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Year 3 Human Disease > Gastroenterology > Flashcards

Flashcards in Gastroenterology Deck (65):

describe each of these 5 structural abnormalities that cause dysphagia
a. pharyngeal pouch
b. oesophagitis (types)
c. benign strictures
d. malignant strictures
e. extrinsic pressure (causes)

a. pharyngeal pouch: pouch forms off oesophagus, food gets stuck in so does not move down oesophagus as normal
b. oesophagitis (types): reflux (due to acid reflux or candida), infective
c. benign strictures: scarring of oesophagus due to acid reflux/ endoscopy
d. malignant strictures: cancer
e. extrinsic pressure (causes): thyroid goitre, aortic aneurysm, lung cancer, lymph nodes


a. dysphagia
b. odynophagia

a. dysphagia: difficulty swallowing
b. odynophagia: pain on swallowing


describe these 6 motility disorders that occur with dysphagia
a. achalasia
b. oesophageal spasm
c. bulbar palsy (eg MND) / pseudobular palsy (eg stroke)
d. systemic sclerosis
e. Chagas' disease

a. achalasia: Auerbach's/myenteric plexus in oesophageal muscle does not work --> no control of peristalsis --> sphincter does not relax --> no passing of food to stomach
b. oesophageal spasm: unco-ordinated peristalsis
c. bulbar palsy (eg MND) / pseudobular palsy (eg stroke): lesion along upper/lower motorneurone to throat
d. systemic sclerosis: fibrosis (scar tissue)
e. Chagas' disease: destruction of ANS plexus due to parasitic infection


difference in symptoms between achalasia and spasm

achalasia pain is constant, spasm comes and goes


what does GORD stand for and what is it

Gastro-oesophageal reflux disease
dysfunction of the lower oesophageal sphincter predisposing to the reflux of gastric acid up in to the oesophagus


7 risk factors for GORD and explain

-obesity: both inc intra-abdominal pressure on oesophagus
-alcohol: blocks Ca2+ channels --> relaxes sphincter muscles
-smoking: alc and smoking are irritants --> inc gastric acid secretion
-hiatus hernia: top bit of stomach hooks up through diaphragm --> lower pressure in diaphragm, acid can come upwards
-helicobacter pylori
-anticholinergic medications eg bladder relaxants


5 GORD symptoms

-odynophagia (painful swallowing)
-waterbrash (excessive salivation)
-acid brash (acid/ bile regurgitation/taste)


4 characteristics of heartburn

-radiation of pain towards mouth
-after meals/racumbency (lying down)
-relief with antacid use


order of preference of 3 types of GORD management

-lifestyle measures
-OGD (endoscopy)


7 lifestyle management techniques for GORD

-weight loss
-smoking cessation
-alcohol cessation
-small regular meals
-raise the head of the bed
-avoid eating just before bed


3 types of GORD medication and why they work

-antacids eg gaviscon: neutralises acid
-proton pump inhibitors eg omeprazole, lansoprazole. inhibit proton pump in gastric acid production
-H2 antagonists eg ranitidine: block histamine receptors on parietal cells


what is barretts oesophagus

metaplastic change of distal oesophageal epithelium from squamous to columnar type when the lower oesophagus tries to protect itself from gastric acid in GORD--> upwards migration of squamocolumnar junction
-inc risk of adenocarcinoma development


management of barret's oesophagus

-yearly endoscopic surveillance and biopsy
-if dysplastic changes found, affected tissue is removed by oesophageal resection/ mucosal ablation


are gastric GU or duodenal ulcers DU more common? by how much

duodenal ulcers 4x more common


where do gastric ulcers occur and why

lesser curvature of stomach
more motile and more exposed to acid (ulcers elsewhere on stomach are suspicous)


3 symptoms of gastric ulcers

-epigastric pain after (GU) or before (DU) meals, relief with antacids
-postprandial epigastric discomfort and fullness, belching, early satiety, nausea


7 causes of peptic ulcer disease

-infection (helicobacter pylori)
-drugs (NSAIDS, steroids, bisphosphonates- inhibit prostaglandins)
-hormonal (Zollinger-Ellison syndrome (tumour of pancreas, secretes gastrin), gastrinoma
-blood group O


structure of helicobacter pylori

gram negative bascilli


4 aspects of intestinal/mucosal physiology affected by helicobacter pylori

-inc gastric acid secretion
-gastric metaplasia
-immune response
-mucosal defense mechanisms


2 enzymes released by h pylori and what they do

-urease. converts urea --> CO2 + ammonia to neutralise pH and protect itself BUT bad for gastric epithelium
-protease. damages our barrier system


what are the symptoms of peptic ulcer disease

-loss of weight
-recent onset, progressive symptoms
-melaena or haematemesis
-swallowing difficulties


2 investigations of peptic ulcers

-helicobacter pylori detection


4 ways to detect h pylori

-breath test (breathe in urea, if there is h pylori you breathe out CO2)
-stoll antigen


5 treatments of peptic ulcer disease

-lifestyle adjustment
-cessation of causative medication
-h pylori eradication
H2 antagonists


when is a peptic ulcer v serious

if it bursts through stomach --> stomach enzymes break down internal organs


2 signs of upper GI bleeding

-haematemesis (vomiting blood)
-melaena (black stools due to inclusion of blood)


9 causes of upper GI bleeds

-Mallory-Weiss tear (excessive drinking/vomiting)
-peptic ulcer disease*
-GI malignancy* *= leave friable epithelial surface prone to bleeding
-oesophageal varices (liver cirrhosis--> less blood flow from hepatic portal vein --> dilated oesophageal vessels/HPV)
-bleeding disorders
-drugs (NSAIDS, steroids, anticoagulants, thrombolytics)


7 ways to manage upper GI bleeds

-Circulation (cannulae, IV fluid, blood transfusion, vit K)
-urgent OGD endoscopy (Rockall score)
-if known varices --> IV terlipressin/ antibiotics, consider surgical banding/ sclerotherapy
-surgical techniques: adrenaline injection, diathermy, laser coagulation
-uncontrolled bleeding --> Sengstaken-Blakemore tubes (inflate in GI tract to stop bleeding like catheter)


what is coeliac disease

auto-immune condition, inflammation of proximal small bowel mucosa with gluten


where is gluten found 3

wheat, rye, barley
(alpha-gliaden component)


what genes cause genetic susceptibility to coeliac disease 2

DQ2. DQ8


skin condition associated with coeliac disease

dermatitis herpetiformis (itchy rash on pressure points eg elbows, bum, occipate, knees)


cell types in upper and lower GI tracts and how this relates to cancers of upper and lower GI tract

upper: squamous cells (--> squamous cell carcinomas, oral causes eg smoking, alcohol, hot drinks)
lower: columnal cells (--> adenocarcinomas, eg caused by gastric reflux)


role of prostaglandins in stomach 4

-increase mucous production
-increase bicarbonate production
-increase blood flow to mucosa
-decrease gastric acid secretion


4 clinical features of coeliac disease

-abdominal pain/bloating
-weight loss
-oral ulceration/angular cheilitis


2 tests for diagnosis of coeliac disease

-BLOOD: endomysial and tissue transglutaminase (TTG) antibodies, anaemia
-BIOPSY: jejunal/ duodenal


treatment of coeliac disease

gluten free diet


3 histological effects of crohns and why they are detrimental

-villous atrophy (flat villi)
-crypt hyperplasia (more goblet cells and mucous)
-chronic inflammatory lymphocytic infiltrate within epithelium
--> reduced surface area for absorption


2 main inflammatory bowel diseases (IBD)

-ulcerative colitis UC


3 interactive causes of IBD

-genetic susceptibility
-environmental factors: smoking, high fat/sugar intake, intestinal microflora
-host immune response (defects in immunoregulation or barrier function)


role of smoking in IBD

protective in ulcerative colitis
damaging in Crohns


prevalence and common area of UC

80-150 per 100 000
more common in Caucasians in western world
M:F 1.2:1
mean age of onset 34 yrs


6 clinical features of UC

-diarrhoea w blood and mucus, 10-20 stools/day
-tenesmus (still need to poo)
-lower abdominal disomfort
-constitutional symptoms eg malaise, lethargy, anorexia, fever
-oral ulceration (aphthous-like ulcers)


prevalence and common area of Crohn's

20-100/100 000
more common in Caucasians in western world
M:F 1:1.2
mean age of onset 26 yrs


6 clinical features of Crohn's

-abdominal pain
-weight loss
-constitutional symptoms eg malaise, lethargy, anorexia, fever
-oral lesions: labial swelling, ulceration in sulcus, angular cheilitis, cobblestoning
-perianal lesions: fissures, skin tags, perianal abscesses, anorectal fistulae


compare gut distribution of UC and crohns

-UC: rectum alone (proctitis)/ proximally to involve sigmoid/descending colon (L sided colitis)/ whole colon (total colitis)
-crohn's: mainly TERMINAL ILEUM/ASCENDING COLON. healthy 'skip lesions' found between bad areas


5 methods of diagnosis of IBD

-blood tests (iron deficiency anaemia, raised CRP/WBC, hypoalbuminaemia
-barium enema/follow through
-colonoscopy (not in acute attacks, as epithelium is v fragile --> may perforate


4 treatment options of crohns

-smoking cessation
-treat diarrhoea/anaemia
-immunosuppressants (steroids, monoclonal ab)
-surgery: stricuroplasty, resection with end-to-end anastamosis


2 treatment options of UC

-surgery: subtotal colectomy with end ileostomy and preservation of rectum in acute flare-ups, later ileorectal or ileoanal anastamosis after the acute flare


compare crohns and UC affected area

crohns: commonly terminal ileum with perianal and oral involvement
UC: limited to colon


compare crohns and UC continuity

crohns: patchy (skip lesions)
UC; continuous proximal extension


compare crohns and UC effect on thickness of gut wall

crohns: transmural (whole wall thickness, caused by deep ulcers crossing muscularis mucosae w fissures, fistulae, abscesses, stricturing)
UC: mucosa/submucosa only (superficial ulceration)


compare crohns and UC granulomas

common in crohns


compare crohns and UC pseudopolyps

common in UC


compare crohns and UC most prominent feature

-crohns: abdominal pain
UC: bloody diarrhoea


skin effects with IBD 5

-erythema nodosum: looks like dark bruises on shins
-uveitis: inflammation of iris
-pyoderma gangrenosum: necrotic skin condition, violet ring surrounding lesion
-arthropathy: inflammation of joint
-primary sclerosing cholangitis: bile ducts fibrose


does IBD increase risk of adenocarcinoma



what is IBS

functional bowel disorder in which no organic cause can be found. disorder of intestinal motility/enhanced visceral perception


4 symptoms of IBS

-abdominal bloating
-central/lower abdominal pain relieved by defacation
-pR mucus
-alternating diarrhoea, constipation


3 treatments of IBS

-treatment of constipation/diarrhoea
-tricyclic ad


what classifies diarrhoea as
a. acute
b. persistent
c. chronic

a. acute: 14 days
c. chronic >3 months


6 common causes of diarrhoea

-coeliac disease
-drugs (antibiotics, laxatives, PPIs, ETOH, NSAIDs)
-colorectal cancer


6 uncommon causes of diarrhoea

-lactose intolerance
-overflow diarrhoea
-ischaemic colitis
-chronic pancreatitis
-addison's disease


6 categories + examples of constipation

-general (poor diet/dehydration, immobility, IBS, elderly)
-anorectal disease (anal fissure, rectal prolapse)
-obstruction (stricture, colorectal carcinoma, diverticulitis, pelvic mass)
-metabolic (hyperthyroididm, hypercalcaemia)
-drugs (opiate analgesics, iron supplements, anticholinegics)
-other (diabetic neuropathy, systemic sclerosis, Hirschprung's disease)


bristol stool chart

1: separate hard lumps (hard to pass)
2: sausage shaped but lumpy
3: sausage w cracks on surface
4: smooth soft sausage (best one)
5: soft blobs, clear edges (passed easily)
6: fluffy pieces with ragged edges (mushy)
7: entirely liquid