Nurs 605 Module 6 Flashcards
1
Q
Describe the alarming/red flag symptoms of a patient presenting with dyspepsia that would warrant an urgent endoscopy
A
VBAD vomiting bleeding/anemia abdominal mass/unintentional weight loss dysphagia (difficulty swallowing) age >55 with above symptoms
2
Q
What are the classes of medications used as cytoprotectants or those that decrease acid production
A
bismuth salts antacids H2 antagonists misoprostol PPIs sulcrafate
3
Q
Describe the mechanism of action of bismuth salts
A
increases prostaglandins = increases mucous and bicarbonate production in the stomach
acts to coat ulcers and erosions as a protective layer
4
Q
What microbe does bismuth salts have some activity against?
A
h. pylori
5
Q
Would you use bismuth salts as monotherapy for H. pylori infection?
A
no- monotherapy has no effect
6
Q
Describe contraindications for use of bismuth
A
can’t use in those who have ASA allergies
not appropriate in renal insufficient patients
7
Q
What are the side effects of bismuth salts?
A
blackening of the stool and tongue
tinnitus at high doses
nausea/vomiting
8
Q
How do drugs affect acid secretion in the stomach?
A
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
9
Q
Describe the mechanism of action of antacids
A
base that neutralizes gastric acid and raises gastric pH
10
Q
What are some adverse effects of antacids
A
hyperkalcemia
can affect absorption of other drugs
constipation
rebound acidity
11
Q
What are the uses of antacids?
A
adjunctive relief for peptic ulcer disease
ineffective in eradication of h. pylori
12
Q
Describe the mechanism of action of sulcrafate
A
cytoprotectant-creates a barrier around the ulcer or erosion to prevent further damage
does not alter gastric pH
13
Q
What is the primary consideration of using sulcrafate?
A
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
14
Q
What are the side effects of sulcrafate?
A
constipation
nausea
dry mouth
headache
15
Q
What are some drug interactions with sulcrafate?
A
decreased activity with PPIs, antacids, and H2 antagonists
decreased absorption of digoxin, phenytoin, warfarin, abx
16
Q
What class of drug is misoprostol?
A
protaglandin analog
17
Q
What is the mechanism of action of misoprostol?
A
enhances mucousal defence and suppressed acid secretion
18
Q
What is the major contraindication for use of misoprostol?
A
can’t use in pregnant women as it is an abortive agent as well
19
Q
At what dosage is misoprostal effective and what is the risk of this?
A
800mcg
can’t tolerate by most people as too many side effects
20
Q
What are the side effects of misoprostol?
A
diarrhea, cramps, uterine contractions=no pregnant women!
21
Q
What is the dosing for bismuth salts?
A
30mL QID
22
Q
Why does tinnitus occur when taking bismuth at high doses?
A
due to salicylates
23
Q
A 14 year old is recovering from the flu; can they take bismuth for dyspepsia?
A
nope!
24
Q
What are common doses of sulcrafate?
A
1 g QID or 2g QID
25
What is the primary use of misoprostol?
used in prevention of dudenal ulcers caused by increased use of NSAIDS
26
What class of drug is misoprostol?
synthetic prostaglandin analog
27
Descibe the mechanism of action for H2 antagonists
blocks h2 receptors in parietal cells = suppresses gastric acid secretion; gastrin and acetylcholine
28
What are some common H2 antagonists?
ranitidine, cimetidine, famotidine
29
What are the side effects of H2 antagonists?
diarrhea, headache, constipation, myalgia
30
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
31
What side effects occur with cimetidine specifically>
men-gynecomastia
| women- galactorrhea
32
Why is cimetidine rarely used?
causes gynecomastia and galactorrhea
| inhibitor of many CYPs include 1A2, 2D6, 3A4 (most drugs) so lots of drug interactions
33
At what approximately percentage are H2 receptor antagonists eliminated?
approx. 70%
34
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
35
Discuss how PPIs irreversibly inhibit acid secretion
inhibits the proton pump irreversibly (last stage of acid production)
36
What is the potency of PPIs?
PPIs are very potent; approx 80-90% reduction of acids
37
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
38
What are some of the PPIs available in Canada?
pantoprazole
rabeprazole
omeprazole
esomeprazole
39
What is the purpose of gastrin the stomach?
stimulated when there is prescence of food in the stomach
| stimulates pepsinogen, histamine
40
What is the purpose of histamine in the stomach?
stimulates acid secretion for breakdown of food
41
What is the purpose of somatostatin in the stomach?
inhibits the secretion of stomach acid; inhibits gastrin (which stimulates acid production)
42
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
43
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
44
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**
45
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
46
What are the clinical manifestations of GERD?
```
heartburn
dyspepsia
nightime cough
regurgitation
globus
belching
```
47
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
48
What are the goals of therapy in those with GERD?
```
reduce or eliminate symptoms
identify triggers
prevent complications
heal ulcers
prevent recurrence
```
49
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
50
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
51
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
52
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
53
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
54
What are some causes of nausea?
many causes
| GI, viruses, illness, neurological causes, psychiatric, opiod induced, cancer or other medical reasons
55
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
56
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
57
What are the side effects of scopolamine?
dry mouth, blurred vision, urinary retention
58
Describe the mechanism of action of antihistminic agents in the use of motion sickness
works at the vestibular apparatus to prevent nausea
59
What is the major side effect of dimenhydrinate and diphenhydramine?
sedating
| gravol and benedryl
60
What are some pharmalogical recommendations to manage nausea and vomiting in pregnant women?
```
dicletin
metoclopramide
dimenhydrinate
ondansetran
promethazine
```
61
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
62
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
63
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)
64
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
65
Which chemotherapy drug is most likely to cause delayed CINV
cisplatin
66
What is the choice of agent in delayed CINV?
dexamthasone 4-8mg BID-QID
apreptant 80mg
metoclopramide or prochlorperazine
67
Name some causes of constipation
diet, poor bowel habits, anxiety, opiods, neurological disorders
68
What are the classes of laxatives?
```
bulk forming
stool surfactant agents
osmotic laxatives
PEG
saline/lubricant laxatives
stimulant laxatives
```
69
Name and describe the mechanism of action of bulk forming laxatives
psysillium
increases stool bulk, softens it and increases water content
stimulates peristalsis movement
70
Name and describe the mechanism of action of stool surfactant agents
docusate sodium/calcium
stool softeners; allows stool to reabsorb water
preventative against straining
71
Name and describe the mechanism of action of osmotic laxatives
lactulose
increase stool liquidity
works quickly
72
describe the mechanism of action of PEG
hyperosmotic laxative
| short term use only
73
Describe the mechanism of action of saline/lubricant laxatives
saline: changes to osmotic gradient so causes stool to express quickly via peristalsis
74
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)
75
Name some dietary recommendations in a patient with constipation
increase fluids
increase fibre
prune juice
discontinue offending foods or drugs
76
Name common anti diarrheal agents
loperamide
| lomotil - diphenoxlate with atropine
77
When should a person seek medical attention when experiencing diarrhea/
>24 hours diarrhea, fever, nausea or vomting, signs of dehydration, blood in stool
78
What is the standard treatment of diarrhea when using loperimide?
max 16mg/day
| 4mg stat, then 2mg after every loose stool
79
What is the standard treatment of diarrhea using lomotil?
2.5mg to 5mg PO q 6 hours
80
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
```
81
A child is less than <2 years of age; are they able to use antidiarrheals?
no, must be greater than 2 years of age
82
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
83
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
84
Describe the non pharmacological and pharmalogical ways to manage chrohns disease
non pharm:
smoking cessation, surgery
pharm:
corticosteroids-prednisone/budesonide
azathioprine
methotrexate
85
Describe the pathophysiology of peptic ulcer disease
erosion of the GI tract
| either gastric or dudodenal ulcers
86
What are some clinical symptoms of PUD?
dyspepsia
87
Whata are the causes of PUD?
etoh, smoking, H. Pylori, NSAID use
88
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
89
Desribe the clinical symptom that is different between gastric and duodenal PUD?
gastric- irritated by food
| duodenal- calms with food
90
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
91
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
92
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
```
93
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
94
This drug is not recommended in the use of NSAID induced ulcer prevention, H. Pylori eradication, and erosive esophagitis
H2 RAs
95
How long does it a take a patient to be on a PPI before noticing any benefit (if any?)
8 weeks
96
What are some noted adverse effects of PPIs?
```
vitamin b12 deficincy
fractures
enteric infections
peritonitis
pneumonia
```
97
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
98
Which PPI has the most drug interactions? the least?
pantoprazole . omeprazole
99
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
100
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
101
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
102
Through what cell and mechanism is acid secreted in the stomach?
parietal cells
proton pump
presence of food stimluates gastrin
