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GI Pharm > GI Perspective > Flashcards

GI Perspective Flashcards

1
Q

Effects of the ANS (PSNS vs SNS) on GI motility?

A

Parasympathetics stimulate GI motility (rest and digest) while Sympathetics inhibit GI motility (fight or flight)

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2
Q

Predominant tone of GI tract smooth muscle?

A

Parasympathetic (muscarinic CHOLINERGIC)

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3
Q

What parasympathetic receptors are found in the GI tract?

A

M3

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4
Q

What is the effect of parasympathetic stimulation on the walls, sphincters, and secretions w/in the GI tract?

A
  1. Walls: contracts
  2. Sphincter: relaxes
  3. Secretions: increase
    =Overall an increase in GI motility via M3’s (rest and digest)
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5
Q

What are the effects of sympathetic stimulation on the walls, sphincters, and secretions of the GI tract? What receptors are involved?

A
  1. Walls: relax via alpha-2 and beta-2 (beta-2 works thru presynaptic inhibition of parasympathetic activity)
  2. Sphincters: contract via alpha-1
  3. No significant effect on secretions
    =Overall a decrease in GI motility (fight or flight)
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6
Q

Effect of ganglionic blockade in the GI system?

A

B/c PSNS is predominant tone:

  1. Reduced GI tone and motility
  2. Constipation
  3. Decreased gastric and pancreatic secretions
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7
Q

Effects of Cholinergic agonists or AchE inhibitors (cholinergic excess)?

A

DUMBBELS

Diarrhea, Urination, Miosis/muscle weakness, Bronchorrhea, Bradycardia, Emesis, Lacrimation, Salivation/Sweating

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8
Q

Effects of muscarinic antagonists (cholinergic deficit)?

A

Opposite of DUMBBELS + Central Effects
Constipation, Urinary retention, Mydriasis/Blurred Vision, Large Bronchiole Dilation, Tachycardia, Antiemesis, Decreased glandular secretions, Hypo/anhidrosis, Restlessness/confusion/delirium/hallucinations

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9
Q

Some medications taken for non-GI conditions have ___________ activity that can lead to _________ as an ADE?

A

Anticholinergic activity that can lead to constipation as an ADE. But, usually, not every drug w/in a given class has this ADE, or another drug class w/out this ADE can be used to provide the same clinical effect.

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10
Q

What are the 4 most significant substances involved in neuronal transmission in the Enteric Nervous System? Why?

A

These are the 5 that are subject to direct modulation by drug therapy:

  1. Ach
  2. Dopamine
  3. Enkephalin and related opioids
  4. Serotonin
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11
Q

Role of Ach in ENS?

A
  1. Excitatory to smooth muscle and secretory cells

2. Major neuron-to-neuron (ganglionic) nt in ENS

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12
Q

Role of Dopamine in ENS?

A

It’s a modulatory nt in the ENS

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13
Q

Role of enkephalin and related opioid peptides in ENS?

A

Present in some secretomotor and interneurons in ENS.

  1. Inhibits Ach release and peristalsis
  2. May stimulate secretion
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14
Q

Role of Serotonin in ENS?

A

Important transmitter or co-transmitter at excitatory neuron-to-neuron junctions in the ENS

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15
Q

What is the overall effect of dopamine and by what two mechanisms is this accomplished?

A

Overall effect= GI relaxant
Mechanisms:
1. Activates D2-R (in LES, stomach)→direct relaxant
2. Activates pre-junctional D2-R→inhibition of Ach release from cholinergic neurons→indirect inhibition of muscular contraction

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16
Q

T/F: Anti-dopaminergics are prokinetic?

A

True

17
Q

Subtypes of Irritable Bowel Syndrome?

A
  1. D-IBS=diarrhea predominant
  2. C-IBS=constipation predominant
  3. Mixed IBS
18
Q

What is implicated in some cases of IBS? How would this be treated?

A

Serotonin disequilibrium: Rx with drugs that modify serotonergic signaling

a. Excess 5-HT (hyperactivity)→D-IBS (Tx w/ 5HT3 antagonist)
b. Insufficient 5-HT release (hypoactivity)→C-IBS (Tx w/ 5HT4 agonist)
c. A partial agonist/antagonist would be better for Tx of IBS as antagonists and agonists completelely block/stimulate causing a pt with diarrhea/constipation to develop the opposite

19
Q

Agonisms of 5-HT4 receptors results in what?

A

Ach release via activation of pre-junctional excitatory 5-HT4-R’s→motility/propulsion

20
Q

Where are 5HT4-R’s located in the GI system?

A
  1. Enteric neurons

2. Smooth muscle

21
Q

Basis for differences in serotonin receptor modulating drug pharmacology?

A

Selectivity for the type of 5-HT receptor it binds to

22
Q

How do probiotics work in the treatment of IBS? (4)

A
  1. Improve epithelial barrier function
  2. Inhibit pathogenic bacteria
  3. Acidify colon
  4. Improve dysmotility
23
Q

What are 2 types of probiotics?

A

a. Nonpathogenic strains of Lactobacillus and Bifidobacterium
b. Fermented dairy products, meats, and vegetables

24
Q

Overall success rate of probiotics in the Rx of IBS?

A

Generally more effective than placebo but not very successful

25
Q

What is a drug target in the treatment of Inflammatory bowel disease (IBD)? Why?

A

TNF-alpha: b/c it plays a pivotal role in the inflammation associated with IBD

26
Q

Rx of IBD?

A

Anti-inflammatory agents and, in certain circumstances, TNF-alpha inhibitors

27
Q

What are three opioid receptors in the GI tract? What are there ligands?

A
  1. Delta-R’s→Enkephalin
  2. Kappa-R’s→Dynorphin
  3. Mu-R’s→Beta-endorphin
28
Q

Where in the GI tract are these 3 opioid receptors located?

A

In the ENS

a. All are located in the Myenteric plexus
b. Mu-R’s are also found in the Submucosal plexus

29
Q

Effects of GI opioid receptor activation?

A

a. All 3→Delayed transit time (gastroparesis)

b. Kappa and Mu also cause visceral antinocioception

30
Q

What is the main ADE in the GI system associated with prescription opioids?

A

CONSTIPATION and incomplete evacuation (hard dry stools)

31
Q

What are two options for opiod antagonists that could be prescribed with opiod analgesics and how do they work?

A
  1. Naloxone - opiod antagonist with low oral bioavailability, so concentration is highest before metabolism - in the GI
  2. Methylnaltrexone: quat. ammonium unable to cross BBB, will only act in other parts of the body
32
Q

What is the mc type of preventable ADE in older ambulatory persons?

A

GI tract events

33
Q

6 types of drug-induced diarrhea?

A
  1. Osmotic diarrhea: drug draws water out
  2. Secretory diarrhea: impaired Na+ absorption and Cl and HCO3 are secreted
  3. Disordered motility: drugs affecting cholinergic tone
  4. Inflammatory diarrhea: direct damage to gastric mucosa or disruption of colonic flora followed by C dif colitis
  5. C dif diarrhea: disruption of acid/base environment or epithelial homeostasis
  6. Fatty diarrhea: maldigestion/malabsorption (ie weight loss products)
34
Q

Describe pill-induced esophagitis?

A

A feeling that pill is stuck in throat from esophageal damage; can lead to perforation/hemorrhage if unhealed

35
Q

Risk factors for pill esophagitis?

A

a. Patient: old age (decreased saliva production), institutionalized, esoph/swallowing disorder, recumbent, neurologic condition, pre-existing GERD or stricture, hiatal hernia
b. Drug: gelatin capsules and extended/sustained-release products, concurrent anticholinergics (decrease saliva production)

36
Q

Rate of oral drug absorption depends on what? (2)

A

a. Drug factors (formulation/physiochemical properties→mucosal permeability)
b. Host factors (intestinal villous blood flow, pH)

37
Q

Where are oral drugs absorbed?

A

Absorption may occur in the oral cavity, esophagus, stomach, or small intestines, depending on the formulation/phyiochemical properties of the drug and the local pH.

GI Pharm (7 decks)

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