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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
PPI MOA
irreversibly inhibit H+/K+ ATPase pump on parietal cell membrane which blocks final step in acid secretion into lumen of stomach
26
PPI AE
generally well tolerated long term: gastric polyps, altered Ca2+ metabolism (↓ bone mineralization), some cardiovascular abnormalities.
27
what are the types of mucosal protectors?
1. Bismuth chelate 2. Sucralafate 3. Misoprostol
28
how do bismuth protectors works?
coats ulcer, enhances prostaglandin synthesis, ↑ gastric mucous epithelial cell growth to protect against H. pylori-induced ulcers
29
how do sucralfates work?
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
How does misprostol work?
synthetic prostaglandin analog (PGE2) that inhibits acid secretion; used to prevent NSAID-induced ulcers.
31
Types of Antiemitic drugs
1. Anticholinergics 2. Antihistamines 3. Neuroleptic drugs 4. Prokinetic drugs 5. Serotonin blockers 6. Neurokinin-1 receptor blockers 7. Cannabinoids
32
MOA for anticholinergic antiemetics
binds to ACh receptors on vestibular nuclei, blocks communication
33
Anticholinergic antiemetics AE
1. dizziness, 2. drowsiness 3. dry mouth 4. blurred vision 5. dilated pupils 6. difficulty with urination
34
Antihistamine antiemetic MOA
inhibit vestibular input to the CTZ
35
Neuroleptic antiemetic drugs MOA
block dopamine receptors in CTZ
36
most important AE for neuroleptic antiemetic drugs
tardive dyskinesia
37
Prokinetic antiemetic drugs MOA
block dopamine in CTZ
38
Prokinetic antiemetic drugs AE
1. sedation 2. diarrhea 3. weakness 4. prolactin release 5. prolonged use causes extrapyramidal signs, motor restlessness
39
Serotonin blockers antiemetic drug MOA
block serotonin receptors in the GI tract, CTZ, and vomiting center
40
Neurokinin-1 receptor blocker antimetic drug MOA
blocks substance P from binding to NK-1 receptor, prevents both central and peripheral stimulation of vomiting centers
41
Which antiemetic drugs are used to prevent vomiting from motion sickness?
1. Anticholinergics 2. Antihistamines
42
Which antiemetic drugs are antipsychotic agents, some have anticholinergic actions and are good for postop vomiting?
Neuroleptic antiemetics
43
Which antiemetic drugs are used to treat vomiting resulting from chemotherapy?
1. Neurokinin-1 receptor blockers 2. Cannabinoids
44
Which antiemetic drug can cause Steven-Johnsons syndrome?
Neurokinin-1 receptor blockers
45
Types of antidirraheal drugs
1. Absorbents 2. Anticholinergics 3. Intestinal flora modifiers 4. Opiates
46
Absorbents MOA
binds to bacteria causing diarrhea and carry them out with feces
47
Absorbents AE
\*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
Anticholinergic Antidirrheal MOA
reduce peristalsis of GI tract
49
Opiates Antidirrheal MOA
decrease GI motility and propulsion (in small doses) Slowing transit time in intestines = absorption of water and electrolytes
50
Opiates antidirrheal AE
1. sedation 2. dizziness 3. constipation 4. nausea 5. vomiting 6. respiratory depression 7. bradycardia 8. hypotension 9. urinary retention
51
Types of Laxatives
1. Bulk-forming 2. Hyperosmotic 3. Saline 4. Emollient 5. Stimulant
52
Bulk forming laxatives MOA
increase water absorption à softens and increases bulk of intestinal contents Distention of colon increases peristalsis
53
hyperosmotic laxatives MOA
creates gradient that draws fluid into colon to increase stool fluid content and stimulate peristalsis
54
Hyperosmotic laxatives AE
1. abdominal bloating 2. rectal irritation 3. electrolyte imbalance
55
Concerns with hyperosmotic laxatives
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
Saline laxatives MOA
similar to hyperosmotic – osmotic pressure pushed water/electrolytes into intestines
57
Saline Laxatives AE
salts may cause issues with individual with diminished cardiac or renal function
58
Emollient laxatives MOA
facilitate water and fat absorption into stool, lubricate fecal matter and intestinal wall
59
what are emollient laxatives also known as?
stool (fecal) softeners or lubricant laxatives
60
Emollient laxatives AE
\*generally well tolerated 1. skin rash 2. decrease vitamin absorption 3. electrolyte imbalance
61
Stimulant laxatives MOA
stimulates peristalsis through enteric nervous system
62
Important consideration with stimulant laxatives
Danger of long-term use: dependence and damage to intestinal cells/loss of colon function
63
Therapeutic concerns with GI agents
1. patient positioning 2. Dehydration 3. Constipation 4. Drug interactions
64
T/F: exercise can facilitate bowel movements and improve gastric emptying?
TRUE
65
T/F: smoking can decrease effectiveness of H2 receptor blockers?
TRUE
66
DDI for Climetidine (tagemet)
Climetidine (tagemet) inhbits CYP450 enzymes

Pharmacology Test 2 (9 decks)

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