David's Gi I Updated

Front 1

What structures are placed next to each other for the cannalicular membrane to work? 2) What cell structures are they dependent on? 3) What ion?

Back 1

Tubulovesicular membrane ahs the H/K ATPase that is placed next to the K/Cl channels on the plasmalemma membrane.

Front 2

How does ACh from vagus affect parietal cells? 2) ECL cells? 3) Chief cells. 4) Antral G cells.

Back 2

1) Through Ma muscarinic receptors to activate IP3/DAG (inc Ca). 2) M1 muscarinic receptors to induce histamine release (affects parietal cells). 3) Release pepsinogen. 4) Release gastrin, but via GRP release

Front 3

Gastrin release from G-Cells via (2)? 2) Affect on parietal cells? 3) On ECL cells?

Back 3

Protein containing food and during cephalic phase from GRP. 2) Gastrin receptors that activate H/K ATPase via IP3 pathway. 3) Histamine release (which affects parietal cells)

Front 4

Histamine acts on what receptors? Result? Secretagogue status?

Back 4

H2 on parietal cells. 2) G-protein coupled with adenylyl cylase that inc cAMP, protein kinase, that opens Cl channels and activates H/K ATPase. 3) It is the most important gastic secretagogue

Front 5

4 inhibitors of Gastric acid secretion in respect to pH? 2) D cells? 3) Prostaglandins (esp oxyntic cells). 4) Enterogastrones

Back 5

1) < 3 pH inhibits. 2) somatostatin inhibits. 3) PGE2 his oxyntic cells which are negatively coupled to adenyl cylase and effects histamine secretion. 4) inhibitory effect (secretin, GIP, PYV, neurotensin)

Front 6

Info! Gastroduodenal mucosal barrier: Mucus, HCO3, transcellular resistance to back diffusion of protons, Reconsitution, maintenance of local blood flow, pancreatic HCO3, and prostaglandins of the E series stimulate secretion of mucus

Back 6

Ya damn straight

Front 7

Peptic ulcer from what 3 things? Causation of GERD?

Back 7

1) H. pylori 2) chronic aspirin or NSAID. 3) Zollinger-Ellison Syndrome. 4) transient inappropriate relaxation of LES

Front 8

3 strategies to protect the gastic mucosa from acid

Back 8

1) inhibit it. 2) prevent contact with it. 3) neutralize it.

Front 9

Name the contraindication for the following antacids. 1) Sodium Bicarbonate. 2) Calcium Carbonate (2). 3) Magnesium Hydroxide. 4) Aluminum hydroxide (3).

Back 9

1) HTN. 2) renal impairment and can have acid rebound. 3) Laxative. 4) produce constipation, deplete phosphate, resorption of bone

Front 10

Antacid effects are additive. 1) what is added for GERD? 2) Al and Mg antacids reduce bioavailability of what two things? 3) Chelate what two drugs?

Back 10

1) alginic acid. 2) weak acids and H2 blockers. 3) tetracycline and digoxin

Front 11

Atropine, propantheline, Isopropamid, and pirenzepine are what? 2) What 2 things do they do?

Back 11

Antimuscarinics. 2) Block motility and secretions throughout GI tract.

Front 12

H2 blockers result in what? What is common side effect that causes relapse?

Back 12

decreased acid secretion after all known stimuli. 2) acid rebound

Front 13

Cimetidine is a what? 2) 3 side effects?

Back 13

H2 blocker. 1) elderly, debilitated and renal impairment very susceptible to mental confusion (seizures), elevated serum creatinine, and hematologic disturbances. 2) Anti-androgen effects (gynecomastia, impotence, galactorrhea). 3) inhibits P450….

Front 14

Ranitidine is a what? 2) what two side effects are greatly reduced compared to others in same class?

Back 14

1) H2 blocker. 2) does NOT bind androgen receptor. Inhibits drug metabolism but less so.

Front 15

Famotidine is a what? 2) two advantages to Ranitidine? 3) 2 big advantages in class?

Back 15

1) H2 blocker. 2) more potent and longer duration. 3) does NOT inhibit hepatic drug metabolism, does NOT bind androgen receptor

Front 16

Nizatidine is a what? 1) Rare side effect? 2) 2 advantages in class?

Back 16

H2 blocker. 1) hepatic toxicity. 2) no drug interaction or androgen receptor binding

Front 17

Misoprostol is a derivative of what and resistant to what? 2) Effect on parietal cell? 3) gastic mucosa? 4) Mucosal blood flow?

Back 17

PGE1 and resistant to principle catabolizing enzyme. 2) inhibits acid secretion by opposing histamine. 3) stimulates. 4) increases

Front 18

Omeprazole, lansoprazole, rabeprazole, and esomeprazole are what? 2) MOA, discuss location too. 3) duration of effect

Back 18

1) proton pump inhibitors (PPI). 2) they are weak bases and are trapped and activated in the secretory canaliculi. At low pH, stable covalent bond with critical site (K+ transport) and H/K ATPase loses activity. 3) prolonged effect

Front 19

PPIs have what two AEs? 2) Contraindicated for what? 3) unusual tissue effect?

Back 19

1) Inc incidence of GI/Respiratory infection and osteoporosis due to calcium malabsorption. 2) Clopidogrel! 3) hypergastrinemia with gastic ECL clustering

Front 20

How do contact agents work?

Back 20

primarily by stimulating mucus secretion

Front 21

What is Sulcrafate? What is it made of? 3) What happens at acidic pH? 4) what does it bind to?

Back 21

Contact protective agent. 2) sulfated sucrose and aluminum hydroxide. 3) undergoes extensive polymerization and crosslinking. 4) exposed protein in ulcer and creates persistent barrier

Front 22

Sulcrafate has what suppressive activity? 2) stimulates mucosal production of what? 3) Inhibits what? 4) Systemic effects? 5) AE?

Back 22

1) H. pylori. 2) PGEs 3) Pepsin activity. 4) not absorbed systemically! 5) constipation

Front 23

What two things does Rebamipide do?

Back 23

Stimulate mucus secretion and scavange free radicals

Front 24

Carbenoxylone does what?

Back 24

Stimulate mucus secretion

Front 25

Bismuth compounds do what 3 things

Back 25

1) mucus secretion. 2) adherence. 3) antibacterial

Front 26

How do you Tx H. pylori?

Back 26

Triple therapy: PPI / amoxicillin / calrythromycin (substituting metronidazole if allergic to amoxicillin). Also: Antimicrobial (metronidazole) + antibacterial (amoxicillin) + bismuth salt

Front 27

Enteric nervous system uses what neurotransmitter? What two receptors does it bind and which is more important?

Back 27

ACh. 2) M2 and M3, M3 being more important

Front 28

Neostigmine does what? 2) DA binds what receptor to do what? 3) Serotonin binds what receptor to do what?

Back 28

1) acetylcholinesterase -> potentiates action of ACh. 2) Binds D2 presynaptic -> inhibits release of ACh. 3) Binds 5HT4 -> excitatory on cholinergic neuron

Front 29

Neostigmine causes stomach to do what? Side effects?

Back 29

Stomach to empty faster. 2) SLUDS

Front 30

Metoclopramide is a what? Effect on ACh? Agnoist for what?

Back 30

DA antagonist. 2) frees ACh from inhibition of DA. 3) 5-HT4 agonist

Front 31

Metoclopramide action on LES? 2) Esophageal clearance? 3) Gastric emptying? 4) Small bowel transit time?

Back 31

1) increase tone. 2) increase clearance. 3) stimulate gastric emptying. 4) decrease transit time

Front 32

Name 4 side effects of metoclopramide

Back 32

1) somnolence. 2) nervousness. 3) dystonic reactions (parkinson's) 4) increase serum prolactin

Front 33

Cisapride and Tegaserod are what? 2) two side effects

Back 33

5-HT4 agonist = prokinetic drug. 2) increased number of bowel movements and potentially fatal cardiac AEs

Front 34

Erythromycin binds to what receptor? 2) Result? 3) Indication? 4) Side effect?

Back 34

nerve and muscle motilin receptors. 2) enhances GI contractions, MMCs, and inc gastric emptying. 3) diabetic gastroparesis. 4) abdominal cramps

Front 35

What do bile acids solubilize?

Back 35

cholesterol

Front 36

Chenodeoxycholic acid MOA (2). 2) Use? 3) three side effects

Back 36

1) dec cholesterol biosynthesis (inhibits HMG-reductase) and inc bile salt pool. 2) gallstone dissolution. 3) diarrhea, liver dysfunction, inc LDL

Front 37

Ursodiol, ursodeoxychlic acid found where? 2) decreases secretion of what two things? 3) differs from our primary bile acid how? 4) Contraindicated?

Back 37

1) POLAR MOTHERFUCKING BEARS. 2) biliary cholesterol and lipid secretion. 3) does not inhibit 7alpha hydroxylase -> so bile salt synthesis and cholesterol metabolism not blocked. 4) contraindicated in chronic liver disease (or bile salt allergy, wtf)

Front 38

Methyl tert-butyl ether (MTBE) infused where? 2) MOA?

Back 38

Directly into gallbladder or bile duct lumen. 2) the ethers are solvents for lipids

Front 39

Monoctanoin is a what? 2) Major consituents of what two things? 3) infused where?

Back 39

semi-synthetic vegetable oil. 2) major constituent of mono- and diglycerides of octanoic and decanoic acid. 3) infused into common bile duct