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3 PHARM SELF > GI > Flashcards

GI Flashcards

1
Q

What are the four sets of GI drugs?

A
  1. Acidity, ulcers GERD
  2. Bowel motility, water flux
  3. Reduce prevent nausea
  4. IBD
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2
Q

What stomach cells secret HCl?

A

parietal

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3
Q

What increases acidity production in the stomach 3 Receptors?

A

ACh receptors
gastrin receptors
histamine receptors

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4
Q

What happens to HCO3 from its dissociation from H+ in the stomach epithelial?

A

exported into blood in exchange for Cl-

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5
Q

What nerve begins cephalic response? acts on what cells?

A

vagus- M receptors of parietal cell and ECL cells (Fundus) which release histamine in a long term manner

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6
Q

Where is G cell located? What cells does gastrin work on?

A

antrum, Parietal and ECL cells

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7
Q

What stims Gastrin release?

A

Increase pH and stretch

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8
Q

How does PGE2 and PGI2 promote protection from gastric acidity?

A

activate Gi and decrease cAMP to decrease acid

also same receptor in epithelial cell causes increased mucus and bicarb secretion

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9
Q

What pumps protons out of the parietal cell?

A

H/K ATPase. K is recycled with Cl antiporter

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10
Q

Does a PPI stop working after its 2 hour activity window (acid labile)? What activates them?

A

No because of irreversible binding

Stomach acid activates

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11
Q

Where does PPI reach the cell?

A

Through blood. It is acid labile and therefore must be protected as it passes through stomach.

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12
Q

What is Zollinger Ellison Syndrome?

A

secretion of Gastrin from tumors of pancreas and intestine.

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13
Q

Where are PPIs cleared? CYP influences?

A

Liver- increase serum warfarin, decrease activation of clopidogrel

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14
Q

What is useful to block for nocturnal acid secretion?

A

H2 receptors blockers (24 hour effectiveness 70%)

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15
Q

How are H2 blockers secreted?

A

Renal- organic cation system

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16
Q

How long does it take tolerance to develop with H2 blockers?

A

3 days–> increased Gastrin

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17
Q

Does sucralfate stick better to gastric or duodenal ulcers? how is it activated?

A

duodenal, acid activated

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18
Q

Is Mg or Al fast acting as an antacids? What is added to reduce case?

A
  1. Mg (stimulates gastric emptying and motility while Al slows)
  2. Surfactant simethicone
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19
Q

Where does muscaranic antagonists work?

A

M1 intramural ganglia!!!!!!

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20
Q

What determines if the H. pylori infection will be pathogenic?

A

Vacuolating endotoxin A

21
Q

What are the 3 types of therapy for H Pylori?

A

triple-PPI+clarithromycin+metronidazole/amoxi/tetra
Quadruple- PPI+metro+ bismuth+ tetra
Quadruple- H2 blocker+bismuth+metro+tetra

22
Q

mechanical stim of Enterochromaffin cells release what?

A

serotonin–> primary afferent–>reflex contracts orally and relax anally

23
Q

Does dopamine generally decrease or increase ACh release?

A

decreasses

24
Q

What cells secrete motilin?

A

enterochromaffic cells and M cells in upper small bowel

25
Q

What are 60% of constipated patients actually complaining about? How to treat?

A 
stool hardness (normal transit times)
Increase fiber
26
Q

T-F–laxatives are really cathartics at lower dosages but act as laxatives when the dose is increased

A

False- opposite is true- cathartic means to purge

27
Q

What type of drugs are best for constipation with associated opioid use?

A

osmotic laxatives

28
Q

Do stool wetting agents increase frequency of defecation?

A

No– just soften the stool

29
Q

Does castor oil actually stimulate smooth muscle? Is the castor bean toxic?

A

Yes, yes due to soluble Ricin fraction

30
Q

How is glycerin administered?

A

rectal suppository- increases water retention and stimulates peristalsis

31
Q

What is one bad thing about fiber laxatives?

A

absorb other drugs

32
Q

Can bulk forming agents be used as a laxative and as antidiarrheal agents?

A

Yes- can be a sponge for antidiarrheal

[colloids or polymères polycarbophil derivatives]

33
Q

Is loperamide more potent than morphine”?

A

yes 40x

34
Q

How do you administer somatostatin or octreotide?

A

parenteral–> combats secretorial diarrhea of tumors, post-surgical gastric dumping

35
Q

What happens to salicylate found in pep to bismol? leads to what?

A

is released in the stomach and is absorbed systemically leading to increased prostanoids and decreased motility

36
Q

T-F– emesis has many inputs? What is it controlled by? What is special about this area?

A
  1. True- CNS, memory, environment, sensors of toxins, gut sensation and movement sensation
  2. Chemoreceptor Trigger Zone in the area postrema at bottom of 4th ventricle & NTS of Vagus nerve
  3. Crosses the BBB and senses blood and CSF
37
Q

Does serotonin promote motility? Is it widely used for chemotherapy induced emesis and nausea? Where are the serotonin receptors located for this ability?

A
  1. Yes
  2. Most widely Used
  3. peripheral small intestine and CTZ and NTS
38
Q

Most serotonin antagonists are secreted by the liver except for which one?

A

Palonosetron which is secreted by kidney

39
Q

Dopamine receptor antagonists block D2 and H1 receptors. Blocking H1 gives what benefit? H1 receptors are found primarily where for anti-emesis effects?

A
  1. anti- motion sickness

2. brainstem and vestibular apparatus

40
Q

How is scopolamine usually administered? What does the drug particular act on for its anti motion sickness effects? Is it effective for chemotherapy induced nausea?

A
  1. Transdermal patch
  2. vestibular apparatus
  3. No, minimal CTZ effects
41
Q

Why is charcoal used more than emetic drugs for poisoning/

A

Danger of aspirating

42
Q

Does syrup of ipecac and apomorphine acton on the CTZ?

A

Yes

43
Q

Is ulcerative colitis or crohns confluent lesions? What are the 3 aims of therapy for these conditions?

A
  1. ulcerative colitis (and is only in anal verge/colon)

2. a. treat acute symptoms b. maintain remissions c. treat super infections.

44
Q

Does TH1 contribute for to Chrons or UC?

A

Crohn’s……UC is TH2

45
Q

What activates sulfasalazine, olsaalazine and balsaalazide? what is the outcome?

A

cleaved by colonic bacterial enzymes at diazo bond to yield mesalamine

46
Q

In Crohn’s is it necessary to select dosage forms that target part of bowel involved?

A

Yes

47
Q

Where are sulfasalazine and olsalazine activated? Where is pH sensitive mesalamine capsules released? what about delayed capsules?

A

In the colon
ileum
jejunum

48
Q

When is cyclosporine used for inflammatory BD?

A

patients failing glucocorticoid therapy [parenteral]

49
Q

Is IBS and IBD the same? What does Tx focus on?

A

No, IBS is alternating constipation and diarrhea with bloating. Tx focuses on motility of the gut

3 PHARM SELF (13 decks)

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