GI Tract Pharmacology Flashcards

1
Q

what is GERD

A

movement of gastric contents into esophagus
caused by relaxation of lower esophageal sphincter

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2
Q

what is PUD

A

peptic ulcer disease
ulcers in upper Gi tract
causes: h. pylori, NSAIDs, stress

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3
Q

Antacid “OIAs”

A

Use: neutralize gastric activity (primarily for acid reflux)
Dosing: frequent
Side Effects: minimal (constipation from aluminum/calcium, diarrhea from magnesium)
Interactions: binds to other drugs/reduces effectiveness

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4
Q

Histamine-2 Receptor Antagonists “OIAs”

A

Uses: Inhibit histamine, gastrin, and ACh stimulated acid release; helps with basal and meal-related acids.
Dosing: Usually once to twice a day dosing.
Side Effects: Diarrhea, dizziness, muscle pain, rashes; Cimetidine has multiple drug interactions.
Interactions: Upregulation of receptors may diminish effectiveness with long-term use; cessation may lead to rebound acid secretion.

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5
Q

Proton Pump Inhibitors (PPIs) “OIAs”

A

Uses: Irreversibly inhibit the H+/K+-ATPase pump on parietal cell membrane, stopping the final step of acid secretion; very effective at healing ulcers and preventing stress ulcer formation.
Dosing: Once daily dosing; need an acidic environment to function.
Side Effects: Similar to H2 Blockers; concerns with long-term use include decreased calcium absorption and increased risk for infection.
concern w/ longterm use causes decrease in calcium absorption/increased risk of infection

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6
Q

neural mechanism for N/V - CTZ

A

chemoreceptor trigger zone
Senses toxins and drugs in blood and cerebrospinal fluid.
Involves dopamine, serotonin (5HT3), neurokinin, and opioid receptors.

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7
Q

neural mechanism for N/V - vestibular

A

Responsible for motion sickness.
Involves muscarinic and histamine-1 receptors

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8
Q

how do anticholinergics work for nausea

A

binds to ACh receptors in vestibular nuclei to block messages in vomiting center

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9
Q

how do neuroleptic drugs work for nausea

A

similar to antipsychotic agents - blocks dopamine in CTZ

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10
Q

how do antihistamines work for nausea

A

H1-blocking agents that inhibit vestibular input to the CTZ, blocks Ach binding to H1 in vestbiular nuclei

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11
Q

how do prokinetic drugs work for nausea

A

block dopamine at CTZ - side use stimulate peristalsis in the stomach

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12
Q

how do serotonin blockers work for nausea

A

blocks serotonin receptors in GI tract, CTZ, and vomiting center

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13
Q

what is diarrhea

A

frequent passage of loose stools, either acute or chronic
mostly due to electrolyte imbalances in intestinal tract
chronic diarrhea have underlying GI conditions

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14
Q

how do adsorbents work for diarrhea

A

coats GI tract, binds to diarrhea causing bacteria and reduces irritation providing relief

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15
Q

how do opiates (lite) work for diarrhea

A

decreases GI motility and propulsion by increasing absorption of electrolytes and water
reduces pain w/ diarrhea

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16
Q

what is constipation

A

movement disorder of colon/rectum = infrequent and painful defecation of sense of incomplete evacuation

17
Q

how do bulk-forming laxatives work for constipation

A

increases water absorption to soften/bulk up stool and stimulates paristalsis

18
Q

how do emollient laxatives work for constipation

A

facilitate water and fat absorption into the stool, reabsorption of water back into the body is blocked

19
Q

how do hyperosmotic laxatives work for constipation

A

works in large intestine by drawing fluid into colon

20
Q

how do saline laxatives work for constipation

A

increases osmotic pressure by increasing electrolyte and water concentrations in small bowel. increases peristalsis but with watery stools

21
Q

how do stimulant laxatives work for constipation

A

stimulates enteric nervous system and peristalsis.

22
Q

key facts about IBS?

A
  • 3 types - IBS-C, IBS-D, IBS-M (rare)
  • idiopathic etiology
  • affects women 2:1, often btwn ages 20-30
  • 10-15% of population has it, but only 15% of that seek help
23
Q

symptoms of IBS

A
  • lower abd. pain
  • bloating
  • diarrhea sx >3 days
  • constipation sx >3 weeks (straining, incomplete)
  • fatigue, anxiety, depression
24
Q

what is IBD?

A

split betwen Crohn’s and Ulcerative Colitis.
chronic inflammatory multisystem condition

25
Q

what is ulcerative colitis

A

confined to rectum and colon
causes continuous lesions affecting mucosa and submucosa

26
Q

what is crohn’s

A

can affect any part of GI tract
causes discontinuous lesions leading to perforations/fistulas

27
Q

sx of UC?

A

cramping, frequent bowel movements, wt loss, arthritis, red nodules, hemorrhoids, fissures

28
Q

sx of crohn’s?

A

malaise/fever, abdom. pain, frequent bowel movements, fistula, wt loss, malnutrition, abdom. mass/tenderness

29
Q

whats the first treatment line for pts w/ UC?

A

aminosalicylates

these are NOT recommended for crohn’s

30
Q

what is Tumor Necrosis Factor (TNF-α)

A

Acts as a pro-inflammatory mediator
• Binds to TNF receptors on immune cells
• Increases activity of helper and regulatory T-Cells
• Contributes to inflammation in Crohn’s disease

31
Q

how do Anti-TINF Monoclonal antibodies work

A

binds to TNF and prevents it from biding to receptors
• Also bind to membrane-bound TNF and reduce its cell signaling

32
Q

What is Reyes Syndrome

A

ages 18 and under
allows viruses to go across the BBB and lead to brain damage and encephalopathy

33
Q

What leads to Reyes Syndrome

A

ages 18 and under taking salicylates (aspirin, pepto-bismol [Bismuth subsalicylate])

34
Q

what GI drugs not to use with pregnant women

A

amitzia/lubiprostone