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Block 10; Week 5-M > GI pharm-Harvey > Flashcards

GI pharm-Harvey Flashcards

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1
Q

What are some important peptic acid diseases?

A

GERD

Peptic ulcer disease

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2
Q

WHat are the defensive forces in peptic ulcer disease?

A 
mucus
bicarb
mucosal blood flow
apical surface membrane transport
epithelial regenerative capacity
elaboration of prostaglandins
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3
Q

What are some things that can predispose or worsen peptic ulcer disease?

A 
H. pylori infection
NSAID
aspirin
cigarettes
alcohol
gastric hyperacidity
duodenal gastric reflux
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4
Q

What are the 5 treatment categories for peptic acid diseases?

A 
antacids
H2 histamine receptor antagonists
proton pump inhibitors
mucosal protective agents
antibiotics
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5
Q

What are some antacids used in peptic acid diseases? What is their MOA?

A 
magnesium hydroxide
aluminum hydroxide
calcium carbonate
sodium bicarbonate
MOA: weak bases that neutralize stomach acid
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6
Q

What are the drawbacks to each type of antacid?

A

**all require frequent dosing
magnesium hydroxide–can cause diarrhea
aluminum hydroxide–can cause constipation
calcium carbonate & sodium bicarb–can cause bloating, metabolic alkalosis, milk alkali syndrome

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7
Q

What are some H2 histamine receptor antagonists used in peptic acid disease?

A

cimetidine
ranitidine
famotidine
nizatidine

MOA: blocks H2 histamine receptors on parietal cells.
**parietal cells secrete gastric acid

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8
Q

Which things do mucous neck cells secrete in the gastric glands of the stomach?

A

mucus

bicarb

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9
Q

What do parietal cells in gastric glands of the stomach secrete? What prompts this secretion?

A

Gastric acid–>activates pepsin
INtrinsic factor–>complexes w/ vit b12
stimulus: ach, gastrin, histamine

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10
Q

What do the enterochromaffin cells of the gastric glands of the stomach secrete? What prompts this secretion? Results?

A

secrete histamine–>increases gastric acid secretion

**stimulus is ach or gastrin

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11
Q

What do chief cells in gastric glands of the stomach secrete? Stimulus?

A

pepsin–digests proteins
gastric lipase–digests fats
**stimulus for release: ach, acid, secretin

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12
Q

What do the D cells in the gastric glands of the stomach secrete? Stimulus & fcn?

A

somatostatin–>inhibits gastric acid secretion

stimulus: acid

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13
Q

What do the G cells in the gastric glands of the stomach secrete? Stimulus & fcn?

A

gastrin–>stimulates gastric acid secretion

stimulus: peptides, AA, Ach

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14
Q

How does the antrum & fundus interact in the stomach?

A

ANTRUM: dietary peptides stimulate the G cell to release gastrin into bloodstream.
luminal acid stimulates D cells to release somatostatin that inhibits G cells.
Vagus nerve releases ACh that inhibits D cells & activates G cells.
FUNDUS: More Ach stimulation of parietal cells & enterochromaffin cells. Gastrin in bloodstream activates enterochromaffin cells to release histamine.
Histamine, Ach, gastrin act on parietal cells to release luminal acid.

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15
Q

What are some possible side effects of H2 receptor antagonists, specifically cimetidine?

A

interfere with hepatic metabolism of other drugs
can cause confusion, hallucinations, and agitation at high doses, especially in the elderly
block androgen receptors causing gynecomastia or impotence in men

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16
Q

How are H2 receptor antagonists metabolized & excreted?

A

liver & kidney

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17
Q

When is cimetidine most effective?

A

more effective for inhibiting nocturnal H+ secretion than meal stimulated H+ secretion.

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18
Q

What is the advantage of H2 receptor antagonists?

A

longer duration of action than antacids

replaced by PPI

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19
Q

What are some PPIs? What is their MOA?

A

omeprazole
esomeprazole
lansoprazole
pantoprazole
rabeprazole
MOA: structurally similar to H2 receptor antagonists
inhibit H+/K+ ATPase (proton pump) specific to gut

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20
Q

What are the side effects of PPIs?

A

can interfere with metabolism of some drugs
reduce absorption of vitamin B12, iron, calcium
increase incidence of respiratory infections
increased gastrin levels (rebound acid production)

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21
Q

How are PPIs metabolized?

A

via hepatic metabolism

have first pass metabolism–short half life (1.5 hours)

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22
Q

Describe how PPIs work in detail.

A

weak bases that are acid labile, so they are enteric coated & are prodrugs that are activated at site of action
@ parietal cells they irreversibly inhibit the proton pump & last for 24 hours

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23
Q

What are some examples of mucosal protection agents for peptic acid diseases?

A

sucralfate
misoprostol
bismuth subsalicylate

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24
Q

What is the MOA of sucralfate?

A

sucrose-sulfated aluminum hydroxide complex
forms viscous paste that selectively binds ulcers
stimulates prostaglandin and bicarbonate secretion

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25
What are some therapeutic considerations w/ sucralfate for peptic acid diseases?
< 3% absorbed used to avoid pH reduction (H2 blockers, PPIs) may cause constipation may impair drug absorption
26
What is the MOA of misoprostol?
analog of prostaglandin E1 (PGE1) activates E3 prostaglandin receptors on parietal and non-parietal epithelial cells inhibits H2 receptor stimulated H+ production stimulates mucus and bicarbonate secretion enhances mucosal blood flow
27
What are some therapeutic considerations when prescribing misoprostol?
readily absorbed orally half-life < 30 min – requires frequent dosing diarrhea, cramping, abdominal pain in 10-20% of patients
28
What is the MOA of bismuth subsalicylate?
coats ulcers creating protective layer direct antimicrobial effects (including H. pylori) absorbs enterotoxins
29
What are some therapeutic considerations when prescribing bismuth subsalicylate?
``` causes blackening of stools can cause constipation GOOD FOR: traveler's diarrhea very safe! in H. pylori treatment combos ```
30
What is the quadruple therapy to great H. Pylori associated ulcers?
PPI clarithromycin amoxicillin or metronidazole bismuth subsalicylate
31
What are the 2 types of gastric motility disorders?
hypomotility: constipation hypermotility: diarrhea
32
What are the 5 treatment categories for hypo motility?
``` laxatives cholinomimetics D2 dopamine receptor antagonists serotonin 5-HT4 receptor agonists opioid receptor antagonists ```
33
What are the different types of laxatives?
bulk forming (psyllium, methylcellulose) stool softeners (docusate, mineral oil, glycerin supp.) osmotics (magnesium hydroxide, magnesium citrate, sodium phosphate) stimulants (phenolphthalein, senna, bisacodyl)
34
What is an example of a cholinomimetic? MOA?
neostigmine acetylcholinesterase inhibition enhances Ach activation of gut smooth muscle muscarinic receptors
35
What is neostigmine used for? What are the negative side effects?
**used in the hospital for acute colonic pseudo-obstruction & a single dose evacuates! SE: salivation, N/V/D, bradycardia (lots of parasympathetic response)
36
Give examples of D2 receptor antagonists used to treat hypo motility. What are their MOA?
metoclopramide domperidone MOA: blocks D2 receptor mediated inhibition of cholinergic smooth muscle contraction
37
Aside from hypo motility, what else are D2 receptor antagonists used for?
increasing gastric emptying in gastroparesis diabetes w/ H2 blocker & PPI for GERD antiemetic
38
What are some side effects to keep in mind w/ prescribing D2 receptor antagonists for Hypomotility?
increases esophageal peristalsis & lower esophageal sphincter pressure restlessness, drowsiness, insomnia, anxiety, agitation galactorrhea, gynecomastia, impotence, menstrual disorders b/c of increased prolactin
39
What is an example of 5-HT4 receptor agonists that are used for treating hypo motility? What is the MOA?
tegaserod MOA: partial agonist @ 5-HT4 receptors acts presynaptically @ primary afferent neurons stimulating release of Ach & increasing smooth muscle contraction in the GI tract.
40
What are some therapeutic considerations when prescribing tegaserod?
good for idiopathic constipation or constipation from IBS
41
What are examples of opioid receptor antagonists? MOA?
methylnaltrexone alvimopan MOA: opioid receptors usu inhibit Ach release from enteric neurons. these meds block that! Allowing Ach release.
42
Therapeutic considerations when prescribing methylnaltrexone or alvimopan?
great for treating constipation in pts being treated w/ opioid analgesics doesn't cross BBB though!
43
What are the treatment categories for hypermotility/diarrhea?
opioid agonists colloidal bismuth bile salt binding resins somatostatin analogs
44
What are some examples of opioid agents used to treat hyper motility? MOA?
loperamide diphenoxylate MOA: activates presynaptic opioid receptors, inhibiting Ach release **increases colonic transit time & fecal water absorption
45
What are the therapeutic considerations for prescribing loperamide?
no analgesic effects b/c doesn't cross BBB | reduces potential for abuse or dependence
46
What are therapeutic considerations for prescribing diphenoxylate?
these preparations also contain atropine
47
What are some examples of colloidal bismuth drugs used to treat hyper motility? MOA?
bismuth subsalicylate bismuth subcitrate potassium MOA: can absorb bacterial enterotoxins
48
What are some examples of bile binding resins used to treat hyper motility? MOA?
cholestyramine colestipol colesevelam MOA: absorbs bile salts that cause colonic secretory diarrhea
49
What are bile binding resins used to treat? SE?
disease of the terminal ileum (crohn's) bc it results in malabsorption of bile salts SE: bloating, flatulence, constipation
50
WHat is an example of a somatostatin analog? MOA?
octreotide MOA: activates somatostatin receptors in gut inhibits gastrin production reduces intestinal fluid secretion
51
Therapeutic considerations in prescribing somatostatin analogs for hypermotility?
short half-life (3 min) administered subcutaneously used to treat secretory diarrhea associated with GI neuroendocrine tumors can inhibit pancreatic secretions leading to steatorrhea and fat soluble vitamin deficiency
52
what is IBS?
Recurring idiopathic condition associated with abdominal discomfort (pain, bloating, cramps), diarrhea and/or constipation.
53
What are the 3 treatment categories for IBS?
anticholinergics serotonin 5-HT3 receptor antagonists serotonin 5-HT4 receptor agonists
54
Give an anticholinergic agent used to treat IBS & its MOA.
dicyclomine | MOA: blocks muscarinic cholinergic receptors in gut, reducing secretions & motility
55
What are the therapeutic considerations with prescribing dicyclomine for IBS?
used for the treatment of diarrhea-predominant IBS not particularly effective higher doses cause significant anticholinergic side effects (dry mouth, blurred vision, urinary retention)
56
GIve an example of a serotonin 5-HT3 receptor antagonist used to treat IBS & its MOA.
alosetron | MOA: blocks 5-HT3 receptors on extrinsic primary afferent neurons
57
What are some important therapeutic considerations for prescribing alosetron?
diarrhea-predominant IBS | **SE: pretty bad constipation
58
Give an example of a serotonin 5-HT4 receptor agonist used to treat IBS. MOA?
tegaserod MOA: partial agonist at 5-HT4 receptor **stimulates release of Ach, GI smooth muscle contraction
59
What are the therapeutic considerations when prescribing tegaserod?
used to treat constipation-predominant IBS
60
What are the treatment types for nausea?
``` serotonin 5-HT3 receptor antagonists neurokinin NK1 receptor antagonists phenothiazines & butyrophenones antihistamines/anticholinergics cannabanoids ```
61
Give an example of a 5-HT3 receptor antagonist used to treat nausea & its MOA.
ondansetron | MOA: blocks 5-HT3 receptors peripherally & centrally (vomiting center & chemoreceptor trigger zone)
62
What are the therapeutic considerations for prescribing ondansetron for nausea?
postop nausea & chemo | not good for other types of nausea
63
Give an example of a neurokinin NK1 receptor antagonist used to treat nausea & its MOA.
aprepitant | MOA: blocks central neurokinin NK1 receptors in the vomiting center & chemoreceptor trigger zone
64
What are the therapeutic considerations for prescribing aprepitant?
used for nausea w/ chemo & taken w/ corticosteroids
65
What are some phenothiazines & butyrophenones used to treat nausea & what is their MOA?
prochlorperazine promethazine droperidol MOA: blocks D2 dopamine receptors in the chemoreceptor trigger zone blocks M1 muscarinic receptors in the vomiting center
66
What are some therapeutic considerations when prescribing phenothiazines & butyrophenones?
used to treat chemotherapy and postoperative nausea also used to treat vertigo may cause extrapyramidal effects (movement disorders
67
What are some antihistamines/anticholinergics used to treat nausea? MOA? NOTE: these are good for motion sickness.
scopolamina diphenhydramine MOA: scop--blocks M1 muscarinic receptor in the vestibular system diphen--blocks H1 histamine receptors in the vomiting center
68
Give an example of a canabanoid & when it is used to treat nausea.
dronabinol | for chemo nausea
69
Describe the symptoms & process of ulcerative colitis.
diffuse mucosal inflammation of the colon | bloody diarrhea, pain, tenesmus
70
Describe the symptoms & process of crohn's disease.
patchy transmural inflammation affecting any part of the GI tract immune response possibly directed against bacteria that attacks the GI tract pain, vomiting, diarrhea, weight loss, intestinal obstruction
71
Give the 4 categories of treatments for inflammatory bowel disease.
aminosalicylates glucocorticoids antimetabolites tumor necrosis factor (TNF) antagonists
72
Give some drugs that are considered aminosalicylates & their MOA.
``` sulfasalazine mesalamine MOA: 5-ASA is the active compound inhibits COX & lipoxygenase pathways **inhibits inflammatory cytokines ```
73
What are aminosalicylates used to treat exactly?
mild-moderate UC | crohn's
74
Give some examples of glucocorticoids used to treat IBD & their MOA.
prednisone, prednisolone, budesonide, hydrocortisone (enema) MOA: inhibits inflammatory cytokines (like TNFalpha) & chemokines inhibits COX-2 dependent production of prostaglandins & leukotrienes
75
When are glucocorticoids used in IBD?
Moderate-->severe UC | crohn's
76
Give some anti-metabolites & their MOA in treatment of IBD.
``` methotrexate azathioprine 6-mercaptopurine MOA: suppresses immune system **interferes w/ IL-1 **increases release of adenosine **stimulates apoptosis of activated T cells **helps with maintenance of remission ```
77
Give some examples of tumor necrosis factor antagonists used to treat IBD & their MOA.
infliximab adalimumab certolizumab MOA: antibodies against the pro inflammatory cytokine TNFalpha
78
When do you use TNF antagonists in IBD?
moderate-severe Crohn's disease that doesn't respond to other meds.
79
Give the meds used for mild & responsive IBD.
budesonide (ileitis) topical corticosteroids (proctitis) antibiotics 5-ASA
80
Give the meds used for moderate IBD.
TNF antagonists oral corticosteroids methotrexate azathioprine/6-mercaptopurine
81
Give the meds used for severe/refractory IBD.
``` surgery natalizumab cyclosporine TNF antagonists IV corticosteroids ```

Block 10; Week 5-M (3 decks)

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