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
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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
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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

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4
Q

What microbe does bismuth salts have some activity against?

A

h. pylori

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5
Q

Would you use bismuth salts as monotherapy for H. pylori infection?

A

no- monotherapy has no effect

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6
Q

Describe contraindications for use of bismuth

A

can’t use in those who have ASA allergies

not appropriate in renal insufficient patients

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7
Q

What are the side effects of bismuth salts?

A

blackening of the stool and tongue
tinnitus at high doses
nausea/vomiting

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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

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9
Q

Describe the mechanism of action of antacids

A

base that neutralizes gastric acid and raises gastric pH

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10
Q

What are some adverse effects of antacids

A

hyperkalcemia
can affect absorption of other drugs
constipation
rebound acidity

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11
Q

What are the uses of antacids?

A

adjunctive relief for peptic ulcer disease

ineffective in eradication of h. pylori

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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

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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

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14
Q

What are the side effects of sulcrafate?

A

constipation
nausea
dry mouth
headache

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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

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16
Q

What class of drug is misoprostol?

A

protaglandin analog

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17
Q

What is the mechanism of action of misoprostol?

A

enhances mucousal defence and suppressed acid secretion

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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

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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

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20
Q

What are the side effects of misoprostol?

A

diarrhea, cramps, uterine contractions=no pregnant women!

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21
Q

What is the dosing for bismuth salts?

A

30mL QID

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22
Q

Why does tinnitus occur when taking bismuth at high doses?

A

due to salicylates

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23
Q

A 14 year old is recovering from the flu; can they take bismuth for dyspepsia?

A

nope!

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24
Q

What are common doses of sulcrafate?

A

1 g QID or 2g QID

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25
Q

What is the primary use of misoprostol?

A

used in prevention of dudenal ulcers caused by increased use of NSAIDS

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26
Q

What class of drug is misoprostol?

A

synthetic prostaglandin analog

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27
Q

Descibe the mechanism of action for H2 antagonists

A

blocks h2 receptors in parietal cells = suppresses gastric acid secretion; gastrin and acetylcholine

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28
Q

What are some common H2 antagonists?

A

ranitidine, cimetidine, famotidine

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29
Q

What are the side effects of H2 antagonists?

A

diarrhea, headache, constipation, myalgia

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30
Q

What side effects occur at high doses of h2 receptor antagonists and why?

A

H2 receptors can cross the blood brain barrier

at high doses can cause confusion, hallucinations

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31
Q

What side effects occur with cimetidine specifically>

A

men-gynecomastia

women- galactorrhea

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32
Q

Why is cimetidine rarely used?

A

causes gynecomastia and galactorrhea

inhibitor of many CYPs include 1A2, 2D6, 3A4 (most drugs) so lots of drug interactions

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33
Q

At what approximately percentage are H2 receptor antagonists eliminated?

A

approx. 70%

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34
Q

Describe the mechanism of action of proton pump inhibitors

A

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

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35
Q

Discuss how PPIs irreversibly inhibit acid secretion

A

inhibits the proton pump irreversibly (last stage of acid production)

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36
Q

What is the potency of PPIs?

A

PPIs are very potent; approx 80-90% reduction of acids

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37
Q

How many days after cessation of PPIs does it take for parietal cells to return to the stomach lining and secrete acid again?

A

approx 2-5 days as cells and the proton pump need to recover and return

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38
Q

What are some of the PPIs available in Canada?

A

pantoprazole
rabeprazole
omeprazole
esomeprazole

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39
Q

What is the purpose of gastrin the stomach?

A

stimulated when there is prescence of food in the stomach

stimulates pepsinogen, histamine

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40
Q

What is the purpose of histamine in the stomach?

A

stimulates acid secretion for breakdown of food

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41
Q

What is the purpose of somatostatin in the stomach?

A

inhibits the secretion of stomach acid; inhibits gastrin (which stimulates acid production)

42
Q

What are prokinetics? Describe their mechanism of action and why they are not used in treatment of GERD

A

prokinetics-drugs that stimulate the motility of gut and the LES
not used in GERD due to lack of evidence supporting use

43
Q

PPIs are an inactive prodrug; what does this mean?

A

delayed activation, stimulated by acid and then begins to work. delayed so that not all cells are destroyed at once

44
Q

In what clinical cases are PPIs used? (these indications have been studied and strong evidence supports use of PPIs in these conditions)

A
uninvestigated GERD
non erosive esophogeal refluex NERD
functional dyspepsia
reflux
esophagitis
H. Pylori eradication

antimicrobial and symptom relief**

45
Q

Describe the pathophysiology of GERD

A

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
Q

What are the clinical manifestations of GERD?

A
heartburn
dyspepsia
nightime cough
regurgitation
globus
belching
47
Q

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?

A

VBAD symptoms require endoscopy ASAP

could be barretts esophagus, esophageal strictures

48
Q

What are the goals of therapy in those with GERD?

A
reduce or eliminate symptoms
identify triggers
prevent complications
heal ulcers
prevent recurrence
49
Q

What are the first choices in treatment of GERD?

A

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
Q

What are some aggravating factors of GERD and how can we modify these factors?

A

obesity, pregnancy (lose weight)
smoking, ETOH (cessation)
dietary changes- no acidic foods/drink
no laying down after eating

51
Q

What pharmacological and non pharmacological options would you suggest to a pregnant woman who has GERD?

A

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
Q

What is the evidence of using PPIs in erosive esophagitis?

A

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
Q

What is the evidence of using PPIs in NERD?

A

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
Q

What are some causes of nausea?

A

many causes

GI, viruses, illness, neurological causes, psychiatric, opiod induced, cancer or other medical reasons

55
Q

Recommend a drug for the prophylaxis of motion sickness

A

motion sickness is caused by vestibular changes and is neurological
choices of treatment are antihistamines and anticholinergics
antihistamines: dimenhydrinate, diphenhydramine
anticholinergics: scopolamine

56
Q

Describe the mechanism of action of scopolamine; include its drug class and what its used for

A

anticholinergic
muscarinic antagonist
prevnetion and treatment of motion sickness

57
Q

What are the side effects of scopolamine?

A

dry mouth, blurred vision, urinary retention

58
Q

Describe the mechanism of action of antihistminic agents in the use of motion sickness

A

works at the vestibular apparatus to prevent nausea

59
Q

What is the major side effect of dimenhydrinate and diphenhydramine?

A

sedating

gravol and benedryl

60
Q

What are some pharmalogical recommendations to manage nausea and vomiting in pregnant women?

A
dicletin
metoclopramide
dimenhydrinate
ondansetran
promethazine
61
Q

Describe the difference between acute and delayed nausea or vomiting in cancer

A

acute: n/v occurs within 24 hours of chemo
delayed: n/v occurs after 24 hours of chemo

62
Q

What are the risk factors contributing to increased risk of nausea and vomiting in cancer?

A

the type of chemotherapy

hx of motion sickness, women >50 years, anxiet

63
Q

What pharmacological options would you use in acute CINV?

A

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
Q

Discuss the management of delayed nausea in CINV

A

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
Q

Which chemotherapy drug is most likely to cause delayed CINV

A

cisplatin

66
Q

What is the choice of agent in delayed CINV?

A

dexamthasone 4-8mg BID-QID
apreptant 80mg
metoclopramide or prochlorperazine

67
Q

Name some causes of constipation

A

diet, poor bowel habits, anxiety, opiods, neurological disorders

68
Q

What are the classes of laxatives?

A
bulk forming
stool surfactant agents
osmotic laxatives
PEG
saline/lubricant laxatives
stimulant laxatives
69
Q

Name and describe the mechanism of action of bulk forming laxatives

A

psysillium
increases stool bulk, softens it and increases water content
stimulates peristalsis movement

70
Q

Name and describe the mechanism of action of stool surfactant agents

A

docusate sodium/calcium
stool softeners; allows stool to reabsorb water
preventative against straining

71
Q

Name and describe the mechanism of action of osmotic laxatives

A

lactulose
increase stool liquidity
works quickly

72
Q

describe the mechanism of action of PEG

A

hyperosmotic laxative

short term use only

73
Q

Describe the mechanism of action of saline/lubricant laxatives

A

saline: changes to osmotic gradient so causes stool to express quickly via peristalsis

74
Q

Name and describe the mechanism of action of stimulant laxatives

A

senna, bisacoydl
stimulate bowel motilitis
increases secretion of fluids
can cause cathartic colon (lazy colon)

75
Q

Name some dietary recommendations in a patient with constipation

A

increase fluids
increase fibre
prune juice
discontinue offending foods or drugs

76
Q

Name common anti diarrheal agents

A

loperamide

lomotil - diphenoxlate with atropine

77
Q

When should a person seek medical attention when experiencing diarrhea/

A

> 24 hours diarrhea, fever, nausea or vomting, signs of dehydration, blood in stool

78
Q

What is the standard treatment of diarrhea when using loperimide?

A

max 16mg/day

4mg stat, then 2mg after every loose stool

79
Q

What is the standard treatment of diarrhea using lomotil?

A

2.5mg to 5mg PO q 6 hours

80
Q

What are the non pharmaceutical recommendations for a person with diarrhea?

A
stop offending drug
small frequent meals
keep hydrated
bulk forming agents may be necessary
avoiding spcity, fatty foods, carbonated drinks and caffeine
81
Q

A child is less than <2 years of age; are they able to use antidiarrheals?

A

no, must be greater than 2 years of age

82
Q

Describe the clinical manifestations of Chrohn’s disease and what part of the intestine it most greatly affects

A
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
Q

Describe the clinical manifestations of ulcerative colitis and what part of the GI tract it affects mostly

A

relapsing blood diarrhea with mucous and pus
abdominal cramping
weight loss
anorexia

affects the colon
ulcerative proctitis affects the rectum only

84
Q

Describe the non pharmacological and pharmalogical ways to manage chrohns disease

A

non pharm:
smoking cessation, surgery

pharm:
corticosteroids-prednisone/budesonide
azathioprine
methotrexate

85
Q

Describe the pathophysiology of peptic ulcer disease

A

erosion of the GI tract

either gastric or dudodenal ulcers

86
Q

What are some clinical symptoms of PUD?

A

dyspepsia

87
Q

Whata are the causes of PUD?

A

etoh, smoking, H. Pylori, NSAID use

88
Q

Why is NSAID use considered a risk factor for PUD?

A

nsaid use, inhibits CoX1- stimulates prostaglandins in the stomach that coats stomach, increased acid production

89
Q

Desribe the clinical symptom that is different between gastric and duodenal PUD?

A

gastric- irritated by food

duodenal- calms with food

90
Q

What is the suggested first line quad therapy for h. pylori eradication?

A

PPI x 10 days BID
first 5 days: amoxicillin 1g BID
second 5 days: clarithromycin 500mg BID + metroniadzole 500mg BID

91
Q

What is the suggested quad therapy for H. pylori eradication after first line therapy has failed?

A

PPI x 14 days
bismuth 2 tabs BID
flagyl 500mg TID
tetracylcine 500mg QID

92
Q

Discuss PPI use in less studied conditions; name these conditions and what the evidence suggests

A
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
Q

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?

A

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
Q

This drug is not recommended in the use of NSAID induced ulcer prevention, H. Pylori eradication, and erosive esophagitis

A

H2 RAs

95
Q

How long does it a take a patient to be on a PPI before noticing any benefit (if any?)

A

8 weeks

96
Q

What are some noted adverse effects of PPIs?

A
vitamin b12 deficincy
fractures
enteric infections
peritonitis
pneumonia
97
Q

Why is it necessary to taper PPIs and for how long?

A

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
Q

Which PPI has the most drug interactions? the least?

A

pantoprazole . omeprazole

99
Q

What are the clinical manifestations of irritable bowel syndrome?

A

abdominal pain with defectation and altered bowel habits without a cause
can be constipation or diarrhea

100
Q

Diarrhea predominant vs. constipation predominant IBS

A

dairrhea prominent - >25% of loose stools mostly (bristol stool 1-2)
constipation prominent >25% of hard/firm stools mosty

101
Q

What are some ways to manage IBS (include pharm and non pharm)

A

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
Q

Through what cell and mechanism is acid secreted in the stomach?

A

parietal cells
proton pump
presence of food stimluates gastrin