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David's lecture > GI anatomy, pathophysiology and pharmacology > Flashcards

GI anatomy, pathophysiology and pharmacology Flashcards

1
Q

The oesophagus delivers food from the mouth to the stomach, but has little active involvement in digestion & absorption. TRUE OR FALSE?

A

TRUE

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2
Q

Absorption mostly takes place in small intestine. TRUE OR FALSE?

A

TRUE

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3
Q

Large intestine reabsorbs water from indigestible products allowing solid waste to be expelled. TRUE OR FALSE?

A

TRUE

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4
Q

The gastric wall Multiple basal layers of

muscle allow churning of contents. TRUE OR FALSE?

A

TRUE

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5
Q

Oxyntic glands contain parietal cells which secrete acid. TRUE OR FALSE?

A

TRUE

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6
Q

What did chief cells secrete?

A

Pepsinogen, gastric lipase

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7
Q

What do G cells and D cells secrete?

A

G cells - Gastrin

D cells - Somatostatin

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8
Q

What does Enterochromaffin

Cells secrete?

A

Atrial natriuretic peptide (ANP)

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9
Q

Pyloric glands secrete gastrin. TRUE OR FALSE?

A

TRUE

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10
Q

How much gastric juice is secreted per day?

A

2000-3000ml

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11
Q

Carbonic anhydrase makes H2CO3 which dissociates into H+ and HCO3. TRUE OR FALSE?

A

TRUE

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12
Q

The Cardia and the pylorus both have sphinches which control entry to and exit to the stomach. TRUE OR FALSE?

A

TRUE

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13
Q

What is the purpose of the mucosa in the GI wall?

A
  • Digestion and absorption of nutrients
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14
Q

What is the purpose of the submucosa in the GI wall?

A
  • Distribution of nutrients to rest of body
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15
Q

What is the purpose of the muscularis in the GI wall?

A
  • For movement of nutrients along the GI tract
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16
Q

Glandular cells that secrte various things and together does not form the gastric glands. TRUE OR FALSE?

A

FALSE

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17
Q 
What do each of these cells secrete? 
Parietal cells
Chief cells 
Mucous cells
ECL Cells
G Cells 
D Cells
Enterochromaffin Cells
A

Parietal cells - HCL, intrinsic factor, vitamin B12
Chief cells - Pepsinogen, Gastric lipase
Mucous cells - Mucous, bicarbonates
ECL Cells - Histamine
G Cells - Gastrin
D Cells - Somatostatin
Enterochromaffin Cells - Atrial natriuretic peptide (ANP)

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18
Q

Oxytinc gland does not secret gastric acid. TRUE OR FALSE?

A

FALSE

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19
Q

K+/H+ ATPase isn’t controlled by calcium and by cAMP. TRUE OR FALSE?

A

FALSE

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20
Q

Gastrin binds to the CCKB receptor and Ach binds to M3 receptor. TRUE OR FALSE?

A

TRUE

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21
Q

CCKB and M3 activation leads to an increase in calcium. TRUE OR FALSE?

A

TRUE

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22
Q

How is gastric acid secretion regulated (Ach and gastrin)?

A

An increase in calcium, incraeses the number of proton K+/H+ ATPase and there by increases the amount of acid that is secreted

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23
Q

How do Prostangladins, histamine and somatostatins regulate gastric acid secretion?

A

Histamine - It binds to H2 receptors, this increases cAMP which leads to increased activity of K+/H+ ATPase, so we obtain more protons pumped out into the lumen of the stomach

Prostangladins - The prostangladins binds to EP2/3R receptors helps to decrease cAMP production this leads to a decrease in K+/H+ ATPase activity and less H+ are pumped into the lumen of the stomach so less gastric production

Somatostatin - Decreases cAMP and there by decreasing the amount of protons being pumped into the lumen of the stomach

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24
Q

Pyloric glands can be stimulated by high pH and by gastirc distention. TRUE OR FALSE?

A

TRUE

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25
Q

High pH and gastric distention leads to pyloric glands secreting gastrin, this causes the oxytinc glands parietal cells to be stimulated by gastrin, leading to an increase in acid secretion. TRUE OR FALSE?

26
Q

The mucous maintains a pH gradient at cell surface. TRUE OR FALSE?

27
Q

What does the hydrophobic layer of mucous prevent? liquid from the stomach getting to the mucous cells

A

liquid from the stomach getting to the mucous cells

28
Q

What does the imbalance between acid poduction and mucosal protection lead to?

A
  • Acid damaging the submucosal layer

- Pepsin digetsion of submucosal layer

29
Q

What is dyspepsia?

A
  • Symptoms associated with upper GI tract e.g heartburn, pain, nausea, patients may describe it as indigestion
30
Q

What are the symptoms of peptic ulcers?

A
  • Crater like wound in mucosa of upper GI tract or stomach

- May lead to haemorrhage and perforations, inflammation

31
Q

What are the two important factors of developing peptic ulcer?

A
  • Helicobacter pyloric infection

- NSAID treatment

32
Q

How does H.pyloric infection lead to the development of peptic ulcers?

A

H.pylori protected in the mucous gel secretes agets causing a persistant inflammation that weakens the mucosal barrier

33
Q

How do NSAIDS cause development of peptic ulcers?

A

Prostanglandins reduce acid secretion incraese mucous and bicarbonates secretion and increases mucosal blood flow. NSAID (COX inhibitors) reduce this

34
Q

How does drug treatment of peptic ulcer aim to promote ulcer healing?

A
  • By reducing acid secretion
  • By increasing mucosal resistance
  • By eradication of H.pylori
35
Q

What is a peptic ulcer?

A

Full thickness breach of mucosa in lower oesophagus, stomach or duodenum that fails to heal over a reasonable period

36
Q

What are some complications of peptic ulcer?

A

Haemorrhage – typically in duodenal ulcers which erode into the gastroduodenal artery leading to haematemesis

Perforation – acute abdominal pain and generalized peritonitis

Fibrous stricture – obstruct gastric outflow

37
Q

Oxytinc glands are predominately in the corpus and pyloric glands are predominately in the pylorus. TRUE OR FALSE?

38
Q

H. Pylori-associated gastritis is the most Most common cause of gastritis; bacterial transmission is from person to person, Lives in the mucus layer of the
stomach. TRUE OR FALSE?

39
Q

H. pylori induced inflammation does not lead to atrophy of oxyntic glands & reduced acid secretion. TRUE OR FALSE?

40
Q

There is an increase risk of cancer if peptic ulcer is due to H.pyloric infection. TRUE OR FALSE?

41
Q

H. pylori induced inflammation leads to increased gastrin secretion and decreased somatostatin secretion parietal cell proliferation and acid hypersecretion (via endocrine effect on oxyntic glands)
TRUE OR FALSE?

42
Q

Excess acid in the duodenum overwhelms mucosal and acid-neutralising protective mechanisms which leads to duodenal ulcers. TRUE OR FALSE?

43
Q

NSAIDs inhibit prostanglandin production. TRUE OR FALSE?

44
Q

What gastroduodenal protective effects does Endogenous prostaglandins have ?

A
  • Reduce HCL prodiction

- Increase mucus and bicarbonate production – better protection of gastric epithelium

45
Q

Aspirin doses as low as 10 mg/day inhibit gastric PG

production and cause stomach damage. TRUE OR FALSE?

46
Q

Proton pump inhibitors, prevents the activity of K+/H+ ATPase. TRUE OR FALSE?

47
Q

GIve an example of PPI drug?

A

-Omeprazole

48
Q

Why does omeprazole accumulate in parietal cells?

A

At neutral pH:

  • Freely membrane permeable
  • Easily enters parietal cells

At pH less than 4:

  • Membrane permeability much reduced
  • Trapped in parietal cells
49
Q

Omeprazole does not covalently bind to H+/K+ ATPase. TRUE OR FALSE?

50
Q

Give an example of a H2 antagonist?

A
  • Cimetidine
51
Q

cimetidine inhibits P450 – potential interaction with several drugs (oral anticoagulats, tricyclic antidepressants)

cimetidine inhibits liver blood flow – so can reduce clearance of drugs that have high hepatic
metabolism, increasing their conc. (eg propanolol)

Are these staments true or false?

52
Q

What are the treatment options of H. pyloric infection?

A
  • Amoxicillin

Triple therapy with PPI plus antibacterial agent for 1 to 2 weeks

53
Q

Give an example of a prostglandin E receptor agonist and some cautions related to this drug?

A
  • Misoprostol
    Cautions:

potent uterine stimulant (has been used to induce abortion)

inflammatory bowel disease; conditions where hypotension might precipitate severe
complications (e.g. cerebrovascular disease,cardiovascular disease)

54
Q

Antacids:

Simplest form of therapy; directly neutralise acids, raising gastric pH. TRUE OR FALSE?

55
Q

What is GORD (reflux oesophagitis) and what is it caused by?

A

is the commonest oesophageal disorder

Cause: reflux of gastric content from stomach to
oesophagus

56
Q

Most patients with GORD will have hiatus hernia (although most patients with hiatus hernia do not have GORD). TRUE OR FALSE?

57
Q

What are the symptoms of Oesophageal Hiatus Hernia?

A
  • Etrosternal pain (heartburn)
  • Any upper abdominal symptoms
    may occur
58
Q

What are the complications of Oesophageal Hiatus Hernia?

A

GORD is a common condition however only a minority develops serious complications:
• Peptic stricture
• Barett’s oesophageus

59
Q

what is Peptic stricture?

A
  • Enign narrowing of oesophagus

- Hould be differentiated from oesophageal carcinoma

60
Q

What is Barrett’s oesophagus?

A
  • Normal squamous epithelia replaced by metaplastic columnar epithelium
  • Recursor lesion of oesophageal adenocarcinoma
61
Q

What are some of the CORD therapy?

A
  • Surgery

Pharmacological Treatment:
– Antacids and alginate
– H2 antagonists
–Proton pump inhibitor

Gastroprokinetic drugs
– increase rate of gastric emptying e.g metoclopramide

David's lecture (13 decks)

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