Gi - Pharm Test 4

Front 1

What are the three common forms of peptic ulcers?

Back 1

-H. Pylori associated
-NSAID – induced
-Stress ulcers or stress related mucosal damage

Front 2

What is H. pylori?

Back 2

-it is a spiral shaped, pH sensitive, gram negative bacteria
-involved in the production of gastric and duodenal ulcers
-it invades the mucous layer of the stomach and attaches to the epithelium,causes breakdown of the mucosal layer

Front 3

How do NSAIDs cause ulcers?

Back 3

They cause direct irritation of gastric mucosa and inhibitprostaglandin synthesis
-related to inhibition of COX-1
-PGs regulate gastric mucous production
-can cause gastric and duodenal ulcers

Front 4

How does stress cause mucosal damage?

Back 4

-mucosal ischemia
-presence of gastric acid, not hypersecretion
-acute/critically ill patients are at risk: trauma, increased ICP, burns, acuteonset (can occur w/in 24hrs of admit)

Front 5

Compare/contrast the three forms of peptic ulcers.

Back 5

Front 6

What are some complications associated with peptic ulcerdisease?

Back 6

Bleeding (d/t artery erosion, 50% of upper GI bleeds) -perforation – obstruction (d/t scarring, edema)

Front 7

What is the acid producing cell in the stomach?

Back 7

the parietal cell

Front 8

Where do proton pump inhibitors work?

Back 8

on the K+/H+ ATPase proton pump, blocking hydrogen ion release (the final pathway)

Front 9

What kid of receptors on the parietal cell do medications to treat peptic ulcer disease work on?

Back 9

-ATPase

-gastrin-cholecystokinin-B receptor

-histamine receptor

-muscarinic receptor

-enterochromaffin-like cell

-somatostatin receptor

Front 10

List some histamine-2 receptor antagonists.

Back 10

Cimetidine – ranitidine – famotidine – nizatidine

Front 11

List some proton pump inhibitors.

Back 11

Omeprazole –esomeprazole – lansorazole – rabeprazole –pantoprazole

Front 12

What are some miscellaneous agents used to treat PUD?

Back 12

Antacids: hydroxide salts of aluminum and magnesium (neutralize acid in the stomach)
mucosal protective agents: sucralfate

Front 13

What is the MOA of H2 antagonists?

Back 13

They bind to and block the H2 receptors located on theparietal cell
-competitive and reversible
-decreases intracellular cAMP synthesis
Decreases histamine stimulated gastric acid secretion

Front 14

What are some adverse effects of H2 antagonists?

Back 14

They are generally well tolerated.
GI upset – headache – drowsiness – hematologic effects (thrombocytopenia)

Front 15

Describe Cimetidine.

Back 15

Available PO or IV. OTC.
Adjust dose for liver and renal dysfxn.
Significant cytochrome P450 inhibition.
AE: antiandrogen effects: gynecomastia and impotence.

Front 16

Describe famotidine.

Back 16

Available PO, IV, OTC.
Adjust dose for renal dysfxn.
No significant cytochrome P450 inhibition.

Front 17

Describe ranitidine.

Back 17

Available PO, IV OTC.
Adjust dose for renal dysfxn.
Little or no cytochrome P450 inhibition.

Front 18

What is the MOA of PPIs?

Back 18

Proton pump is the final common pathway in acid secretion.
Converted to active drug in acid environment (intracellularly)
Creates sulfhydryl bond with proton pump (non-competitive, irreversible)
Only act on proton pumps secreting acid (take before meal to maximize number ofactive pumps.

Front 19

What are some adverse effects of PPIs?

Back 19

Overall well tolerated
GI effects – headache – drowsiness

Front 20

What are some adverse effects of long term use of PPIs?

Back 20

May decrease B12 absorption – hypomagnesemia (muscle spasms,arrhythmias, tremors, seizures) - gastric tumors

Front 21

Which PPI is most likely to inhibit cytochrome P450 enzymes?

Back 21

Omeprazole
drug interactions uncommon for all PPIs

Front 22

What PPI may require dosage adjustment if there is liverfailure?

Back 22

All of them but especially lansoprazole

Front 23

What is the MOA of Sucralfate?

Back 23

Binds electrostatically to positively charged proteinmolecules in the ulcer crater ( forms a protective barrier)
stimulates endogenous prostaglandins
may suppress H. pylori
no effects on acid secretion
minimal systemic absorption (given orally and has local effects)

Front 24

What are the adverse effects of sucralfate?

Back 24

Constipation, hypophosphatemia, aluminum toxicity in renalfailure pts due to aluminum
binds tetracyclines and fluoroquinolones

Front 25

Where does each class of drugs for treatment of PUD work?

Back 25

Front 26

How do you treat H. pylori?

Back 26

Combination regimen
antibiotics: amox, clarithromycin, tetracycline, metronidazole (test forabsence of H.pylori 4 weeks later)
decrease acid production (to promote healing): H2 receptor antagonists, PPIs
bismuth preparations: subsalicylate, ranitidine bismuth citrate
Treatment reduces risk of recurrence to < 10% at 1 year

Front 27

What is the first line regimen recommended for H. pyloritreatment?

Back 27

Carithromycin-based triple therapy:
PPI BID + Clarithro BID + amoxi or metronid BID

Front 28

What is the Bismuth quadruple therapy?

Back 28

Second line treatment for H. pylori.
PPI or H2 antag BID + bismuth subsalicylate QID + metron QID + tetra QID

**not tolerated well**

Front 29

What is a third option for H. pylori treatment?

Back 29

PPI BID + amox BID x5d then PPI BID + clarit BID +tinidazole x 5 d

Front 30

What is the treatment for active duodenal/gastric ulcers?

Back 30

-conventional tx with H2 receptor antag, sucralfate orantacids (heals 90% duodenal ulcer at 8 weeks)
-PPIs show comparable healing rates at 4 weeks
-higher doses or longer therapy usually needed to heal gastric ulcer
-don't use antacids as monotherapy d/t dosing inconvenience

Front 31

What are some things that play a part in refractory ulcers?

Back 31

Poor pt compliance – antimicrobial resistance – smoking –nsaid use – gastric acid hypersecretion – H2 receptor antag tolerance

Front 32

How do you treat refractory ulcers (sx still there at 8weeks –duodenal – or 12 weeks - gastric?

Back 32

Test for H.pylori
high dose PPI
Combo therapy - PPI/H2 antag and sucralfate

Front 33

Who needs maintenance therapy for PUD and how do you do it?

Back 33

Pts with frequent recurrences
duodenal: low dose H2 antag or PPIs
gastric: full dose H2 antag or PPIs

Front 34

How do you treat NSAID induced ulcers?

Back 34

Stop the NSAID
-pts who need NSAIDS may need to reduce dose or add PPI
most will resolve with standard treatment

Front 35

What is misoprostol?

Back 35

Synthetic prostaglandin E analog
moderately inhibits acid secretion, enhances mucosal defense
causes diarrhea in 30%
expensive

Front 36

What is used for prophylaxis of NSAID induced ulcers?

Back 36

Misoprostol
high dose H2-antagonists or PPIs
switch to cox-2 specific agents

Front 37

What is used for prophylaxis of stress ulcers?

Back 37

H2 antagonists or PPIs

Front 38

Describe the pathophysiology of nausea and vomiting.

Back 38

Triggered by afferent impulses to the vomiting center whichis located in the medulla
impulses are received from sensory centers: chemoreceptor trigger zone,cerebral cortex, visceral afferents from the pharynx and GI tracts
Efferent impulses go from the vomiting center -> salivation center, respcenter, pharyngeal, GI and abdominal muscles -> vomiting

Front 39

What kind of neurotransmitter receptors are located in thevomiting center, CTZ and GI tract?

Back 39

Cholinergic – serotonergic – histaminic – dopaminergic –opiate

Front 40

What are some locally-mediated etiologies of N/V?

Back 40

Bowel obstruction – ulcers – surgery – drugs (irritation ofGI mucosa)

Front 41

What are some centrally-mediated etiologies of N/V?

Back 41

Drugs (CTZ stimulation: antineoplastic agents, ipecac,opioids, general anesthetics)
Increased ICP
Sepsis
Organ failure (uremia d/t renal failure, liver failure)

Anticipatory
Other stimuli (sight, smell, taste)

Front 42

How common is post-op nausea/vomiting?

Back 42

20-30% in general surgical population
70-80% in high risk populations

Front 43

What are some adverse effects of post-op nausea/vomiting?

Back 43

Patient distress/morbidity: wound dehiscence, esophagealrupture, aspiration, dehydration, increased ICP, pneumothorax
Increased health care costs

Front 44

What are some risk factors for PONV?

Back 44

Female (3x males) - history of PONV or motion sickness –nonsmoker – younger age (<50) - general vs regional anesthesia – inhalationanesthetics and nitrous – intra or post op opioid analgesics – duration ofsurgery/anesthesia (30mins increases risk 60%) - type of surgery (lap, gyne,abdominal)

Front 45

List some anti-dopaminergics.

Back 45

Butyrophenones – droperidol, haloperidol
Phenothizines – perphenazine
Misc – metoclopramide

Front 46

List some antihistaminic/anticholinergic used for PONV

Back 46

Promethazine – diphenhydramine – dimenhydrinate – meclizine– hydroxyzine – scopolamine

Front 47

List some serotonin antagonists.

Back 47

Dolasetron – granisetron – ondansetron – palonosetron

Front 48

List a benzodiazepine used for PONV.

Back 48

Lorazepam

Front 49

List a corticosteroid used for PONV.

Back 49

Dexamethaxone

Front 50

List a neurokinin-1 receptor (substance P) antagonist usedfor PONV.

Back 50

Aprepitant – expensive but may last longer, give 40mg w/in 3hrs of induction

Front 51

What is the MOA of antidopaminergic agents?

Back 51

Dopamine-receptor antagonism at the CTZ
droperidol is the prototype

Front 52

What are some adverse effects of antidopaminergic agents?

Back 52

Extrapyramidal effects – dysphoria – sedation – hypotension– QT prolongation and torsades

Front 53

What is the MOA of serotonin receptor antagonists?

Back 53

They bind to and block serotonin receptors involved in theemetic pathway
-they have high affinity
-they have local and central effects

Front 54

What are some adverse effects of serotonin receptorantagonists?

Back 54

Headache, lightheadedness, constipation
injectable dolasetron asso with severe arrhythmias in cancer pts (they are onhigh doses)

Front 55

How does dexamethasone work to help PONV?

Back 55

Exact mechanism unknown
efficacy similar to serotonin receptor antagonists and droperidol
used in combo with other antiemetics is more effective than either alone
single doses not asso with sig adverse effects

Front 56

What anti-emetics would you give at induction?

Back 56

Aprepitant – dexamethasone – palonosetron

Front 57

Which anti-emetics would you give at end of surgery?

Back 57

Droperidol – ephedrine – granisetron – ondansetron –dolasetron

Front 58

Which anti-emetic would you give the prior evening or 2hours before?

Back 58

Scopolamine

Front 59

What are some strategies to reduce baseline risk for PONV?

Back 59

Avoidance of general anesthesia by using regional
use of propofol for induction and maintenance
avoid nitrous
avoid volatile anesthetics
minimize intra and post op opioids
minimize neostigmine
adequate hydration

Front 60

What is the PONV risk if a patient has 0 risk factors? 1? 2?3? 4? Treatment?

Back 60

Low 10% ---> wait and see
Mild 21%
Moderate 39% ----> pick 1 or 2 interventions
High 61% ----> >2 interventions/multimodal
Extremely high 79%

Front 61

Which medications do you not readminister for PONV?

Back 61

Dexamethasone or scopolamine
do not readminister if < 6 hrs after PACU