Module 10 Quiz

Question 1

How do ulcers develop?

Answer 1

Secondary to imbalance b/w host defenses and aggressive factors

Question 2

What are our defenses

Answer 2

Mucosal barrier, bicarbonate, prostaglandins, perfusion to mucous membranes

Question 3

List Aggressors

Answer 3

H. Pylori
NSAIDS
Pepsin
Gastric Acid

Question 4

Where do ulcers occur

Answer 4

Lesser curvature of stomach and duodenum

Question 5

What are some complications from PUD

Answer 5

perforation, peritonitis, hemmorhage

Question 6

Goals of drug therapy

Answer 6

1. symptoms alleviation
2. promotion of healing
3. Preventing complications/recurrence

Question 7

Antibiotics

Answer 7

Indication: H. Pylori AND PUD
(Not for assymptomatic people)
-must employ combo therapy
-2-3 abx +PPI or H2 antagonist
-10-14 days
-SE: nausea/diarrhea

Question 8

H2 receptor antagonist

Answer 8

Prototype: Cimetidine
Action: Promotes healing gastric/duodenal selectively blocks H2 receptors=volume reduction/acidity of acid
length: 4-12 weeks
SE: anticholinergic symptoms, PNA
Drug-drug interactions: inhibits Hepatically metabolized drugs (warfarin), antacids decrease absorption (take 1 hr apart)

Question 9

PPI

Answer 9

Prototype: Omeprazole
Indication: duodenal/gastric ulcers, gerd, erosive esophogitis
Action: inhibit gastric acid secretion
Length: 4-8 weeks
SE: acid rebound, FX, PNA, C-diff
drug-drug interactions: increased w/ plavix, decrease absorption of HIV meds and antifungals

Question 10

Anti-ulcer drugs: Sucralfate

Answer 10

Action: Creates physical barrier
SE: constipation, may impede absorption of other meds

Question 11

Ant Acids

Answer 11

Indications: PUD, symptomatic relief of heartburn
Action: form neutral/low acid salts when exposed to gastric acid + decreased mucosal wall destruction
SEs: constipation, diarrhea, sodium loading (be careful in pts with renal failure or HF)
Drug-drug interaction: Can effect dissolution and absorption of medications (Give 1 hour apart)

Question 12

Non drug therapy for PUD

Answer 12

-5-6 meals a day, avoid large meals
-reduce fluctuation in gastric pH=May facilitate recovery
-avoid NSAIDS and smoking

Question 13

Constipation causes and treatment

Answer 13

2 or < BMs a week (can be pathological but in US frequently associated w/ lifestyle factors)

Causes: poor diet (low fiber), caffeine abuse, ETOH, sedentary/inactive, medications

Treatment: improved nutrition and exercise (first line)
-laxatives only after attempting above, used as adjuncts NOT monotherapy

Question 14

Laxative abuse

Answer 14

habitual self prescribing
erroneous belief of what “normal” bowel habits are
-AEs: decrease defacatory reflexes, electrolyte imbalances, dehydration, colitis
-Recommend abrupt cessation, address misconceptions, quality more important than quantity, stress increase consumption of fiber containing food

Question 15

Bulk forming laxative

Answer 15

Prototype: Pysillium
Actions: similar to dietary fiber, works over 1-3 days
-Nonabsorbable, nondigestable substance that results in stool swelling and with water–>increased mass/softening and increase colonic transit

AEs: can result in obstruction if not taken with a full glass of water

Question 16

Surfactant laxatives

Answer 16

Prototype: Docusate
Actions: alters stool consistency by changing surface tension–>water penatrates feces
Onset: 3-6 hours, intermediate onset

Among the most frequently abused

Question 17

Stimulant laxatives

Answer 17

Pprototype: Bisacodyl
Action: stimulates motility and increases water and electrolytes in the intestine by reducing intestinal absorption

commonly abused

Only indicated for constipation r/t opioids or slowed intestinal transit

Question 18

Osmotic laxatives

Answer 18

Prototype: Polyethylene glycol
Actions: pull water into intestines. Not systemically absorbed. Results in rapid fluid evacuation

Indications: bowel prep

AE: dehydration, sodium retention (may exacerbate HF)

Question 19

Antiemetics

Answer 19

N/V is a complex reflex involving multiple recpetors (serotonin, dopamine, histamine, acetylcholine)
-Vomitting center: nulcleus of neurons in medulla oblangota

Center can be activated:
1. directly (anticipation, fear, pain, noxious stimuli)
2. Indirectly (signals from stomach/sm intestine or emetogenic compounds-chemo, ipecac, opioids)

Question 20

Serotonin Receptor Antagonist

Answer 20

Prototype: Ondansetron
Actions: block serotonin receptors in the CTZ and neurons in upper GI tract.

Most effective we have for chemo induced n/v

Excellant for monotherapy (++++ w. dexamethasone)

SEs: QT prolongation/torsades

Question 21

Dopamine antgonists

Answer 21

Phenothiazines: Prototype: Prochlorperazine

Action: block domapine 2 receptors in CTZ

Adverse: EPS reactions, anticholinergic effects, hypotension, sedation

Question 22

Glucocorticoids

Answer 22

Prototype: Dexamethasone

Actions: unknown

IV or PO

AE: none really secondary to short term use

Question 23

Cannabinoids

Answer 23

Prototype: Dronabinol

Actions: activation of canabanoid receptors around the vomiting center

Indications: chemo induced n/v, second line drug

Schedule III

Adverse: sedation, psychiatric effects, tachycardia, hypotension

Question 24

Anti-ulcer drug: Misoprostol

Answer 24

Indication: Only for proph r/t long term NSAID related ulcers
Action: Prostaglandin E analog
SE: abdominal pain, spotting
Contraindication: pregnancy=contraction

Question 25

Butyrophenones

Answer 25

Prototype: haldol

Actons: block dopamine 2 receptors in CTZ

Indications: post op N/V, and chemo
AEs: EPS reactions, sedation, hypotension, anticholinergic effects

Question 26

Metoclopramide

Answer 26

Actions: A prokinetic agent
Indications: chemo, radiation, opioids, toxins

Question 27

Phenergan

Answer 27

-Most widely used.
-1st gen histamine H1 antagonist
-Dangerous respiratory depression in kids & tissue injury/necrosis/abscess with extravasation