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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
Synthetic Opioids
Anti-motility agents (a type of anti-diarrhoeal)
26
Synthetic Opioids - mechanism
Agonist of opioid receptors expressed by enteric neurons >> inhibit the enteric nervous system >> decreased peristalsis, increased segmentation >> increased fluid absorption OVERALL CONSTIPATING EFFECT
27
Synthetic Opioids names
Loperamide (imodium) **used most often because has little CNS effect Codeine phosphate Diphenoxylate
28
Synthetic Opioids - contraindications
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)
29
Rehydration Therapy - mechanism
Na+ and glucose in the rehydration salts is absorbed via SGLT1 - water follows them and is absorbed too
30
Constipation
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
Constipation - common causes
Lack of fibre and fluid intake Lack of physical activity Drugs (e.g. opioids) Obstruction
32
Laxatives - categories
1) Bulking 2) Osmotic 3) Stimulant
33
Laxatives should only be used ----------
for a short time and where other interventions (e.g. exercise, diet change) have failed
34
Bulking laxatives - mechanism
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
Bulking laxatives names
**Ispaghula husk** Methylcellulose Sterculia
36
Bulking laxatives - contraindications
Bowel obstruction | Ileus (lack of movement of the intestine)
37
Osmotic laxatives - mechanism
``` Cause osmosis (sugars, alcohols) → by osmosis, water travels into the stool ↑bulk of the stool → peristalsis is stimulated ```
38
Osmotic laxatives names
Lactulose (treats hepatic encephalopathy) Macrogols Phosphate enema Citrate enema
39
Osmotic laxatives - contraindications
Bowel obstruction | Heart failure, ascites, electrolyte disturbances (phosphate enema)
40
Stimulant laxatives - mechanism
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
Stimulant laxatives names
``` **Senna** Glycerol suppository Bisacodyl Docusate sodium Sodium picosulfate ```
42
Stimulant laxatives - contraindications
Bowel obstruction | Prolonged used → atonic colon
43
Stimulant laxatives - side effects
abdominal pain
44
Drugs to control gastric acid secretion
1) Proton pump inhibitors 2) H2 receptor antagonists 3) Compound alginates
45
Drugs to treat diarrhoea
1) Anti-diarrhoeals/anti-motility drugs: synthetic opioids | 2) Rehydration therapy
46
Drugs to treat constipation
Laxatives
47
Nausea
Unpleasant sensation normally felt in throat and stomach. Can involve pallor, sweating, salivation. Can be acute or chronic.
48
Retching
Rhythmic reverse peristalsis Involuntary abdominal and diaphragm contraction Dry (no vomitus)
49
Emesis
Forceful expulsion of gastric/intestinal contents out the mouth
50
Events of vomiting
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
Stimulation of vomiting
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
Iatrogenic vomiting can be caused by:
chemo, general anaesthetics, certain drugs especially morphine and SSRIs
53
Consequences of vomiting
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
5-HT3 antagonists names
“setrons” | Ondansetron, palonosetron
55
5-HT3 antagonists - mechanism
Block 5-HT3 receptors to reduce nausea in the vomiting centre
56
5-HT3 antagonists - uses
nausea due to chemo
57
Muscarinic acetylcholine - uses
prophylaxis of motion sickness
58
Muscarinic acetylcholine names
Hyosine, scopolamine
59
Muscarinic acetylcholine - mechanism
Mechanism unclear - combination of CNS effect and reduced gastric motion
60
Histamine H1 antagonists names
Cyclizine, cinnarizine
61
Histamine H1 antagonists - uses
prophylaxis of nausea due to inner ear pathology
62
Histamine H1 antagonists - mechanism
Blocks H1 in the vestibular nuclei
63
Dopamine receptor antagonists names
Domperidone, metoclopramide
64
Dopamine receptor antagonists - uses
drug induced vomiting
65
Dopamine receptor antagonists - mechanism
Complex mechanism: blocks D2/3, acts as a prokinetic
66
Metoclopramide is given with ------------- very commonly
morphine
67
NK1 antagonists names
Aprepitant
68
NK1 antagonists - uses
Used with 5-HT3 antagonists for severe chemo induced nausea
69
Cannabinoid receptor agonists
Nabilone
70
Cannabinoid receptor agonists - uses
Used for those unresponsive to other anti-emetics
71
Cannabinoid receptor agonists - mechanism
Stimulation of the brain (? opiate receptors) causes a decrease in vomiting
72
Antiemetics - classes
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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