Nurs 605 Module 6 Flashcards
Describe the alarming/red flag symptoms of a patient presenting with dyspepsia that would warrant an urgent endoscopy
VBAD vomiting bleeding/anemia abdominal mass/unintentional weight loss dysphagia (difficulty swallowing) age >55 with above symptoms
What are the classes of medications used as cytoprotectants or those that decrease acid production
bismuth salts antacids H2 antagonists misoprostol PPIs sulcrafate
Describe the mechanism of action of bismuth salts
increases prostaglandins = increases mucous and bicarbonate production in the stomach
acts to coat ulcers and erosions as a protective layer
What microbe does bismuth salts have some activity against?
h. pylori
Would you use bismuth salts as monotherapy for H. pylori infection?
no- monotherapy has no effect
Describe contraindications for use of bismuth
can’t use in those who have ASA allergies
not appropriate in renal insufficient patients
What are the side effects of bismuth salts?
blackening of the stool and tongue
tinnitus at high doses
nausea/vomiting
How do drugs affect acid secretion in the stomach?
dependent on the drug-many mechanisms of actions
increased prostaglandin to increase mucous and bicarbonate
acts on histamines that suppresses gastrin production
irreversibly binds to proton pump to prevent gastric secretions=decreases acid secretion
neutralizes acids
Describe the mechanism of action of antacids
base that neutralizes gastric acid and raises gastric pH
What are some adverse effects of antacids
hyperkalcemia
can affect absorption of other drugs
constipation
rebound acidity
What are the uses of antacids?
adjunctive relief for peptic ulcer disease
ineffective in eradication of h. pylori
Describe the mechanism of action of sulcrafate
cytoprotectant-creates a barrier around the ulcer or erosion to prevent further damage
does not alter gastric pH
What is the primary consideration of using sulcrafate?
needs a very acidic/gastric environment to work
not used often due to drug interactions
most GI drugs limit acid secretion
must use 2 hours prior to other drugs
What are the side effects of sulcrafate?
constipation
nausea
dry mouth
headache
What are some drug interactions with sulcrafate?
decreased activity with PPIs, antacids, and H2 antagonists
decreased absorption of digoxin, phenytoin, warfarin, abx
What class of drug is misoprostol?
protaglandin analog
What is the mechanism of action of misoprostol?
enhances mucousal defence and suppressed acid secretion
What is the major contraindication for use of misoprostol?
can’t use in pregnant women as it is an abortive agent as well
At what dosage is misoprostal effective and what is the risk of this?
800mcg
can’t tolerate by most people as too many side effects
What are the side effects of misoprostol?
diarrhea, cramps, uterine contractions=no pregnant women!
What is the dosing for bismuth salts?
30mL QID
Why does tinnitus occur when taking bismuth at high doses?
due to salicylates
A 14 year old is recovering from the flu; can they take bismuth for dyspepsia?
nope!
What are common doses of sulcrafate?
1 g QID or 2g QID
What is the primary use of misoprostol?
used in prevention of dudenal ulcers caused by increased use of NSAIDS
What class of drug is misoprostol?
synthetic prostaglandin analog
Descibe the mechanism of action for H2 antagonists
blocks h2 receptors in parietal cells = suppresses gastric acid secretion; gastrin and acetylcholine
What are some common H2 antagonists?
ranitidine, cimetidine, famotidine
What are the side effects of H2 antagonists?
diarrhea, headache, constipation, myalgia
What side effects occur at high doses of h2 receptor antagonists and why?
H2 receptors can cross the blood brain barrier
at high doses can cause confusion, hallucinations
What side effects occur with cimetidine specifically>
men-gynecomastia
women- galactorrhea
Why is cimetidine rarely used?
causes gynecomastia and galactorrhea
inhibitor of many CYPs include 1A2, 2D6, 3A4 (most drugs) so lots of drug interactions
At what approximately percentage are H2 receptor antagonists eliminated?
approx. 70%
Describe the mechanism of action of proton pump inhibitors
inhibits the transportation of hydrogen ions in the proton pump= no exchange for K in the intestinal lumen= no acid secretion
increases gastric pH and is an inactive prodrug
Discuss how PPIs irreversibly inhibit acid secretion
inhibits the proton pump irreversibly (last stage of acid production)
What is the potency of PPIs?
PPIs are very potent; approx 80-90% reduction of acids
How many days after cessation of PPIs does it take for parietal cells to return to the stomach lining and secrete acid again?
approx 2-5 days as cells and the proton pump need to recover and return
What are some of the PPIs available in Canada?
pantoprazole
rabeprazole
omeprazole
esomeprazole
What is the purpose of gastrin the stomach?
stimulated when there is prescence of food in the stomach
stimulates pepsinogen, histamine
What is the purpose of histamine in the stomach?
stimulates acid secretion for breakdown of food
What is the purpose of somatostatin in the stomach?
inhibits the secretion of stomach acid; inhibits gastrin (which stimulates acid production)
What are prokinetics? Describe their mechanism of action and why they are not used in treatment of GERD
prokinetics-drugs that stimulate the motility of gut and the LES
not used in GERD due to lack of evidence supporting use
PPIs are an inactive prodrug; what does this mean?
delayed activation, stimulated by acid and then begins to work. delayed so that not all cells are destroyed at once
In what clinical cases are PPIs used? (these indications have been studied and strong evidence supports use of PPIs in these conditions)
uninvestigated GERD non erosive esophogeal refluex NERD functional dyspepsia reflux esophagitis H. Pylori eradication
antimicrobial and symptom relief**
Describe the pathophysiology of GERD
low esophageal sphincter pressure
“refluxes” and allows stomach acid to return up the esophagus
can lead to delayed gastric emptying and possible barrett’s esophagus
What are the clinical manifestations of GERD?
heartburn dyspepsia nightime cough regurgitation globus belching
A patient presents with vomting, heartburn, unintential weight loss, bleeding, and dysphagia; what would be your next steps and what could these potential be an indicator of?
VBAD symptoms require endoscopy ASAP
could be barretts esophagus, esophageal strictures
What are the goals of therapy in those with GERD?
reduce or eliminate symptoms identify triggers prevent complications heal ulcers prevent recurrence
What are the first choices in treatment of GERD?
H2 receptor antagonists and PPIs
PPIs are superior over H2 receptor antagonists for tx outcomes but ok to try either one first
antacids can also be used as adjunctive therapy for symptom relief
What are some aggravating factors of GERD and how can we modify these factors?
obesity, pregnancy (lose weight)
smoking, ETOH (cessation)
dietary changes- no acidic foods/drink
no laying down after eating
What pharmacological and non pharmacological options would you suggest to a pregnant woman who has GERD?
antacids
H2 RAs and PPIs are all safe in pregnancy
lifestyle modifications-smaller meals, not laying in bed after eating, raising the head of the bed
What is the evidence of using PPIs in erosive esophagitis?
unclear evidence supporting the use of long term PPIs in prevention of complications such as barretts or strictures
is possible that PPIs are used lifelong in those with exisiting severe barretts
What is the evidence of using PPIs in NERD?
overall, decreased symptoms of NERD
increased % of patients that didn’t benefit (some are non responders)
no evidence that supported PPIs are better than H2RAs
What are some causes of nausea?
many causes
GI, viruses, illness, neurological causes, psychiatric, opiod induced, cancer or other medical reasons
Recommend a drug for the prophylaxis of motion sickness
motion sickness is caused by vestibular changes and is neurological
choices of treatment are antihistamines and anticholinergics
antihistamines: dimenhydrinate, diphenhydramine
anticholinergics: scopolamine
Describe the mechanism of action of scopolamine; include its drug class and what its used for
anticholinergic
muscarinic antagonist
prevnetion and treatment of motion sickness
What are the side effects of scopolamine?
dry mouth, blurred vision, urinary retention
Describe the mechanism of action of antihistminic agents in the use of motion sickness
works at the vestibular apparatus to prevent nausea
What is the major side effect of dimenhydrinate and diphenhydramine?
sedating
gravol and benedryl
What are some pharmalogical recommendations to manage nausea and vomiting in pregnant women?
dicletin metoclopramide dimenhydrinate ondansetran promethazine
Describe the difference between acute and delayed nausea or vomiting in cancer
acute: n/v occurs within 24 hours of chemo
delayed: n/v occurs after 24 hours of chemo
What are the risk factors contributing to increased risk of nausea and vomiting in cancer?
the type of chemotherapy
hx of motion sickness, women >50 years, anxiet
What pharmacological options would you use in acute CINV?
low risk of vomiting: dexamethaxone (steroid)
metoclopramide if steroid contraindicated
mod: ondansetron (serotonin blocker)
high riks: aprepitant (for chemo at high risk of n/v)
Discuss the management of delayed nausea in CINV
control nausea in the acute phase
regular antemetics for 2-5 days if at high risk
lower risk? 1-2 days of antiemetics
PRN antiemetics
Which chemotherapy drug is most likely to cause delayed CINV
cisplatin
What is the choice of agent in delayed CINV?
dexamthasone 4-8mg BID-QID
apreptant 80mg
metoclopramide or prochlorperazine
Name some causes of constipation
diet, poor bowel habits, anxiety, opiods, neurological disorders
What are the classes of laxatives?
bulk forming stool surfactant agents osmotic laxatives PEG saline/lubricant laxatives stimulant laxatives
Name and describe the mechanism of action of bulk forming laxatives
psysillium
increases stool bulk, softens it and increases water content
stimulates peristalsis movement
Name and describe the mechanism of action of stool surfactant agents
docusate sodium/calcium
stool softeners; allows stool to reabsorb water
preventative against straining
Name and describe the mechanism of action of osmotic laxatives
lactulose
increase stool liquidity
works quickly
describe the mechanism of action of PEG
hyperosmotic laxative
short term use only
Describe the mechanism of action of saline/lubricant laxatives
saline: changes to osmotic gradient so causes stool to express quickly via peristalsis
Name and describe the mechanism of action of stimulant laxatives
senna, bisacoydl
stimulate bowel motilitis
increases secretion of fluids
can cause cathartic colon (lazy colon)
Name some dietary recommendations in a patient with constipation
increase fluids
increase fibre
prune juice
discontinue offending foods or drugs
Name common anti diarrheal agents
loperamide
lomotil - diphenoxlate with atropine
When should a person seek medical attention when experiencing diarrhea/
> 24 hours diarrhea, fever, nausea or vomting, signs of dehydration, blood in stool
What is the standard treatment of diarrhea when using loperimide?
max 16mg/day
4mg stat, then 2mg after every loose stool
What is the standard treatment of diarrhea using lomotil?
2.5mg to 5mg PO q 6 hours
What are the non pharmaceutical recommendations for a person with diarrhea?
stop offending drug small frequent meals keep hydrated bulk forming agents may be necessary avoiding spcity, fatty foods, carbonated drinks and caffeine
A child is less than <2 years of age; are they able to use antidiarrheals?
no, must be greater than 2 years of age
Describe the clinical manifestations of Chrohn’s disease and what part of the intestine it most greatly affects
non bloody diarrhea/steatorrhea 5-6x day abdominal cramping fevers anemia -lack of vitamin b12 weight loss malnutrition- due to lack of absoprtion of essential vitamins
chrons can affect any part of the GI tract
Describe the clinical manifestations of ulcerative colitis and what part of the GI tract it affects mostly
relapsing blood diarrhea with mucous and pus
abdominal cramping
weight loss
anorexia
affects the colon
ulcerative proctitis affects the rectum only
Describe the non pharmacological and pharmalogical ways to manage chrohns disease
non pharm:
smoking cessation, surgery
pharm:
corticosteroids-prednisone/budesonide
azathioprine
methotrexate
Describe the pathophysiology of peptic ulcer disease
erosion of the GI tract
either gastric or dudodenal ulcers
What are some clinical symptoms of PUD?
dyspepsia
Whata are the causes of PUD?
etoh, smoking, H. Pylori, NSAID use
Why is NSAID use considered a risk factor for PUD?
nsaid use, inhibits CoX1- stimulates prostaglandins in the stomach that coats stomach, increased acid production
Desribe the clinical symptom that is different between gastric and duodenal PUD?
gastric- irritated by food
duodenal- calms with food
What is the suggested first line quad therapy for h. pylori eradication?
PPI x 10 days BID
first 5 days: amoxicillin 1g BID
second 5 days: clarithromycin 500mg BID + metroniadzole 500mg BID
What is the suggested quad therapy for H. pylori eradication after first line therapy has failed?
PPI x 14 days
bismuth 2 tabs BID
flagyl 500mg TID
tetracylcine 500mg QID
Discuss PPI use in less studied conditions; name these conditions and what the evidence suggests
GERD symptoms (cough, asthma, laryngx)- little evidence to support PPI use; can try as last resort if needed NSAID preventative ulcers- studies show misoprostol at high doses showed good effect; can try in high risk individuals (prev. GI bleed, h. pylori, on meds that required NSAID use) Antiplatelet ulcers-no strong evidence to support PPI use to prevent ulcers
Describe where COX1 and COX2 are found and what their roles are. Why is the inhibition of COX1 in NSAIDs a risk factor for developing PUD?
COX1- kidneys, prostaglandins in the GI for protection; platelet aggregation and tissue perfusion
COX2- inflammatory cytokines
No COX1= no GI protection, increased bleeding due to decreased platelet aggregration
This drug is not recommended in the use of NSAID induced ulcer prevention, H. Pylori eradication, and erosive esophagitis
H2 RAs
How long does it a take a patient to be on a PPI before noticing any benefit (if any?)
8 weeks
What are some noted adverse effects of PPIs?
vitamin b12 deficincy fractures enteric infections peritonitis pneumonia
Why is it necessary to taper PPIs and for how long?
may cause rebound acidity if abruptly stopped
taper over 4-8 weeks
can use H2RA or antacids but don’t take at the same time
Which PPI has the most drug interactions? the least?
pantoprazole . omeprazole
What are the clinical manifestations of irritable bowel syndrome?
abdominal pain with defectation and altered bowel habits without a cause
can be constipation or diarrhea
Diarrhea predominant vs. constipation predominant IBS
dairrhea prominent - >25% of loose stools mostly (bristol stool 1-2)
constipation prominent >25% of hard/firm stools mosty
What are some ways to manage IBS (include pharm and non pharm)
non pharm-life style changes; dietary modifactions FODMAPS, gluten free etc; prebiotics, probiotics
pharm: dependent on diarrhea or constipation type
diarrhea? loperimide, lomotil
constipation? laxatives
Through what cell and mechanism is acid secreted in the stomach?
parietal cells
proton pump
presence of food stimluates gastrin
