GI Flashcards

(146 cards)

1
Q

Conditioned response before chemotherapy, triggered by fear of nausea/vomiting.

A

anticipatory n/v

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2
Q

Drugs used to prevent/treat nausea and vomiting from various causes (surgery, pain, motion sickness, chemotherapy, pregnancy, etc.) but may be contraindicated if they delay diagnosis or mask symptoms.

A

anti-emetics

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3
Q

derivative of marijuana used for anti-nausea purposes

A

cannabinoid

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4
Q

Central area relaying stimuli to the vomiting center

A

chemoreceptor trigger tone (CTZ)

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5
Q

Stomach contents expelled during vomiting

A

emesis

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6
Q

Ability to cause vomiting.

A

emetogenic

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7
Q

Rapid body motion stimulates inner ear receptors, triggering vomiting.

A

motion sickness

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8
Q

Abdominal discomfort with an urge to vomit

A

nausea

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9
Q

Used when initial antiemetic treatment fails.

A

rescue emetic

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10
Q

Expulsion of stomach contents through the esophagus/mouth

A

vomiting

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11
Q

Located in the medulla oblongata, controls the vomiting reflex

A

vomiting center

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12
Q

causes of nausea and vomiting

A
  • GI disorders: Infections, inflammation, overeating, GI motility issues
  • Other conditions: Cardiovascular, neurologic, infectious, and metabolic disorders
  • Drugs: Common with alcohol, aspirin, anticancer drugs, etc.
  • Other factors: Pain, unpleasant stimuli, emotional stress, radiation, surgery, pregnancy, migraines
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13
Q
  • Protects against NSAID-induced ulcers by mimicking prostaglandin E
  • contraindicated in women of childbearing age unless using contraception, as it may cause abortion or birth defects
A

misopristol

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14
Q

Requires multiple-drug therapy to eradicate the infection and prevent ulcer recurrence.

A

tx of h. pylori infection

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15
Q

Forms a barrier over ulcers to protect them from gastric acid

A

sucralfate

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16
Q

Block acid production by inhibiting the gastric proton pump (e.g., omeprazole, esomeprazole).

A

proton pump inhibitors (PPIs)

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17
Q

Reduce gastric acid secretion (e.g., cimetidine, famotidine)

A

Histamine 2 Receptor Antagonists (H2RAs):

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18
Q
  • Neutralize gastric acid and reduce pepsin production
  • types: aluminum, magnesium, calcium
A

antacids

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19
Q

May cause constipation

A

aluminum antacids

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20
Q

May cause diarrhea and hypermagnesemia.

A

magnesium antacids

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21
Q

Fast-acting but can cause rebound acidity and hypercalcemia

A

calcium antacids

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22
Q
  • Chronic condition where stomach acid or bile refluxes into the esophagus.
  • Causes: Incompetent lower esophageal sphincter (LES), certain foods (e.g., chocolate, fats), alcohol, smoking, and medications.
  • Symptoms: Heartburn (pyrosis) that worsens when lying down, acid regurgitation, and sometimes esophagitis or esophageal ulceration.
A

Gastroesophageal Reflux Disease (GERD)

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23
Q
  • Ulcers form in the esophagus, stomach, or duodenum due to exposure to gastric acid and pepsin.
  • Main causes: H. pylori infection and NSAID use are attributed to a balance between cell-destructive (acid, H. pylori, NSAIDs) and cell-protective (mucus, bicarbonate) effects.
  • Other factors: Stress, older age, smoking, and imbalance between destructive (acid, pepsin, H. pylori) and protective (mucus, bicarbonate, prostaglandins) effects in the stomach.
A

peptic ulcer disease (PUD)

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24
Q

Excessive gastric acid secretion due to gastrin-secreting tumors, often causing ulcers.

A

Zollinger-Ellison Syndrome:

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25
Develop in critically ill patients; lesions are linked to mucosal ischemia, acidosis, and decreased GI motility.
Stress Ulcers
26
Damage caused by NSAIDs (Advil, Aleve, Aspirin), leading to gastric or duodenal ulcers and GI bleeding
NSAID Gastropathy
27
Cause heartburn, stomach pain, and burning sensations, often worse when the stomach is empty.
duodenal ulcers
28
Dull aching pain, often right after eating. Symptoms include bloating, indigestion, and nausea.
gastric ulcers
29
Inflammation caused by alcohol, NSAIDs, or H. pylori. Chronic gastritis is usually due to H. pylori infection.
gastritis
30
Low or absent production of gastric acid in the stomach
achlorhydria
31
The part of the stomach that connects to the esophagus
cardia
32
Inflammation of the esophagus.
esophagitis
33
inflammation of the gastric mucosa, either acute or chronic
gastritis
34
Gram-negative bacterium found in the gastric mucosa of most patients with chronic gastritis.
heliobacter pylori (h. pylori)
35
Enzyme system responsible for producing gastric acid.
hydrogen, potassium adenosine triphosphatase
36
Enzyme that helps digest protein.
pepsin
37
Heartburn
pyrosis
38
when do we want to avoid antidiarrheals
In cases of toxin-related diarrhea (e.g., food poisoning) to allow the body to expel the irritants.
39
in what type of patient would we want to monitor for loperamide toxicity
hepatic impairment
40
octreotide bismuth subsalicylate (pepto-bismal) antibacterial drugs
adjuvant drugs
41
Used to treat diarrhea caused by bacterial infections (e.g., E. coli).
antibacterial drugs
42
Controls traveler’s diarrhea and cramping.
Bismuth Subsalicylate (Pepto-Bismal)
43
Decreases GI secretion and motility for conditions like HIV/AIDS-related diarrhea.
octreotide
44
* A synthetic opioid that decreases GI motility. It is available without a prescription but should not exceed 16 mg/day under medical supervision. (Over the Counter) * Paregoric: Contains morphine, increases intestinal muscle tone, and decreases peristalsis. * FDA Warning: Overuse can cause torsades de pointes, cardiac arrest, and death.
loperamide (imodium)
45
Slows peristalsis by acting on intestinal muscles. (Prescription required)
diphenoxylate w/ atropine (lomotil)
46
opioid related antidiarrheals
lomotil (diphenoxylate w/ atropine) imodium (loperamide)
47
non-pharmacologic therapy for diarrhea
* Fluid Replacement: Replace fluids and electrolytes using clear liquids (e.g., broth, ginger ale) and bland foods (e.g., rice, soup). * Diet: Resume a normal diet after 2-3 days.
48
* **Pathophysiology:** results from increased bowel motility or fluid retention in the intestines. It is a symptom of various conditions like infections or irritants. * **Clinical Manifestations**: -Acute: Often the body’s defense mechanism to rid itself of toxins, usually resolving in 24-48 hours. -Chronic: Can cause malnutrition and anemia. * **Symptoms:** Fever, vomiting, bloody stools, and fluid/electrolyte imbalances. * **Etiology**: -Laxative Abuse: Often associated with eating disorders. Infections: From bacteria like E. coli, Salmonella, or viruses like rotavirus. -Food Contamination: Common causes include undercooked meat or contaminated water. -Conditions: IBS, inflammatory bowel disorders, and antibiotic-associated colitis (e.g., C. difficile).
diarrhea
49
Increased stool liquidity or defecation frequency (more than 3 stools per day).
diarrhea
50
Conditions where inflamed mucous membranes release fluids, mucus, proteins, and blood into the intestines.
inflammatory bowel disorders
51
A functional disorder affecting intestinal motility without inflammation or tissue changes.
Irritable Bowel Syndrome (IBS)
52
loose, fatty stool
steatorrhea
53
Caused by the enterotoxigenic strain of E. coli from contaminated food or water.
traveler's diarrhea
54
increases intestinal fluid secretion, stimulates bowel movements.
Lubiprostone (Amitiza)
55
* taken on an empty stomach to improve bowel motility. * FDA Warning: Contraindicated in children under 6 due to dehydration risk.
linaclotide
56
Activated by various stimuli via the CTZ, cerebral cortex, sensory organs, and vestibular apparatus.
vomiting center
57
receptors involved in vomiting reflex
* Muscarinic (M1) * Dopamine (D2) * Histamine (H1) * Serotonin (5-HT3) * Substance P (NK1)
58
Emetogenic drugs cause ---------- release, activating 5-HT3 receptors, triggering vomiting.
serotonin
59
* **Mechanism:** Act by blocking neurotransmitters (dopamine, serotonin, etc.) in the vomiting center, CTZ, and GI tract that are stimulated by emetogenic drugs or toxins involved in nausea and vomiting. * **Forms:** Oral (often preventive), parenteral or rectal (often treatment). * **Most Effective Timing:** Best when administered before nausea occurs. * **Pregnancy**: Use antiemetics only with healthcare provider guidance; some can be harmful to the fetus.
anti-emetics
60
types of anti-emetic drugs
* Phenothiazines (e.g., prochlorperazine, promethazine) * H1 antihistamines * corticosteroids * 5-HT3 antagonists * substance P antagonists * benzodiazepines * cannabinoids * scopolamine
61
* Block dopamine receptors; treat nausea from drugs, radiation, surgery; not effective for motion sickness. * FDA Warning: Promethazine contraindicated for children under 2 years (risk of fatal respiratory depression); avoid subcutaneous administration.
phenothiazines (e.g. prochlorperazine, promethazine)
62
Anticholinergic properties; prevent/treat motion sickness
H1 antihistamines
63
Mechanism unknown; used alone or with other drugs for chemotherapy-induced nausea
Corticosteroids (e.g., dexamethasone)
64
Block serotonin receptors; prevent/treat nausea from chemotherapy, radiation, or surgery
5-HT3 Antagonists (e.g., ondansetron)
65
Block neurokinin 1 receptor; manage chemotherapy-induced nausea.
substance p antagonists (e.g. aprepitant)
66
Relaxation and anxiety relief; used for anticipatory nausea in chemotherapy.
benzodiazepines (e.g. lorazepam)
67
Manage chemotherapy-induced nausea; Schedule II drugs due to potential abuse.
Cannabinoids (e.g., dronabinol, nabilone)
68
Anticholinergic; used for motion sickness and cancer radiation therapy-induced nausea.
scopolamine
69
merely acts as a relay station, transmitting stimuli to the vomiting center which initiates the vomiting reflex. It does not directly involve in release of serotonin, blocking receptors or managing symptoms, which are generally functions of drugs
chemoreceptor trigger zone
70
nursing interventions for n/v
* **Prevention and Minimization:** Use measures to prevent or reduce nausea and vomiting. * **Identifying Triggers:** Help patients identify situations and avoid stimuli that may cause or worsen nausea and vomiting. * **Pain Management:** Administer analgesics before diagnostic tests or other procedures that may cause pain and trigger nausea. * **Timing of Antiemetics:** Administer antiemetic drugs 30-60 minutes before events like chemotherapy or travel. * **Adjust Drug Timing:** Modify the timing of any oral drugs that may cause nausea, taking them with or after food if necessary. * **Assess Condition:** Report recurring nausea and vomiting to healthcare providers. Discontinue or adjust drugs if needed (e.g., digoxin, antibiotics). * **Pregnancy Tips:** Suggest that pregnant women eat dry crackers before getting up and consume small, frequent protein meals to reduce nausea. * **Avoid Oral Intake:** Avoid giving food, fluids, or medications during acute vomiting episodes to reduce the risk of worsening nausea or fluid imbalance. * **Fluid and Electrolyte Replacement:** Provide small amounts of fluids and food orally when tolerated. * **Monitor Patient:** Record vital signs, intake/output, and body weight if vomiting occurs frequently. * **Environmental Control:** Reduce environmental stimuli like noise and odors. Let patients rest in bed if nauseated. * **Oral Care:** Help patients rinse their mouth after vomiting to reduce bad taste and protect tooth enamel. * **Nonpharmacologic Remedies:** Offer non-drug remedies like cool washcloths to the face/neck. * **Patient Education:** Educate patients about drug therapy and prevention strategies.
71
A symptom, not a disease, involving infrequent, painful bowel movements/expulsion of hard, dry stools.
constipation
72
Normal bowel elimination stimulated by GI tract movements.
defecation
73
Hard mass of stool in the rectum due to chronic constipation.
fecal impaction
74
expulsion of gas thru the rectum
flatulence
75
Mild effect, promotes soft stool
laxative
76
Strong effect, causes elimination of liquid/semiliquid stool
cathartic
77
* **Etiology:** Often no specific cause, but associated with age, diet, physical inactivity, and certain medications. * **Risk Factors:** Female sex, older age, low education/income, and nonwhite status increase the risk. * **Physiology:** Defecation reflex controlled by the cerebral cortex; ignoring the urge weakens the reflex and causes constipation.
constipation
78
clinical manifestations of diarrhea
* Adults: Less than three bowel movements per week, along with symptoms like straining and hard stools. * Children (Under 4): Fewer than two stools per week, painful bowel movements, large stool masses. * Bowel Transit Time: Testing sometimes used to diagnose constipation but its usefulness is debated.
79
nonpharmacologic tx of diarrhea
* fiber, fluids, behavioral therapy (biofeedback) * increased fruits, vegetables, and whole grains reduce bowel transit time * prune and pear juice for infants
80
general constipation management
* fluid intake, fiber, and exercise are preferred treatments over medications. * Be Aware of Laxative/Cathartic Abuse: Common in eating disorders and strict weight control. * Caution: Avoid laxatives with undiagnosed abdominal pain or potential intestinal obstruction.
81
Often combined with Kayexalate for hyperkalemia management.
sorbitol
82
Used to treat constipation and hepatic encephalopathy by reducing ammonia levels.
lactulose
83
Lubricate stool and slow water absorption but can interfere with vitamin absorption.
lubricant laxatives
84
* Strongest, can lead to electrolyte imbalance. (e.g., Bisacodyl) * **MOA:** Irritates the GI mucosa, pulls water into the bowel, produces watery stool. * **Use:** Constipation immediate relief or bowel preparation for surgery. * **Pharmacokinetics:** Poorly absorbed; mainly excreted in feces.
stimulant cathartics
85
Rapid bowel evacuation for procedures
polyethylene glycol solution
86
Increase osmotic pressure in the intestines, resulting in semifluid stool
saline laxatives
87
Soften stools by allowing water/fat to penetrate.
surfactant laxatives
88
* allows stomach acid to back up into the esophagus * four major symptoms are heartburn, regurgitation, dysphagia, and waterbrash.
GERD
89
is a general term that refers to ulcer formation in the esophagus, stomach, or duodenum
peptic ulcer disease (PUD)
90
is a gram-negative, spiral bacterium that weakens the protective mucous lining of the stomach and duodenum
heliobacter pylori
91
how do we treat H. pylori
* **Acid reduction** – Proton pump inhibitor twice daily (healing dose) * **Antimicrobial combinations:** Clarithromycin + Amoxicillin; Bismuth subsalicylate + Metronidazole + Tetracycline (Bismuth subsalicylate can cause tongue discoloration, black stools) [need usually more than 1 drug]
92
* sulfated sucrose/aluminum compound that provides a protective coating in stomach * May cause hypophosphatemia
sucralfate
93
* prostaglandin analog that is cytoprotective in the setting of NSAID use (which reduces naturally occurring protective prostaglandin E) * Contraindicated in pregnancy (used in medical abortions w/ mifepristone) * Diarrhea * Not indicated in children ## Footnote gives back good prostaglandins taken away by NSAIDs
misoprostol (cytotec)
94
* BEERS list * risk of bone changes in animal studies * interacts w/ high-dose methotrexate, CYP2C19 - clopidogrel; mycophenolate ## Footnote IV Push 40mg over > 2 min (10ml NS) IV Infusion 40mg over 15 min Oral 30 minute before meal cannot be given via NGT
pantoprazole (protonix) | PPI prototype
95
* **MoA:** Decrease HCl production by parietal cells in stomach * IV, PO * **Side Effects:** Diarrhea, bone fracture, hypomagnesemia, headache, acute interstitial nephritis, C. Diff risk * **Major Interactions:** omeprazole CYP inhibitor * PPIs on BEERS list for risk of CDI * stronger than H2RA prototype (famotidine)
proton pump inhibitors (omeprazole, pantoprazole)
96
* **MoA:** Decrease HCl production by blocking histamine-2 * IV, PO * **Adverse effects:** diarrhea, dizziness, drowsiness, headache, confusion * **Major Interactions** – cimetidine CYP inhibitor, medications that require acidic environment * Pearls for Geriatrics, Peds, Preg/Lactating – renally eliminated and require dose adjustment
histamine 2 receptor antagonists (H2RA) | -itidines ## Footnote e.g. famotidine
97
* **MoA:** Neutralization of Stomach Acid (HCl), Oral liquid, chewable tablets * Al – constipation, Mg- diarrhea, electrolyte disturbance * Major Interactions: Cation: chelation; Inc pH - solubility * Major Monitoring/Education – chronic aluminum exposure, osteomalacia, hypophosphatemia * Older patients may be more prone to neurotoxicity of Aluminum * safe in pregnancy
antacids
98
classes of medications used to treat GERD/peptic ulcer disease
* Decrease Gastric Acidity: **Antacids** (Aluminum Hydroxide, Magnesium Hydroxide, Calcium Carbonate) -Tums®, Maalox®, Rolaids®, Mylanta®; **Proton-Pump Inhibitors** (Omeprazole, Prilosec®) * **Histamine-2 Receptor Antagonists** (Famotidine, Pepcid®) * Cytoprotection: **Misoprostol, Sucralfate**
99
what is the typical presentation/diagnosis for peptic ulcer disease
* Pain usually 1-4 hrs after eating and usually relieved by food * Pain is not necessary for diagnosis - some asymptomatic * Diagnosis dependent on endoscopic visualization of ulcer * Helicobacter pylori testing – endoscopic, urea breath test, fecal antigen, blood antibody
100
risk factors for PUD
* **Stress:** Shock, Burns, Surgery, Head injury, Trauma, Medical illness * **Psychological stress** * **Cigarette smoking (nicotine)** * **Medications:** NSAIDS, antineoplastic agents, corticosteroids
101
causes of diarrhea
viruses bacteria food medications
102
mechanisms of diarrhea
* secretory: increased gi secretions * osmotic: brings fluid into GI tract * exudative: caused by inflammation and damage to the intestinal lining, which results in the leakage of blood, pus, and mucus into the stool * altered intestinal transit: maybe d/t surgical intervention
103
how do we evaluate diarrhea
* Assess for contraindication to treatment; e.g. fever, hypotension, blood * Assess for dehydration – skin turgor, mucous membranes * Assess history of substance abuse - sign of withdrawal * Assess beliefs about bowel habits * Educate on rapid reduction of anti-diarrheal when diarrhea dissipates - short term tx only
104
how do we manage diarrhea non-pharmacologically
oral rehydration solutions that containsn carbs, Na, K+, bicarb, Cl, citrate * pedialyte * enfalyte
105
list of meds we should avoid in pediatric pts to keep them safe
KIDs list
106
pharmacologic management of diarrhea
* loperamide (imodium) * diphenoxylate (lomotil) * paregoric * tincture of opium | loperamide most common ## Footnote last 3 are opiate derivatives
107
108
* Prolong intestinal transit, increase gut capacity, prolonging contact and absorption, and stimulate water absorption * **Loperamide (Imodium®):** Also Anti-secretory, oral capsules and solution (OTC); abuse potential – euphoria with high doses→ cardiovascular problems * **Diphenoxylate/Atropine (Lomotil®):** Atropine component to curb abuse potential, Tablet and solution, adverse effects of atropine - blurred vision, dry mouth, dizziness and urinary hesitancy (anticholinergic effects of atropine)
109
classifies and grades stool appearance
bristol stool scale
110
inclination to vomit or feeling that emesis is imminient
nausea
111
ejection or expulsion of gastric contents - often forceful
vomiting
112
most common adverse effects of drug therapy
nausea and headache
113
causes of n/v
* post-op * mechanical/obstructive * MI * DKA * migraine * vestibular disorders * uremia * pancreatitis * noxious odors * pregnancy * drug withdrawal
114
pathophys of n/v
* Impulses from Chemoreceptor Trigger Zone (CTZ), cerebral cortex and visceral afferents from pharynx and GI tract to * Vomiting Center (VC) coordination results in: Salivation, brief pharynx closure, respiratory stop and abdominal muscles→vomiting * CTZ stimulation: Chemotherapy, pregnancy * Neurotransmitters involved: cholinergic, histaminic. dopaminergic, opiate. serotonergic, neurokinin. benzodiazepine
115
etiology of n/v
* Mechanical obstruction * Gastroparesis or GERD * Pancreatitis * Gastroenteritis * Myocardial Infarction * Migraine * Vestibular Disorders * DKA * Uremia (renal disease) * Medications * Drug withdrawal * Pregnancy * Noxious odors * Post-operative nausea/vomiting
116
medications used to counteract n/v
* **phenothiazines:** promethazine, prochlorperazine (compazine); ADEs: blurred vision, urinary retention, dry mouth, photosensitivity, drowsiness, confusion (not great for elderly) * **antihistamines:** hydroxyzine, dimehydrinate, diphenhydramine; not great for elderly; ADEs: drowsiness, dizziness, confusion, dry mouth, blurred vision, urinary retention (meclazine), tachycardia * **5-HT3 receptor antagonists:** ondansetron (zofran), ADEs: diarrhea, headache, dizziness, constipation, fatigue, pain at injection site; great for chemo + post-op n/v * **substance P/neurokinin antagonist:** aprepitant; ADEs: fatigue, weakness, dizziness, headache, hiccups, arrhythmia
117
how do we treat n/v in special populations
* Children – Promethazine contraindicated children < 2years * Elderly - Hydroxyzine, dimenhydrinate, diphenhydramine, promethazine – BEERS list * Post-Op Nausea – drugs like ondansetron – drugs of choice
118
how do we assess for n/v
* Identify risk factors: disorders, medications * Get specifics: Frequency, duration, precipitating factors, accompanying signs/symptoms, amount, color, odor, presence of blood, measures that relieved nausea
119
nursing interventions for n/v
* Identify triggers * Avoid stimuli – odors, sights; excessive ingestion of food, alcohol, NSAIDs * Premedication with analgesics before painful procedures (pain can precipitate n/v) * Administer anti-emetic medication 30-60 minutes prior to inciting events (radiation, chemotherapy, travel) * Can oral medications be taken with food? depends on med * Assess and report – does a medication need to be changed? Does patient have gastroparesis? Ileus? * Pregnancy - Small frequent meals; Crackers/toast before rising in morning * Supportive care; mouth rinsing; cool, wet washcloth to face/neck * Replacement fluids/electrolytes * Decrease environmental stimuli; motion
120
pharmacologic management of diarrhea that increases bulk in stool; adsorbent
* kaolin-pectin (kapectolin) * polycarbophil (fibercon) * attapulgite (di-gon II, diarrest)
121
* anti-secretory pharmacologic managment of diarrhea * warning - salicylate content: aspirin allergy, ulcers, anticoag use * side effect: black tongue, black stools
bismuth subsalicylate (kaopectate) | we do not use aspirin or salicilate sin children
122
miscellaneous pharmacologic management of diarrhea
* lactase (lactaid) - enzyme replacement * lactobacillus acidophilus, bulgaricus - bacterial replacement * octreotide (for vip) - secreting tumor diarrhea
123
* defined as difficult or infrequent passage of stool; characterized by straining and incomplete defecation * quantification: less than 3 bm/week * causes: diet, hypothyroidism, medications, obstruction (may have vomiting and inability to take anything in PO)
constipation
124
risk factors for constipation
* low activity * female * non-white * advanced age * low level income/education
125
medications that cause constipation
* anticholinergics * opiates * CCBs * aluminum * iron * phenothiazines * 5-HT3 receptor antagonists
126
medical causes of constipation
* IBS * tumors * DM * hypothyroidism * HF * pregnancy * spinal cord injury * parkinsons
127
primary function is the reabsorption of water from intestinal content more time here = drier fecal matter
colon
128
normal defecation physiology
* Controlled by cerebral cortex (“training” → acceptable times/places) * Voluntary control: contracts sphincter to prevent defecation; inhibits external anal sphincter to allow defection * Extended contraction of external sphincter - “holding it”; defecation reflex dissipates; "urge” does not recur until additional feces enter rectum – several hours later ## Footnote Preventing constipation is the first thing we want to do besides tx
129
what are our tx paths for IBS
* Constipation – Predominant: Dietary Fiber/Fluid, osmotic laxatives linaclotide, plecanitide, tenapanor, lubiprostone; Serotonin-4 agonist (tegaserod) * Diarrhea - Predominant: Limit lactose, caffeine, alcohol food/drug triggers; loperamide; rifaximin/eluxadine/TCA; serotonin-3 antagonists (alosetron)
130
* affects 10% of adults * chronic abd pain w/ altered bowel habits and no other cause * either C or D dominant * ROME IV Criteria * Recurrent abd pain/discomfort >3days/mo in last 3 mo and 2 of the following: * Relieved with defecation, Onset associated with change in stool frequency, Onset associated with change in stool appearance
irritable bowel syndrome (IBS)
131
laxatives
* bisacodyl * mag citrate * psyllium * docusate
132
* Irritate mucosa→H20 into colon→peristalsis * ADEs: Watery stool, fluid/electrolyte, acid-base imbalance * Abdominal pain, cramping
bisacodyl
133
* Osmotic effect→H20 into colon→distension→peristalsis * Fluid/electrolyte imbalance; avoid in renal failure (Mg)
magnesium citrate
134
* Add mass→peristalsis→defecation * Must be taken with water
psyllium
135
Decrease surface tension of feces → water/fats penetrate→ softer, easier to expel
docusate
136
laxatives
* Bulk-forming: Psyllium * Emollients: Docusate (Colace) * Osmotic (slow): Lactulose, Sorbitol, Polyethylene glycol 3350 (Miralax®) * Stimulants/Cathartics: Senna, bisacodyl (oral) * Osmotic(fast): magnesium citrate, magnesium hydroxide (Milk of Magnesia), bisacodyl (rectal) (Dulcolax) * Intestinal secretagogues: Lubiprostone, linaclotide (linzess), plecanatide * Opioid antagonists: Methylnaltrexone, naloxegol
137
non-pharmacologic approaches to constipation
* activity/exercise * dietary fiber (fruit, vegetables) * fluid intake (48-80 oz/day, approx 1.5-2.4L/day) (if not contraindicated) * establish bowel routine: avoid delays
138
* common complication of diabetes; decrease motility or made erratic; decreasing GI function * gastric surgery (vagotomy, gastric resection)
gastroparesis
139
* MoA: Dopamine blockade in CTZ; ↑LES tone, ↑ gastric emptying, ↑ small bowel transit Dosage forms: IV/IM 5mg/ml; Oral – tablet/ODS/solution – 5mg, 10mg; 5mg/5ml; Nasal spray (15mg) * adverse effects/cautions: extrapyramidal symptoms, tardive dyskinesia; beers list; KIDs List; renally dosed
Metoclopramide (Reglan®)
140
how do we treat ulcerative disease
* Acid Reduction * Cytoprotection * Risk Mitigation
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# ``` ``` * Gastroesophageal Reflux Disease (GERD) * Peptic Ulcer Disease (PUD) * Stress-Related Mucosal Damage (SRMD)
ulcerative disease
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* Estimated 20% of adults suffer GERD on a weekly basis * Characterized by regurgitation of gastric contents into esophagus * Symptoms: “heartburn”, dysphagia, belching, hypersalivation, odynophagia; also chest pain, hoarseness, chronic cough * May result in tissue damage due to gastric acid and pepsin * Tissue injury includes esophagitis, Barrett’s esophagus, strictures, adenocarcinoma
GERD
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pathophys of GERD
* Reflux of gastric contents into esophagus/mouth * Caused by incompetent lower esophageal sphincter (at the junction of esophagus and stomach) * change in stomach acidity
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risk factors of GERD
* Obesity * Age >40-50 years * Pregnancy * Smoking * Alcohol consumption * Medications * Foods * Other contributing factors: gastric distention; recumbent position
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treatment strategies for GERD
* non-pharmacologic: dietary changes, small meal size, weight loss, smoking cessation, remaining upright after eating, elevating head of bed * pharmacologic: decrease acidity; PPIs, H2RAs, antacids
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* Distinct from Gastritis in that ulcers are larger (>5mm) and deeper (into muscularis mucosa) * Usually occur in the stomach (gastric ulcer) or intestine (duodenal ulcer), but can occur in esophagus, jejunum, ileum or colon: (Helicobacter pylori +, NSAID-induced, stress-related mucosal damage (SRMD) * Other risks: smoking, alcohol use, hypersecretory conditions, medication non-adherence, chemotherapy, radiation
peptic ulcer disease (PUD)