessel walls in the pancreas leading to the leakage of fluid into the tissues causing oedema, inflammation and hypovolaemia (as extracellular fluid is trapped in the gut, peritoneum and retroperitoneum)
destruction of blood vessels by enzymes causes haemorrhage
destruction of the adjacent islets of Langerhans can result in hyperglycaemia as beta cells will be destroyed resulting in less insulin
lipolytic enzymes cause fat necrosis, which can result, if extensive and involving the anterior abdominal wall, in skin discolouration (Grey Turner’s sign)

Answer 353

A

the released fatty acids bind to Ca2+ ions, forming white precipitates in the necrotic fat
if this is very severe, it can result in hypocalcaemia, presenting with tetany

Answer 354

A

acute pancreatitis is a differential diagnosis in any patient with upper abdominal pain
gradual or sudden severe epigastric or central abdominal pain that radiates to the back; sitting forward may relieve this
anorexia, nausea and vomiting
tachycardia
fever
jaundice
dehydration
hypotension
abdominal guarding and tenderness on examination
Cullen’s sign
Grey Turner’s sign

Answer 355

A

periumbilical ecchymosis (skin discolouration due to blood under the skin due to bruising) 
- seen in acute pancreatitis

Answer 356

A

left flank bruising (skin discolouration due to blood under the skin due to bruising)
- seen in acute panreatitis

Answer 357

A

• raised serum amylase - 3-fold the upper limit of normal
- note: may be normal even in severe pancreatitis as levels fall after 3-5 days of acute event and other things can cause raised amylase e.g. upper GI perforation
• raised urinary amylase; may be diagnostic as levels remain elevated over long time period
• raised serum lipase; more sensitive and specific for pancreatitis than amylase
• CRP level for monitoring severity and prognosis

Answer 358

A

essential to exclude gastroduodenal perforation, which also raises serum amylase
may show gallstones or pancreatic calcification

Answer 359

A

to identify extent of pancreatic necrosis

Answer 360

A

identifies degree of pancreatic damage

* useful in differentiating fluid and solid inflammatory masses

Answer 361

A

used as a predictor of severity and prognostic tool
Glasgow and Ranson scoring systems
APACHE II (Acute Physiology And Chronic Health Evaluation)

Answer 362

A

uses various factors such as; age, neutrophils, calcium and blood glucose etc to predict a severe attack
80% sensitive, although only after 48 hours from presentation

Answer 363

A

Acute Physiology And Chronic Health Evaluation

used to assess severity
based on common physiological and laboratory values, age and presence/absence of chronic conditions e.g. obesity
has a high sensitivity and can be applied as early as 24 hours after symptom onset

Answer 364

A

severity assessment is essential
nil by mouth - nasogastric tube for dietary supplements (as less pancreatic enzymes are released so need to support patients nutritionally!) to decrease pancreatic stimulation
urinary catheter
analgesia e.g. IM pethidine or IV morphine
drainage of collections may be required
prophylactic antibiotics e.g. cefuroxime or metronidazole to reduce risk of infected pancreatic necrosis

Answer 365

A

systemic inflammatory response syndrome (SIRS)

Answer 366

A

systemic inflammatory response syndrome

proinflammatory state
any two of: tachycardia, tachypnoea, pyrexia with temp >38, high WCC

Answer 367

A

debilitating continuing inflammatory process of the pancreas resulting in progressive loss of exocrine pancreatic tissue which is replaced with by fibrosis

Answer 368

A

worldwide prevalence is around 4-5%
males affected more than females
median age of presentation is 51

Answer 369

A

commonest cause in the developed world is long-term alcohol excess (60-70%)
chronic kidney disease
hereditary: defects in the trypsinogen gene or cystic fibrosis
autoimmune pancreatitis - raised IgG4 (seen in many autoimmune disorders) triggers pancreatitis
idiopathic
trauma
recurrent acute pancreatitis

Answer 370

A

obstruction or reduction in bicarbonate secretion, which produces an alkaline pH which in turn stabilises trypsinogen, leads to the activation of trypsinogen as pH rises making it more unstable and causing its activation into trypsin which leads to pancreatic tissue necrosis with eventual fibrosis
abnormalities of bicarbonate excretion can be the result of functional defects at the level of the cellular wall e.g. cystic fibrosis or mechanical as in trauma
increased intrapancreatic enzyme activity leads to the precipitation of proteins within the duct lumen in the form of plugs
these plugs then become calcified resulting in ductal obstruction and further pancreatic damage
alcohol increases trypsinogen activation and also causes proteins to precipitate in the ductal structure of the pancreas leading to local pancreatic dilatation and fibrosis
note: the vast majority of people drinking excess alcohol do not develop pancreatitis - this suggests that the disease process is a complex interaction of different mechanisms

Answer 371

A

epigastric pain that ‘bores’ through to the back:
• can be episodic or unremitting; can be relieved by sitting forward
• exacerbated by alcohol
nausea and vomiting
decreased appetite
exocrine dysfunction
endocrine dysfunction

Answer 372

A

epigastric pain that bores through to the back
• can be episodic or unremitting; can be relieved by sitting forward
• exacerbated by alcohol

Answer 373

A

malabsorption (presenting feature in absence of pain) with:

weight loss
diarrhoea
steatorrhoea (pale, loose, fatty, foul smelling stools that float)
protein deficiency

Answer 374

A

pancreatic malignancy - lots of common symptoms should be thought of especially when there is a short history and pancreatic mass

Answer 375

A

serum amylase and lipase: may be elevated, but in advanced disease, there may not be sufficient residual acinar cells to produce elevation
faecal elastase will be abnormal in majority of patients with moderate-severe disease
abdominal ultrasound and contrast-enhance CT:
• detects pancreatic calcification and a dilated pancreatic duct to confirm diagnosis
MRI with MRCP to identify more subtle abnormalities

Answer 376

A

alcohol cessation
abdominal pain:
• NSAIDs
• opiates e.g. oral tramadol
• tricyclic antidepressants e.g. amitryptiline
duct drainage
shock wave lithotripsy to fragment gallstones in the head of pancreas
steatorrhea:
• pancreatic enzyme supplements
• PPIs help supplement pass stomach
diabetes: insulin

Answer 377

A

chronic pancreatic inflammation which results from an autoimmune process

Answer 378

A

high prevalence in Japan

Answer 379

A

presentation is very similar to normal chronic pancreatitis
there are elevated levels of serum gammaglobulins and immunoglobulin G (IgG) levels - IgG4
autoantibodies such as antinuclear cytoplasmic antibody (ANCA) and rheumatoid factor may also be elevated

Answer 380

A

this condition is steroid responsive with glucocorticoid therapy e.g. oral prednisolone for 4-6 weeks

Answer 381

A

the ALT/AST ratio is a useful clinical indicator.
in viral hepatitis, ALT > AST unless cirrhosis is present, when AST > ALT.
in alcoholic liver disease and steatohepatitis the AST is often greater than the ALT.
thus in patients with viral hepatitis, an AST/ALT ratio > 1 indicates cirrhosis, and in patients without cirrhosis in whom AST > ALT, alcohol or obesity should be considered the most likely cause.

Answer 382

A

the origin can be determined by electrophoretic separation of isoenzymes or bone-specific monoclonal antibodies.
however, if the γ-GT is also abnormal, the ALP is presumed to come from liver

Answer 383

A

this is a microsomal enzyme present in liver and many other tissues.
activity can be induced by drugs such as phenytoin, warfarin and alcohol.
if the ALP is normal, a raised serum γ-GT can be a useful guide to alcohol intake.
however, mild elevation of γ-GT is common, even with minimal alcohol consumption, but it is raised in fatty liver disease.
in the absence of other liver function test abnormalities, a slightly raised γ-GT can safely be ignored

Answer 384

A

the globulin fraction is often raised in autoimmune hepatitis and a fall indicates successful therapy.

Answer 385

A

hepatocellular injury

Answer 386

A

indicates a cholestatic disorder such as primary biliary cirrhosis, primary sclerosing cholangitis or extrahepatic bile duct obstruction

Answer 387

A

most likely due to Gilbert’s disease

Answer 388

A

careful history (alcohol consumption, exposure to hepatotoxic drugs, risk factors for chronic liver disease)
physical examination (features of chronic liver diseases)
simple laboratory tests (viral hepatitis, metabolic and autoimmune liver disease)
ultrasound

Answer 389

A

lack of digestive enzymes - decetive intraluminal digestion

Answer 390

A

pancreatic insufficiency - pancreatitis + - defective bile secretion - bile obstruction + ileal reesection - bacterial overgrowth

Answer 391

A

gliadin in wheat presented to APC -> formation of toxic T cells + gliadin antibodies –> enterocyte injury -> loss of epithelial cells –> malabsorption due to loss of absorptive area.

Answer 392

A

IBS - bowel 2. functional dyspepsia - stomach

Answer 393

A

chronic GI symtpoms in the absence of organic disease to explain the symptoms

Answer 394

A

True linked to hormonal changes

Answer 395

A

gastric symptoms in the upper abdomen

Answer 396

A

gastric symptoms in the upper abdomen

Answer 397

A

chronic frequent abdo pain - altered bowel habit - bloating communly associated

Answer 398

A

True - IBS symptoms are v similar to coeliac, so should be ruled out

Answer 399

A

ovarian - Ca-125 test - coeliac TTA/G??

Answer 400

A

Age >45 years
Short history of symptoms
Documented unintentional weight loss
Nocturnal symptoms
Family history of Gl cancer/IBD
GI Bleeding
Palpable abdominal mass or lymphadenopathy
Evidence of iron deficiency anemia on blood testing
Evidence of inflammation on blood/stool testing

Answer 401

A

FALSE

IBD pts will experience symptoms all through the night while IBS pts won’t as its a disorder linking the brain and the gut so one the brain sleep so does the gut

Answer 402

A

marker of gut inflammation

Answer 403

A

IBS that occurs after an bout of gastroenteritis.

Answer 404

A

abdominal pain at least 1 day per week with 2 or more of these symptoms:
- symptoms related to defecation
- associated with change in frequency of stools
- associated with change in forms of stools

Answer 405

A

alcohol
tobacco use
Barretts oesophagus
obesity
acid reflux
physical activity.

Answer 406

A

oesophageal motility disorder where there is no peristalsis in the oesophagus + the lower oesophageal sphincter is unable to relax in response to swallowing.

Answer 407

A

non-progressive dysphagia - difficulty swallowing solids + liquids
chesty retro-sternal pain
cough caused by regurgitation
cough when laying down
- weight loss due to reduced intake

Answer 408

A

initially: CCBs and nitrates to help lower pressure around LOS - usually ineffective and just while pt waits for definitive tx:

surgery
endoscopic balloon stent

Answer 409

A

ischamia of the colon’s arterial supply → colonic inflammation due to hypoperfusion

Answer 410

A

the inferior mesenteric artery

Answer 411

A

non-occlusive: reduced perfusion = most common
- heart failure due to reduced cardiac output
- septic shock
- PVD
- cocaine use
- recent CABG
occlusive
- thrombus
- embolus
- tumour, volvulus, hernia

Answer 412

A

transient LLQ pain
bright bloody stool
may have signs of hypovolaemic shock

Answer 413

A

GS = colonoscopy + biopsy

other: AXR= not diagnostic but may show ‘thumbprinting

Answer 414

A

depends on presentation but usually

non-occlusive cause improves with supportive management
- IV fluids
- ABX
- nil by mouth + NG tube
- treatment of underlying cause.
occlusive causes may need surgery
gangrene → surgery

Answer 415

A

ischamia of the small intestine caused by thrombus or embolus blocking the superior mesenteric artery.
types:
- acute → acute attack
- chronic → lasts over months

Answer 416

A

Foregut
- Stomach and part of duodenum, biliary system, liver, pancreas
- Celiac artery
Midgut
- Duodenum to 1st half of transverse colon
- Superior mesenteric artery
Hindgut
- 2nd half of transverse colon to rectum
- Inferior mesenteric artery

Answer 417

A

symptoms
- abdominal pain
  - Acute ischaemia: severe, out of proportion to abdominal signs
  - Chronic ischaemia: colicky, intermittent, post-prandial and described as ‘intestinal angina’.
- N+V
- diarrhoea
- fever
signs
- NO abdominal signs e.g. guarding or rebound tenderness.
- severe pain not proportional to clinical findings
- hypotension + tachycardia - rapid hypovolemic shock.
- bleeding on rectal exam

Answer 418

A

CT angiogram = gold standard: shows the site of occlusion + the extent of necrosis and ischeamia.
ECG: as AF is the most common cause of acute mesenteric ischaemia.
FBC + ABG: looking for anaemia + persistent metabolic acidosis

Answer 419

A

chronic = management of CVD risk +/or elective procedures
acute
- initial management
  - fluid resus, ABX, IV heparin
- definitive management
  - surgery: especially for infarcted/ necrotic bowel

Answer 420

A

bowel infarction +/or perforation
strictures
*

Answer 421

A

internal originate above the rectal plexus [dentate line]
- ∴ less painful as there is much less sensory supply.
- may feel tenesmus
external originate below the dentate line
- ∴ extremely painful as there is more innervation.
  - pts struggle to sit

Answer 422

A

bright red PR blood
PAIN
mucus discharge
itching
swelling

Answer 423

A

swollen veins around the anus disrupting the anal cushions and potentially causing prolapse of anal cushions through the anal passage.

Answer 424

A

1st degree / mild
- Increase fibre and fluid intake
- Stool softeners
- Topical analgesia
- Topical steroids for short periods
2nd/ 3rd degree / definitive tx
- non-surgical = rubber band ligation
- surgery

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GI Flashcards

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