Pharm- Gi

Front 1

Chemorecepto trigger zone (CTZ)

Back 1

contained in the area postrema on the floor of the IV ventircle in medulla. BBB is poorly developed here so readily available for emesis stimuli.

Front 2

Vomiting Center (VC)

Back 2

integrates the emetic response. Located in dorsolateral border of the reticular formation of the medulla.

Front 3

Ipecacuanha

Back 3

Emetic drug that is used to treat non-corrosive poisoning when the patient is conscious. Only effective when vomiting stimulant in still in the upper GI.

Front 4

Apomorphine

Back 4

emesis causing drug that acts on CTZ. Patient must be awake to give to them. Only effective while emesis stimulant is still in upper GI

Front 5

What are some minor drugs that can cause emesis.

Back 5

L-DOPA, cardiac glycosides, Cu sulfate.

Front 6

Cinnarizine, Cyclizine, promethazine.

Back 6

H1-receptor antagonist. Effective in motion sickness and against substances acting locally in stomach but not against those working on CTZ. Act at vestibular nucleus in the medulla.

Front 7

Hyoscine

Back 7

Muscarinic-receptor antagonist. Acts on vestibular nucleus and vomiting center and blocks visceral afferents activated by stimuli in the stomach. Ineffective on CTZ stimulants.

Front 8

Ondansetron and granisetron

Back 8

Serotonin receptor antagonists. Immense value in treating vominting caused by cytotoxic drugs. Synergestic effects with dexamethasone.

Front 9

Nabilone

Back 9

Synthetic cannabinol derivative. Reduces vomiting due to substance which stimulate the CTZ. Can get some drowsiness and dizziness but very effective.

Front 10

Risk factors for peptic ulcer.

Back 10

Coffee (caffein is acid stimulant), alcohol, tobacco (Slows healing), salicylates, heredity, NSAIDs, age.

Front 11

Symptoms of ulcer

Back 11

Gnawing or burning pain in the epigastrium. Typically occurs when the stomach is empty, between meals, and early morning. Relieved by antacids and eating. Can have nausea, vomiting, and loss of appetite. Can get anemia.

Front 12

H2 Receptor Antagonists

Back 12

Acid suppression agents. Treat GERD and peptic ulcers. Decrease flor of stomach acid to aid in healing process known as esophagitis. Useful in Zolllinger-Ellison syndrome.

Front 13

Suffic for H2 Receptor Antagonist

Back 13

tidine

Front 14

Cimetidine

Back 14

Classic H2 receptor antagonist. Reduces acid secretion for 4-5 hours which is rough. Can have GI problems and confusion. Androgen receptor antagonist can give guys boobs and impotence and excess prolactin release in women. Inhibitor of microsomal enzymes. Antacids reduce bioavailability.

Front 15

Ranitidine (Zantac)

Back 15

10x potency of cimetidine. No anti-androgenic properties. Doesn't bind to testosterone receptors. Famotidine is 2x potency of ranitidine.

Front 16

Cholinergic antagonists
(Propantheline, Isopropamide, Scopolamine)

Back 16

Cause a decreased Ach stimulated secretion and motility along the gastrointestinal tract. Rarely used along but in patients resistant to H2 receptor antagonists. Not high enough dose for systemic doses.

Front 17

Antacids

Back 17

Weak bases that only partially neutralize gastric acid. Reduce pain associated with ulcers and promote healing. Can result in alkalosis.

Front 18

Aluminum hydroxide

Back 18

Antacid. Not absorbed by GI. Can cause constipation. Binds bile acids and stimulates mucus secretion. That is most important point.

Front 19

Sodium Bicarbonate

Back 19

Systemic absorption. Not for long term therapy. Don't give with HTN patients.

Front 20

Calcium carbonate

Back 20

Stimulates gastrin release. Causes rebound acid production. Don't give to renal disease patients. Overuse can give hypercalcemia.

Front 21

Magnesium hydroxide

Back 21

Antacid. Frequent long lasting diarrhea. Hypotention maybe.

Front 22

Antacid drug interactions

Back 22

Can alter bioavailability by changing pH. Also can chelate other drugs like digoxin and tetracyclines.

Front 23

Proton pump inhibitors

Back 23

Rapidly heal erosive esophagitis. Not only symptom relief but elimination of symptoms in most cases. 6-8 weeks is great prognosis for healing.

Front 24

Omeprazole
(Losec)

Back 24

Inhibits parietal cell proton pump directly. Hypertrophy of gastrin producing cells. Inhibits microsomal enzymes and has been shown to cause tumors in animals at high doses. Long half life.

Front 25

Urogastone and Enterogastonr

Back 25

Polypeptides that causes marked cecrease in basal and stimulated acid secretion. New drugs that we dont' know much about.

Front 26

Sulcralfate

Back 26

Protective drug. Complex polysaccharide complexed with aluminum hydroxide that crosslinks as a result of acidic gastic pH. Polymer has affinity for exposed proteins in peptic ulcers. Requires the acid for activation.

Front 27

H. Pylori

Back 27

Spiral shaped bacterium found in gastric mucus layer or adherent to epithelial lining of the stomach. 90% of duodenal and 80% of gastric. Antibiotics to cure. Produce urease. Provides organism an alkaline environment. Disrupts membrane. Chronic infection and usually a lifetime flora. Can also cause atrophic gastritis and gastric cancer and MALT lymphoma.

Front 28

H. Pylori diagnosis

Back 28

IgG antibodies in blood can determine positive infection. Breath test: patient given labeled urea and H. pylori metabolizes it quickly and the labeled carbon on urea comes out in breath. Culture and biopsy as well.

Front 29

H. Pylori treatment

Back 29

Antibiotics. Use combination to take out DNA and the cell wall. 2 week therapy. Also give other ulcer drug to get largest chance of healing.