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316 Pharmacology > Final: Gastrointestinal system > Flashcards

Final: Gastrointestinal system Flashcards

1
Q

Accessory organs to GI

A

Pancreas, Liver, Gallbladder

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2
Q

Major activities of the GI system

A

Secretion
Digestion
Absorption
Motility

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3
Q

Enteric nervous system allows what kind of control

A

Allows local control to the contents of GI tract

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4
Q

The enteric system is also innervated by

A

ANS (sympathetic/parasympathetic)

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5
Q

Chief cells secrete

A

pepsinogen

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6
Q

Parietal cells secrete

A

Hydrochloric acid and intrinsic factor

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7
Q

Hydrochloric acid converts

A

Pepsinogen to pepsin

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8
Q

Hydrochloric acid converts

A

Pepsinogen to pepsin

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9
Q

Enteroendocrine cells (G cells) secrete

A

Hormone gastrin

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10
Q

What does gastrin do

A

Stimulates secretion of HCL & pepsinogen, which increases motility of GI tract; helps keep LES closed

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11
Q

Mucous cells secrete

A

an alkaline mucus that protects the epithelium against shear stress, acid and pepsin

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12
Q

What reflects the condition of ENTIRE tract

A

Mucosa

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13
Q

The process of digestion begins in the _____ with the ___ secreted from the _____

A

The process of digestion begins in the mouth with the enzymes secreted from the salivary glands

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14
Q

What produces chyme

A

Food, gastric hydrochloric acid, and pepsin

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15
Q

digestion continues in the proximal portion of the small intestine by the action of the pancreatic enzymes, intestinal enzymes, and bile salts.

A
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16
Q

Nutrients are absorbed via

A

Active transport diffusion or facilitated diffusion

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17
Q

Where does digestion and absorption of all major nutrients and drugs occur in

A

small intestine

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18
Q

Peristalsis

A

Mass movement; strong wavelike rhythmic muscular contractions

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19
Q

Haustral segmentation

A

Churning. Slow segmenting movements in which the colonic wall rolls back and forth.

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20
Q

Neural reflexes

A

Gastocolic reflex

ileogastric reflex

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21
Q

Large intestine include

A

Cecum

Appendix

Colon

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22
Q

parts of the colon

A

Ascending
Transverse
Descending

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23
Q

Gi disorders are often due to factor such as

A

diet, stress, and medication side effects

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24
Q

Examples of GI disorders

A 
Gastroesophageal Reflux Disease (GERD)
Peptic Ulcer Disease (PUD)
Constipation
Diarrhea
Nausea and vomiting
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25
Q

GERD

A

Transient relaxation of lower esophageal sphincter, which causes acid to back up into esophagus, leading to pyrosis, dyspepsia, and pain

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26
Q

Common triggers for acid reflux

A
  • Large meals, overeating
  • Increased intraabdominal pressure
  • —Exertion after a meal
  • —Pregnancy
  • —Overweight
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27
Q

What can decrease lower esophageal sphincter and be a trigger for acid reflux

A

Caffeine, nicotine, alcohol, fatty and fried foods

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28
Q

Lifestyle modifications for Gastroesophageal reflux disease

A 
Lose weight
Eat small meals
Avoid foods that exacerbate gerd
Elevate HOB if gerd s/s worsen 
Avoid eating 3 hours before sleeping 
smoking cessation 
avoid ALCOHOL
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29
Q

Pharacological management for GERD

A

Antacids
OTC H2RA
OTC PPI
Prokinetic medication (Rx)

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30
Q

Peptic ulcers include

A

Gastric ulcers and duodenal ulcers

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31
Q

Risk factors for peptic ulcer disease

A 
Increasing age
Smoking
Long term NSAID use
Long term steroid use
Alcohol
Spicy foods
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32
Q

Peptic ulcer disease results in a

A

balance between the aggressive factors and the defensive mechanisms is disrupted

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33
Q

Examples of aggressive factors

A

H pylori infections, gastric acid production, NSAIDs, alcohol, pepsin and bile salts

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34
Q

Examples of defensive mechanisms

A

as gastroduodenal mucosal defense, tight intercellular junctions, mucus, mucosal blood flow, and epithelial renewal.

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35
Q

Symptoms of peptic ulcer disease

A
  • Burning, gnawing pain
  • Frequently occurs when stomach is empty
  • Pain often felt midline near xyphoid
  • May radiate below costal margins
  • Relieved by food or antacids
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36
Q

Complications of peptic ulcer disease

A
  • Hemorrhage,
  • Perforation, or obstruction
  • Bleeding may be sudden, severe, without warning or insidious, producing only occult blood in the stool
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37
Q

Causes of peptic ulcer disease

A
  • Bacterial infection by Helicobacter pylori
  • Increased Hal and pepsin
  • Zollinger-Ellison syndrome (Gastrinoma -> increased pepsin and acid)
  • inadequate mucosal defense against gastric acid
  • Long-term NSAID/steroid use
  • Stress
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38
Q

Urea Breath Test

A

1st line non-invasive test to dx H. pylori infection

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39
Q

How is a urea breath test done

A

Patient drinks liquid urea which makes urease, which hydrolyze urea.

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40
Q

What confirms the presence of H. Pylori

A

CO2

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41
Q

does a negative test automatically rule out the presence of H. pylori

A

No.

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42
Q

Do false positives or negatives happen more often?

A

No false positives, false negatives are possible

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43
Q

Treatment for peptic ulcer disease

A
  • Lifestyle changes
  • Eradicate H. pylori infection
  • Decrease secretion of gastric acid
  • Neutralize gastric acid once it is secreted
  • Protect gastric mucosa from damage
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44
Q

Pharmacologic treatments for peptic ulcer disease

A 
Histamine 2 antagonists 
Proton pump inhibitors 
Prostaglandins 
Antacids 
Mucosal protectants
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45
Q

For PUD causes by H.pylori is treated with

A

triple therapy: Proton Pump Inhibitor + 2 antibiotics

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46
Q

What do histamine-2 antagonists do

A

decrease the amount of HCL produced

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47
Q

What do prostaglandins do

A

Inhibit the secretion of gastrin and increase the secretion of the mucus lining of the stomach

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48
Q

What do antacids do

A

interact with acids at the chemical level to neutralize gastric pH

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49
Q

What do mucosal protectants do

A

Coat injured area in the stomach to prevent further injury from acid

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50
Q

Examples of histamine-2 receptors antagonists

A

Cimetidine
Ranitidine
Famotidine
Nizatidine

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51
Q

Cimetidine is the

A

first drug in this class to be developed

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52
Q

Ranitidine is more ___ than cimetidine

A

longer acting and more potent than cimetidine

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53
Q

What is nizatidine

A

Newest drug in the H2 antagonists, similar to ranitidine; indicated for patients with liver dysfunction

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54
Q

H2 antagonists antagonist

A

Prevention and tx of GERD, PUD, esophagitis, GI bleeding due to stress, ulcers, and Zollinger-Ellison syndrome

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55
Q

H2 antagonist MoA

A

Blocks H2 receptors on the surface of parietal cell to decrease the production of gastric acid

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56
Q

Side effects of H2 antagonists

A

Headaches, dizziness, metal confusion, delirium, coma depression, muscle aches, fatigue, skin rash, fever, diarrhea, constipation

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57
Q

Cimetidine has been associated with

A

Androgen like effects like gynecomastia, impotence, and decreased libido

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58
Q

Nursing considerations of H2 antagonists

A
  • Neuro side effects common among elderly and impaired renal function
  • some hepatic metabolism
  • Ive administration requires dilution and administration over at least 2 minutes
  • —- IM administration does not require dilution, but administered into large muscle groups
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59
Q

Cimetidine is metabolized

A

eliminated INTACT by kidneys

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60
Q

When cimetidine is given IV, it can cause

A

Dysrhythmias and hypotension

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61
Q

Cimetidine drug interactions

A
  • Antacids decrease absorption of cimetidine, separate by 2 hrs
  • Inhibits 1st pass effect of alc
  • Cimetidine inhibits hepatic drug metabolizing enzymes and interferes with metabolism of other drugs (warfarin, lidocaine, phenytoin, theophylline, metformin)
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62
Q

Ranitidine

A
  • More potent than cimetidine
  • Produces fewer side effects
  • Has fewer drug interactions (weak inhibitor of cytochrome P-450 system)
  • Is absorbed at the same rate in the presence or absence of food
  • Antacids have small effect on ranitidine absorption
  • Poor penetration of BBB
  • Does not bind to androgen receptors
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63
Q

Proton Pump Inhibitors indication

A
  • Used alone or with other drugs in the treatment of gastric ulcers, GERD, Zollinger- Ellison syndrome; reduce risk of NSAID-associated gastric ulcerations
  • Prophylaxis of stress-induced ulcers, GI bleeding
  • Relief of symptoms of heartburn, acid indigestion (OTC preparations)
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64
Q

Proton pump inhibitors MoA

A

suppress gastric acid secretion by blocking the proton pump (H+,K+-ATPase enzyme system) that pumps hydrogen ions into the secretory surface of the gastric parietal cells

65
Q

Iansoprazole may effect

A

Vitamin B12 absorption

66
Q

Iansoprazole common adverse effects

A

Diarrhea, abdominal pain, nausea

-Hypomagnesemia

67
Q

OTC PPI has what kind of warning

A

Osteoporosis and fracture warning

68
Q

Misoprostol drug class

A

Prostaglandin E1 analog

69
Q

MoA of misoprostol

A

Inhibits secretion of gastric acid and stimulates secretion of mucus, providing cytoprotective effects on integrity of the gastric mucosa

70
Q

Misoprostol adverse effects

A

Diarrhea, nausea, abdominal discomfort, fever

-Also used with mifepristone as an abortifacient (induces abortion)

71
Q

Misoprostol unlabeled uses

A

Postpartum hemorrhage, induction of labor (very risky); treatment of incomplete/missed abortion (miscarriage)

72
Q

Misoprostol boxed warning

A
  • Not used in women of childbearing unless they comply with effective contraceptives
  • do not give to other people
73
Q

Antacids

A

Act in the stomach to neutralize the gastric acid and prevent or relieve pain/ discomfort associated with GERD, esophagitis, heartburn, gastritis, GI bleeding and stress ulcers. Alkaline compounds that neutralize acid (neutralize stomach acid to pH >5)

74
Q

Types of antacids

A 
Aluminum hydroxide (Amphojel)
Calcium carbonate (Tums)
Magnesium salts (Milk of Magnesia) 
Sodium bicarbonate (Alka-Seltzer)
75
Q

Nursing considerations of antacids

A

With the exception of sodium bicarbonate, antacids are minimally absorbed systemically

76
Q

Antacids may affect the absorption of other drugs (Chelation), administer

A

2 hours before or after other drugs

77
Q

Antacids adverse effects

A
  • Aluminum & calcium salts tend to be constipating
  • Magnesium salts tend to loosen stools and tend to produce diarrhea
  • Calcium carbonate has greatest potential to produce kidney stones
  • Preparations that combine these agents aid in normalizing bowel function
78
Q

Magnesium hydroxide drug class

A

Antacid, magnesium salt; laxative

79
Q

Magnesium hydroxide moA

A

Works in small & large intestine to attract & retain water in the intestinal lumen, thereby increasing pressure within intestine which stimulates peristalsis

80
Q

Magnesium hydroxide adverse effects in large doses

A

Cramps, diarrhea, nausea

81
Q

Antacids precautions

A
  • Renal insufficiency: about 15-30% is absorbed from small intestine
  • Acute abdomen of unknown origin
  • Neuromuscular disorders
82
Q

Sucralfate drug class

A

Mucosal protective agent

83
Q

Sucralfate aids healing

A

of ulcers; used for long-term prevention of ulcer recurrence

84
Q

Sucralfate MoA

A

forms a viscous, sticky gel that adheres to normal & necrotic mucosa, forming a protective coating over the eroded stomach lining; creates a physical barrier that impairs diffusion of Hal and prevents degradation of mucus by pepsin and acid

85
Q

Nursing considerations of sucralfate

A

Can decrease absorption of some other drug: administer 2 hours before or after other drugs

86
Q

Is constipation a disease

A

Not a disease, but a symptom of an underlying disorder

87
Q

Constipation is broadly described as an

A

Abnormally infrequent of difficult passage of hard, dry feces

88
Q

normal bowel movement

A

3 times a day, or 3 times a week depending on person

89
Q

Hard and dry stool of constipation occur when

A

the colon absorbs too much water or if intestinal muscle contractions are slow or sluggish, causing stool to move through colon too slowly

90
Q

Diseases that cause constipation slow

A

movement of stool through the colon, rectum, or anus

91
Q

Neurological disorders than cause constipation

A

Multiple Sclerosis, Parkinson’s disease, chronic idiopathic intestinal pseudo-obstruction, stroke, spinal cord injuries

92
Q

Metabolic and endocrine conditions that cause constipation

A

Diabetes, hypothyroid, hypercalcemia

93
Q

systemic disorders that cause constipation

A

Amyloidosis, systemic lupus erythematous (SLE),

scleroderma

94
Q

Miscellaneous disorders causing constipation

A

Intestinal obstruction, scar tissue (adhesions), diverticulosis, tumors, colorectal stricture, Hirschsprung’s disease, or cancer can compress, squeeze, or narrow the intestine and rectum and cause constipation

95
Q

Medications that increase risk of constipation

A 
Opioids 
Antacids that contain Aluminum
Blood pressure medications (calcium channel blockers) 
Anticholinergic drugs
Antidiarrheal drugs
Iron supplements 
Diuretics
96
Q

Indications for use of laxatives

A

Short-term relief of constipation (to avoid cathartic dependence)
Prevent straining when it is clinically undesirable (avoid valsalva manuever)
Evacuate the bowel for diagnostic procedures
Remove ingested poisons from the lower GI tract
As an adjunct in anthelmintic therapy

97
Q

All laxatives are contraindicated if

A

THERE IS A GI OBSTRUCTION OR ABDOMNIAL PAIN OF UNKNOWN ORIGIN

98
Q

Goal of treatment for laxatives

A

passage of a soft, formed bowel movement within 12 to 24 hours

99
Q

Bulk forming laxatives indications

A
  • Acute & chronic constipation; the only laxatives indicated for use
  • Prophylaxis of constipation in patients that should not strain during defecation
  • Also an antidirrheal
  • Investigational: GI disorders such as IBS, inflammatory bowel disease
100
Q

Examples of laxatives

A

Polycarbophil
Psyllium
Methylcellulose
What dextrin

101
Q

Bulk forming moA

A

Soluble fiber absorbs water which forms emollient gel/viscous solutions causing fecal matter to increase in bulk, then bulky mass increases peristalsis and decreases transit time

102
Q

Bulk forming laxative must be taken with

A

Plenty of water to AVOID FECAL IMPACTION

103
Q

BULK FORMING LAXATIVES MAY CAUSE

A

BLOATING AND FLATULENCE

104
Q

psyllium is contraindicated with

A

intestinal obstruction or fecal impaction; acute abdomen of unknown origin

105
Q

Most common side effects of psyllium

A

Bloating, flatulence, and cramp

106
Q

Stool softeners/ Emollients moA

A

for emollient laxatives (stool softeners): decreases surface tension of the liquid contents in the bowel and promotes incorporation of liquid into stool, which is a softer mass and easier passage of stool

107
Q

Docusate drug class

A

Stool softeners/emollients

108
Q

Docusate is most effecting in preventing

A

Straining in high risk patients

109
Q

Docusate side effects

A

May cause diarrhea, flatulence, abdominal cramps

110
Q

Docusate may take up to

A

3 days to produce soft stool

111
Q

Lubricant laxatives; mineral oil indicated for

A

acute, softening of fecal impaction, softening of fecal mass for patients with painful anorectal conditions

112
Q

Mineral oil moA

A

Coat and soften stool which prevents reabsorption of water from the stool

113
Q

Saline/ Osmotic Agents moA

A

Draw water into laxatives through osmosis which increases intestinal motility

114
Q

Types of saline laxative

A
  • magnesium citrate (Citrate of Magnesia)
  • magnesium hydroxide (Milk of Magnesia)
  • polyethylene glycol solution (Miralax)
  • polyethylene glycol-electrolyte solution (GoLYTELY)
  • sodium phosphate enema (Fleet)
115
Q

Can you use stimulant laxatives long term

A

No, stimulant laxatives are not used for long term

116
Q

Why aren’t stimulant laxatives used for long term

A

May induce loss of normal bowel function and laxative dependence

117
Q

Stimulant laxatives moA

A

produce propulsive movements by direct chemical irritation &/or stimulation of intestinal wall &/or mesenteric plexus; increasing fluid & electrolytes within the intestinal lumen

118
Q

Stimulant laxative examples

A
  • Bisacodyl
  • Senna
  • Castor oil
119
Q

Bisacodyl is a very popular OTC laxative and is drug of choice to

A

empty the bowel before surgery

120
Q

Bisacodyl is indicated for

A

Acute constipation; bowel preparation for diagnostic and surgical procedures

121
Q

Bisacodyl adverse effects

A

nausea, vomiting, abdominal cramps; possible F&E imbalance (especially potassium)

122
Q

Is Diarrhea a a disease

A

No, it is is symptom of an underlying condition

123
Q

Diarrhea is characterized as

A

Loose, watery stool during a limited time period

124
Q

Acute diarrhea is usually due to

A

Bacterial or viral origin

125
Q

Diarrhea is caused by

A

any factor that decreases fluid absorption in the small or ;large bowel, increases fluid secretion, and alters bowel motility or is associated with mucosal injury

126
Q

Diarrhea can cause dehydration:

A

Particularly dangerous in children and in the elderly, must be treated promptly

127
Q

Diarrhea may be accompanied by

A
  • cramping abdominal pain
  • bloating
  • nausea
  • urgent need to use the bathroom
  • fever
  • bloody stools
128
Q

Acute diarrhea lasts

A

< 2 weeks; bacterial, viral, or parasitic infection

129
Q

Chronic diarrhea lasts

A

> 4 weeks; usually related to functional disorders like irritable bowel syndrome or inflammatory bowel diseases

130
Q

Bacterial infections that cause diarrhea

A

common culprits include Campylobacter, Salmonella, Shigella, and E. coli

131
Q

Viral infections that cause diarrhea

A

rotavirus, Norwalk virus, cytomegalovirus, herpes simplex virus, & viral hepatitis

132
Q

Parasites that cause diarrhea

A

Giardia lamblia, Entamoeba histolytica, & Cryptosporidium

133
Q

Other things that can cause diarrhea

A

Food intolerances
Adverse drug effects
Intestinal diseases
Functional bowel disorders

134
Q

Pharmacologic tx for diarrhea

A

Ioperamide
Diphenoxylate + Atropine
Paregorgic

135
Q

What does loperamide do

A

structural analog of meperidine; has opioid-like actions on gut (inhibits gastric motility)

136
Q

what does diphenoxylate + atropine (Lomotil) do

A

structural analog of meperidine; has opioid-like actions on gut (inhibits gastric motility)

137
Q

What does paregoric do?

A
  • -Increase muscular tone and inhibit peristalsis in GI tract
  • -Schedule III drug alone and Schedule IV when combined in small amounts with other medications; only recommended for short term use
138
Q

Ioperamide indications

A
  • Acute or chronic diarrhea

- Reduce the volume of discharge from ileostomy

139
Q

Ioperamide moA

A
  • Structural analog of meperidine that has a direct effect on the nerves of the intestinal wall and slows peristalsis
  • Decreased volume and increased viscosity of stool leading to decreased fluid and electrolyte loss
140
Q

Ioperamide common adverse effects

A

Abdominal cramps, constipation

141
Q

Ioperamide nursing considerations

A
  • Contraindicated in diarrhea caused by infections that penetrate intestinal mucosa or pseudomembraneous colitis (implicated in toxic megacolon)
  • Use cautiously in patients with hepatic impairment: encephalopathy
  • Do not give to patients with abdominal pain of unknown origin
142
Q

Nausea and vomitting is an emetic response that is a

A

Complex reflex after activating vomiting center in medulla oblongata

143
Q

Pharmacologic prevention and tx for nausea and vomitting

A

Phenothiazines
Antihistamines
5-HT3 receptor antagonists
Prokinetic

144
Q

Prochlorperazine class

A

dopamine antagonists; phenothiazines

145
Q

Prochlorperazine Moa

A

Block dopamine2 receptors in CTZ

146
Q

Prochlorperazine indications

A

Prevention and Tx of nausea and vomitting related to surgery, cancer, chemotherapy, and toxin

147
Q

Prochlorperazine side effects

A

Extrapyramidal rx
Anticholinergic effects
Hypotension and sedation

148
Q

medications for nausea and vomitting are known as

A

Antiemetics

149
Q

Antihistamine examples for nausea and vomiting

A

Hydroxyzine

Promethazine

150
Q

Hydroxyzine, Promethazine moA

A

Block H1 receptors and the muscarinic receptors in the pathway from the inner ear to the vomiting center

151
Q

Hydroxyzine, Promethazine indications

A

Nausea and vomitting associated with motion sickness

152
Q

Hydroxyzine, Promethazine side effects

A 
Anticholinergic effects (dry mouth, tachycardia, urinary retention, blurred vision, thickened respiratory secretions)
Dizziness, confusion
153
Q

Ondansetron drug classification

A

5-HT3 receptor antagonist

154
Q

Ondansetron indiction

A

Prevention of CINV, radiation-induced emesis, post-operative n/v, hyperemesis gravies

155
Q

Ondansetron nursing nursing considerations

A
  • More effective at preventing CINV than at suppressing CINV (therefore should not be given prn but on a scheduled basis)
  • **Caution: Risk for ECG changes: no single dose should exceed 16 mg (typically 4-8 mg)
156
Q

Metoclopramide drug class

A

Dopamine receptor antagonist, prokinetic, GI stimulant

157
Q

Metoclopramide indications

A

Relief of post-operative or chemotherapy-induced N/V, diabetic gastroparesis, GERD, delayed gastric emptying; unlabeled: persistent hiccups

158
Q

Metoclopramide adverse effects

A

Extrapyramidal (EPS) effects with chronic use [secondary to central dopaminergic blockade]

159
Q

Metoclopramide black box warning

A

may cause tardive dyskinesia, often irreversible (duration of tx & cumulative dose associated with increased risk)

316 Pharmacology (19 decks)

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