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Bloc E - GI & Metabolism > Feb22 M3-Antacids and prokinetic drugs > Flashcards

Feb22 M3-Antacids and prokinetic drugs Flashcards

1
Q

ulcers cause+consequence and therapeutic goal

A

cause: bacterial infections
consequence: higher acidity in stomach
goal: stop excessive acid in stomach

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2
Q

direct way of reducing stomach acid

A

PPI blocks H (out) K (in) ATPase on luminal surface of parietal cell

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3
Q

4 receptors on parietal cell basal side regulating HCl secretion + effect

A
  • M3 (muscarinic R): activates Ca dep pathway to release more HCl
  • gastrin R (Ca dep pathway too)
  • histamine R (activates cAMP dep pathway to release more HCl)
  • PG R (blocks Ca dep pathway)
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4
Q

drugs acting indirectly on parietal cell to reduce acid secretion and one acting to increase it

A
  • musc antag
  • CCK2 (gastrin) R antag
  • histamine R antag
  • NSAIDs increase it
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5
Q

direct way of neutralizing stomach acid

A

bases (chemistry). many drugs like that

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6
Q

final problem of stomach acidity (why block it)

A

acid activates pepsin. overtime destroys wall of stomach = ulcers

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7
Q

drug blocking stomach wall

A

sucralfate (helps mucous layer)

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8
Q

how to tackle main cause of peptic ulcer

A

Abx (bacterial infection): bismuch, metro, tetracycline

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9
Q

(imp?) 5 drugs used for ULCER therapy

A
  1. antacids to neutralize
  2. cimetidine (H2i)
  3. propantheline (M1 M3 blocker)
  4. adenylate cyclase blockers (cAMP = histamine pathway)
  5. PPI
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10
Q

problems with cimetidine + alternative

A

ranitidine (better H2i). less anti-androgenic effects, longer action, no drug interaction (no p450 interaction)

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11
Q

omeprazole (PPI) advantages (2)

A
  1. activated when needed only (more acid in stomach = activated more)
  2. forms disulfide bridge with the pump and changes its chemistry = acts longer
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12
Q

omeprazole side effects

A

gastric mucosa hyperplasia (to compensate): may lead to gastric CA (hyperplasia stim by gastrin release in response to high pH)

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13
Q

2 kinds of antacids

A
  1. systemic (bioavailable): bicarb.

2. nonsystemic (poorly absorbed): Ca, Mg, Al

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14
Q

systemic antacids side effect

A

alkaline blood

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15
Q

what makes antacids diff from one another

A

onset time, duration of action, constipation or laxative effect

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16
Q

4 kinds of antacids + how to choose

A

-Na and K
-Ca
-Mg
-Al
choose depending on medical condition

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17
Q

long and short acting antacids

A 
long = Ca and Mg
short = Na, K
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18
Q

sucralfate (mucosa protecting drug) mech of action

A

complexes with proteins on ulcer side to provide coating for mucosa (+ binds to pepsin)

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19
Q

gastroparesis def + condition where cna happen

A

damage to gastric nerves or SM (ex, diabetes) = more acidity in stomach bc delayed gastric emptying

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20
Q

workforce to drive GI tract is why

A

Ach innervation to SM (Ach on musc Rs)

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21
Q

prokinetic drugs acting in synaptic cleft

A 
M3 agonists (bethanechol)
AChEi (neostigmine)
22
Q

prokinetic drugs acting downstream on the presynpatic neuron

A

D2R inhibitors (dopamine) (metoclopramide) so the negative effect of this pathway on Ach release is blocked

23
Q

prokinetic drugs acting upstream on neuron presynaptic

A
  • erythromycin (motilin R bindors): positive regul of firing

- serotonin R agonists (cisapride) positive effect on firing

24
Q

bethanecol (musc agonist) side effect and prob

A

non specific .. heart relaxation (M2)

25
Q

cholinergic drugs (bethanecol and neostigmine: M agonists and AChEi) side effects

A

stim GI secretions (acid included) (not just mvmt), reflex and asthma are problematic and exacerbated by them and heart prob too.

26
Q

classical D2Ri drug and one more used now

A

metoclopramide. (acts on CNS so not too good) domperidone better

27
Q

D2Ri drugs other effect (benefits that it’s non specific)

A

blocks emesis, more GI coordination, etc.

28
Q

D2Ri side effects

A

increase prolactin and breast tenderness (gynecomastia, galactorhea, etc.)

29
Q

serotonin agonist used upstream on neuron (prokinetic)

A

metoclopromide (also D2 antagonist) and it has a mixed 5HT4 agonist, 5HT3 antag effect

30
Q

why cisapride not used as serotonin $ agoist

A

activates arrhythmia channel in the heart. can cause death + galactorrhea + extrapyr effects in the brain

31
Q

5HT4 R signal transduction

A

GPCR activates cAMP, higher Ca in the cell

32
Q

5HT4 R agonist side effects and why

A

-more stim of bladder (R is on SM too) and adrenals

33
Q

good thing in cisapride and metoclopromide

A

block 5HT3 (and also D2 for metoclopromide) in CTZ = block emesis

34
Q

serotonin agonists effects on GI tract

A
  • more gastric contractions
  • more gastroduod coordination
  • lower sphincter in stomach contracts more
35
Q

motilin R agonists (erythromycin) effect on GI tract

A

more LES contraction, GI contraction

36
Q

paresis meaning

A

lack of GI movement

37
Q

most important factor in how food moves down GI tract

A

how liquid the food is

38
Q

constipation 3 causes

A
  • functional disorders (damage to enteric nerves or muscles)
  • drug treatments (opiates)
  • low residue diet (residue = attracts water)
39
Q

5 types of laxatives (SSELB)

A
  • secretory or stimulant
  • saline
  • emollient
  • lubricant
  • bulk forming
40
Q

principle of laxatives

A

goal is to activate Cl channels in GI tract (their pumping of Cl in lumen is what keeps water in lumen)

41
Q

secretory laxatives (castor oil) mech (2)

A
  1. activate the PG receptor EP3 (Cl channels more active)

2. inhib water reabso in lower intestine

42
Q

secretory laxative used in IBS and opioid induced constipation

A

lubiprostone

43
Q

saline laxatives mech + examples

A

draw water in intestine by osmosis (Mg hydroxide, sodium phosphate, sodium sulfate)

44
Q

emollient laxatives mech

A

attract water to stool (anionic surfactants. lower surface tension of stool)
EX: DOCUSATE

45
Q

lubricant laxatives mech + ex

A

retard water abso, smooth transit, less transit TIME (faster velocity)
ex: mineral oil

46
Q

bulk forming agents laxatives mech + example

A

form large hydrophilic masses (less viscosity of content + more bulk and water content)
Ex: Bran (fibres) OR psyllium husk

47
Q

4 problems of laxatives

A
  • damage to myenteric plexus + habituation (bc ENS used to working less)
  • colonic atony
  • too much Ca loss
48
Q

order of things to do when need laxatives

A
  • increase diet fibers and water
  • bulk agents
  • osmotic laxatives
  • stimulants (secretory): more pharma ones are last resort
49
Q

antidiarrheal drugs mech of action

A

act on intestinal neurons: more abso, less fluid secretion, more segmental contractions, less propulsive contractions + act on CNS

50
Q

ex of antidiarrheals

A

opioids, morphine, codeine

51
Q

morphine and codeine good and bad

A

good: segmental contractions more and propulsive less
bad: act on CNS… (crosses BBB)
SO ARE NOT USED for diarrhea in enteric infections

52
Q

drugs used as antidiarrheal and why

A

loperamide and diphenoxylate (no CNS effects)

Bloc E - GI & Metabolism (58 decks)

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