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Clinical Physiology > Gastrointestinal disorders > Flashcards

Gastrointestinal disorders Flashcards

1
Q

List some examples of GIT disorders

A
  • Peptic ulcer disease
  • Osmotic and secretory diarrhoea
  • Gluten and lactose intolerance
  • Inflammatory bowel disorders
  • Cirrhosis
  • Acute pancreatitis
  • Gallstones
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2
Q

What causes mumps?

A

Viral infection of the salivary glands

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3
Q

What is a possible consequence of mumps particular to males?

A

Orchitis (testicular inflammation) that may cause infertility in adult males

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4
Q

Name the three types of gastric exocrine cells and the substances they excrete

A
  • Mucous cell
  • Parietal cell — HCL, intrinsic factor
  • Chief cell — digestive enzymes (most notably pepsinogen; converts to pepsin which breaks down proteins)
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5
Q

Name the three types of stomach endocrine cells and the substances they secrete

A
  • G-cells — release gastrin into blood
  • Enterochromaffin-like cells — secrete histamine (paracrine — effects only in the area of the gland secreting it)
  • D-cells (found mainly in duodenum but also pyloris) — secrete somatostatin (signals body to stop producing excess acid)
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6
Q

Gastrin is released from G-cells in response to what?

A

Distension of antrum/vagus nerve stimulation

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7
Q

What is the function of G-cells?

A

Promotes secretion of HCl and pepsinogen, as well as stomach motility

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8
Q

What inhibits gastrin secretion from G-cells?

A

Low pH (<4) and the hormone somatostatin

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9
Q

What does omeprazole do?

A

Shuts down acid production by proton pump inhibitors

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10
Q

What prevents the stomach digesting itself?

A

A mucous layer trapping HCO3- (local alkaline pH), giving a neutral buffer effect.

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11
Q

List four protective factors of gastroduodenal mucosa

A
  • HCO3- and mucous
  • Prostaglandins
  • Mucosal blood flow
  • Growth factors
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12
Q

List six damaging factors for gastroduodenal mucosa

A
  • H+ and pepsin
  • H. pylori
  • NSAIDs
  • Stress
  • Smoking
  • Alcohol
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13
Q

Ulcers cannot be present without ____.

A

Acid

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14
Q

What is the main cause of peptic ulcer disease?

A

Helicobacter pylori infection

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15
Q

List three contributing factors for peptic ulcer disease

A
  • Stress
  • NSAIDs
  • Alcohol
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16
Q

True or false: stress, NSAIDs, and alcohol are causal factors for peptic ulcer disease.

A
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17
Q

How does H. pylori cause peptic ulcer disease?

A

H. pylori has the enzyme urease which digests urea to produce NH3. It creates a small local area with favourable pH to withstand the harsh environment of the stomach.

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18
Q

Explain why peptic ulcer disease is so common in the duodenum

A
  • H. pylori infects the antrum of the stomach
  • This inhibits somatostatin secretion, leading to excess gastrin secretion
  • Increased H+ is delivered to the duodenum as acidic food boluses, causing the ulcer
  • The duodenum normally responds by secreting HCO3-, but this is inhibited by the H. pylori infection
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19
Q

Name two tests used to dx peptic ulcer disease

A

Urea breath test and endoscopy

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20
Q

Explain the urea breath test

A
  • The pt ingests urea with a small amount of radioactive carbon
  • H. pylori metabolises it to NH3 and radioactive CO2
  • The amount of radioactive CO2 exhaled is measured
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21
Q

Describe the rx for peptic ulcer disease

A
  • Omeprazole (proton pump inhibitor)
  • Antibiotics for H. pylori
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22
Q

What is Zollinger-Ellison syndrome?

A

Peptic ulcer disease caused by a tumour (gastrinoma)

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23
Q

Where is the gastrinoma often located?

A

Head of the pancreas

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24
Q

How does a gastrinoma cause peptic ulcer disease?

A

The tumour secretes large amounts of gastrin into the blood, inducing excessive H+ secretion by parietal cells

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25
Q

Describe three tests for dx of peptic ulcer disease that is not caused by a tumour

A
  • Serum gastrin levels — tested after fasting on at least three separate occasions (levels should be low)
  • Pentagastrin test — infusion of a gastrin homologue while H+ is monitored; normally would increase acid but if a gastrinoma already has levels extremely high there is little change
  • Secretin stimulation test — secretin stimulates gastrin secretion from a gastrinoma but not from healthy G-cells, i.e. gastrin increases when a tumour is present
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26
Q

Small intestine absorption is predicated on what factor?

A

Having a large surface area

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27
Q

Name the three sections of the small intestine

A

Duodenum, jejunum, and ileum

28
Q

Pts with celiac disease are intolerant of ____.

A

Gluten

29
Q

Celiac is an ____ condition.

A

Autoimmune

30
Q

What results from inflammation triggered by gluten ingestion in pts with celiac disease?

A

Damages villi, decreasing surface area and leading to malabsorption

31
Q

What is lactose intolerance, and what causes it?

A

Little/no lactase, a brush border enzyme that digests lactose. It is either genetic or acquired (after diarrhoea/gastroenteritis — may be temporary).

32
Q

What happens to lactose intolerance pts who ingest lactose or sorbitol?

A

Osmotic diarrhoea, and metabolism creates methane gas and H2

33
Q

How is lactose intolerance dx?

A
  • H2 breath test
  • Extra solutes in stool (increased faecal osmolar gap)
34
Q

What is the rx for lactose intolerance?

A

Lactase tablets, avoid lactose ingestion

35
Q

Name the four subtypes of diarrhoea

A
  • Osmotic — e.g. lactose intolerance
  • Rapid transit — hypermotility, bypass surgery
  • Inflammatory — inflammation of intestine
  • Secretory — increased secretion of fluid
36
Q

What causes secretory diarrhoea?

A

Bacterial; vibrio cholerae causing cholera or enterotoxigenic E. coli

37
Q

Explain the mechanism of secretory diarrhoea

A
  • Bacterial toxins bind receptors on secretory crypt cells
  • Irreversible activation of adenylate cyclase produces excess cAMP
  • Causes increased chloride secretion; water follows, causing severe dehydration and hypovolaemia
38
Q

How is secretory diarrhoea dx?

A

Identified bacteria in faeces

39
Q

What is used to rx secretory diarrhoea?

A

PO or IV rehydration solution (PO preferred — contains glucose which stimulates water uptake in small intestine)

40
Q

Describe the aetiology of IBD

A
  • Persistent specific infection
  • Dysbiosis
  • Defective mucosal barrier
  • Defective microbial clearance
  • Abnormal immunoregulation
41
Q

Explain dysbiosis

A
  • An altered balance of beneficial vs aggressive bacteria leading to a more pro-inflammatory intestinal flora
    • Aggressive bacteria include e. coli, bacteroides, and klebsiella
    • Beneficial bacteria include lactobacillis and bifidobacterium species
42
Q

List four functions of the liver

A
  • Metabolism — gets first pass of intestinal blood
  • Detoxification — making urea from nitrogen
  • Protein synthesis — albumin (retain fluid in capillaries), clotting factors (∴ bleeding disorders)
  • Excreting bile — bilirubin, bile salts (fat absorption)
43
Q

What is the purpose of the hepatic portal vein?

A

Not a true vein, it cleans the blood straight after absorption of nutrients in the intestine

44
Q

What causes jaundice?

A

Excess bilirubin due to liver dysfunction

45
Q

What is the source of bilirubin, and how is it excreted?

A

Produced by metabolism of haemoglobin (metabolism of old RBCs in spleen); extracted from blood by the liver and excreted in bile

46
Q

What causes neonatal jaundice?

A

Increased bilirubin ∴ immature liver not keeping up

47
Q

Increased bilirubin in blood, even in absence of obvious jaundice, can indicate what two things?

A

Liver disease or blockages such as gallstones

48
Q

What is hepatic steatosis?

A

Increased build-up of fat in the liver

49
Q

What is cirrhosis?

A

Chronic liver damage leading to scarring and liver failure

50
Q

Lack of coagulation factors (bleeding) and portal hypertension are indicative of what?

A

Liver failure

51
Q

What is ascites?

A

Fluid in the abdomen (peritoneum)

52
Q

Name two things that can cause cirrhosis

A

Liver inflammation and alcohol (not always)

53
Q

How does cirrhosis develop?

A

Normal liver cells die by necrosis and are replaces by connective tissue (fibrosis)

54
Q

What are bile salts?

A

Bile acids (cholesterol-based) conjugated to amino acids

55
Q

What is the meaning of ‘amphiphatic’?

A

Soluble in both fat and water

56
Q

How are bile salts recycled?

A

They are taken up by the enterohepatic circulation and transported back to the liver.

57
Q

Explain the link between ileal resection and bile salts

A
  • Bile salts are not recycled (bile salt malabsorption) and are left in the faeces
  • Leads to secretion of Cl- and water in the large intestine; secretory diarrhoea
58
Q

What is the common term for cholelithiasis?

A

Gallstones

59
Q

How is cholelithiasis dx?

A

Ultrasound

60
Q

What is the rx for cholelithiasis?

A

Surgical resection of the gallbladder

61
Q

What are the functions of the large intestine?

A
  • Absorption of water and some electrolytes
  • Synthesis of vitamins by ‘good bacteria’ (vitamin K, essential for coagulation)
  • Temporary storage of faeces before excretion
62
Q

What is diverticulosis?

A

Diverticula in the large intestine that are easy areas for bacteria to occupy

63
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulitis involves inflammation

64
Q

What causes diverticulosis?

A

Low fibre diet

65
Q

What is the enteric nervous system?

A

A division of the autonomic nervous system that governs the GIT

Clinical Physiology (11 decks)

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