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GI 1 Flashcards

1
Q

What are some causes of GORD?

A

Hiatus hernia (sliding 80%, rolling 20%)

Loss of oesophageal peristaltic function

Abdominal obesity

Gastric acid hypersecretion

Slow gastric emptying

Overeating

Smoking

Alcohol

Pregnancy

Drugs

Systemic sclerosis

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2
Q

How does GORD present?

A

Heartburn

Belching

Food/Acid regurg

Increased salivation

Odynophagia (pain on swallowing)

Nocturnal asthma

Chronic cough

Laryngitis

Sinusitis

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3
Q

How would you investigate GORD?

A

trial PPI

oesophagogastroduodenoscopy (OGD)

ambulatory pH monitoring

Oesophageal manometry

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4
Q

How would you manage GORD?

A

PPI - omeprazole

Lifestyle changes : weight loss, head-of-bed elevation, avoid late night eating

H2 antagonist - ranitidine

Nissen fundoplication

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5
Q

What are some complications of GORD?

A

Peptic Stricture - inflamm of oesophagus = causes narrowing and a stricture

Barrett’s oesophagus - metaplasia from squamous to columnar (premalignant for adenocarcinoma of the oesophagus)

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6
Q

Where does a Mallory-Weiss tear occur? What are some causes?

A

mucosal tear occurring at the oesophagogastric junction produced by a sudden increase in intra-abdominal pressure

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7
Q

What are some risk factors for Mallory-Weiss tear?

A

Alcoholism

Forceful vomiting

Eating disorders

Male

NSAID abuse

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8
Q

How would you investigate a Mallory-Weiss tear?

A

FBC - initial evaluation of patient with bleed

Urea - should be high in patient with ongoing bleeding

LFTs - liver disease may predispose a patient to oesophageal varices

Prothrombin time

Oesophagogastroduodenoscopy - after bleed stabilisation

cross-match/blood grouping

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9
Q

How would you manage Mallory-Weiss tear?

A

IV fluids (PPI in high risk patients)

Phytomenadione (vit K) - if prolonged PT/INR

Hemoclip placement

Adrenaline

Endoscopic band ligation

anti-emetic - ondansetron

Sengstaken-Blackmore tube

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10
Q

What are the two sphincters of the stomach?

A

gastro-oesophageal sphincter

pyloric sphincter - controls gastric contents into the duodenum

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11
Q

What cells are present in the muscosa in the upper 2/3rds of the stomach?

What are their functions?

A

Parietal cells - secrete HCL

Chief cells - pepsinogen and initiate proteolysis

Enterochromaffin-like cells - releases histamine (stimulates acid release)

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12
Q

What cells are found in the antral muscosa of the stomach?

What are their functions?

A

Mucus secreting cells - secrete mucin (protect gastric mucosa) and bicarb

G cells - secrete gastrin - stimulates acid release

D cells - secrete somatostatin - suppressant of acid secretion

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13
Q

What glands in the duodenum release alkaline mucus?

A

Brunner’s glands - in combination with pancreatic and biliary secretions = neutralise the acid secretion from the stomach

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14
Q

What are peptic ulcers? Where are duodenal ulcers and gastric ulcers found?

A

Break in the superficial epithelial cells penetrating down to the muscularis mucosa

Duodenal ulcers are more commonly found in the dueodenal cap

Gastric ulcers are most commonly seen on the lesser curve of the stomach

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15
Q

What are some causes of peptic ulcers?

A

Helicobacter pylori infection

Drugs - NSAIDs, steroids and SSRIs

Smoking

Delayed gastric emptying

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16
Q

Which is more common? Duodenal or gastric ulcers?

A

Duodenal ulcers more common

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17
Q

How do peptic ulcers present?

A

Recurrent burning epigastric pain

Duodenal ulcers = night and worse when hungry

Nausea

Anorexia and weight loss - particularly with gastric ulcers

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18
Q

What are some red flag symptoms to be aware when investigating peptic ulcers?

A

Unexplained weight loss

Anaemia

GI bleeding - melena or hematemesis

Dysphagia

Upper Abdominal mass

Persistent vomiting

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19
Q

How would you investigate peptic ulcers?

A

H.pylori urea breath test or stool antigen test

Upper GI endoscopy

FBC - microcytic anaemia

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20
Q

How would you treat a peptic ulcer?

A

PPI - omeprazole

H2 antagonist - ranitidine

If H.pylori positive - TRIPLE THERAPY = PPI, clarithromycin, metronidazole

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21
Q

What are causes of gastrointestinal varices?

A

All due to portal hypertension

  1. Alcoholism
  2. Viral cirrhosis
  3. Pre-hepatic - thrombosis in portal or splenic vein
  4. Intra-hepatic - cirrhosis, schistosomiasis, sarcoid, congenital hepatic fibrosis
  5. Post-hepatic - budd-chiari syndrome, right heart failure, constrictive pericarditis
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22
Q

How would a oesophago-gastric varices present?

A

if ruptured:
Haematemesis

Abdo pain

Shock

Fresh rectal bleeding

Hypotension and tachycardia

Pallor

signs of chronic liver damage : splenomegaly

ascites

hyponatraemia

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23
Q

How would you investigate an oesophago-gastric varices?

A

FBC - microcytic anaema or thrombocytopenia

LFTs - elevated transaminases, Alk phos and bilirubin

Urea and creatinine

Oesophagogastroduodenoscopy (OGD)

blood typing/cross-matching

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24
Q

How would you manage an oesophago-gastric varices?

A

Vasoactive drugs - terlipressin

Prophylatic abx - ceftriaxone

TIPS - trans-jugular intrahepatic porto-systemic shint

25
Q

What is Achalasia? What causes it?

A

Oesophageal aperistalsis and impaired relaxation of the lower oesophageal sphincter

caused by degeneration of mesenteric plexus of the oesophagus

26
Q

How does Achalasia present?

A

Dysphagia for fluids and solids

Regurg of food particularly at night

Substernal cramps

27
Q

How would you investigate Achalasia?

A

Endoscopy

Barium swallow - loss of peristalsis and delayed oesophageal emptying

Oesophageal manometry

28
Q

How would you treat achalasia?

A

Nifedipine

Pneumatic dilation

Injection of botulinum toxin A

Laparoscopic cardiomyotomy

29
Q

What is the difference between gastritis and gastropathy?

A

Gastritis = inflammation assoc with muscosal injury

Gastropathy = indicates epithelial cell damage and regeneration WITHOUT
inflammation - commonest cause is mucosal damage associated with Aspirin/
NSAIDs

30
Q

What are some causes of gastritis?

A

H.Pylori infection

Autoimmune gastritis

Viruses - CMV, herpes simplex

Duodenogastric reflux

Mucosal ischaemia

Increased acid

Aspirin and NSAIDs

Alcohol

31
Q

How does gastritis present?

A

Nausea or recurrent upset stomach

Abdo bloating

Epigastric pain

Vomiting

Indigestion

Hematemesis

32
Q

How do you investigate Gatritis?

A

H.pylori urea breath test

H.pylori faecal antigen test

FBC

33
Q

How would you manage gastritis?

A

Ranitidine

H.pylori - triple therapy

Autoimmune - cyanocobalamin

34
Q

What are some causes of malabsorption?

A

Pancreatic insufficiency

Defective bile secretion

Bacterial Overgrowth

Coeliac disease

Crohn’s

Giardia Lamlia

Surgical resection of bowel

Lack of digestive enzymes

Defective epithelial transport

Lymphatic obstruction

35
Q

What is coeliac disease ?

A

T-cell mediated autoimmune disease of the small bowel in which PROLAMIN intolerance causes villous atrophy and malabsorption

36
Q

What are some forms of Prolamin?

A

Gliadin = wheat

Hordeins = barley

Secalins = rye

37
Q

What are some risk factors for coeliac disease?

A

Type 1 diabetes

Thyroid disease

Sjogrens

IgA deficiency

Breast feeding

Age of introduction to gluten into diet

Rotavirus infection in infancy

38
Q

Which part of the bowel is most affected by coeliac disease? What is the consequence of this part being affected?

A

proximal small bowel

Meaning B12, folate and iron cannot be absorbed = anaemia

39
Q

How does coeliac disease present?

A

1/3 asymptomatic

steatorrhoea

diarrhoea

abdominal pain

bloating

nausea & vomiting

angular stomatitis

weight loss

fatigue

anaemia

osteomalacia

40
Q

How would you investigate coeliac disease?

A

Small bowel histology - gold-standard

FBC and blood smear - low Hb and microcytic red cells

IgA-tTg - increased titre

endomysial antibody - alt to IgAtTG with greater specificity and lower sensitiviy

skin biopsy - IgA dermal deposits

Endoscopy -

41
Q

How would you manage coeliac disease?

A

gluten-free diet

calcium and iron supplements

correct electrolytes

prednisolone

42
Q

What are histological findings on biopsy that would indicate coeliac disease?

A

villous atrophy

crypt hyperplasia

increased intraepithelial white cell count

43
Q

What are the forms of Ulcerative Colitis?

A

Proctitis - just rectum - 50%

Left-sided colitis - rectum and left colon - 30%

Entire Colon/up to ileocaecal valve- pancolitis/extensive colitis - 20%

44
Q

What are some risk factors for UC?

A

Fam Hx

NSAIDs

smoking is protective

chronic stress and depression trigger flares

45
Q

How does UC present?

A

runs a course of remissions and exacerbations

restricted pain usually in lower left quadrant

episodic or chronic diarrhoea with blood and mucus

cramps

in acute UC - may be fever, tacycardia and tender distened abdomen

46
Q

What are some extra intestinal signs of UC?

A

clubbing

apththous oral

ulcers

erythema nodusum

amyloidosis

47
Q

How would you investigate UC?

A

Stool studies - faecal calprotectin

ESR/CRP - suggestive of flare-ups

flexible sigmoidoscopy

colonoscopy

biopsy

48
Q

What are some macroscopic findings of UC?

A

only colon up to ileocaecal valve

begins in the rectum and extends

NO skip lesions

49
Q

What are some microscopic findings of UC?

A

mucosal inflammation ONLY - it is not transmural

depleted goblet cells

increased crypt abscesses

50
Q

How would you manage UC?

A

Acute - methylprednisolone
IV fluids
ciclosporin

non-acute - mesalazine (5ASA)

prednisolone

ciclosporin

colectomy

51
Q

Which part of the GI tract is affected by Crohn’s?

A

Any part of the gut from mouth to anus

Esp. terminal ileum and proximal colon

There are parts of unaffected bowel = skip lesions

52
Q

What are some risk factors for Crohn’s?

A

genetic association (mutation in NOD2)

smoking

NSAIDs may exacerbate

Fam Hx

Chronic stress and depression

Appendictomy may increase risk

53
Q

What are macroscopic features of Crohn’s?

A

not continuous = skip lesions

involved bowel is usually thickend and often narrowed

Cobblestone appearance due to ulcers and fissures

54
Q

What are some microscopic features of Crohn’s?

A

Transmural inflammation = through all layers

lymphoid hyperplasia

granulomas present - non-caseating epitheloid cells

goblet cells present

55
Q

How does Crohn’s present?

A

diarrhoea with urgency

bleeding

pain - acute right iliac fossa pain

weight loss

malaise

lethargy

perinal abscess

anal strictures

56
Q

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

A

apthous ulcers, clubbing, skin, joint and eye problems

57
Q

How would you investigate Crohn’s?

A

FBC

Iron studies

B12 and folate

ESR and CRP

CT scan

Colonoscopy and biopsy

58
Q

How would you treat Crohn’s?

A

Budesonide/Mesalazine

Azathioprine

MTX

Gastro (4 decks)

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