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Pharm Y2S2 Patient > GI Physiology and Therapeutics > Flashcards

GI Physiology and Therapeutics Flashcards

1
Q

What does the alimentary canal comprise of?

A

Specialised organs, tissues and accessory structures

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2
Q

What is the GIT made up of?

A 
Mouth 
Pharynx
Oesophagus
Stomach 
Small intestine (duodenum, jejunum, ileum)
Large intestine 
Rectum 
Colon
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3
Q

What are the functions of the salivary glands?

A
  • Secrete amylase and lipase

- produce mucin to help with lubrication

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4
Q

What are the 3 sets of salivary glands?

A

Sublingual
Submandibular
Parotid

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5
Q

What is mumps?

A

An infection of glands including salivary, testes and pancreas

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6
Q

How is swallowing coordinated?

A

Through complex tactile receptors that relay information to the medullar oblongata

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7
Q

Which nerves re involved in swallowing?

A 
Trigeminal
Facial 
Glossopharyngeal 
Vagus 
Spinal accessory  
Hypoglossal
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8
Q

What can happen in stroke patients in terms of swallowing?

A

If there is damage to the nerves it can result in dysphagia

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9
Q

How does food get to the diaphragm?

A

From the oesophagus - leads to the top of the stomach

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10
Q

What kind of cells is the oesophagus lined with?

A

squamous epithelial cells

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11
Q

What is the purpose of the oesophageal sphincter?

A

Contracts and seals the top of the stomach preventing acid / enzymes from passing into the oesophagus

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12
Q

What is Barrett’s oesophagus?

A

Erosion of the oesophagus cells which occurs when exposed to stomach fluid - the cells are replaced with abnormal cells which are pre-cancerous

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13
Q

What happens to abnormal cells in Barrett’s oesophagus is reflux is controlled?

A

The oesophagus heals but the abnormal cells remain - high risk of adenocarinoma

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14
Q

What is a hiatus hernia?

A

Hernia that occurs when the stomach gets through the diaphragm - associated with acid reflux

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15
Q

What do G cells do?

A

secrete gastrin

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16
Q

What do chief cells do?

A

secrete pepsinogen / lipase

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17
Q

What is pepsinogen?

A

an inactive form of pepsin

- acid cleaves pepsinogen to produce pepsin

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18
Q

What do parietal cells do?

A

secret HCl

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19
Q

What effect does the sight or smell of food have?

A

Triggers impulses causing a reaction in the stomach, Ache is released - this binds to a receptor leading to the release of HCl

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20
Q

What does distention of the stomach cause?

A

Release of histamine which binds to its receptor causing HCl release

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21
Q

What do H2 antagonists do?

A

Bind to histamine receptor / inhibit the effects of histamine

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22
Q

Give examples of 2 H2 antagonists

A

Limetidine

Ranitidine

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23
Q

Which drug is used to inhibit the gastric proton pump?

A

Omeprazole

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24
Q

What is the process of HCl production / release

A
  • HCl needs to get from blood and into the lumen.
  • Cl- moves out of the blood and into the cell, they diffuse across the cytosol.
  • CO2 + H20 (from living cells) - the reaction is catalysed by carbonic anhydrase to prodcce carbonic acid. This splits to carbonate ions (taken out of the cell) and H+.
  • The protons are pumped out of the cell.
  • H+ and Cl- combine to form HCl
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25
Q

What is the pH of the stomach and why is this a problem ?

A

1-2 - leads to drug inactivation

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26
Q

What is the stomach made up of?

A

Proteases and pepsinogen

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27
Q

What is the purpose of pepsinogen?

A

It prevents self-digestion - the cells are not exposed to the active protease

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28
Q

Why doesn’t the stomach digest itself?

A
  1. Foveolar cells produce mucus which is alkaline so neutralises HCl
  2. Tight junctions: protein complexes lock epithelial cells together which restricts movement of acid / protease
  3. High cell turnover: damaged ells are replaced every 2-3 days
29
Q

What would happen if the mucus barrier of the stomach broke down?

A

Stomach / duodenal cells would be exposed to HCl / pepsin leading to a gastric / duodenal ulcer

30
Q

How is peritonitis caused?

A

When food secretions and bacteria move into the peritoneal cavity - in case of perforated ulcer

31
Q

What does Helicobacter pylori do?

A

Infects gastric mucosa reduced barrier efficacy - leads to an ulcer. If eradicated ulcer recurrence is low.

32
Q

What is the treatment for H.pylori?

A

2 antibiotics and a PPI

  • Clarithromycin, amoxicillin or metronidazole
  • Omeprazole (or esomeprazole, lansoprazole etc)
33
Q

How can H.pylori be detected?

A
  1. Urea breath kit - patient swallows 13C labelled urea solution, urease activity by the organism produces labelled CO2
  2. Mucosal biopsies test urease
  3. Histopathology
  4. Cultures
34
Q

What do high antibody titres (H.pylori) indicate?

A

There is an active infection

35
Q

How long should H.pylori treatment last?

A

7 days

Max of 2 months if symptoms recur

36
Q

What is chyme?

A

Contents of stomach emptied into the duodenum

37
Q

What is peristalsis?

A

a wave of muscular contraction that goes through the intestines

38
Q

What do circular muscles of the small intestine do?

A

Contract to narrow lumen preventing back flow

39
Q

What do longitudinal muscles of the small intestine do?

A

contract to squeeze bolus along the GIT

40
Q

What does a gastric sleeve leave?

A

~15% of the original stomach

41
Q

What does a gastric band do?

A

Reduces stomach capacity - the top part of the stomach is bound

42
Q

What is diarrhoea?

A

Excessive fluid and ion loss

43
Q

What is the myenteric plexus?

A

A layer of the intestine containing nerves. Inhibits reduce longitudinal muscle.

44
Q

How does loperamide work?

A

Targets µ opioid receptors of MP which reduces muscle tone

It ↑ salt and water reabsorption by reducing motility of gut muscles

45
Q

Where does bile acid synthesis happen and where are they stored?

A

Synthesised in the liver

Stored in the gall bladder

46
Q

What do bile acids do?

A

Emulsify lipids allowing them to be absorbed

47
Q

How is the small intestine adapted for digestion and absorption?

A
  1. Pilcae increase surface area
  2. Epithelium is only one cell thick
  3. Enzymes conver macromolecules into small molecules
48
Q

What does SGLT1 transport?

A

Glucose and galatose into enterocytes - it is a Na+ dependent process

49
Q

What does GLUT5 transport?

A

Fructose - not sodium dependent

50
Q

How are monosaccharides transported out of enterocytes?

A

By transporters in the basolateral membrane

51
Q

What does PEPT1 transport?

A

Small peptides and amino acids - H+ dependent

52
Q

What do drug efflux transporters do?

A

Remove drugs from cells, they are effluxes into the gut lumen resulting in reduced absorption

53
Q

Give examples of 2 efflux transporters

A

P-glycoprotein

Breast cancer resistance protein

54
Q

What is extravasation?

A

When a drug leads out of capillaries and comes in contact with tissue - leads to cell death

55
Q

What is GORD?

A

Gastro oesophageal reflux disease, it causes chronic heart burn symptoms, it can cause chronic cough, laryngitis and is associated with asthma

56
Q

The danger eliminations of GORD?

A 
Anaemia
loss of weight 
anorexia 
recurrent problems
melaena / haematemsis
swallowing
57
Q

What can give symptomatic relief from GORD?

A
  • Alginates, they have antacid properties

- Antacids

58
Q

What effects can alienates and antacids have?

A

Can affect absorption of other drugs if taken at the same time. They increase pH which can damage enteric coating

59
Q

What are the side effects of H2 antagonists?

A

Headaches
Diarrhoea
Dizziness

60
Q

What does cimetidine interact with?

A

Warfarin - inhibits metabolism
Phenytoin, carbamazepine and valproate - ↓ metabolism
Theophylline - ↓ metabolism
Sildenafil - ↑ plasma concs

61
Q

What is the treatment for NSAID associated ulcers?

A

If H.pylori negative stop NSAID but if still needed:

  • PPI long term at same dose
  • PPI and when healed which to misoprotol
  • PPI and switch to selective COX2 inhibitor (ibuprofen)
  • Give combo of naproxen / esomeprazole OR ketoprofen / omeprazole
62
Q

What are the types of stool on the Bristol Stool Chart?

A
  • Type 1 & 2 → indicate constipation
  • Type 3 & 4 → easiest to pass
  • Type 5 & 6 → symptomatic of diarrhoea
  • Type 7 → sign of cholera or food poisoning
63
Q

What is diarrhoea caused by?

A
  • Failure to absorb fluids (infective cause or IBD)
  • Osmotic effects (unabsorbed food / enzyme deficiencies)
  • Motility problem
64
Q

What are red flag diarrhoea symptoms?

A
  • Unexplained weight loss
  • Rectal bleeding
  • Persistent diarrhoea
  • Systemic illness
  • Recent hospital
  • Following foreign travel
65
Q

What could travellers diarrhoea be caused by?

A
  • Enterotoxigenic E.coli
  • Campylobacter
  • Salmonella
  • Shigella
  • Parasites
  • Viruses
66
Q

What is the aim of diarrhoea treatment?

A

Prevent / revere fluid and electrolyte loss and manage dehydration

67
Q

What properties should ORS solutions have?

A
  • Enhance absorption
  • Replace electrolytes
  • Simple to use
  • Be palatable and acceptable
  • Readily available
68
Q

What function does dextrose or rice powder have in ORS?

A

Act as carbohydrates for active absorption of electrolytes

69
Q

Which 2 drugs can be used as treatment for diarrhoea?

A

Naloxone and Loperamide

Pharm Y2S2 Patient (2 decks)

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