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Block 10 week 5 > GI pharm-Harvey > Flashcards

GI pharm-Harvey Flashcards

1
Q

What are the peptic acid diseases?

A

GERD

PUD

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2
Q

What are the tx categories for peptic acid diseases?

A
  1. antacids
  2. H2 histamine receptor antagonists
  3. proton pump inhibitors
  4. mucosal protective agents
  5. antibiotics
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3
Q

What are the major antacid agents for peptic acid diseases?
What are 2 other antacids used for peptic acid diseases?
What is the MOA of these agents?

A

Magnesium hydroxide
Aluminum hydroxide

calcium carbonate
sodium bicarbonate

weak bases that neutralize stomach acid

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4
Q

Antacids require (blank) dosing.
Aluminum hydroxide can cause (blank)
Magnesium hydroxide can cause (blank)
Calcium carbonate and sodium bicarbonate can cause (blank x 3)

A

frequent
constipation
diarrhea
bloating, metabolic alkalosis, milk alkali syndrome

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5
Q

What are the H2 histamine receptor antagonists used for peptic acid disease?
What is the MOA of these drugs?

A

Cimetidine (main)

  • ranitidine
  • famotidine
  • nizatidine

-Blocks H2 histamine receptors on parietal cells

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6
Q

Where do you find G and D cells?

Where do you find parietal cels?

A

antrum

fundus

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7
Q

When should you give H2 receptor antagonists for peptic acid disease?

A

-more effective at inhibiting noctural H+ secretion

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8
Q

What has a longer duration of actions, antacids or H2 receptor antagonists?

A

H2 receptor antagonists

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9
Q

H2 receptor antagonists have been replaced by (blank).

How are H2 receptor antagonists eliminated?

A

proton pump inhibitors

hepatic metabolism and renal filrtation/secretion

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10
Q

H2 receptor antagonists are considered very safe however (blank) can interfere with hepatic metabolism of other drugs, can cause confusion, hallucinations, and agitation at high doses, especially in the elderly.

A

cimetidine

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11
Q

(blank) can block androgen receptors causing gynecomastia or impotence in men

A

Cimetidine

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12
Q

What are the proton pump inhibitors?

What is the mechanism of action?

A

omeprazole

inhibit H+/K+ ATPase (proton pump) specific to gut

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13
Q

Omeprazole (PPIs) are (blank) labile so oral formulas are (blank) coated. It is a weak (acid/base) so it will be concentrated in acidic compartments (i.e parietal cells)

A

acid
enteric
base (pKa 4-5)

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14
Q

PPIs are (blank) drugs that are activated at site of action. How do they work? Does it reversibly or irreversibly work?

A

pro-drugs
covalently modify proton pump
IRREVERSIBLY inhibits the proton pump

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15
Q

What is the duration of action of PPIs?
How are they eliminated?
What is the half life like?

A

24 hours
hepatic metabolism
short half life (1.5 hrs) due to first pass metabolism

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16
Q

PPIs have a high therapeutic index but can interfere with (blank), reduce (blank), increase (blank) and (blank)

A
  • metabolism of some drugs
  • absorption of vit B12, iron, calcium
  • incidence of respiratory infections
  • gastrin levels (rebound acid production)
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17
Q

Which works the best, H2 blockers or PPIs?

A

PPIs

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18
Q

What are the mucosal protective agents?

A
  • sucralfate
  • misoprostol
  • bismuth subsalicylate
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19
Q

Sucralfate forms a (blank) complex that forms a viscous paste that selectively binds (blank) and stimulates (blank and blank) secretion

A

sucrose-sulfated aluminum hydroxide complex

ulcers

prostaglandin and bicarbonate secretion

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20
Q

Only (blank) percent or less of sucralfate is absorbed. It is used to avoid (blank) reduction (H2 blockers, PPIs).

A

3%

pH

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21
Q

What may sucralfate cause and what may it impair?

A

constipation

impair drug absorption

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22
Q 
What is misoprostol?
What does it activate?
What does it inhibit?
What does it stimulate?
What does it enhance?
A

Mucsoal protector->analog of prostaglandin E1 (PGE1)

E3 prostaglandin receptors on parietal and non-parietal eptihelial cells

H2 receptor stimulated H+ production

mucus and bicarb secretion

mucosal blood flow

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23
Q

Can you give misoprostol orally?
What is the half life and what does this indicate about dosing?
What are the adverse SEs?

A

Yes-> readily absorbed orally
less than 30 minutes-> requires frequent dosing
Diarrhea, cramping, abdominal pain in 10-20% of patients

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24
Q

What is bismuth subsalicylate?

What is the mechanism of action?

A

mucosal protector

  • coats ulcers creating protective layer, direct antimicrobial effects (including H. pylori)
  • absorbs enterotoxins
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25
Q

What do you use bismuth subsalicylate for?
Is it safe?
Causes (blank) of stools
and can cause (blank)

A

dyspepsia and travelers diarrhea
Really safe!
blackening of stools
constipation

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26
Q

Bismuth + (blank or blank) can be used to treat H. pylori

A

tetracycline or metronidazole

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27
Q

What do you use antibiotics for with peptic diseases?
What is the goal?
What is the triple therapy?
What is quadruple therapy?

A
  • H pylori associated ulcers
  • eradicate organism and heal the ulcer

PPI + Clarithromycin+ amoxicillin or metronidazole

+bismuth

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28
Q

What are the 5 categories of drugs used to treat hypomotility?

A
  1. laxatives
  2. cholinomimetics
  3. D2 dopamine receptor antagonists
  4. serotonin 5-HT4 receptor agonists
  5. opioid receptor antagonists
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29
Q

What are the four classes of laxatives?

A
  • bulk forming
  • stool softeners
  • osmotics
  • stimulants
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30
Q

What are the bulk forming laxatives?

A

psyllium

methylcellulose

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31
Q

What are the stool softener laxatives?

A

docusate, mineral oil, glycerin supp.

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32
Q

What are the osmotic laxatives?

A

magensium hydroxide, magnesium citrate, sodium phosphate

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33
Q

What are the stimulant laxatives?

A

phenolphthalein, senna, bisacodyl

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34
Q

What are the cholinomimetics for hypomotility?

What is the MOA?

A

neostigmine

  • acetylcholineterase inhibition
  • enhances Ach activation of gut SM muscarinic receptors
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35
Q

What do you use neostigmine for?

A

hospitalized patient with acute colonic pseudo-obstruction

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36
Q

A single dose of (blnk) causes prompt evacuation

A

neostigmine

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37
Q

What are the SEs of neostigmine?

A
  • Salivation
  • n/v
  • diarrhea
  • bradycardia
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38
Q

What are the D2 receptor antagonists used for hypomotility?

What is the MOA?

A

metoclopramide

-blocks D2 receptor mediated inhibition of cholinergic SM stimulation

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39
Q

D2 receptor antagonists increase (blank) and (Blank).
Enhances (blank)
Is a potent (blank)

A

esophageal peristalsis
lower esophageal sphincter pressure

gastric emptying (no effect on small or large intestines)

antiemetic

40
Q

What do you use D2 receptor antagonists for?

A

treat delayed gastric emptying (gastroparesis), commin in diabetic patients

41
Q

Use D2 receptor antagonists with (blank or blank) to treat GERD

A

H2 block or PPI

42
Q

What are the SEs of D2 receptor antagonists?

A

restlessness, drowsiness, insomnia, anxiety, and agitation in 10-20% of patients
elevated prolactin levels

43
Q

Since D2 receptor antagonists can cause elevated prolactin levels, what will be the SEs associated with this?

A

galactorrhea
gynocomastia
impotence
menstrual disorders

44
Q

What is a serotonin 5-HT4 receptor agonists?

A

tegaserod

stimulates the release of ACh, which causes GI smooth muscle contraction

45
Q

tegaserod is a partial agonist at (blank) receptors. It acts presynaptically on (blank) stimulating the release of ACh, which causes GI smooth muscle contraction

A 
5HT4 
IPANs (intrinsic primary afferent neurons)
46
Q

What is tegaserod used to treat?

Why dont you want to use it really?

A

idiopathic constipation and constipation associated with IBS

CV side effects

47
Q

What are the opoid receptor antagonists used to treat hypomotility?
What is the mechanism of action?

A
  • methylnaltrexone
  • alvimopan

Blocks presynaptic opoid receptors which normally act to inhibit ACh release from enteric neurons

48
Q

Will opoid receptor antagonists (methylnaltrexone, alvimopan) affect your mood?
What do you use them to treat?

A

no because it doesnt cross the BBB.

constipation in patients with opoid analgesics

49
Q

What are the four categories of hypermotility drugs?

A

Opoid agonists
Colloidal bismuth
Bile salt binding resins
Somatostatin analogs

50
Q

What are the opoid agents used in hypermotility issues?

A

loperamide (imodium)

diphenoxylate

51
Q

What is the mechanism of action of opoid agents?

A

-activates presynaptic opoid mu receptors on cholinergic nerves inhibiting ACh release and increase colonic transit time and fecal water absorption

52
Q

(blank) is an opoid agonist that has no analgesic effects (does not cross the BBB) reducing potential for abuse or dependence

A

Loperamide

53
Q

(blank) preparations contain atropine to minimiz abuse potentia and aid in slowing GI motility

A

diphenoxylate

54
Q

What are the colloidal bismuth agents used for hypermotility issues?
How does it work?
What do you use it to treat?

A

Bismuth subsalicylate
Bismuth subcitrate potassium

Can absorb bacterial enterotoxins

gastric irritation, diarrhea and travelers diarrhea

55
Q

What are the bile binding resins used to treat hypermotility?
What is the MOA?
What are the SEs?

A
  • cholestyramine
  • colestipol
  • colesevelam

absorbs bile salts that cause colonic secretory diarrhea

bloating, flatulence, constipation and prevent absorption of many drugs

56
Q

What do you use to treat diseases of terminal ileum (chrons disease)?

A

Bile binding resins

57
Q

What are the somatostatin analogs used to treat hypermotility?

A

octreotide

58
Q

What is the mechanism of action of octreotide (somatostatin analog)?

A

activates somatostatin receptors in the gut, inhibiting gastrin production-> reduces intestinal fluid secretion and inhibits GI motility at high doses

59
Q

Does octreotide have a long or short half-life?
How do you administer it?
What do you use it to treat?
What can it inhibit leading to steatorrhea and fat soluble vitamin deficiency?

A

short half life (3 min)
subQ
secretory diarrhea associated with GI neuroendocrine tumors
pancreatic secretions

60
Q

What is this:
Recurring idiopathic condition associated with abdominal discomfort (pain, bloating, cramps), diarrhea and/or constipation.

A

IBS

61
Q

WHat are the three classes of drugs you use to treat IBS?

A
  1. anticholinergics
  2. serotonin 5-HT3 receptor antagonists
  3. serotonin 5-HT4 receptor agonists
62
Q

What are the anticholinergic agents used to treat IBS?

What is the MOA?

A

dicyclomine

block muscarinic cholinergic receptors in gut, reducing secretions and motility

63
Q

What do you use dicyclomine for?
Is it effective?
what are the SEs?

A

tx of diarrhea-predominant IBS
Not really
Higher doses cause significant anticholinergic SEs (dry mouth, blurred vision, urinary retention)

64
Q

What are the serotonin 5-HT3 receptor antagonists?

A

alosetron

65
Q

What is the MOA of alosetron (serotonin 5-HT3 receptor antagonists)?

A

blocks 5-HT3 receptors on extrinsic primary afferent neurons (EPANs)

66
Q

What do you use Alosetron for? What are the SEs?

A
  • tx of diarrhea predominant IBS

- constipation (sometimes serous enough for constipation)

67
Q

What are the serotonin 5-HT4 receptor agonists? What is the MOA?

A

Tegaserod
-partial agonist at 5HT4 receptors act presynaptically on IPANs to stimulate release of ACh, which causes GI SM contraction

68
Q

What does tegaserod treat?

Why does it have limited use?

A

constipation -predominant IBS

because of CV SEs

69
Q

What are the drug categories used to treat nausea?

A
  • serotonin 5HT3 receptor antagonists
  • neurokinin NK1 receptor antagonists
  • Phenothiazines and butyrophenones
  • antihistamines/anticholinergics
  • canabanoids
70
Q

What are the serotonin 5HT3 receptor antagonists?

What is the MOA?

A

ondansetron

Blocks 5-HT3 receptors peripherally (EPANs in gut) and centrally (vomiting centers and chemoreceptor trigger zone)

71
Q

When do you use odanestron?

A

for postop nausea and chemotherapy

not effective for other types of nausea (i.e motion sickness)

72
Q

What are the neurokinin NK1 receptor antagonists?

A

aprepitant

73
Q

What is the moa of aprepitant?

A

Blocks central neurokinin NK1 receptors (vomiting center and chemoreceptor trigger zone)

74
Q

When do you use aprepitant?

A

used with corticosteroids for nausea associated with chemotherapy

75
Q

What are the phenothiazines and butryophenes used for nausea?

A

Prochlorperazine (MAIN)
promethazine
droperidol

76
Q

What is the MOA of prochlorperazine?

A

Blocks D2 dopamine receptors in the chemoreceptor trigger zone
Blocks M1 muscarinic receptors in the vomiting center

77
Q

What do you use prochlorperazine for?

What are some SEs?

A

-used to treat chemotherapy and postoperative nausea and vertigo

Extrapyramidal effects (movement disorders)

78
Q

What are the antihistamines/anticholinergics used to treat nausea?

A

scopolamine

diphenhydramine

79
Q

What is the MOA of scopolamine?

What is the MOA of diphenhydramine?

A

blocks M1 muscarinic in the vestibular system

blocks H1 histamine receptors in the vomiting center

80
Q

What do you use scopolamine or diphenhydramine for?

A

motion sickness

81
Q

What are the canabanoid agents used for nausea?

What do you use it for?

A

dronabinol (THC)

nausea associated with chemotherapy

82
Q

Ulcerative colitis has (blank) mucosal inflammation of the (blank) and has what three major clinical findins

A

diffuse
colon
bloody diarrhea, pain, tenesmus

83
Q

Chron’s disease has (blank) inflammation affecting (blank) part of the GI tract. Immune response possibly directed against (blank) that attacks GI tract. What are the main clinical findings?

A

patchy transmural
any
bacteria

pain, vomiting, diarrhea, weight loss, intestinal obstruction

84
Q

What are the treatment categories for tx of inflammatory bowel disease?

A
  1. aminosalicylates
  2. glucocorticoids
  3. antimetabolites
  4. tumor necrosis factor (TNF) antagonists
85
Q

What are the aminosalicylates?

A

sulfasalazine

mesalamine

86
Q

What is the MOA of aminosalicylates?

A

inhibition of COX and LOX pathways

may also inhibit production of inflammatory cytokines

87
Q

Wht is the active compound in aminosalicylates?

A

5-aminosalicyclic acid (5-ASA)

88
Q

What do you use aminosalicylates for (sulfasalazine, mesalamine)?

A

mild to moderate ulcerative colitis and Chron’s disease

89
Q

What are the glucocorticoids used for IBD?

What is the MOA?

A

prednisone, prednisolone, budesonide, hydrocortisone (enema)

inhibit production of inflammatory cytokines (TNF-alpha) and chemokines
-inhibit COX dependent production of prostaglandins and leukotrienes

90
Q

What do you use glucocorticoids for?

A

moderate to severe ulcerative colitis and Chron’s disease

91
Q

What are the antimetabolites used to treat IBD?

A

methotrexate
azathioprine
6-mercaptopurine (6-MP)

92
Q

What is the MOA of antimetabolites?

A

immune suppressant effects

  • > interferes with IL-1 effects
  • > increases release of adenosine
  • > stimulates apoptosis of activated T-cells
93
Q

What do you use antimetabolites for?

A

induction and maintenance of remission

94
Q

What are the TNF antagonists used in IBD?

A

infliximab
adalimumab
certolizumab

95
Q

What is the MOA of TNF antagonists?

A

antibodies against the proinflammatory cytokine TNF-alpha

96
Q

What do you use TNF antagonists for?

A

moderate to severe Crohn’s disease that has not responded to conventional therapy

Block 10 week 5 (3 decks)

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