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GI- Week 1 > GI Pharm Intro > Flashcards

GI Pharm Intro Flashcards

1
Q

What is the predominant ANS tone in the GI?

A

Parasympathetic

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2
Q

What is the effect of sympathetic input into the GI on the walls? What receptors mediate this?

A

the walls of the GI relax via a2 and B2 binding

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3
Q

What is the effect of sympathetic input into the GI on the sphincters? What receptors mediate this?

A

they contract via a1 binding

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4
Q

What is the effect of sympathetic input into the GI on secretions?

A

There is none

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5
Q

What is the effect of parasympathetic input into the GI on the walls? What receptors mediate this?

A

contraction via M3 receptors (parasympathetics also cause sphincters to relax via M3 binding and secretions to increase via M3 binding)

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6
Q

What are the effects of cholinergic (Ach) agonists (or AchE inhibitors)?

A

SLUDGE BBB

Salivation

Lacrimation

Urination

Defecation

GI symptoms

Emesis

Bronchorrhea, Bronchospams, Bradycardia

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7
Q

What are the effects of cholinergic (Ach) antagonists (or AchEs)?

A

constipation and urinary retention

blurred vision

large bronchiole dilation

tachycardia

antiemesis

decreased glandular secretions

restlessness, confusion, delirium, hallucinations

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8
Q
A
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9
Q

What is the enteric nervous system?

A

The ENS is involved in sensorimotor control of the GI and this consists of both afferent sensory neurons and a number of motor nerves and interneurons that are organized principally into two nerve plexuses: the myenteric (Auerbach’s) plexus and the submucosal (Meissner’s) plexus.

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10
Q

Where is the myenteric plexus located and what does it do?

A

It’s located bettwen the longitudinal and circular muscle layers of the GI wall and plays an important role in the contraction and relaxation of GI smooth muscle

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11
Q

What does Meissner’s plexus do?

A

It’s involved in secretory and absorptive functions of the GI epithelium, local blood flow, and neuroimmune activities

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12
Q

What is the primary neurotransmitter of the ENS?

A

Ach

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13
Q

What other neurotransmitters are involved in ENS control/modulation?

A

Dopamine (pre- and postsynaptically inhibit Ach release and relax the esophageal sphincter)

Enkephalin and related opiod peptides

Serotonin (5-HT) (promote Ach release)

ATP, CGRP, CCK

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14
Q

What is Metoclopramide?

A

A drug used to treat N/V and gastroparesis via its gastrokinetic actions

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15
Q

How does Metoclopramide work?

A

This drug possesses both dopaminergic (inhibits pre and postsynatic D2 receptors to promote Ach release and prevent relaxation of the esophageal sphincter and stomach) and serotonergic modulatory activity (stimulatory to promote Ach release), leading to coordinated contractions that enhance motility in the upper GI tract

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16
Q

What is the major downside of Metoclopramide?

A

it causes tardive dyskinesia (involuntary movements of the tongue, lips, face, trunk, and extremities) and

akathisia (movement disorder characterized by a feeling of inner restlessnes and a compelling need to be in constant motion)

  • cardiac arrhythmias and bradycardia
  • hyperprolactinemia
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17
Q

What part of Metoclopramide causes BOTH tardive dyskinesia and akathisia?

A

the dopamine modulation

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18
Q

What are the main types of laxatives?

A

dietary fiber and bulk-forming

surfactant

osmotic

stimulant

miscellaneous

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19
Q

How do antidiarrheals work?

A

they work to decrease stool fluidity (i.e. water absorbers), to antagonize cholinergic NS activity, or to activate the opiate receptors in the ENS

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20
Q

What is Inflammatory Bowel Disease?

A

this is a term that encompasses ulcerative colitis and Crohn’s disease

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21
Q

What causes IBD?

A

There is suggested dysbiosis of normal intestinal homeostatic relationship between intestinal mucosa and normal commensals, leading to inflammation (including TNFa)

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22
Q

What are some TNFa-antagonists used in the tx of IBD?

A

Infliximab

Adalimumab

Certolizumab pegol

Golimumab

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23
Q

What are natalizumab and vedolizumab?

A

these bind the a4B7 integrin on T cells in the bloodstream, blocking its interaction with MAdCAM-1, which is mainly expressed on gut endothelial cells, to prevent extravasation of T cells into tissue (mostly used for UC)

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24
Q
A
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25
Q

What are the AEs of a4B7 integrin inhibitors (natalizumab and vedolizumab)?

A
  • immunosuppression (avoid giving live vaccines during tx)
  • progressive multfocal leukoencephalopathy
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26
Q

What causes the rare progressive multfocal leukoencephalopathy seen with a4B7 integrin inhibitors?

A

JC virus, which is normally present and kept under control by the immune system

27
Q

How would mild UC be treated initially?

A

Sulfasalazine, and its metabolite 5-ASA, as anti-inflammatories in the gut (note that these work primarily in the gut because they are poorly absorbed)

28
Q

How should you procede if Sulfasalazine doesnt work for initial UC tx?

A

systemic glucocorticoids (note that if UC or CD are moderate to severe at presentation, you can start tx with this)

29
Q

How should you procede if systemic glucocorticoids work but then the UC pt. relapses?

A

try immunomodulators like thiopurine, and then go to TNF-a inhibitors

30
Q

How should mild CD be tx initially?

A

topical glucocorticoids (distal colonic disease) or budesonide (distal ileal involvement)

31
Q
A
32
Q

One of the most significant and consistent AEs to chronic opiate use is what?

A

constipation

33
Q
A
34
Q

How do opiates affect the gallbladder?

A

they promote contraction, spasm of the sphincter of Oddi and decreased secretions, leading to biliary pain and delayed digestion

35
Q

How do opiates affect the gastroduodenum?

A

they decreased gastric emptying and increase pyloric tone

initially increase duodenal motiltiy followed by quiescence

increased gastric acid secretion

all promoting anorexia and N/V

36
Q

How do opiates affect the small bowel and colon?

A

they increased tone, increase transit time, and increase absorption

and decrease secretion

all promoting constipation, cramps, and delayed digestion leading to hard, dry stool

37
Q

How do opiates affect the anorectum?

A

they decrease rectal sensitivity and increase internal sphincter tone

leading to incomplete evacuation

38
Q

What are some ways that drugs can induce diarrhea?

A
  • osmotic diarrhea by drawing water into the GI
  • secretory diarrhea by imparing Na+ absorption (e.g. NSAIDs), causing Cl- and HCO3- to be secreted into the GI
  • affecting cholinergic tone
  • inflammatory diarrhea
39
Q

What is inflammatory diarrhea?

A

disruption of colonic flora precipitating C. difficle colitis or damaging thr gastric mucosa, usually via antimicrobials or drugs that affect intestinal pH

40
Q

How does C. difficile diarrhea occur?

A

disruption of the acid-base environment or epithelial homeostatsis is in the case of PPIs, H2 antagonists, and immunosuppressants

41
Q

What drugs produce diarrhea by virtue of their MOA?

A

orlistat (weight-loss) and cholestyramine (for hypercholesterolemia)

42
Q

What other drugs list diarrhea as an AE?

A
  • octreotide
  • metformin via decreased glucose absorption (aka osmotic diarrhea)
43
Q

What are some drugs that frequently cause C. difficile diarrhea?

A

ampicillin, amoxicillin

clindamycin

1st, 2nd, and 3rd gen cephalosporins

imipenem/cilastatin

44
Q

What are some drugs that cause noninfectious watery diarrhea?

A

a-glucoside inhibitors such as acarbose and miglitol

45
Q

What are some drugs that cause noninfectious secretory diarrhea?

A

ABX, anticholinergics

metformin

digoxin

calcitonin

NSAIDs

simvastin

theophylline

46
Q

What are some drugs that cause noninfectious diarrhea via altered motility?

A

cholinergic drugs, macrolides, and metoclopramide

47
Q

What are some drugs that cause noninfectious fatty diarrhea?

A

metformin

HIV medications

octreotide

orlistat

cholestyramine

tetracyclines

48
Q
A
49
Q

What are some drug classes most likely to cause constipation?

A

antacids

anticonvulsants

antipsychotics

CCBs

dopamine agonists

50
Q

T or F. Decreased intestinal P-gp activity would lead to dramatically increased drug bioavailability

A

T.

51
Q

What is the pH of the stomach?

A

~2

52
Q

How do NSAIDs affect the GI?

A

they inhibit the production of prostaglandinds which results in increased gastric acid secretion and reduction of secretion of protective mucus and bicarbonate by epithelial cells

53
Q

How does the use of antacids affect the co-administration of oral drugs?

A

some drugs, like doxycycline, tetracycline, and fluoroquinolones, require an acidic environment for absorption and antacids can chelate them (dont administer at the same time)

54
Q

What drugs require an acid environment for absorption and are less bioavailable in the presence of H2 blockers?

A

ampicillin,

itra/ketoconazole

cephalosporins

sulfonylureas

55
Q

Famotidine inhibits clearance of what drug?

A

Theophylline

56
Q

All PPIs are substrates what what CYP?

A

2C19, and all but dexlansoprazole exert some degress of 2C19 inhibition, with pantoprazole being the weakest

57
Q

What drug would be less effective if given with a PPI?

A

Clopidogrel, which requires metabolic (2C19) activation

58
Q

How does cholestryamine work?

A

it sequesters bile salts in the GI tube and prevents absorption to lower cholesterol

59
Q

How do opiate receptors work?

A

presynaptically they inhibits release of neurotransmitter by acting as a CCB, and postsynaptically they hyperpolarize potassium channels making it less responsive to neurotransmitter to modulate cholinergic activity

60
Q

How does erythromycin affect the GI?

A

it stimulates motilin receptors in the duodenum to “clean” the stomach after a meal (releases cyclically) as IV eryhtromycin lactobionate

used commonly before surgery to avoid aspiration pneumonia durign surgery

61
Q
A
62
Q

What drug can be used to reverse opitae induced constipation but doesnt affect the analgesic effects of opiates?

A

methylnaltrexone

63
Q
A

GI- Week 1 (20 decks)

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