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
GERD
Transient relaxation of lower esophageal sphincter, which causes acid to back up into esophagus, leading to pyrosis, dyspepsia, and pain
26
Common triggers for acid reflux
- Large meals, overeating - Increased intraabdominal pressure - ---Exertion after a meal - ---Pregnancy - ---Overweight
27
What can decrease lower esophageal sphincter and be a trigger for acid reflux
Caffeine, nicotine, alcohol, fatty and fried foods
28
Lifestyle modifications for Gastroesophageal reflux disease
``` 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 ```
29
Pharacological management for GERD
Antacids OTC H2RA OTC PPI Prokinetic medication (Rx)
30
Peptic ulcers include
Gastric ulcers and duodenal ulcers
31
Risk factors for peptic ulcer disease
``` Increasing age Smoking Long term NSAID use Long term steroid use Alcohol Spicy foods ```
32
Peptic ulcer disease results in a
balance between the aggressive factors and the defensive mechanisms is disrupted
33
Examples of aggressive factors
H pylori infections, gastric acid production, NSAIDs, alcohol, pepsin and bile salts
34
Examples of defensive mechanisms
as gastroduodenal mucosal defense, tight intercellular junctions, mucus, mucosal blood flow, and epithelial renewal.
35
Symptoms of peptic ulcer disease
- 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
36
Complications of peptic ulcer disease
- Hemorrhage, - Perforation, or obstruction - Bleeding may be sudden, severe, without warning or insidious, producing only occult blood in the stool
37
Causes of peptic ulcer disease
- 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
38
Urea Breath Test
1st line non-invasive test to dx H. pylori infection
39
How is a urea breath test done
Patient drinks liquid urea which makes urease, which hydrolyze urea.
40
What confirms the presence of H. Pylori
CO2
41
does a negative test automatically rule out the presence of H. pylori
No.
42
Do false positives or negatives happen more often?
No false positives, false negatives are possible
43
Treatment for peptic ulcer disease
- Lifestyle changes - Eradicate H. pylori infection - Decrease secretion of gastric acid - Neutralize gastric acid once it is secreted - Protect gastric mucosa from damage
44
Pharmacologic treatments for peptic ulcer disease
``` Histamine 2 antagonists Proton pump inhibitors Prostaglandins Antacids Mucosal protectants ```
45
For PUD causes by H.pylori is treated with
triple therapy: Proton Pump Inhibitor + 2 antibiotics
46
What do histamine-2 antagonists do
decrease the amount of HCL produced
47
What do prostaglandins do
Inhibit the secretion of gastrin and increase the secretion of the mucus lining of the stomach
48
What do antacids do
interact with acids at the chemical level to neutralize gastric pH
49
What do mucosal protectants do
Coat injured area in the stomach to prevent further injury from acid
50
Examples of histamine-2 receptors antagonists
Cimetidine Ranitidine Famotidine Nizatidine
51
Cimetidine is the
first drug in this class to be developed
52
Ranitidine is more ___ than cimetidine
longer acting and more potent than cimetidine
53
What is nizatidine
Newest drug in the H2 antagonists, similar to ranitidine; indicated for patients with liver dysfunction
54
H2 antagonists antagonist
Prevention and tx of GERD, PUD, esophagitis, GI bleeding due to stress, ulcers, and Zollinger-Ellison syndrome
55
H2 antagonist MoA
Blocks H2 receptors on the surface of parietal cell to decrease the production of gastric acid
56
Side effects of H2 antagonists
Headaches, dizziness, metal confusion, delirium, coma depression, muscle aches, fatigue, skin rash, fever, diarrhea, constipation
57
Cimetidine has been associated with
Androgen like effects like gynecomastia, impotence, and decreased libido
58
Nursing considerations of H2 antagonists
- 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
59
Cimetidine is metabolized
eliminated INTACT by kidneys
60
When cimetidine is given IV, it can cause
Dysrhythmias and hypotension
61
Cimetidine drug interactions
- 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)
62
Ranitidine
- 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
63
Proton Pump Inhibitors indication
- 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)
64
Proton pump inhibitors MoA
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
Iansoprazole may effect
Vitamin B12 absorption
66
Iansoprazole common adverse effects
Diarrhea, abdominal pain, nausea | -Hypomagnesemia
67
OTC PPI has what kind of warning
Osteoporosis and fracture warning
68
Misoprostol drug class
Prostaglandin E1 analog
69
MoA of misoprostol
Inhibits secretion of gastric acid and stimulates secretion of mucus, providing cytoprotective effects on integrity of the gastric mucosa
70
Misoprostol adverse effects
Diarrhea, nausea, abdominal discomfort, fever | -Also used with mifepristone as an abortifacient (induces abortion)
71
Misoprostol unlabeled uses
Postpartum hemorrhage, induction of labor (very risky); treatment of incomplete/missed abortion (miscarriage)
72
Misoprostol boxed warning
- Not used in women of childbearing unless they comply with effective contraceptives - do not give to other people
73
Antacids
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
Types of antacids
``` Aluminum hydroxide (Amphojel) Calcium carbonate (Tums) Magnesium salts (Milk of Magnesia) Sodium bicarbonate (Alka-Seltzer) ```
75
Nursing considerations of antacids
With the exception of sodium bicarbonate, antacids are minimally absorbed systemically
76
Antacids may affect the absorption of other drugs (Chelation), administer
2 hours before or after other drugs
77
Antacids adverse effects
- 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
Magnesium hydroxide drug class
Antacid, magnesium salt; laxative
79
Magnesium hydroxide moA
Works in small & large intestine to attract & retain water in the intestinal lumen, thereby increasing pressure within intestine which stimulates peristalsis
80
Magnesium hydroxide adverse effects in large doses
Cramps, diarrhea, nausea
81
Antacids precautions
- Renal insufficiency: about 15-30% is absorbed from small intestine - Acute abdomen of unknown origin - Neuromuscular disorders
82
Sucralfate drug class
Mucosal protective agent
83
Sucralfate aids healing
of ulcers; used for long-term prevention of ulcer recurrence
84
Sucralfate MoA
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
Nursing considerations of sucralfate
Can decrease absorption of some other drug: administer 2 hours before or after other drugs
86
Is constipation a disease
Not a disease, but a symptom of an underlying disorder
87
Constipation is broadly described as an
Abnormally infrequent of difficult passage of hard, dry feces
88
normal bowel movement
3 times a day, or 3 times a week depending on person
89
Hard and dry stool of constipation occur when
the colon absorbs too much water or if intestinal muscle contractions are slow or sluggish, causing stool to move through colon too slowly
90
Diseases that cause constipation slow
movement of stool through the colon, rectum, or anus
91
Neurological disorders than cause constipation
Multiple Sclerosis, Parkinson's disease, chronic idiopathic intestinal pseudo-obstruction, stroke, spinal cord injuries
92
Metabolic and endocrine conditions that cause constipation
Diabetes, hypothyroid, hypercalcemia
93
systemic disorders that cause constipation
Amyloidosis, systemic lupus erythematous (SLE), | scleroderma
94
Miscellaneous disorders causing constipation
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
Medications that increase risk of constipation
``` Opioids Antacids that contain Aluminum Blood pressure medications (calcium channel blockers) Anticholinergic drugs Antidiarrheal drugs Iron supplements Diuretics ```
96
Indications for use of laxatives
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
All laxatives are contraindicated if
THERE IS A GI OBSTRUCTION OR ABDOMNIAL PAIN OF UNKNOWN ORIGIN
98
Goal of treatment for laxatives
passage of a soft, formed bowel movement within 12 to 24 hours
99
Bulk forming laxatives indications
- 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
Examples of laxatives
Polycarbophil Psyllium Methylcellulose What dextrin
101
Bulk forming moA
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
Bulk forming laxative must be taken with
Plenty of water to AVOID FECAL IMPACTION
103
BULK FORMING LAXATIVES MAY CAUSE
BLOATING AND FLATULENCE
104
psyllium is contraindicated with
intestinal obstruction or fecal impaction; acute abdomen of unknown origin
105
Most common side effects of psyllium
Bloating, flatulence, and cramp
106
Stool softeners/ Emollients moA
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
Docusate drug class
Stool softeners/emollients
108
Docusate is most effecting in preventing
Straining in high risk patients
109
Docusate side effects
May cause diarrhea, flatulence, abdominal cramps
110
Docusate may take up to
3 days to produce soft stool
111
Lubricant laxatives; mineral oil indicated for
acute, softening of fecal impaction, softening of fecal mass for patients with painful anorectal conditions
112
Mineral oil moA
Coat and soften stool which prevents reabsorption of water from the stool
113
Saline/ Osmotic Agents moA
Draw water into laxatives through osmosis which increases intestinal motility
114
Types of saline laxative
- magnesium citrate (Citrate of Magnesia) - magnesium hydroxide (Milk of Magnesia) - polyethylene glycol solution (Miralax) - polyethylene glycol-electrolyte solution (GoLYTELY) - sodium phosphate enema (Fleet)
115
Can you use stimulant laxatives long term
No, stimulant laxatives are not used for long term
116
Why aren't stimulant laxatives used for long term
May induce loss of normal bowel function and laxative dependence
117
Stimulant laxatives moA
produce propulsive movements by direct chemical irritation &/or stimulation of intestinal wall &/or mesenteric plexus; increasing fluid & electrolytes within the intestinal lumen
118
Stimulant laxative examples
- Bisacodyl - Senna - Castor oil
119
Bisacodyl is a very popular OTC laxative and is drug of choice to
empty the bowel before surgery
120
Bisacodyl is indicated for
Acute constipation; bowel preparation for diagnostic and surgical procedures
121
Bisacodyl adverse effects
nausea, vomiting, abdominal cramps; possible F&E imbalance (especially potassium)
122
Is Diarrhea a a disease
No, it is is symptom of an underlying condition
123
Diarrhea is characterized as
Loose, watery stool during a limited time period
124
Acute diarrhea is usually due to
Bacterial or viral origin
125
Diarrhea is caused by
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
Diarrhea can cause dehydration:
Particularly dangerous in children and in the elderly, must be treated promptly
127
Diarrhea may be accompanied by
- cramping abdominal pain - bloating - nausea - urgent need to use the bathroom - fever - bloody stools
128
Acute diarrhea lasts
< 2 weeks; bacterial, viral, or parasitic infection
129
Chronic diarrhea lasts
>4 weeks; usually related to functional disorders like irritable bowel syndrome or inflammatory bowel diseases
130
Bacterial infections that cause diarrhea
common culprits include Campylobacter, Salmonella, Shigella, and E. coli
131
Viral infections that cause diarrhea
rotavirus, Norwalk virus, cytomegalovirus, herpes simplex virus, & viral hepatitis
132
Parasites that cause diarrhea
Giardia lamblia, Entamoeba histolytica, & Cryptosporidium
133
Other things that can cause diarrhea
Food intolerances Adverse drug effects Intestinal diseases Functional bowel disorders
134
Pharmacologic tx for diarrhea
Ioperamide Diphenoxylate + Atropine Paregorgic
135
What does loperamide do
structural analog of meperidine; has opioid-like actions on gut (inhibits gastric motility)
136
what does diphenoxylate + atropine (Lomotil) do
structural analog of meperidine; has opioid-like actions on gut (inhibits gastric motility)
137
What does paregoric do?
- -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
Ioperamide indications
- Acute or chronic diarrhea | - Reduce the volume of discharge from ileostomy
139
Ioperamide moA
- 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
Ioperamide common adverse effects
Abdominal cramps, constipation
141
Ioperamide nursing considerations
- 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
Nausea and vomitting is an emetic response that is a
Complex reflex after activating vomiting center in medulla oblongata
143
Pharmacologic prevention and tx for nausea and vomitting
Phenothiazines Antihistamines 5-HT3 receptor antagonists Prokinetic
144
Prochlorperazine class
dopamine antagonists; phenothiazines
145
Prochlorperazine Moa
Block dopamine2 receptors in CTZ
146
Prochlorperazine indications
Prevention and Tx of nausea and vomitting related to surgery, cancer, chemotherapy, and toxin
147
Prochlorperazine side effects
Extrapyramidal rx Anticholinergic effects Hypotension and sedation
148
medications for nausea and vomitting are known as
Antiemetics
149
Antihistamine examples for nausea and vomiting
Hydroxyzine | Promethazine
150
Hydroxyzine, Promethazine moA
Block H1 receptors and the muscarinic receptors in the pathway from the inner ear to the vomiting center
151
Hydroxyzine, Promethazine indications
Nausea and vomitting associated with motion sickness
152
Hydroxyzine, Promethazine side effects
``` Anticholinergic effects (dry mouth, tachycardia, urinary retention, blurred vision, thickened respiratory secretions) Dizziness, confusion ```
153
Ondansetron drug classification
5-HT3 receptor antagonist
154
Ondansetron indiction
Prevention of CINV, radiation-induced emesis, post-operative n/v, hyperemesis gravies
155
Ondansetron nursing nursing considerations
- 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
Metoclopramide drug class
Dopamine receptor antagonist, prokinetic, GI stimulant
157
Metoclopramide indications
Relief of post-operative or chemotherapy-induced N/V, diabetic gastroparesis, GERD, delayed gastric emptying; unlabeled: persistent hiccups
158
Metoclopramide adverse effects
Extrapyramidal (EPS) effects with chronic use [secondary to central dopaminergic blockade]
159
Metoclopramide black box warning
may cause tardive dyskinesia, often irreversible (duration of tx & cumulative dose associated with increased risk)