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Pharmacology Test 2 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

what are the phases of digestion?

A

cephalic phase

gastric phase

intestinal phase

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2
Q

what occurs during the intestinal phase of digestion?

A

chyme enters the duodenum release of bicarbonate solution and pancreatic enzymes

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3
Q

T/F: the neuronal control of digestions is mostly cholinergic and excitatory?

A

True

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4
Q

what is peptic ulcer disease (PUD)?

A

ulcerations of the mucosal lining of the esophagus, stomach and/or duodenum

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5
Q

T/F: H pylori infection can cause chronic gastritis, PUD, GERD, and gastric cancer?

A

TRUE

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6
Q

how is H pylori infection treated?

A

antacid + antibiotic

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7
Q

T/F: one should discontinue use of NSAIDs during H. pylori infection if possible

A

TRUE

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8
Q

what regulates vomiting?

A

chemoreceptor trigger zone (CTZ) and the Vomiting center

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9
Q

where is the CTZ?

A

floor of the 4thh ventricle in cerebrum

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10
Q

what does the CTZ respond to?

A

toxins/drugs in blood and CSF

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11
Q

what does the vomiting center do?

A

integrates signals from multiple places including: CTZ, GI tract, pharynx, vestibular system

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12
Q

what is the typical cause of diarrhea?

A

from water and electrolyte imbalance in intestinal tract

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13
Q

common pathologies that can lead to diarrhea?

A
  1. IBS
  2. Crohn’s disease
  3. Ulcerative colitis
  4. Bowel impaction with overflow
  5. Bacterial overgrowth
  6. Bile acid malabsorption
  7. Celiac disease
  8. Short bowel syndrome
  9. Laxative abuse can lead to diarrhea
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14
Q

what is constipation?

A

movement disorder of the colon; infrequent/painful defecation, hard stools, incomplete evacuation

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15
Q

what are some causes of constipation?

A
  1. Bowel impaction
  2. Endocrine or neurogenic condition
  3. Sedentary lifestyle
  4. Poor diet (limited roughage, dehydration)
  5. Medications
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16
Q

drug classes indicated for acid reflux

A
  1. antacid
  2. H2 receptor antagonist
  3. proton pump inhibitors (PPI)
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17
Q

Drug classes that heal/treat ulcers that form from gastric acid

A
  1. H2 receptor antagonists
  2. PPI
  3. Mucuosal protectors
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18
Q

which drug classes that treat acid reflux also help heal ulcers?

A
  1. H2 receptor blocker
  2. PPI (more effective of the two)
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19
Q

MOA of antacids

A

neutralizes stomach acidity by increasing stomach pH

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20
Q

AE of antacids

A
  1. Effervescent types (i.e. Alka-Seltzer) have high Na+ content – if pt has hypertension they should probably avoid this one
  2. Magnesium products à diarrhea
  3. Aluminum and calcium à constipation
  4. Drug-Drug interactions
  5. Alters absorption of electrolytes from GI tract à electrolyte imbalance
  6. Avoid taking within 2 hours of other oral medications
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21
Q

how do antacids have DDIs?

A

↑ absorption of basic drugs and ↓ absorption of acidic drugs

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22
Q

MOA of H2 receptor anatagonists

A

reduce secretion of stimulated acid

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23
Q

T/F: H2 receptor antagonists are best taken HS (at bedtime)

A

TRUE

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24
Q

H2 receptor antagonist AE

A
  1. diarrhea
  2. muscle pain
  3. rashes
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25
Q

PPI MOA

A

irreversibly inhibit H+/K+ ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach

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26
Q

PPI AE

A

generally well tolerated

long term: gastric polyps, altered Ca2+ metabolism (↓ bone mineralization), some cardiovascular abnormalities.

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27
Q

what are the types of mucosal protectors?

A
  1. Bismuth chelate
  2. Sucralafate
  3. Misoprostol
28
Q

how do bismuth protectors works?

A

coats ulcer, enhances prostaglandin synthesis, ↑ gastric mucous epithelial cell growth to protect against H. pylori-induced ulcers

29
Q

how do sucralfates work?

A

an Al salt of sucrose that forms a protective coating over the ulcer; used for high-risk causes (trauma, burns, ARDS, major surgery, etc.)

30
Q

How does misprostol work?

A

synthetic prostaglandin analog (PGE2) that inhibits acid secretion; used to prevent NSAID-induced ulcers.

31
Q

Types of Antiemitic drugs

A
  1. Anticholinergics
  2. Antihistamines
  3. Neuroleptic drugs
  4. Prokinetic drugs
  5. Serotonin blockers
  6. Neurokinin-1 receptor blockers
  7. Cannabinoids
32
Q

MOA for anticholinergic antiemetics

A

binds to ACh receptors on vestibular nuclei, blocks communication

33
Q

Anticholinergic antiemetics AE

A
  1. dizziness,
  2. drowsiness
  3. dry mouth
  4. blurred vision
  5. dilated pupils
  6. difficulty with urination
34
Q

Antihistamine antiemetic MOA

A

inhibit vestibular input to the CTZ

35
Q

Neuroleptic antiemetic drugs MOA

A

block dopamine receptors in CTZ

36
Q

most important AE for neuroleptic antiemetic drugs

A

tardive dyskinesia

37
Q

Prokinetic antiemetic drugs MOA

A

block dopamine in CTZ

38
Q

Prokinetic antiemetic drugs AE

A
  1. sedation
  2. diarrhea
  3. weakness
  4. prolactin release
  5. prolonged use causes extrapyramidal signs, motor restlessness
39
Q

Serotonin blockers antiemetic drug MOA

A

block serotonin receptors in the GI tract, CTZ, and vomiting center

40
Q

Neurokinin-1 receptor blocker antimetic drug MOA

A

blocks substance P from binding to NK-1 receptor, prevents both central and peripheral stimulation of vomiting centers

41
Q

Which antiemetic drugs are used to prevent vomiting from motion sickness?

A
  1. Anticholinergics
  2. Antihistamines
42
Q

Which antiemetic drugs are antipsychotic agents, some have anticholinergic actions and are good for postop vomiting?

A

Neuroleptic antiemetics

43
Q

Which antiemetic drugs are used to treat vomiting resulting from chemotherapy?

A
  1. Neurokinin-1 receptor blockers
  2. Cannabinoids
44
Q

Which antiemetic drug can cause Steven-Johnsons syndrome?

A

Neurokinin-1 receptor blockers

45
Q

Types of antidirraheal drugs

A
  1. Absorbents
  2. Anticholinergics
  3. Intestinal flora modifiers
  4. Opiates
46
Q

Absorbents MOA

A

binds to bacteria causing diarrhea and carry them out with feces

47
Q

Absorbents AE

A

*aspirin product: use with caution in children recovering from flu/chickenpox, increased bleeding time, GI bleed, tinnitus

*decrease effectiveness of many drugs (digoxin, hypoglycemic drugs, anticoagulants)

48
Q

Anticholinergic Antidirrheal MOA

A

reduce peristalsis of GI tract

49
Q

Opiates Antidirrheal MOA

A

decrease GI motility and propulsion (in small doses)

Slowing transit time in intestines = absorption of water and electrolytes

50
Q

Opiates antidirrheal AE

A
  1. sedation
  2. dizziness
  3. constipation
  4. nausea
  5. vomiting
  6. respiratory depression
  7. bradycardia
  8. hypotension
  9. urinary retention
51
Q

Types of Laxatives

A
  1. Bulk-forming
  2. Hyperosmotic
  3. Saline
  4. Emollient
  5. Stimulant
52
Q

Bulk forming laxatives MOA

A

increase water absorption à softens and increases bulk of intestinal contents

Distention of colon increases peristalsis

53
Q

hyperosmotic laxatives MOA

A

creates gradient that draws fluid into colon to increase stool fluid content and stimulate peristalsis

54
Q

Hyperosmotic laxatives AE

A
  1. abdominal bloating
  2. rectal irritation
  3. electrolyte imbalance
55
Q

Concerns with hyperosmotic laxatives

A

do not take if a pt is on diuretics or is at CV risk.

The electrolyte imbalance puts them at risk for cardiac arrhythmias

56
Q

Saline laxatives MOA

A

similar to hyperosmotic – osmotic pressure pushed water/electrolytes into intestines

57
Q

Saline Laxatives AE

A

salts may cause issues with individual with diminished cardiac or renal function

58
Q

Emollient laxatives MOA

A

facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall

59
Q

what are emollient laxatives also known as?

A

stool (fecal) softeners or lubricant laxatives

60
Q

Emollient laxatives AE

A

*generally well tolerated

  1. skin rash
  2. decrease vitamin absorption
  3. electrolyte imbalance
61
Q

Stimulant laxatives MOA

A

stimulates peristalsis through enteric nervous system

62
Q

Important consideration with stimulant laxatives

A

Danger of long-term use:

dependence and damage to intestinal cells/loss of colon function

63
Q

Therapeutic concerns with GI agents

A
  1. patient positioning
  2. Dehydration
  3. Constipation
  4. Drug interactions
64
Q

T/F: exercise can facilitate bowel movements and improve gastric emptying?

A

TRUE

65
Q

T/F: smoking can decrease effectiveness of H2 receptor blockers?

A

TRUE

66
Q

DDI for Climetidine (tagemet)

A

Climetidine (tagemet) inhbits CYP450 enzymes

Pharmacology Test 2 (9 decks)

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