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Year 3 Human Disease > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

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

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

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2
Q

define

a. dysphagia

b. odynophagia

A

a. dysphagia: difficulty swallowing

b. odynophagia: pain on swallowing

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3
Q

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

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

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4
Q

difference in symptoms between achalasia and spasm

A

achalasia pain is constant, spasm comes and goes

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5
Q

what does GORD stand for and what is it

A

Gastro-oesophageal reflux disease

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

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6
Q

7 risk factors for GORD and explain

A
  • pregnancy
  • 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
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7
Q

5 GORD symptoms

A
  • heartburn
  • odynophagia (painful swallowing)
  • waterbrash (excessive salivation)
  • acid brash (acid/ bile regurgitation/taste)
  • belching
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8
Q

4 characteristics of heartburn

A
  • discomfort
  • radiation of pain towards mouth
  • after meals/racumbency (lying down)
  • relief with antacid use
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9
Q

order of preference of 3 types of GORD management

A
  • lifestyle measures
  • medication
  • OGD (endoscopy)
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10
Q

7 lifestyle management techniques for GORD

A
  • weight loss
  • smoking cessation
  • alcohol cessation
  • small regular meals
  • raise the head of the bed
  • avoid eating just before bed
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11
Q

3 types of GORD medication and why they work

A
  • 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
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12
Q

what is barretts oesophagus

A

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

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13
Q

management of barret’s oesophagus

A
  • yearly endoscopic surveillance and biopsy

- if dysplastic changes found, affected tissue is removed by oesophageal resection/ mucosal ablation

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14
Q

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

A

duodenal ulcers 4x more common

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15
Q

where do gastric ulcers occur and why

A

lesser curvature of stomach

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

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16
Q

3 symptoms of gastric ulcers

A
  • epigastric pain after (GU) or before (DU) meals, relief with antacids
  • heartburn
  • postprandial epigastric discomfort and fullness, belching, early satiety, nausea
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17
Q

7 causes of peptic ulcer disease

A
  • infection (helicobacter pylori)
  • drugs (NSAIDS, steroids, bisphosphonates- inhibit prostaglandins)
  • hormonal (Zollinger-Ellison syndrome (tumour of pancreas, secretes gastrin), gastrinoma
  • alcohol
  • smoking
  • stress
  • blood group O
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18
Q

structure of helicobacter pylori

A

gram negative bascilli

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19
Q

4 aspects of intestinal/mucosal physiology affected by helicobacter pylori

A
  • inc gastric acid secretion
  • gastric metaplasia
  • immune response
  • mucosal defense mechanisms
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20
Q

2 enzymes released by h pylori and what they do

A
  • urease. converts urea –> CO2 + ammonia to neutralise pH and protect itself BUT bad for gastric epithelium
  • protease. damages our barrier system
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21
Q

what are the symptoms of peptic ulcer disease

A

ALARMS

  • Anaemia
  • loss of weight
  • anorexia
  • recent onset, progressive symptoms
  • melaena or haematemesis
  • swallowing difficulties
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22
Q

2 investigations of peptic ulcers

A
  • endoscopy

- helicobacter pylori detection

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23
Q

4 ways to detect h pylori

A
  • breath test (breathe in urea, if there is h pylori you breathe out CO2)
  • stoll antigen
  • serology
  • biopsy
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24
Q

5 treatments of peptic ulcer disease

A

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

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25
Q

when is a peptic ulcer v serious

A

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

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26
Q

2 signs of upper GI bleeding

A
  • haematemesis (vomiting blood)

- melaena (black stools due to inclusion of blood)

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27
Q

9 causes of upper GI bleeds

A
  • Mallory-Weiss tear (excessive drinking/vomiting)
  • oesophagitis*
  • 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
  • angiodysplasia
  • drugs (NSAIDS, steroids, anticoagulants, thrombolytics)
28
Q

7 ways to manage upper GI bleeds

A
  • Airways
  • Breathing
  • 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)
29
Q

what is coeliac disease

A

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

30
Q

where is gluten found 3

A

wheat, rye, barley

alpha-gliaden component

31
Q

what genes cause genetic susceptibility to coeliac disease 2

A

DQ2. DQ8

32
Q

skin condition associated with coeliac disease

A

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

33
Q

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

A

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

34
Q

role of prostaglandins in stomach 4

A
  • increase mucous production
  • increase bicarbonate production
  • increase blood flow to mucosa
  • decrease gastric acid secretion
35
Q

4 clinical features of coeliac disease

A
  • diarrhoea/steatorrhoea
  • abdominal pain/bloating
  • weight loss
  • oral ulceration/angular cheilitis
36
Q

2 tests for diagnosis of coeliac disease

A
  • BLOOD: endomysial and tissue transglutaminase (TTG) antibodies, anaemia
  • BIOPSY: jejunal/ duodenal
37
Q

treatment of coeliac disease

A

gluten free diet

38
Q

3 histological effects of crohns and why they are detrimental

A
  • villous atrophy (flat villi)
  • crypt hyperplasia (more goblet cells and mucous)
  • chronic inflammatory lymphocytic infiltrate within epithelium
  • -> reduced surface area for absorption
39
Q

2 main inflammatory bowel diseases (IBD)

A
  • crohn’s

- ulcerative colitis UC

40
Q

3 interactive causes of IBD

A
  • genetic susceptibility
  • environmental factors: smoking, high fat/sugar intake, intestinal microflora
  • host immune response (defects in immunoregulation or barrier function)
41
Q

role of smoking in IBD

A

protective in ulcerative colitis

damaging in Crohns

42
Q

prevalence and common area of UC

A

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

43
Q

6 clinical features of UC

A
  • diarrhoea w blood and mucus, 10-20 stools/day
  • tenesmus (still need to poo)
  • urgency
  • lower abdominal disomfort
  • constitutional symptoms eg malaise, lethargy, anorexia, fever
  • oral ulceration (aphthous-like ulcers)
44
Q

prevalence and common area of Crohn’s

A

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

45
Q

6 clinical features of Crohn’s

A
  • abdominal pain
  • diarrhoea
  • 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
46
Q

compare gut distribution of UC and crohns

A
  • 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
47
Q

5 methods of diagnosis of IBD

A
  • 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
  • MRI
  • biopsy
48
Q

4 treatment options of crohns

A
  • smoking cessation
  • treat diarrhoea/anaemia
  • immunosuppressants (steroids, monoclonal ab)
  • surgery: stricuroplasty, resection with end-to-end anastamosis
49
Q

2 treatment options of UC

A
  • immunosuppressants
  • surgery: subtotal colectomy with end ileostomy and preservation of rectum in acute flare-ups, later ileorectal or ileoanal anastamosis after the acute flare
50
Q

TABLE OF CROHNS/UC COMPARISON

compare crohns and UC affected area

A

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

51
Q

compare crohns and UC continuity

A

crohns: patchy (skip lesions)

UC; continuous proximal extension

52
Q

compare crohns and UC effect on thickness of gut wall

A

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

53
Q

compare crohns and UC granulomas

A

common in crohns

54
Q

compare crohns and UC pseudopolyps

A

common in UC

55
Q

compare crohns and UC most prominent feature

A

-crohns: abdominal pain

UC: bloody diarrhoea

56
Q

skin effects with IBD 5

A
  • 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
57
Q

does IBD increase risk of adenocarcinoma

A

yes

58
Q

what is IBS

A

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

59
Q

4 symptoms of IBS

A
  • abdominal bloating
  • central/lower abdominal pain relieved by defacation
  • pR mucus
  • alternating diarrhoea, constipation
60
Q

3 treatments of IBS

A
  • antispasmodics
  • treatment of constipation/diarrhoea
  • tricyclic ad
61
Q

what classifies diarrhoea as

a. acute
b. persistent
c. chronic

A

a. acute: 14 days

c. chronic >3 months

62
Q

6 common causes of diarrhoea

A
  • gastroenteritis
  • IBS
  • IBD
  • coeliac disease
  • drugs (antibiotics, laxatives, PPIs, ETOH, NSAIDs)
  • colorectal cancer
63
Q

6 uncommon causes of diarrhoea

A
  • hyperthyroidism
  • lactose intolerance
  • overflow diarrhoea
  • ischaemic colitis
  • chronic pancreatitis
  • addison’s disease
64
Q

6 categories + examples of constipation

A
  • 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)
65
Q

bristol stool chart

A

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

Year 3 Human Disease (28 decks)

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