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Clinical Biochemistry & Endocrinology 3 > GI Function and Tests > Flashcards

GI Function and Tests Flashcards

1
Q

What does the stomach do?

A

physical digestion - mechanical churning to make chyme

chemical digestion - gastric juice (acid and pepsin)

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2
Q

How are peptic ulcers formed?

A

H. pylori infection
weakens mucous coating of stomach and duodenum
stomach exposed to acid

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3
Q

How is H. pylori able to protect itself from stomach acid?

A

secretes urease which is alkaline

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4
Q

How do we diagnose peptic ulcers?

A

urea breath test (measure 13C labelled CO2 in breath - high concentration is positive)
serological tests for Ab to H-pylori
faecal antigen testing

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5
Q

How are peptic ulcers treated?

A

histamine antagonists
protein pump inhibitors
antibiotics to end infection

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6
Q

What is the Zollinger Ellison Syndrome?

A

gastrin producing tumours

–> gastric acid production –> ulceration

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7
Q

How is Zollinger Ellison syndrome diagnosed?

A

high gastrin

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8
Q

What are the 3 parts of the small intestine?

A

duodenum, jejunum, ileum

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9
Q

What are the common causes of acute pancreatitis?

A

alcoholism, gall stones

both cause interrupted blood flow to pancreas

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10
Q

How is acute pancreatitis confirmed clinically?

A

elevated serum amylase (5x ULN)
acute abdominal pain
low amylase =/= no pancreatitis

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11
Q

What are other causes of a high serum amylase?

A

peptic ulcer rupture, ectopic pregnancy, acute abdominal condition

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12
Q

What is acute pancreatitis?

A

acute inflammation of pancreas

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13
Q

What is chronic pancreatitis?

A

impaired secretion of pancreatic enzyme –> malabsorption

chronic inflammation

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14
Q

How do we test for chronic pancreatitis?

A

low faecal elastase (pancreas specific enzyme)

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15
Q

How do we treat chronic pancreatitis?

A

give pancreatic enzyme supplements

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16
Q

What is the function of bile salts?

A

digestion, absorption of lipids and fat-soluble vitamins

17
Q

What is bile salt malabsorption and its causes?

A

impaired reabsorption of bile salts - excess delivery into colon
produces toxic bile salts
leads to water diarrhoea
many causes

18
Q

How do we diagnose BSM using the 75-SeHCAT test?

A

75-SeHCAT bile acid is administered and retention is measured by gamma camera after 7 days
low retention is abnormal

19
Q

How do we use serum cholestenone to diagnose BSM?

A

measure levels in blood

if high indicates BSM as it is a BS synthesis metabolite

20
Q

What is malabsorption?

A

failure of the normal digestion and/or absorption of nutrients

21
Q

What are the consequences of malabsorption?

A

weight loss, failure to thrive, abdominal distension (nutrients ferment in stomach –> bloating), anaemia, bone disease (vit D, calcium deficiencies), diarrhoea

22
Q

How do we investigate malabsorption generally?

A 
clinical history
simple lab tests
- LFTs, 
- iron/anaemia testing
- calcium/mg test
- CRP 
- TFTs (metabolic rate)
- coeliac
23
Q

What are the specific tests of malabsorption?

A 
tissue transglutaminase Ab - coeliac
faecal calportectin - IBD
faecal elastase - pancreatic insufficiency
laxative screen (abuse)
urinary 5-HIAA - carcinoid
and imaging
24
Q

What is coeliac disease?

A

autoimmune disorder with sensitivity to gliadin component of gluten (wheat, barley, rye)

25
Q

What is the mechanism of coeliac disease?

A

exposure to gluten cause T-cell mediated response against transglutaminase
causes small intestine cell damage (villous atrophy)

26
Q

How do we diagnose coeliac disease?

A

presence of IgA tissue transglutaminase Ab in blood

definitive - endoscopy and intestinal sample examination

27
Q

What is the treatment for coeliac disease?

A

no gluten in diet

28
Q

What are 2 examples of inflammatory bowel disease?

A

Crohn’s and Ulcerative colitis

29
Q

What is Crohn’s disease?

A

chronic inflammation of bowel

30
Q

What is ulcerative colitis?

A

ulcers in small intestine

31
Q

How do we test for inflammatory bowel disease?

A

calprotectin in faeces due to GI inflammation

distinguishes IBD and IBS

32
Q

What is the mechanism of VIPoma/Verner Morrison Syndrome?

A

VIP (vasointestinal polypeptide) increases water/electrolyte secretion, increasing GI tract motility
(WDHA - watery diarrhoea, hypokalaemia, achlorhydria)

33
Q

What is the cause of Verner Morrison?

A

pancreatic tumours secreting excess VIP

34
Q

What is carcinoid syndrome?

A

tumours in GI tract, %-HT secretion,

lead to excretion of excess water/electrolytes, facial flushing (vasodilation)

35
Q

How do test for carcinoid syndrome?

A

measure 5-HIAA in urine

5-HIAA is a serotonin (5-HT metabolite)

36
Q

Why is more serotonin produced in carcinoid patients?

A

more tryptophan is metabolised through the 5-hydroxyindole pathway (increased serotonin and 5-HIAA production)

Clinical Biochemistry & Endocrinology 3 (7 decks)

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