GI Flashcards
what does the upper GI tract involve
mouth, oesophagus, stomach and duodenum
what is the most common problem with the oesophagus
Barrett’s oesophagus (and oesophageal cancer )
what stops reflux into the oesophagus (2)
cardiac sphincter
diaphragm constricting around the lower oesophagus
why is it important that we prevent acid reaching the oesophagus
mucous is needed to protect epithelium from acid
only glandular epithelium has mucous (stomach)
if acid reaches non-mucous lined squamous epithelium of the oesophagus, it is destroyed and acid then can ulcerate the tissue
compare the epithelium of the oesophagus and the stomach
oesophagus = non-keratinised stratified squamous epithelium
stomach= non-keratinized simple columnar epithelium with mucous glands
how might we diagnose barrettes disease (4)
endoscopy
normal oesophageal tissue is white and reflective
if red tissue is found in the lower oesophagus, this is columnar epithelium from the stomach growing
what is barrettes oesophagus
where we get metaplasia from stratified squamous epithelium in the oesophagus to columnar epithelium from the stomach
what is another name for barretts oesophagus
columnar lined lower oesophagus - CELLO
explain the mechanism of barrettes oesophagus
IF the acid refluxes, acid goes into the oesophageal epithelium and these cells cannot cope with low pH so they die.
This leads to no epithelium, ulceration and pain.
Squamous epithelial CAN regrow but if the acid keeps refluxing, then we get metaplasia or growth from epithelium from the stomach into the oesophagus.
what might barrettes oesophagus predispose and why
barrettes oesophagus has columnar epithelium in the oesophagus
This is not meant to be and is genetically unstable so predisposes oesophageal cancer
constant acid attack will constantly damage tissue and also increase chances of cancer
why is adenocarcinoma of the oesophagus infinitely increased chances with people with barrettes oesophagus
people without barrettes oesophagus cannot get oesophageal adenocarcinomas as this is cancer of glandular tissue
normal oesophageal tissue is not glandular so cannot get adenocarcinoma
what are some risk factors for barrettes oesophagus (3)
increased wieght = abdominal pressure increase on stomach contents
male
late age >50
why might oesophageal cancers be eligibly on the rise (2)
ageing population and old onset so more diagnosis
no longer grouped with gastric cancers
in asia and africa there are very high levels of oesophageal cancers. compare this cancer to the type of oesophageal caner found in europe.
Asia and Africa are commonly squamous cell carcinomas due to alcohol and smoking
Europe are usually barrettes related = adenocarcinomas
compare oesophageal adenocarcinomas and squamous cell carcinomas
AC = barrettes oesophagus, reflux, weight, age, europe
SCC = asia, africa, smoking and alcohol
give 2 reasons why oesophageal cancer has low prognosis
often not diagnosed until late stage so low prog
very close to important structures e.g. trachea, aorta, vena cava so can have very bad consequences if metastatic
what is Helicobacter Gastritis caused by
Helicobacter Pylori H. Pylori
what is the strcutre of H.Pylori (3)
rod shaped bacilli
motile
flagellum
how is Helicobacter Gastritis caused (3)
hide in the mucous layer of stomach
This bacteria produces chemicals that attract in inflammatory cells eg. neutrophils into the stomach, causing acute inflammation.
This causes ulceration in the stomach allowing acid to reach under the epithelium.
where do H.Pylori live
mucous layer of the stomach
how do we treat Helicobacter Gastritis
1 week
Antibiotic e.g. metronidazole
why is the incidence of gastric cancer reducing with time (2)
oesophageal cancer no longer included in ‘gastric cancers’ and they made up a large proportion of this
less frying with cast rion pans that = nitrosamines = carcinogen
where do we find high gastric cancer incidence, why?
east asia and eastern europe
high amounts of smoked and pickled foods - acidic
how do we treat acid reflux (3)
anti-acids e.g. Gaviscon
proton pump inhibitors e.g. Omeprazole or Lansoprazole
surgery
what are some side effects of proton - pump inhibitors
prolonged use = kidney damage
alcoholics should not take
diarrhea
what carcinogen is produced by frying in cast iron
Nitrosamines
what 3 main things lead to intestinal metaplasia
smoked/pickled foods, helicobacter pylori (gastritis) pernicious anaemia
why is intestinal metaplasia of the stomach bad (3)
where intestinal epithelium grows into the distal stomach
genetically unstable epithelium that is not protected by mucous = high damage
predisposes dyplasia and cancer
what is another name for coeliac disease
Gluten sensitive enteropathy
what 3 changes to the intestines do we see with coeliac disease
villous atrophy
crypt hyperplasia
increased neutrophil count on surface epithelium
how does coeliac disease work (4)
autoimmunity to gliadin protein
Gliadin protein from gluten is absorbed
Gliadin is presented to APCs causing
Activation of toxic T cells
On second gluten exposure = toxins that kill epithelial cells and cause: crypt hyperplasia, villus atrophy and leukocytes in epithelium
what is the prevalence and treatment for coeliac
1% of population
avoidance of gluten
What are the 2 major chronic idiopathic inflammatory bowel diseases
Crohns disease
Ulcerative Colitis
what can inflammatory bowel disease be divided into (2)
chronic idiopathic (ulcerative colitis and crohns disease)
other
what is crohns disease (3)
chronic idiopathic IBD
patchy discontinuous inflammation of the bowel
affecting all parts of the GI tract from mouth to anus and all layers of the bowel (transmural)
where does Crohns disease effect
all segments of the bowel from mouth to anus and all layres of the bowel = transmureal
what histological markers are there of crohns disease
grnauloma inflammation
These are characterised by pinkish ‘epithelioid’ macrophages surrounded by lymphocytes, also found in TB.
a histological section shows granuloma tissue with pink epithelioid macrophages, what diseases might this be
TB - likely to be lungs
Crohns - GI
what clinical representations of the bowel might we see in Crohns disease (3)
patchy inflammation
Aphthous ulcers (can present in mouth)
cobblestoned effect on bowel due to fibrosis
what are some signs and symptoms of Crohns disease
abdominal pain
diarrhoea
fibrosis of bowel
aphthous ulcers in Gi tract and mouth
where does ulcerative colitis affect
This disease only affects the MUCOSA of the COLON.
It will start at the rectum and then extend further up the bowel. This, as opposed to crohn’s disease, is always continuous and can affect the whole colon.
what is a distincitve feature of ulcerative colitis inflammation
There will be a very distinct cut off between normal and inflamed mucosa. This disease only affects the mucosa of the large colon, it doesn’t spread into the submucosa, muscle or fat.
compare the location of inflammation between Crohns disease and Ulcerative Colitis
C: non-continuous, whole GI tract, all layers of tissue
UC: continuous, starts at anus, only affects colon, only affects mucosa
a patient has ulceration on their tongue and soft tissues and then an endoscopy shows ulceration in the oesophagus, what is the likely diagnosis and how could we confirm this
Crohn disease
biopsy showing granuloma formation ?
what is the treatment for ulcerative colitis
anti-inflammatories
immunosuppressants
what is Diverticular Disease
diverticular - outpouching of the mucosa - tending to occur in the sigmoid colon which is the part of the colon just before the rectum
where is diverticular disease likely to act
sigmoid colon - just next to the rectum
what is a diverticular
outpouching in the mucosa - affecting sigmoid colon within diverticular disease of the colon
how does diverticular disease occur
The bowel wall has small perforations for blood vessels to enter and supply the bowel.
A lack of fibre in the diet leads to a raised pressure in the bowel and this can cause diverticular disease. The less fibre in the bowel, the more pressure the muscles have to put on the contents to push it along and when the mucosa is pushed down into these perforations, they enter the muscular perforations forming outpouches.
what is a major risk factor for diverticular disease
lack of fibre in the diet
And age
why is diverticular disease dangerous
blind ended sacs which can get clogged up with faeces and get inflamed and possibly rupture which is very bad as faeces is released into the peritoneal cavity causing
Faecal peritonitis
what is a major risk factor for faecal peritonitis
diverticular disease
blind ended sacs which can get clogged up with faeces and get inflamed and possibly rupture which is very bad as faeces is released into the peritoneal cavity
what is faecal peritonitis
where faeces and contents of colon are released into the peritoneal space causing infection
how could we diagnose faecal peritonitis
found commonly on elderly patients complaining of abdominal pain. On gentle probing, there is a rigid structure in the abdomen = Faecal peritonitis
how do we treat faecal peritonitis
surgery to remove faeces
if too severe and urgent, colostomy bag above the rupture until surgery can be done
why might colorectal cancer be low in africa
life expectancy lower due to malnutrition and lack of vaccination and health control e.g. HIV
colorectal cancer only becomes prelevent over age of 60
why is colorectal prognosis increasing with increasing incidence
This is likely to do with fibre optic colonoscopes, along with CT scans, aiding early diagnosis greatly leading to increased prognosis
what are polyps
adenomas
benign growths that predispose adenocarcinomas
how many people over 60 have colorectal polyps
1/3
explain the TMN staging
for cancer
N = if it has spread to lower or higher nodes
T = invasion depth
M = presence of metastasis
what is a possibly prevention strategy against adenoma polyps
low dose aspirin
how can we remove polyps
if colorectal, endoscopic resection
how do we treat colorectal adenocarcinomas
surgical resection
how do we treat colorectal metastatic adenocarcinomas
palliative care and chemotherapy
often non-treatable
what liver metastasis are surgically removable and not trstable
if within 1 half of the liver, surgical removal is often viable as the liver regenerates. after both halves have been infiltrated, prognosis is very low
what genetic disease leads to huge increased risk of adenocarinoma of the colorectal or GI tract
Familial Adenomatous Polyposis
Autosomal dominant genetic condition that affects young adults where they have healthy GI but in early adulthood gain thousands of small adenomas.
what is familiar adenomatous polyposis
Autosomal dominant genetic condition that affects young adults where they have healthy GI but in early adulthood gain thousands of small adenomas.
where does colorectal cancer often involve
Mainly occurs in rectum and sigmoid
but 13% in the caecum near the small intestine which requires a very flexible endoscope.
why is cancer in the caecum hard to diagnose
in the colon very close to the small intestine
need a very flexible endoscope to reach this point
what is Gastroentrinitis
Syndrome characterised by GI-symptoms including nausea, vomiting, diarrhoea and abdominal pain
what is dehydration
Abnormal faecal discharge characterised by frequent and/or fluid stool. Associated with increased fluid and electrolyte loss- often disease of small intestine - bacteria, dehydration
what is dysentery
Abnormal inflammation of GI-tract: often blood and pus in faeces and pain, fever, abdominal cramps- often disease of large intestine
what is enterocolitis
Inflammation of mucosa of small and large intestine
explain how the GI tract defends against infection
normal bacterial flora
saliva in mouth
rapid shedding of epithelium in mouth, small intestine and colon
pH in stomach
slow of fluid and peristalsis
mucous
what is food poisoning
This strictly refers to ingestion of toxins or poisons in food: e.g. bacterial toxins or heavy metals causing vomiting, diarrhea and other symptoms
Bacteria grow and multiply in food
Cooking kills bacteria but toxin still active – intoxication
what foods have risk of staph aureus food poisnoning
mainly dairy and cooked meats
pre-packed snadwhiches
things prepared and kept e.g. salsas at KFC
how does staph aureus food poisoning present
3-6h of severe vomiting- self-limiting- complete recovery
does cooking thouroughly prevent staph aureus food poisoning
not always
50% of strains produce heat-stable enterotoxins – also resistant to stomach acid and digestive enzymes
where might we find botulism toxin
tinned foods, cheese sauce,
what happens with botulism toxin
blockage of acetyl choline neurotransmitter
flaccid paralysis
death
who is most likely to get botulism
infant botulism
what bacteria causes ‘fried rice syndomre’
Bacillus Cereus
explain how Bacillus Cereus causes infection (4)
spores found on most grains e.g rice, wheat
when cooked bacteria die but spore survive
if left to cool, spores germinate and produce toxin
heat stable toxin survives reheating and is ingested
what is bacillus cereus found in
most pulses
rice and wheat products
spores found in ground
what type of bacteria is bacillus cereus (3)
gram positive, spore forming bacillus rod
how do helicobacter pylori survive in the stomach and what do they cause
bacteria produce urease
convert urea to ammonia
ammonia neutralised the low pH acid
forming an alkaline environment for long enough to implement self into mucin layer
cause inflammation of mucosa and destroy epithelium
cause stomach ulceration
how do we test for helicobacter pylori food poisoning (3)
give high urea food diet
bacteria produce urease urea–> ammonia
ammonia breath test
which part of the stomach does H. Pylori infect
lower stomach mucous membrane
how do we treat H. Pylori gastric ulcers
proton-pump inhibitor e.g. omeprazole
PLUS metronidazole/ amoxicillin and Clarithromycin
what two classifications of H.Pylori are there and why is this relevent (3)
CagA positive and negative
cytotoxin-associated gene A present or not
CagA is related to gastric cancers
how do we treat severe diarrhea and what do we NOT do
Fluid and electrolyte replacement is essential and time to recover
Antibiotic treatment often not successful and may worsen problem- as wipes out competing organisms…. or stimulates toxin production (C.diff)
what is some relevent history to dysphagia
Duration - progressive = structural cause malignancy, intermittent = motility e.g. spasm
Solids or liquids or both
Pain (odynophagia) = oesophagitis
Weight loss = red flag for malignancy
Previous medical history
Medications
Cigarettes and alcohol
what are the three causes of dysphagia
1) Oropharyngeal Problem
2) Oesophageal Problem
3) Gastric problem
what is Sjogrens syndrome and relate this to GI problems
autoimmune disease affecting fluid outputs like tears and saliva
reduced salivary flow = oropharyngeal dysphagia
describe some causes of oropharyngeal dysphagia
Sjorgrens syndrome or polypharmacy= reduced saliva
neurone disorders e.g. ALS/parkinsons = lack of tongue control
hypothyroidism = enlarged thyroid = obsturction
describe some causes of oesophageal dysphagia
peptic stricture (long standing reflux = narrowing oesophagus)
oesophageal pouch
achalasia
oesophageal carcinomas
oesophageal spasms = motility disorders
what is a peptic stricture
stricture is a narrowing of a lumen
peptic strictures are narrowing’s of the oesophagus due to constant irritation, reflux or other damage
can cause oesophageal dysphagia
what is achalasia
In achalasia, the muscles in the oesophagus do not contract correctly and the ring of muscle can fail to open properly, or does not open at all. Food and drink cannot pass into the stomach and becomes stuck. It is often brought back up.
what are some signs of pharyngeal pouch (3)
regurgitation
halitosis
dysphagia
but most asymptomatic
how do we diagnose pharyngeal pouch
barium swallow with xray helps identify a pouch
can be done by endoscopy but this can perforate pouch
what is a pharyngeal pouch
Defect between the constrictor and the transverse cricopharyngeal muscle
diverticulum formation lateral to the pharynx
Very rare, 1 in 100,000 people
how would we diagnose achalasia
bird beaks sign of the oesophagus, xray
constriction of distal portion of oesophagus
what is the bird beaks sign
constriction of the distal portion of the oesophagus
tell-tale sign of achalasia
what gastric problems can cause dysphagia
Carcinoma
Outlet obstruction- peptic ulceration
how do we manage dysphagia
manage underlying problems
If nutritionally deplete, may require supplementation – oral supplements, NG, PEG feeding
what is GORD
gastro-oesophageal reflux disease
what percent of people have GORD
30%
what are some signs and symptoms of GORD
Heartburn, epigastric pain, acid reflux, waterbrash, nausea, vomiting, tooth decay, asthma
give some risk factors of GORD
Excessive relaxation of lower oesophageal sphincter
raised intra-abdominal pressure - obesity
hiatus hernia
delayed oesophageal clearance
dietary = alcohol, tea, coffee, acidic foods
how do we manage GORD
PPI (omeprazole, lansoprazole)
anti-acids e.g. Gaviscon
H2 antagonists
Lifestyle advice (weight loss, smoking cessation, reduce alcohol) - avoid acidic and late meals, raise head in bed e.g. 2 pillows
what non-medication management of GORD is there
Lifestyle advice (weight loss, smoking cessation, reduce alcohol) - avoid acidic and late meals, raise head in bed e.g. 2 pillows
surgery = fundoplication
what is a fundoplication
wrapping part of the fundus of the stomach around the base of the oesophagus, to reinforce the sphincter and relieve inflammation caused by reflux
what is a hiatus hernia
A hiatus hernia is when part of your stomach moves up into your chest. It’s very common if you’re over 50.
It does not normally need treatment if it’s not causing you problems. Causes reflux due to pressure gradient being lost between abdominal and thoracic cavities
what are the three types of hiatus hernia
pre-stage = oesophagus stomach angle is obtuse
sliding hiatus hernia = constriction is in upper stomach in thorax
paraoesophageal type = pouch of stomach in thorax
what pH is indicative of acid reflux in the oesophagus
<4pH
how do we differentiate a gastric and duodenal ulcer
gastric is worsened by eating
duodenal is made better by eating
give sings/symptoms of peptic ulcer
taking NSAIDs
H. Pylori infection
epigastric pain possibly radiating to back
pain/better on eating
vomiting or haematemesis
why might peptic ulcers cause haematemesis and vomiting
Vomiting/ Hematemesis (due to gastric ulcer (=hematemesis) or pyloric outlet obstruction due to duodenal ulceration(=vomiting)).
how many people over 50 are infected with H.Pylori
50%
how do we treat H.Pylori (4)
PPI e.g. omeprazole
2 antibiotics
IF BLEEDING = endoscopic treatment
if this fails, surgical tx
what are the symptoms of gastric cancer and when is this investigated
Epigastric pain, weight loss, vomiting
Must be suspected in anyone over 50 years with new onset symptoms
Epigastric pain
Weight loss
Vomiting
Early cancer can be asymptomatic
what investigations do we undergo for gastric cancer
Gastrectomy
If positive, CT scan or endoscopic ultrasound
how would we differentiate pancreatic cancer to gastric cancer
both would cause epigastric pains
pancreatic will be related to chronic Hep or liver problems, jaundice
severe pain and high blood amylase. what is this
pancreatitis
what are the common causes of pancreatitis
commonest cause alcohol > gallstones > pancreatic trauma, drugs, hypercalcamia / lipidaemia, familial
how do we differentiate acute and chronic abdominal pain
chronic will be localised due to inflammation reaching pericardium
acute will be generalised
unless puncture/trauma where this will be localised
chronic is > 6 weeks
what are these drugs for: cyclizine, metaclopramide
anti-emetics
what causes acute diarrhoea
Infection (gastroenteritis: bacterial or viral)
Campylobacter, Salmonella, Shigella, E. Coli
Drugs
Antibiotics, PPIs, food intolerances, alcohol
Food allergy / intolerance
what classes as chronic diarrhoea
> 6 weeks
name the three main types of cause for chronic diarrhoea
Small bowel disease
lactase deficiency
Coeliac disease
Crohn‘s disease
Pancreatic disease
pancreatic insufficiency
pancreatic carcinoma
cystic fibrosis
Colonic disease
ulcerative colitis
Crohn’s disease
carcinoma
what are the three histological features of coeliac disease
when on a gluten containing diet:
-Intraepithelial leukocytes increased in intestine
-crypt hyperplasia
-villous atrophy
how common is coaeliac disease
1 in 100
what are some signs and symptoms of coeliac disease
GI problems e.g. abdominal pain, diarrhoea
iron deficency
b12 anaemia
fatigue
how do we investigate Coaelic disease
when on gluten diet blood test for high IgA
if high, endoscopy to look for scalloping
what is Dermatitis Herpetiformis closely linked with and what is it
Itchy blisters on knees, backs and buttocks
closely related to coaeliac disease
treated by gf diet
compare diarrhoea related to small bowel/pancreatic and from the colon (4)
Small bowel:
-floating, hard to flush stool
-throughout day
-pain is variable
-not relived by defication
colon:
-blood or mucous in stool
-usually in morning
-pain is during defication
-pain releived by defication
what are some signs of ulcerative colitis
abdominal pain
diarrhoea and bleeding on defecation
Weight loss, fever, and anaemia
what are some associated diseases with IBD
Vascular - thrombosis common so when admitted to hospital, prophylactic LMWH given
Liver - cirrhosis, CAH, pericholangitis. U.C: primary sclerosing cholangitis
Skin - erythema nodosum, pyoderma gangrenosum
Mouth - ulcers. Crohn’s: lips, buccal mucosa
Joints - arthritis, ankylosing spondylitis
Eyes - episcleritis, uveitis
what is erythema nodosum
red markings on the skin e.g. legs
commonly associated with IBD
if pt has gangrenosum on the legs, what might we suspect
IBD
what are some risks for colon cancer
Polyps – Cancer
Over 50 more risk
Red meats, saturated fats, lack of fibre and fruit n veg
Polyps are a risk factor and removed if found endoscopically
Long standing IBD or acromegaly
Obesity and smoking
compare rectal hameroiids anal bleeding to colorectal cancer
haemorrhoids cause bright red bleeding
cancer will be darker red/black
what are some symptoms of colon cancer
None!! (Bowel Cancer Screening – FIT stool testing and if positive, colonoscopy )
Rectal Bleeding (may be hemorrhoids if bright red bleeding, with history of constipation and tx with creams or surgical intervention)
Altered Bowel Habit
Lethargy/ Weight Loss
what is cholangitis
inflammation of the bile duct
what might cause post hepatic jaundice
gallstones (with pain, fever)
cholangitis
bile duct stricture
pancreatic carcinomas (constant pain radiating to back, weight loss)
what pain is specific to pancreatic carcinomas
constant abdominal pain radiating to the back
what two antibiotic often cause hepatic jaundice
augmentin, flucloxacillin
what are some signs of hepatic jaundice
Malaise
lethargy
anorexia
distaste for cigarettes
jaundice
pale stools (no conjugation)
dark urine (more renal excretion)
right upper quadrant discomfort
compare stool and urine and bilirubin blood levles in pre- hepatic and post jaundice
pre:
-high unconjugated
-
hepatic:
-high unconjugated
-low conjugated
-pale stool
-dark urine (more renal excretion)
give some causes of hepatic jaundice
liver infection e.g. Hep C and hep B or EBV
drugs e.g. Augmentin or flucloxacillin
alcohol hepatitis = high alcohol
chronic hepatitis or cirrhosis = Wilsons syndrome
what is Wilsons syndrome and what might be a sign of this
increased copper deposits in the brain and liver
may present as jaundice causing hepatic jaundice
what causes pre-hepatic jaundice
haemolytic anaemia, splenomegaly, sickle cell
What can frying in cast iron cause (2)
Gastric cancer
Production of nitrosamines
