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GI > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Making HCl in the parietal cell

A

1) Carbonic acid is produced by water + CO2 via carbonic anhydrase
2) HCO3- and H+ are produced
3) HCO3- is pumped out of the cell in exchange for Cl- which is pumped into the canaliculus
4) H+ is pumped into the canaliculus
5) H+ and Cl- make HCl

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2
Q

Transport protein that moves HCl into the canaliculus

A

Proton pump

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3
Q

Canaliculus

A

Small channel found on gastric parietal cells to increase surface area for secretion.
Together, many canaliculi form an extensive secretory network on the cell surface.

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4
Q

Secretagogues (causing HCl secretio) act via the 3 receptors

A

ACh&raquo_space;> M3
Gastrin&raquo_space; G/CCK2
Histamine&raquo_space; H2

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5
Q

Mechanism of increasing HCl secretion by ACh

A

ACh binds to the receptor :↑cAMP, ↑proton pumps, ↑ acid secretion

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6
Q

Mechanism of increasing HCl secretion by gastrin

A

Gastrin bind to the receptor: ↑Ca2+, ↑ proton pumps, ↑ acid secretion

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7
Q

Mechanism of increasing HCl secretion by histamine

A

Histamine binds to the receptor: ↑cAMP, ↑ proton pumps, ↑ acid secretion

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8
Q

Proton Pump Inhibitors (PPIs) - mechanism

A

Irreversibly inhibits proton pump (H+/K+ATPase) to decrease HCl production.

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9
Q

Why must PPIs be taken 20 minutes before eating?

A

They do not work on proton pumps in the tubulovesicle, so must be taken 20 minutes before eating because this is the same time frame for proton pumps to move to the canalicular membrane before digestion.

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10
Q

PPI names

A

Omeprazole
Lanosprazole
Pantoprazole

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11
Q

PPI - adverse effects

A

Less acidic stomach environment reduces defence against infection (C.diff)
Masks symptoms of gastric malignancy
Risk of osteoporosis

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12
Q

H2 Receptor Antagonists - mechanism

A

Blocks H2 receptors so histamine cannot act on the parietal cell, to decrease HCl production.

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13
Q

Why are H2 receptor antagonists less effective than PPIs?

A

PPIs block the proton pumps directly, whereas with H2 receptor antagonists only the histamine-mediated component of acid secretion is blocked (ACh and gastrin are still capable of causing acid secretion)

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14
Q

H2 Receptor Antagonists names

A

Ranitidine
Cimetidine
Famotidine
Nizatidine

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15
Q

H2 Receptor Antagonists - adverse effects

A

masks symptoms of gastric malignancy

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16
Q

Compound Alginates - mechanism

A

Have antacid and alginate function:

1) Buffer HCl and make stomach pH more neutral
2) Increase viscosity of gastric juice, react with acid to produce a foam layer that protects the oesophagus

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17
Q

Compound Alginates names

A

Peptac
Gaviscon
Mucogel (antacid only)

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18
Q

NSAIDs - effect on gastric acid secretion

A

Inhibit COX-1, which affects prostaglandin production. Less prostaglandin is available so ↑HCl
INCREASED RISK OF PEPTIC ULCER

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19
Q

NSAIDs names

A

Aspirin
Ibuprofen
Diclofenac
Naproxen

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20
Q

What does NSAID stand for?

A

non-steroidal anti-inflammatory drug

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21
Q

Prostaglandins and somatostatin - effect on gastric acid secretion

A

Reduce the effect of the secretagogues and inhibit gastric acid secretion

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22
Q

Prophylaxis for NSAID induced peptic ulcer

A

Misoprostol (prostaglandin E1 analogue)

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23
Q

Diarrhoea

A

loss of fluid and solutes from the GI tract making stool loose and watery (>3 loose stools in 24hrs) → leads to dehydration

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24
Q

Diarrhoea - causes

A

1) Activation of CFTR e.g. by bacterial enterotoxins
(more Cl- is secreted, Na+ and water follow)
2) Impaired absorption of NaCl
(water can’t follow NaCl into blood)
3) Non-absorbable/poorly absorbable solutes
e.g. malabsorption syndromes
4) Hypermotility
(Lumenal contents progress too rapidly, reduced absorption)

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25
Q

Synthetic Opioids

A

Anti-motility agents (a type of anti-diarrhoeal)

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26
Q

Synthetic Opioids - mechanism

A

Agonist of opioid receptors expressed by enteric neurons&raquo_space; inhibit the enteric nervous system&raquo_space; decreased peristalsis, increased segmentation&raquo_space; increased fluid absorption
OVERALL CONSTIPATING EFFECT

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27
Q

Synthetic Opioids names

A

Loperamide (imodium) **used most often because has little CNS effect
Codeine phosphate
Diphenoxylate

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28
Q

Synthetic Opioids - contraindications

A

ABCD
Acute UC (risk of megacolon/perforation)
Babies (don’t give to children)
C.diff colitis (these drugs can make it worse)
**don’t use in hospitals until C.diff is ruled out
Dysentery (bloody diarrhoea)

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29
Q

Rehydration Therapy - mechanism

A

Na+ and glucose in the rehydration salts is absorbed via SGLT1 - water follows them and is absorbed too

30
Q

Constipation

A

passage of ≤2 bowel movements a week, often passed with difficulty, straining or pain and a sense of incomplete evacuation.
(delay in defaecation + enhanced absorption of water) → presence of hard, dried faeces within colon

31
Q

Constipation - common causes

A

Lack of fibre and fluid intake
Lack of physical activity
Drugs (e.g. opioids)
Obstruction

32
Q

Laxatives - categories

A

1) Bulking
2) Osmotic
3) Stimulant

33
Q

Laxatives should only be used ———-

A

for a short time and where other interventions (e.g. exercise, diet change) have failed

34
Q

Bulking laxatives - mechanism

A

Indigestible by the small intestine so add to faecal mass, and cause the stool to absorb water.
↑ bulk of the stool → peristalsis is stimulated

35
Q

Bulking laxatives names

A

Ispaghula husk
Methylcellulose
Sterculia

36
Q

Bulking laxatives - contraindications

A

Bowel obstruction

Ileus (lack of movement of the intestine)

37
Q

Osmotic laxatives - mechanism

A 
Cause osmosis (sugars, alcohols) → by osmosis, water travels into the stool
↑bulk of the stool → peristalsis is stimulated
38
Q

Osmotic laxatives names

A

Lactulose (treats hepatic encephalopathy)
Macrogols
Phosphate enema
Citrate enema

39
Q

Osmotic laxatives - contraindications

A

Bowel obstruction

Heart failure, ascites, electrolyte disturbances (phosphate enema)

40
Q

Stimulant laxatives - mechanism

A

Stimulate intestinal motility and intestinal secretion
(by increasing mucosal electrolyte/water secretion, + stimulating enteric nerves)
↑bulk of the stool → peristalsis is stimulated
↑intestinal motility → ↑stool movement through the intestine

41
Q

Stimulant laxatives names

A 
**Senna**
Glycerol suppository
Bisacodyl
Docusate sodium
Sodium picosulfate
42
Q

Stimulant laxatives - contraindications

A

Bowel obstruction

Prolonged used → atonic colon

43
Q

Stimulant laxatives - side effects

A

abdominal pain

44
Q

Drugs to control gastric acid secretion

A

1) Proton pump inhibitors
2) H2 receptor antagonists
3) Compound alginates

45
Q

Drugs to treat diarrhoea

A

1) Anti-diarrhoeals/anti-motility drugs: synthetic opioids

2) Rehydration therapy

46
Q

Drugs to treat constipation

47
Q

Nausea

A

Unpleasant sensation normally felt in throat and stomach. Can involve pallor, sweating, salivation.
Can be acute or chronic.

48
Q

Retching

A

Rhythmic reverse peristalsis
Involuntary abdominal and diaphragm contraction
Dry (no vomitus)

49
Q

Emesis

A

Forceful expulsion of gastric/intestinal contents out the mouth

50
Q

Events of vomiting

A

1) intestinal slow wave activity stops
2) retrograde contraction from ileum to stomach
3) glottis is closed, breathing stops (prevents aspiration)
4) lower oesophageal sphincter relaxes
5) diaphragm and abdominal muscles contract
6) gastric contents is ejected
* *NOT STOMACH CONTRACTION

51
Q

Stimulation of vomiting

A

1) Toxic materials/drugs in blood stimulate brain directly (affected areas lack a blood/brain barrier)
2) Mechanical stimuli (GI tract pathology)
3) Vestibular system (inner ear)
4) CNS stimulation (pain, repulsion, fear, psychological)

52
Q

Iatrogenic vomiting can be caused by:

A

chemo, general anaesthetics, certain drugs especially morphine and SSRIs

53
Q

Consequences of vomiting

A

1) Dehydration
2) Loss of gastric protons and chloride
(metabolic alkalosis)
This also causes hypokalaemia (don’t worry why)
3) Oesophageal damage (Mallory-Weiss tear)

54
Q

5-HT3 antagonists names

A

“setrons”

Ondansetron, palonosetron

55
Q

5-HT3 antagonists - mechanism

A

Block 5-HT3 receptors to reduce nausea in the vomiting centre

56
Q

5-HT3 antagonists - uses

A

nausea due to chemo

57
Q

Muscarinic acetylcholine - uses

A

prophylaxis of motion sickness

58
Q

Muscarinic acetylcholine names

A

Hyosine, scopolamine

59
Q

Muscarinic acetylcholine - mechanism

A

Mechanism unclear - combination of CNS effect and reduced gastric motion

60
Q

Histamine H1 antagonists names

A

Cyclizine, cinnarizine

61
Q

Histamine H1 antagonists - uses

A

prophylaxis of nausea due to inner ear pathology

62
Q

Histamine H1 antagonists - mechanism

A

Blocks H1 in the vestibular nuclei

63
Q

Dopamine receptor antagonists names

A

Domperidone, metoclopramide

64
Q

Dopamine receptor antagonists - uses

A

drug induced vomiting

65
Q

Dopamine receptor antagonists - mechanism

A

Complex mechanism: blocks D2/3, acts as a prokinetic

66
Q

Metoclopramide is given with ————- very commonly

67
Q

NK1 antagonists names

A

Aprepitant

68
Q

NK1 antagonists - uses

A

Used with 5-HT3 antagonists for severe chemo induced nausea

69
Q

Cannabinoid receptor agonists

70
Q

Cannabinoid receptor agonists - uses

A

Used for those unresponsive to other anti-emetics

71
Q

Cannabinoid receptor agonists - mechanism

A

Stimulation of the brain (? opiate receptors) causes a decrease in vomiting

72
Q

Antiemetics - classes

A

1) 5-HT3 antagonists (chemo)
2) Histamine H1 antagonists (inner ear)
3) Muscarinic acetylcholine (motion sickness)
4) Dopamine receptor antagonists (drug-induced)
5) NK1 antagonists (severe chemo nausea)
6) Cannabinoid receptor agonists (unresponsive nausea)

GI (9 decks)

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