Pharm: Acid Suppress Etc; Sm And Lg Bowel D/os

Front 1

4 classes of anti-secretory agents

Back 1

1) H2 - receptors blockers
2) Proton pump inhibitors
3) Prostaglandin analogs
4) Muscarinic antagonists

Front 2

When acid secretion across the apical membrane occurs, there is a rise in the pH of the parietal cell. What happens for there to be more acid to pump out via the H/K/ATPase?

Back 2

CO2 and H20 enters the cell, and good ol' carbonic anhydrase catalyzes the reaction to get H+ + HCO3-.

HCO3- exits the basolateral membrane via the HCO3/Cl exchanger.

The exchanger provides the Cl for net HCL movement across the apical membrane. Rseults in alkaline tide if there is increased gastric acid secretion.

Front 3

What is "alkaline tide?"

Back 3

Lots of HCO3- being released into the bloodstream due to the secretion of excess stomach acid. It occurs because of the carbonic anhydrase reaction of turning CO2 and H20 into HCO3- and H+

Front 4

T/F Stimulation of the parietal cell causes the surface area of the parietal cell to increase and H/K/ATPases to fuse into the canalicular membrane

Back 4

T

Front 5

Histamine H2 Receptor Antagonists end in what?

Back 5

-tidine

(ranitidine; cimetidine; famotidine)

Front 6

2 ways histamine can be released from the ECL cells

Back 6

1) Direct vagus stimulation (ACh to muscarinic receptors)

2) Gastrin stimulation of CCK receptors

Front 7

What type of receptor is the H2 receptor on the parietal cell?

Back 7

G protein coupled, causes activation of cyclic AMP which leads to phosphorylation of the H/K/ATPase pump. H2RA blocks actions of histamine.

Front 8

What is the preferred dosing for H2 receptor blockers?

Back 8

Evening because the most prominent effect on H2Rantagonists is on BASAL acid secretion.

Front 9

indications for H2 receptor blockers

Back 9

1) Gastric ulcer
2) Duodenal ulcer
3) GERD
4) Pathological hypersecretory conditions (Zollinger-Ellison)
5) Heartburn/acid indigestion/sour stomach - OTC

Front 10

T/F Prevention of NSAID-induced gastric damage, and elimination of H pylori (part of a regimen) are unlabelled uses of H2 receptor blockers

Back 10

T

Front 11

What is an important interaction/metaoblic consequence with cimetidine?

Back 11

Cimetidine binds to androgen receptors and inhibits CYP450 - drug interactions mainly from CYP problems

Front 12

Proton pump inhibitors end in what?

Back 12

-prazole

Front 13

Most effective acid suppressors

Back 13

PPIs

Front 14

Why do PPIs require an acid environment?

Back 14

They are prodrugs that are catalyzed into active drug into the gastric parietal cell (which is why they only work in the parietal cell)

The activated form binds to and inhibits the H/K/ATPase that pumps acid into stomach lumen.

Front 15

Why should PPIs be taken with or before a meal?

Back 15

Because their activation requires acid, and food stimulates parietal cells to produce acid.

Front 16

What is the major adverse effect of PPIs?

Back 16

Rebound acid secretion following termination of treatment due to excess gastrin (lack of FB inhibition)

Front 17

Indications of PPIs

Back 17

1) Treatment of Gastric and duodenal ulcers

2) GERD

Front 18

Prototype of prostaglanding analog (antisecretory and protective)

Back 18

misoprostol

Front 19

PGE2 and PGI2 are major prostaglandins synth'd by the gastric mucosa that provide protection by inhibition acid secretion by binding to the ____ receptor on the parietal cell.

Back 19

EP3

Front 20

What changes does binding to the EP3 receptor cause in the parietal cell?

Back 20

Inhibition of adenylyl cyclase and decreased levels of cAMP via the Gαi pathway.

Front 21

MOA of misoprostol (prostaglandin analog)

Back 21

Synthetic analog of prostaglandin.

Does all the protective effectso f the prostaglandins

Front 22

Indications for prostaglandin analogs

Back 22

Reduction of NSAID-induced mucosal damage.

Front 23

Adverse effects of prostaglandin analog misoprostol

Back 23

Diarrhea, abdominal pain/cramps

Contraindicated during pregnancy because it increases uterine contractility

Front 24

Muscarinic antagonists - what are they used for?

Back 24

They were developed before better drugs to treat peptic ulcer. Not used very much anymore.

Front 25

What is sucralfate?

Back 25

A protective agent that becomes a sticky polymer that adheres to epithelial cells and ulcer craters. Stimulates prostaglandin production and epidermal growth factor.

Use has declined.

Front 26

sucralfate : adverse effects

Back 26

Constipation, may inhibit absorption of other drugs

Front 27

What are the antacids?

Back 27

They all neutralize stomach acid.

Calcium carbonate; Magnesium salta; Aluminum salts

Front 28

What are adverse effects of antacids?

Back 28

Can cause an increase in alkali and sodium load

Front 29

What is the combination therapy generally used to treat H pylori infection?

Back 29

1) Antibiotics

2) PPIs

3) Bismuth-based products

Front 30

Adverse effect of cimetidine

Back 30

Gynecomastia/galatorrhea (effects at androgen receptor)

Front 31

What are 5HT3 receptor antagonists used for?

Back 31

anti-emetic, especially due to chemotherapy

Front 32

What do the 5HT3 receptor antagonists end in?

Back 32

-etron

(eg, ondansetron, granisetron)

Front 33

What is metoclopramide (reglan)?

Back 33

A dopamine receptor antagonist that is used to ameliorate nausea and vomiting.

Front 34

What is the chemo-receptor trigger zone (CTZ)?

Back 34

The emetic center.

Promotes vomiting/nausea. Things that stimulate it provoke nausea/vomiting.

Front 35

What stimulates the chemo receptor trigger zone (CTZ?)

Back 35

5HT3, D2, M1

Front 36

Side effects of metoclopramide?

Back 36

Extrapyramidal including parkinson-like symptoms

Front 37

Principal MOA of Dopamine receptor antagonist (metoclopramide)

Back 37

D2 receptor antagonism at the CTZ. For cancer chemo-induced emsis

Front 38

How are antihistamines used in motion sickeness?

Back 38

block input from the vestibular apparatus to the CTZ.

Front 39

Antihistamines (except diphenhydramine) end in what?

Back 39

-zine

Eg, promethazine, cyclizine, hydroxyzine)

Front 40

How are anticholingergics used in motion sickness?

Back 40

Block muscarinic receptors at the CTZ from getting vestibular input.

Front 41

What anticholingeric is used to treat motion sickness?

Back 41

scopolamine

Front 42

What is delta-9-tetrahydrocannabinol?

Back 42

Naturally occurring cannadinoid from THC plant. Stimulation of CB1 receptor neurons in CTZ. Useful in cancer chemotherapy

Front 43

Adverse effects of delta-9-tetrahydrocannabinol

Back 43

Central sympathomimetic effects, including palpitations, tachycardia, vasodilation, hypotension. Marijuana "highs". Can induce withdrawal symptoms on cessation.