GI

Question 1

What are the four sets of GI drugs?

Answer 1

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

Question 2

What stomach cells secret HCl?

Answer 2

parietal

Question 3

What increases acidity production in the stomach 3 Receptors?

Answer 3

ACh receptors
gastrin receptors
histamine receptors

Question 4

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

Answer 4

exported into blood in exchange for Cl-

Question 5

What nerve begins cephalic response? acts on what cells?

Answer 5

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

Question 6

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

Answer 6

antrum, Parietal and ECL cells

Question 7

What stims Gastrin release?

Answer 7

Increase pH and stretch

Question 8

How does PGE2 and PGI2 promote protection from gastric acidity?

Answer 8

activate Gi and decrease cAMP to decrease acid

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

Question 9

What pumps protons out of the parietal cell?

Answer 9

H/K ATPase. K is recycled with Cl antiporter

Question 10

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

Answer 10

No because of irreversible binding

Stomach acid activates

Question 11

Where does PPI reach the cell?

Answer 11

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

Question 12

What is Zollinger Ellison Syndrome?

Answer 12

secretion of Gastrin from tumors of pancreas and intestine.

Question 13

Where are PPIs cleared? CYP influences?

Answer 13

Liver- increase serum warfarin, decrease activation of clopidogrel

Question 14

What is useful to block for nocturnal acid secretion?

Answer 14

H2 receptors blockers (24 hour effectiveness 70%)

Question 15

How are H2 blockers secreted?

Answer 15

Renal- organic cation system

Question 16

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

Answer 16

3 days–> increased Gastrin

Question 17

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

Answer 17

duodenal, acid activated

Question 18

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

Answer 18

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

Question 19

Where does muscaranic antagonists work?

Answer 19

M1 intramural ganglia!!!!!!

Question 20

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

Answer 20

Vacuolating endotoxin A

Question 21

What are the 3 types of therapy for H Pylori?

Answer 21

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

Question 22

mechanical stim of Enterochromaffin cells release what?

Answer 22

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

Question 23

Does dopamine generally decrease or increase ACh release?

Answer 23

decreasses

Question 24

What cells secrete motilin?

Answer 24

enterochromaffic cells and M cells in upper small bowel

Question 25

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

Answer 25

``` stool hardness (normal transit times) Increase fiber ```

Question 26

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

Answer 26

False- opposite is true- cathartic means to purge

Question 27

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

Answer 27

osmotic laxatives

Question 28

Do stool wetting agents increase frequency of defecation?

Answer 28

No-- just soften the stool

Question 29

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

Answer 29

Yes, yes due to soluble Ricin fraction

Question 30

How is glycerin administered?

Answer 30

rectal suppository- increases water retention and stimulates peristalsis

Question 31

What is one bad thing about fiber laxatives?

Answer 31

absorb other drugs

Question 32

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

Answer 32

Yes- can be a sponge for antidiarrheal | [colloids or polymères polycarbophil derivatives]

Question 33

Is loperamide more potent than morphine"?

Answer 33

yes 40x

Question 34

How do you administer somatostatin or octreotide?

Answer 34

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

Question 35

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

Answer 35

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

Question 36

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

Answer 36

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

Question 37

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

Answer 37

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

Question 38

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

Answer 38

Palonosetron which is secreted by kidney

Question 39

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

Answer 39

1. anti- motion sickness | 2. brainstem and vestibular apparatus

Question 40

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?

Answer 40

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

Question 41

Why is charcoal used more than emetic drugs for poisoning/

Answer 41

Danger of aspirating

Question 42

Does syrup of ipecac and apomorphine acton on the CTZ?

Answer 42

Yes

Question 43

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

Answer 43

1. ulcerative colitis (and is only in anal verge/colon) | 2. a. treat acute symptoms b. maintain remissions c. treat super infections.

Question 44

Does TH1 contribute for to Chrons or UC?

Answer 44

Crohn's……UC is TH2

Question 45

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

Answer 45

cleaved by colonic bacterial enzymes at diazo bond to yield mesalamine

Question 46

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

Answer 46

Yes

Question 47

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

Answer 47

In the colon ileum jejunum

Question 48

When is cyclosporine used for inflammatory BD?

Answer 48

patients failing glucocorticoid therapy [parenteral]

Question 49

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

Answer 49

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