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Class 9: GI Flashcards

1
Q

Types of acid-controlling drugs

A

Antacids, histamine-2 (H2) antagonists & proton pump inhibitors

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2
Q

Acid-related pathophysiology

A

-The stomach secretes: HCl, bicarbonate, pepsinogen, intrinsic factor, mucus & prostaglandins (anti-inflammatory)
-Hyperacidity

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3
Q

Antacids MOA

A

-Neutralize stomach acid
-Promote gastric mucosal defence mechanisms

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4
Q

Antacids promote secretion of…

A

-Mucus; a protective barrier against HCl
-Bicarbonate; helps buffer HCl
-Prostaglandins; prevent activation of proton pump

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5
Q

Antacids DO NOT…

A

Prevent the overproduction of acid

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6
Q

Antacids DO..

A

Neutralize the acid once it is in the stomach

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7
Q

Antacid effects

A

-Reduce acid associated pain
-Raising gastric pH by 0.3 neutralizes 50% of the gastric acid
-Raising gastric pH one point neutralizes 90% of the gastric acid

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8
Q

Antacids are used…

A

Alone or in combination with aluminum salts, magnesium salts, calcium salts or sodium bicarbonate

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9
Q

Aluminum salts

A

-Almagel (with magnesium hydroxide)
-Combination products (aluminum and magnesium): Maalox, mylanta

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10
Q

Magnesium salt

A

-Carbonate salt: Magmix
-Hydroxide salt: Milk of magnesia
-Oxide salt: Magnesium oxide
-Trisilicate salt: Gasulsol Tablets
-Combination product: Calmax, maalox

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11
Q

Calcium salt are used to..

A

Prevent or treat calcium deficiency (calcium acetate, calcium liquid, and calcium carbonate (tums))

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12
Q

Calcium salts are used in pt with

A

Kidney failure to bind dietary phosphate and reduce the amount of phosphorus absorbed from food

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13
Q

Calcium salts used in pt with kidney failure include…

A

Aluminum hydroxide, calcium acetate, calcium carbonate, calcium liquid and sevelamer [Renagel]

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14
Q

Sodium bicarbonate

A

-Is highly soluble
-Buffers the acidic properties of HCl
-Has a quick onset but short duration

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15
Q

Sodium bicarbonate may cause..

A

-Metabolic alkalosis
-Problems in patients with HF, HTN, or renal insufficiency because of the high Na+ content

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16
Q

Antacid contraindications

A

-Severe kidney failure or electrolyte disturbances (because of the potential toxic accumulation of electrolytes in the antacids themselves)
-GI obstruction

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17
Q

Adverse effects of antacids

A

Minimal and depend on the compound used

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18
Q

Aluminum & calcium adverse effects

A

Constipation

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19
Q

Magnesium adverse effects

A

Diarrhea

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20
Q

Calcium carbonate adverse effects

A

Produces gas and belching; combining it with simethicone reduces discomfort

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21
Q

Antacid interactions + adsorption of other drugs

A

Adsorption of other drugs to antacids reduces the ability of the other drug to be absorbed into the body

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22
Q

Antacid interactions + increased stomach pH

A

Increases the absorption of basic drugs & decreases the absorption of acidic drugs

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23
Q

Antacid interactions + urinary pH

A

-Increased excretion of acidic drugs & decreased excretion of basic drugs

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24
Q

Antacid nursing implications

A

-Assess for allergies and pre-existing conditions that may restrict the use of antacids, such as fluid imbalances, pregnancy & renal disease

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25
Q

Antacid nursing implications cont’d

A

-Many drug interactions; most drugs should be given 1 to 2 hours after giving an antacid
-Antacids may cause premature dissolving of enteric-coated medications resulting in stomach upset

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26
Q

Antacid adverse effects to monitor for…

A

-N/V, diarrhea & abdominal pain
-With calcium-containing products monitor for constipation, acid rebound
-Therapeutic response

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27
Q

About histamine-2 (H2) antagonists

A

-Reduce acid secretion
-Are available OTC in lower dosage forms
-The most popular drugs for treatment of acid-related disorders

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28
Q

Types of histamine-2 (H2) antagonists

A

-FNRC-H, “dines”
-Cimetidine
-Famotidine
-Nizatidine
-Ranitidine

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29
Q

Histamine-2 (H2) antagonist MOA

A

-Block histamine at the H2 receptors of acid-producing parietal cells
-Reduce production of hydrogen ions, resulting in decreased production of HCl
-Suppresses secretion of stomach acid

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30
Q

H2 antagonist indications

A

GERD, PUD, erosive esophagitis, adjunct therapy in control of upper GI bleeding, and pathological gastric hypersecretory conditions

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31
Q

H2 antagonist adverse effects

A

-Very few adverse effects
-Cimetidine: Impotence & gynecomastia
-Headaches, lethargy, confusion, diarrhea, urticaria, sweating, flushing

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32
Q

H2 antagonist interactions

A

-Cimetidine binds with P-450 microsomal oxidase system in the liver and inhibits oxidation of many drugs and increases drug levels
-Inhibits absorption of drugs that require an acidic environment for absorption
-Smoking decreases the effectiveness of H2 blockers

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33
Q

Nursing implications of H2 antagonists

A

-Assess for allergies and impaired renal or liver function
-Use with caution in patients who are confused and in older adults
-Give 1 hour before or after antacids

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34
Q

Proton pump

A

-Parietal cells release +hydrogen ions (protons) during HCl production
-This process is called the “proton pump”
-H2 blockers & antihistamines do not stop the action of the pump

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35
Q

Proton Pump Inhibitors (PPIs)

A

-Irreversibly bind to the hydrogen–potassium–ATPase enzyme preventing the movement of hydrogen ions
-Results in achlorhydria; blockage of gastric acid secretion

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36
Q

To return to normal acid secretion following achlorhydria…

A

The parietal cell must synthesize new hydrogen–potassium–ATPase

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37
Q

PPI drug effect

A

-Total inhibition of gastric acid secretion
-GERD maintenance therapy
-Short-term tx of active duodenal & gastric ulcers
-Tx of H. pylori induced ulcers, given with an antibiotic
-Tx of Zollinger-Ellison syndrome

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38
Q

Types of PPIs

A

-“prazoles” LORRPE
-Lansoprazole
-Omeprazole magnesium
-Rabeprazole & rabeprazole sodium
-Pantoprazole
-Esomeprazole

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39
Q

PPI drug effect safety & approval

A

-Safe for short-term therapy & adverse effects are uncommon
-Some approved for long-term therapy

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40
Q

PPI nursing implications + pantoprazole

A

-Pantoprazole is the only proton pump inhibitor available for parenteral administration and can be used in pt that are unable to take PO medications

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41
Q

PPI + diazepam or phenytoin

A

PPIs may increase serum levels of diazepam or phenytoin and cause increased chance for bleeding with warfarin (Coumadin)

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42
Q

PPIs work best when..

A

Taken 30-50 minutes before meals

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43
Q

Other antacids

A

Sucralfate, misoprostol & simethicone

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44
Q

Sucralfate

A

-A cytoprotective drug used for stress ulcers & PUD

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45
Q

Sucralfate MOA

A

-Binds to the base of ulcers & erosions forming a protective barrier
-Protects these areas from pepsin which normally breaks down proteins and makes ulcers worse
-Absorbs little from the gut

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46
Q

Sucralfate adverse effects

A

Constipation, nausea & dry mouth

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47
Q

Sucralfate nursing interactions

A

-May impair absorption of other drugs—give other drugs at least 2 hours before giving sucralfate
-Should not be administered with other medications

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48
Q

Sucralfate + phosphate

A

Binds with phosphate; may be used in chronic renal failure to reduce phosphate levels

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49
Q

Misoprostol

A

-A synthetic prostaglandin analogue
-Prostaglandins have cytoprotective functions

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50
Q

Prostaglandin cytoprotetive functions

A

-Protect gastric mucosa from injury by enhancing local production of mucus or bicarbonate
-Promote local cell regeneration & help to maintain mucosal blood flow

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51
Q

Misoprostol indications

A

Prevention of NSAID–induced gastric ulcers

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52
Q

Misoprostol dosing considerations

A

Doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps, diarrhea

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53
Q

VC & CTZ

A

-Vomiting Centre (VC) & Chemoreceptor Trigger Zone (CTZ)
-Both are located in the brain and once stimulated, induce the vomiting reflex

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54
Q

Slide 36

A
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55
Q

Antiemetic drug MOA

A

Most work by blocking one of the vomiting pathways

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56
Q

Slide 38

A
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57
Q

Antiemetic drug indications

A

Prevention and reduction of N/V

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58
Q

Antiemetic drug classes

A

-Anticholinergics, antihistamines, neuroleptics, prokinetics, serotonin blockers and tetrahydrocannabinol

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59
Q

Anticholinergics

A

Block ACh receptors in the vestibular nuclei & reticular formation

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60
Q

Antihistamines

A

Block H2 receptors thereby preventing ACh from binding to receptors in the vestibular nuclei

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61
Q

Neuroleptics

A

Block dopamine in the CTZ and may also block ACh

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62
Q

Prokinetics

A

Block dopamine in the CTZ or stimulate ACh receptors in the GI tract

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63
Q

Serotonin blockers

A

Block serotonin recepetors in the GI tract, CTZ & VC

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64
Q

Tetrahydrocannabinol

A

Have inhibitory effects on the reticular formation, thalamus & cerebral cortex

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65
Q

Anticholinergics (ACh blockers): Other indications

A

-Bind to and block acetylcholine (ACh) receptors in the inner ear labyrinth
-Block transmission of nauseating stimuli to CTZ & from the reticular formation to the VC

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66
Q

Anticholinergics include…

A

Scopolamine; used for motion sickness

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67
Q

MOA & other indications of antihistamine drugs

A

-Inhibit ACh by binding to H1 receptors
-Prevent cholinergic stimulation in vestibular and reticular areas, thus preventing N/V
-Also used for motion sickness, nonproductive cough, allergy symptoms & sedation

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68
Q

Antihistamine (H1 receptor blocker) drugs

A

-DPMD
-Dimenhydrinate, diphenhydramine, meclizine & promethazine

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69
Q

MOA & other indications of neuroleptic drugs

A

-Block dopamine receptors on the CTZ
-Also used for psychotic disorders & intractable hiccups

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70
Q

Neuroleptic drugs

A

-CPP, “azines”
-Chlorpromazine, promethazine & perphenazine

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71
Q

MOA & other indications of prokinetic drugs

A

-Block dopamine in the CTZ
-Desensitize CTZ to impulses it receives from the GI tract
-Stimulate peristalsis in GI tract, enhancing emptying of stomach contents
-Can also be used for used for GERD & delayed gastric emptying

72
Q

Prokinetic drugs

A

Metoclopramide

73
Q

MOA & other indications of serotonin blockers

A

-Block serotonin receptors in the GI tract, CTZ, and VC
-Used for N/V in patients receiving chemotherapy and in the postoperative period

74
Q

MOA & other indications of tetrahydrocannabinoids (THC)

A

-Alter mood and body’s perception of its surroundings
-Used for N/V associated with chemotherapy & anorexia associated with weight loss in patients with AIDS

75
Q

Tetrahydrocannabinoids

A

Dronabinol & nabilone

76
Q

Adverse effects of antiemetics

A

Stem from their nonselective blockade of various receptors

77
Q

Slide 48

A
78
Q

Nursing implications of antiemetics

A

-Can cause severe drowsiness
-Can cause CNS depression when taken with alcohol
-Change positions slowly to avoid orthostatic hypotension

79
Q

Antiemetic nursing implications cont’d

A

Given 1 to 3 hours before a chemotherapy drug

80
Q

Age-related considerations of N/V

A

Older adult patients experiencing nausea and vomiting require careful assessment and monitoring, particularly during periods of fluid loss and subsequent rehydration therapy

81
Q

Age-related considerations of N/V cont’d

A

-They are more likely to have cardiac or renal insufficiency that places them at greater risk for life-threatening fluid & electrolyte imbalances
-Excessive replacement of fluid & electrolytes may result in adverse consequences in older adults with HF or renal disease

82
Q

Acute diarrhea

A

-Occurs suddenly in a previously healthy person
-Lasts from 3 days to 2 weeks
Is self-limiting
-Resolves without sequelae

83
Q

Categories of antidiarrheals

A

Probiotics & intestinal flora modifiers, adsorbents, anticholinergics and opiates

84
Q

Adsorbents

A

Activated charcoal, aluminum hydroxide, bismuth subsalicylate, cholestyramine & polycarbophil

85
Q

Anticholinergics

A

Atropine sulphate & hyoscyamine

86
Q

Opiates

A

Opium tincture, paregoric, codeine phosphate, diphenoxylate & kepramide hydrochloride

87
Q

Probiotics & intestinal flora modifiers

A

Lactobacillus acidophillus, lactobacillus GG & saccharomyces boulardii

88
Q

Adsorbents MOA

A

-Coat the walls of the gastrointestinal (GI) tract
-Bind to the causative bacteria or toxin, which is then eliminated through the stool

89
Q

Types of adsorbents

A

Bismuth subsalicylate, activated charcoal & attapulgite

90
Q

Anticholinergic MOA

A

-Decrease intestinal muscle tone and peristalsis of GI tract
-Slow the movement of fecal matter through the GI tract

91
Q

Anticholinergic drug types

A

Belladonna alkaloids, atropine, hyoscyamine & hyoscine

92
Q

Antimotility drugs: Opiates MOA

A

-Decrease bowel motility and relieve rectal spasms (reduces pain)
-Decrease transit time through the bowel, allowing more time for water and electrolytes to be absorbed

93
Q

Antimotility drugs: Opiate drugs

A

Paregoric, opium tincture, codeine, loperamide & diphenoxylate

94
Q

Antidiarrheals: Intestinal flora modifiers

A

-Are also known as probiotics or bacterial replacement drugs
-Are bacterial cultures of Lactobacillus organisms
-Includes L. acidophilus

95
Q

Lactobacillus organisms work by…

A

-Supplying missing bacteria to the GI tract
-Suppressing the growth of diarrhea-causing bacteria

96
Q

Antidiarrheal combination products

A

Diphenoxylate with subtherapeutic amounts of atropine which discourages recreational opiate drug use

97
Q

Large doses of diphenoxylate & atropine result in…

A

Extreme anticholinergic effects such as dry mouth, blurred vision, abdominal pain & tachycardia

98
Q

Adverse effects of antidiarrheal adsorbents

A

-Increased bleeding time, constipation, dark stools, confusion & twitching
-Hearing loss, tinnitus, metallic taste & blue gums

99
Q

Adverse effects of antidiarrheal anticholinergics

A

-Urinary retention, hesitance & impotence
-Headache, dizziness, confusion, anxiety & drowsiness
-Dry skin, rash & flushing
-Blurred vision, photophobia & increased intraocular pressure
-Hypotension, HTN, bradycardia & tachycardia

100
Q

Adverse effects of antidirrheal opiates

A

-Drowsiness, dizziness, sedation, lethargy, N/V, anorexia & constipation
-Respiratory depression, bradycardia, palpitations & hypotension
-Urinary retention, flushing, rash, urticaria

101
Q

Antidiarrheal adsorbent interactions

A

-Adsorbents decrease the absorption of digoxin, clindamycin, quinidine & hypoglycemic drugs
-Adsorbents cause increased bleeding time and bruising when given with anticoagulants

102
Q

Antacids + anticholinergic antidiarrheals

A

Antacids can decrease the effects of anticholinergic antidiarrheal drugs

103
Q

Antidiarrheal nursing considerations

A

-Do NOT give bismuth subsalicylate (Pepto-Bismol) to children or teenagers with chickenpox because of the risk of Reye’s syndrome
-Teach patients to take medications exactly as prescribed and to be aware of their fluid intake and dietary changes

104
Q

Antidiarrheal administration considerations

A

Assess fluid volume status, intake & output, and mucous membranes before, during, and after treatment

105
Q

Slide 65

A
106
Q

Bulk forming laxatives

A

Psyllium, methylcellulose & polycarbophil

107
Q

Emolient laxatives

A

Docusate sodium & mineral oil

108
Q

Hyperosmotic laxatives

A

Polyethylene glycol (PEG), lactulose, sorbitol & glycerin

109
Q

Saline laxatives

A

Magnesium sulphate, magnesium citrate, magnesium hydroxide, magnesium phosphate & sodium phosphate

110
Q

Stimulant laxatives

A

Senna, biscodyl, cascara sagrada & castor oil

111
Q

Bulk forming laxative MOA

A

High in fibre, absorb water to increase bulk and distend bowel to initiate reflex bowel activity

112
Q

Emolient laxative MOA

A

-AKA stool softeners and lubricants
-Promote more water and fat in the stools, lubricate fecal material & intestinal walls

113
Q

Hyperosmotic laxative MOA

A

-Increase fecal water content resulting in bowel distention, increased peristalsis & evacuation
-Used for diagnostic & surgical preparation

114
Q

Lactulose liquid is also used to..

A

Reduce elevated serum ammonia levels

115
Q

Saline laxative MOA + use

A

-Increase osmotic pressure within the intestinal tract, causing more water to enter the intestines
-Results in bowel distention, increased peristalsis & evacuation
-Used for diagnostic and surgical prep and removal of helminths and parasites

116
Q

Stimulant laxative MOA

A

Increase peristalsis via intestinal nerve stimulation

117
Q

All laxatives

A

-Increase peristalsis and water & focal mass
-Softens fecal mass

118
Q

All laxatives increasesecretion of water & electolytes in the small bowel except..

A

Hyperosmotics

119
Q

All laxatives inhibit absorption of water in the small bowel except…

A

Hyperosmotics

120
Q

All laxatives increase wall permeability in the small bowel except…

A

Hyperosmotics & saline

121
Q

All laxatives act only in the large bowel except…

A

Saline & stimulants

122
Q

Laxative contraindications

A

-Use with caution with:
-Acute surgical abdomen, appendicitis symptoms such as N/V and fecal impaction (mineral oil enemas excepted)
-Intestinal obstruction & undiagnosed abdominal pain

123
Q

All laxatives can cause..

A

Electrolyte imbalances

124
Q

Bulk forming laxative adverse effects

A

Impaction, fluid overload & esophageal blockage

125
Q

Emolient laxative adverse effects

A

Skin rashes & decreased absorption of vitamins

126
Q

Hyperosmotic adverse effects

A

Abdominal bloating & rectal irritation

127
Q

Saline laxative adverse effects

A

Magnesium toxicity (with renal insufficiency), cramping, diarrhea & increased thirst

128
Q

Stimulant laxative adverse effects

A

Nutrient malabsorption, skin rashes, rectal & gastric irritation

129
Q

Laxative interactions

A

-Because laxatives alter intestinal function they can interact with other drugs quite readily
-Each category can alter the effect of specific drugs
-Some laxatives may interact with food such as milk and juices

130
Q

Patients should not take a laxative or cathartic if they are…

A

Experiencing N/V or abdominal pain

131
Q

Assessments before administering a laxative

A

Assess fluid and electrolytes before initiating therapy

132
Q

Take laxative tablets with…

A

180 to 240mL of water

133
Q

Take bulk forming laxatives with…

A

240mL of water

134
Q

Alternatives to laxatives..

A

A high-fibre diet and increased fluid intake is preferred to laxative use

135
Q

Long-term laxative use often…

A

Results in decreased bowel tone and may lead to dependency

136
Q

All laxative tablets should be…

A

Swallowed whole, not crushed or chewed, especially if enteric coated

137
Q

Bisocodyl & cascara sagrada should be…

A

Given with water due to interactions with milk, antacids and juices

138
Q

Contact physician if a pt experiences blank when taking laxatives

A

Severe abdominal pain, muscle weakness, cramps, or dizziness which may indicate possible fluid or electrolyte loss

139
Q

Disorders of the stomach & upper small intestine

A

GERD, acute gastritis, upper GI bleed & PUD

140
Q

GERD pt teaching

A

Smoking cessation, elevate head of bed 30 degrees, avoid lying down for 2 to 3 hours after eating and avoid late-night eating

141
Q

Upper GI bleed collaborative care

A

Endoscopic, surgical & drug therapy

142
Q

Upper GI bleed nursing implementations

A

Health promotion, acute intervention & ambulatory and home care

143
Q

PUD drug therapy

A

H2‑receptor blockers, PPIs, antibiotics, antacids, anticholinergics & cytoprotective drug therapy

144
Q

PUD nursing implementation

A

-Health promotion
-Acute intervention of: Hemorrhaging, perforation & gastric outlet obstruction
-Ambulatory and home care

145
Q

PUD postoperative complications

A

Dumping syndrome, postprandial hypoglycemia & bile reflux gastritis

146
Q

Age related considerations with PUD

A

-Recent increased incidence in >60 years of age d/t the use of NSAIDS
-Pain may not be the first symptom, look for frank gastric bleeding (hematemesis/melena) or a decreased hematocrit
-Higher morbidity/mortality rates d/t comborbidities & decreased ability to withstand hypovolemia

147
Q

Acute abdominal pain acute interventions

A

Preoperative & postoperative care

148
Q

Abdominal trauma emergency management

A

-Focuses on establishing an airway & adequate breathing, fluid replacement, and prevention of hypovolemic shock
-Establish IV access and administer volume expanders or blood if the pt is hypotensive

149
Q

Types of intestinal obstruction

A

Mechanical & nonmechanical

150
Q

Slide 94

A
151
Q

Disorders of the liver

A

Viral hepatitis, toxic and drug-induced hepatitis, nonalcoholic fatty liver disease and nonalcoholic steatohepatitis

152
Q

Hepatitis drug therapy goals

A

-Decrease viral load & liver enzyme levels
-Decrease rate of disease progression: a-interferon, nucleoside and nucleutide analogs

153
Q

Acute intervention of hepatitis

A

Jaundice & rest

154
Q

Nonalcoholic fatty liver disease (NAFLD)

A

-A spectrum of disease that ranges from simple fatty liver that causes no hepatic inflammation to severe liver scarring
-Characterized by hepatic steatosis associated with other causes

155
Q

Hepatic steatosis

A

Accumulation of fat in the liver

156
Q

Diagnositic studies of liver cirrhosis

A

Liver biopsy & noninvasive fibrosis markers

157
Q

Collaborative care of liver cirrhosis

A

-Drug therapy
-Ascites may require a peritoneovenous shunt

158
Q

Acute intervention of liver cirrhosis

A

-Ruptured esophageal varices
-Hepatic encephalopathy

159
Q

Collaborative care of acute pancreatitis

A

Conservative, surgical, drug & nutritional therapy

160
Q

Etiology of bleeding tendencies

A

Lack of or decreased absorption of vitamin K resulting in decreased production of prothrombin

161
Q

Etiology of clay-coloured stools

A

Blockage of flow of bile salts out of the liver

162
Q

Etiology of dark amber urine that foams when shaken

A

Soluble bilirubin in the urine

163
Q

Etiology of intolerance to fatty foods (nausea, sensation of fullness & anorexia)

A

No bile in the small intestine for fat absorption

164
Q

Etiology of no urobilinogen in the urine

A

No bilirubin reaching the small intestine to be converted to uroglobilinogen

165
Q

Etiology of obstructive jaundice

A

No bile flow into the duodenum

166
Q

Etiology of pruritis

A

Deposition of bile salts in the skin tissues

167
Q

Etiology of steatorrhea

A

No bile salts in the duodenum preventing fat emulsion & digestion

168
Q

Collaborative care of cholethiases & cholesystitis

A

Conservative, surgical, transhepatic biliary catheter, drug & nutritional therapy

169
Q

Cholecystectomy

A

Removal of the gallbladder

170
Q

Cholecystostomy (usually an emergency procedure)

A

Incision into gallbladder (usually for the removal of gallstones)

171
Q

Choledocholithotomy

A

Incision into the common bile duct for removal of stones

172
Q

Cholescystogastrostomy

A

Anastomosis between the stomach & gallbladder

173
Q

Cholecystoduodenostomy

A

Anastomosis between the gallbladder & duodenum to relieve obstruction at the distal end of the common bile duct

174
Q

Laproscopic cholecystectomy

A

Removal of the gallbladder via laparoscopy through the use of a dissecting laser

175
Q

Laparoscopic cholecystectomy postoperative care

A

-Remove bandages the day after surgury, bathe or shower
-Notify the surgeon of any redness, swelling, bile-coloured drainage or pus, severe abdominal pain, N/V, fever & chills
-AAT, return to work within 1 week
-DAT, low-fat is typically tolerated better

488 (16 decks)

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