Module 10 Quiz Flashcards
How do ulcers develop?
Secondary to imbalance b/w host defenses and aggressive factors
What are our defenses
Mucosal barrier, bicarbonate, prostaglandins, perfusion to mucous membranes
List Aggressors
H. Pylori
NSAIDS
Pepsin
Gastric Acid
Where do ulcers occur
Lesser curvature of stomach and duodenum
What are some complications from PUD
perforation, peritonitis, hemmorhage
Goals of drug therapy
- symptoms alleviation
- promotion of healing
- Preventing complications/recurrence
Antibiotics
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
H2 receptor antagonist
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)
PPI
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
Anti-ulcer drugs: Sucralfate
Action: Creates physical barrier
SE: constipation, may impede absorption of other meds
Ant Acids
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)
Non drug therapy for PUD
-5-6 meals a day, avoid large meals
-reduce fluctuation in gastric pH=May facilitate recovery
-avoid NSAIDS and smoking
Constipation causes and treatment
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
Laxative abuse
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
Bulk forming laxative
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
Surfactant laxatives
Prototype: Docusate
Actions: alters stool consistency by changing surface tension–>water penatrates feces
Onset: 3-6 hours, intermediate onset
Among the most frequently abused
Stimulant laxatives
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
Osmotic laxatives
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)
Antiemetics
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)
Serotonin Receptor Antagonist
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
Dopamine antgonists
Phenothiazines: Prototype: Prochlorperazine
Action: block domapine 2 receptors in CTZ
Adverse: EPS reactions, anticholinergic effects, hypotension, sedation
Glucocorticoids
Prototype: Dexamethasone
Actions: unknown
IV or PO
AE: none really secondary to short term use
Cannabinoids
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
Anti-ulcer drug: Misoprostol
Indication: Only for proph r/t long term NSAID related ulcers
Action: Prostaglandin E analog
SE: abdominal pain, spotting
Contraindication: pregnancy=contraction
Butyrophenones
Prototype: haldol
Actons: block dopamine 2 receptors in CTZ
Indications: post op N/V, and chemo
AEs: EPS reactions, sedation, hypotension, anticholinergic effects
Metoclopramide
Actions: A prokinetic agent
Indications: chemo, radiation, opioids, toxins
Phenergan
-Most widely used.
-1st gen histamine H1 antagonist
-Dangerous respiratory depression in kids & tissue injury/necrosis/abscess with extravasation
