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NURS 2514 > 5 - Upper GI Problems > Flashcards

5 - Upper GI Problems Flashcards

1
Q

Define nutrition

A

process by which food and nutrients affect cellular function, growth and development, + health and disease.

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2
Q

Define elimination

A

elimination: excretion of waste products primarily through the urinary + GI system

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3
Q

Identify the 4 histological layers of the GI tract (from inside –> outside)

A
  1. mucosa
  2. submucosa
  3. muscularis externa
  4. serosa
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4
Q

Describe the mucosa of the GI tract in terms of its composition and function

A

epithelial layer

produces mucus + some digestive enzymes + absorbs nutrients

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5
Q

Describe the submucosa of the GI tract in terms of its composition + what it contains

A

CT layer

contains nerves, blood, + lymph vessels

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6
Q

Describe the muscularis externa of the GI tract in terms of its structure and function

A

sm muscle layer involved in the mixing + turning of ingested material

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7
Q

Describe the serosa of the GI tract in terms of its structure + function

A

outer CT layer; forms the visceral peritoneum

wraps around the bowel wall + forms a flap called the mesentary which allows the bowel to be attached to the abdomnal cavity where it attaches to its blood + nerve supply

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8
Q

Compare nausea + vomiting

A

nausea is a sensation: a feeling of discomfort w a conscious desire to vomit.

vomiting is a reflex: the forceful ejection of emesis from the upper GI tract

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9
Q

Which part of our body controls n + v?

A

The emetic center of the medulla

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10
Q

Identify the 4 parts of our body in which the emetic center receives input from

A

CTZ
Vestibular System
Vagal + Enteric Nervous System
CNS

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11
Q

What is the function of the CTZ (chemoreceptor trigger zone)? Where is it located? What does it have receptors for?

A
  • lies outside the blood brain barrier
  • senses toxins in the blood and will trigger reflex sensory receptors
  • has receptors for dopamine, serotonin, opiates, acetylcholine, substance P
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12
Q

What is the function of the vestibular system?

A
  • sends info to the brain via cranial nerve VIII (8)
  • motion sickness
  • rich in muscarinic receptors [which is blocked by motion sickness drugs]
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13
Q

What is the function of the vagal + enteric nervous system? What will trigger this pathway? How can we help N + V in this pathway?

A
  • inputs information regarding the state of the GI system via cranial nerve 10
  • something that irritates the gut will trigger the pathway; irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the serotonin receptors
  • help N + V by blocking serotonin receptors
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14
Q

What is the function of the CNS in inputting N + V receptors to the medulla?

A
  • mediates vomiting that arises from psychiatric disorders and stress from higher brain cells; “psychological vomiting”
  • unpleasant, sights, smells
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15
Q

Which nerve / pathway is stimulated to result in vomiting in the digestive tract?

A

vagus nerve / serotonin-based pathway is stimulated

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16
Q

What are the causes of vomiting that stem from the digestive tract?

A
  • gastritis (inflammation of the gastric wall)
  • gastroenteritis + food poisoning
  • GERD
  • pyloric stenosis, bowel obstruction, peritonitis, ileus
  • overeating
  • food allergies
  • cholecystitis
  • pancreatitis
  • appendicitis
  • hepatitis
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17
Q

What are the causes of vomiting that stem from the sensory system and brain?

A
  • motion sickness
  • concussions
  • cerebral hemorrhage
  • migraine
  • brain tumors + ICP
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18
Q

Which 4 drug classes produce N + V as a side effect?

A
  • chemotherapy
  • alcohol
  • opioids
  • SSRIs
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19
Q

Why is aspiration a potential complication of vomiting?

A

Vomiting can lead to the passage of gastric contents into airways

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20
Q

Why are mallory-weiss tears (tears in esophageal lining) a potential complication of vomiting?

A

Throwing up or dry heaving is a large muscular effort

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21
Q

What is alkaline tide?

A

loss of Hcl, K+, and increased production of HCO3- by gastric mucosa

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22
Q

Why can prolonged vomiting result in metabolic acidosis?

A

There are 2 reasons for this:

  • physical losses of HCO3- in the vomit
  • chemical consumption of HCO3- due to lactic acid production and ketoacidosis
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23
Q

What is the MOA of anticholinergic drugs (Ach blockers) as antinausea drugs?

ex - scopolamine (buscopan)

A
  • bind to and block Ach receptors in the inner ear which therefore blocks the transmission of nauseating stimuli to the CTZ + emetic center
  • also used for motion sickness via transdermal patch
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24
Q

Provide an example of an anticholinergic drug.

A

Scopolamine (buscopan)

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25
Q

Describe the MOA of antihistamines (H1 receptor blockers) as antiemetic + antinausea drugs

A

inhibit Ach by binding to M receptors in the inner ear

prevent cholinergic stimulation therefore preventing N + V

also used for motion sickness, non-prod coughs, allergy symptoms, + sedation

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26
Q

Provide 2 examples of antihistamine drugs

A

dimenhydrinate (Dramamine, Gravol)

diphenhydramine (Benadryl)

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27
Q

Describe the MOA of serotonin blockers as antinausea and antiemetic drugs

A

block serotonin receptors in the GI tract, CTZ, and emetic center of the medulla

used for n + v in pts receiving chemo and postoperative n + v

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28
Q

Provide 2 examples of serotonin blockers

A

dolasetron (Anzemet)

ondansetron (Zofran)

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29
Q

What is the MOA of glucocorticoids as antinausea + antiemetic drugs?

A

used to treat N + V associated w some chemo drugs

increases antiemetic effect of serotonin blockers like ondansetron

can be combined w

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30
Q

What is the MOA of tetracannabinoids?

A
  • used for n + v associated w chemo + anorexia associated w weight loss in aids pts
  • increase appetite
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31
Q

provide an example of a tetracannabinoid

A

ex - cannabidoil (Sativex)

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32
Q

how can ginger (a herbal product) help treat n + v? what are some potential adverse effects? drug interactions?

A

help w n + v caused by chemo, morning sickness, motion sickness

s/e’s: anorexia, n + v, skin rxns

drug interactions: increase abs of orla meds, increased bleeding risk w anticoagulants

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33
Q

What is diarrhea?

A

Having 3+ loose or liquid stools per day; having more stools than normal

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34
Q

What does diarrhea result from?

A
  • excess secretions (ex - enterotoxins)
  • malabsorption (leading to bacterial growth)
  • inflammation
  • exudate (increased bulk of liquid in the GI tract)
  • invasion (results in bleeding, dysentery)
  • increased osmotic pressure (caused by deficiency in some tpe of digestive enzyme)
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35
Q

Why does diarrhea lead to metabolic acidosis and hyperkalemia?

A

b/c GI secretions are rich in HCO3- and K+

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36
Q

What are the causes of diarrhea?

A
  • infections –> gastroenteritis
  • malabsorption due to:
  • -> enzyme deficiencies (celiac, lactose intolerance)
  • -> loss of pancreatitis secretions r/t cystic fibrosis or pancreatitis
  • -> loss of bile acids (can’t emulsify + digest fat)
  • -> structural defects or short bowel syndrome
  • inflammatory bowel diseases
  • IBS (idiopathic)
  • chronic ethanol ingestion
  • ischemic bowel disease
  • radiation enteropathy following treatment for pelvic + abdominal cancers
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37
Q

What are the 2 potential risks associated w diarrhea?

A

rapid dehydration + hypovolemic shock

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38
Q

describe the MOA of adsorbent drugs and provide an example

A

adsorbent drugs are a class of antidiarrheal drugs

coat the walls of the GI tract to calm it, bind to the causative bacteria or toxin + eliminates it thru the stool

ex - bismuth subsalicylate (Pepto Bismol)
ex - activated charcoal
ex - aluminum hydroxide

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39
Q

Describe the side effects of Bismuth subsalicylate (Pepto-Bismol)

A
  • increased bleeding time (so not good for bleeding stomach ulcers)
  • constipation
  • dark stools
  • confusion, twitching
  • hearing loss, tennitus
  • metallic taste
  • blue gums
  • toxic to kidneys in high doses
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40
Q

provide 2 examples of antimotility drugs

A

anticholinergics + opioids

41
Q

Describe anticholinergics as antimotility drugs and provide an example

A
  • anticholinergics decrease intestinal muscle tone + peristalsis of GI tract
  • therefore slow the mvmt of fecal matter through the GI tract
  • example: belladonna alkaloids (atropine)
42
Q

Describe opiates as antimotility drugs and provide 2 examples

A
  • decrease bowel motility + relieve rectal spasms therefore reduce pain
  • decrease the transit time through the bowel therefore allow more time for water and electrolytes to be absorbed
  • often combined w atropine
  • ex: loperamide (imodium OTC)
  • diphenoxylate / atropine (Lomotil)
  • that’s why a common side effect is constipation
43
Q

define constipation

A

infrequent or hard-to-pass bowel mvmts

44
Q

what is obstipation?

A

failure to pass stools or gas

45
Q

describe severe constipation

A

includes onstipation and fecal impaction, which can progress to bowel obtruction and become life threatening

46
Q

what is primary / functional constipation?

A

idiopathic; ongoing symptoms of constipation > 6 mo w no other cause

47
Q

which medication classes can cause constipation (7)?

A

1) antidepressants
2) anticonvulsants
3) antihistamines
4) diuretics
5) aluminum / calcium antacids
6) calcium channel blockers
7) opioids

48
Q

identify the 6 metabolic + muscular causes of constipation

A

1) hypercalcemia
2) hypothyroidism
3) dm
4) cystic fibrosis
5) celiac disease
6) mucular dystrophy

49
Q

identify the 5 structural + functional abnormalities that can result in constipation

A

1) spinal cord lesions
2) parkinson’s
3) colon cancer
4) anal fissures
5) paralytic ileus

50
Q

What is a common side effect across all 6 classes of laxatives?

A

electrolyte imbalances

51
Q

describe the MOA of bulk forming laxatives and provide 2 examples

A
  • high fiber
  • absorb water to increase bulk
  • distend bowel to initiate reflex bowel activity
  • psyllium (Metamucil)
  • methylcellulose (Citrucel)
52
Q

describe the MOA of emollient laxatives and provide 2 examples

A
  • stool softeners + lubricants
  • promote more water + fat in the stools
  • lubricate the fecal material and intestinal walls
  • docusate salts (stool softeners)
  • mineral oil (lubricants)
53
Q

describe the moa of hyperosmotic drugs and provide 3 examples

A
  • increase fecal water content
  • results in bowel distension, increased peristalsis, + evacuation

ex - polyethylene glycol (PEG-lyte, Lax-a-Day)

ex - sorbitol, glycerin

ex - lactulose

54
Q

describe the moa of saline drugs and provide an example

A
  • increase the op w/in the intestinal tract therefore causing more water to enter the intestines
  • results in bowel distenition, increased peristalsis, + evacuation

ex - magnesium hydroxide (milk of magnesia)

55
Q

describe the moa of stimulant drugs and provide 2 examples

A

increases peristalsis via intestinal nerve stimulation

ex - senna
ex - bisacodyl (Dulcolax)

56
Q

describe the MOA of peripherally acting opioid antagonists and provide 2 examples

A
  • used to treat constipation related to opioid use and bowel resection theraoy
  • block entrance of opioids into the bowel
  • strict regulations for use
  • allow bowel function normally w continued opioid use

ex - methylnaltrezone (relistor)
ex - naloxegol (movantik)

57
Q

identify 3 esophageal disorders

A

GERD
hiatal hernia
esophageal cancer

58
Q

define GERD

A

condition where gastric contents move into the esophagus creating the sensation of heartburn and / or esophagitis

59
Q

identify the potential causes of GERD

A
  • weak or incompetent lower esophageal sphincter (LES) < 10 MMhg (NORMAL 10-30)
  • hiatal hernia
  • decreased esophageal peristalsis
  • decreased saliva function
  • increased gastric acid production or delayed stomach emptying (pressure in stomach is greater than LES)
60
Q

identify the clinical manifestations of GERD

A
  • heartburn

- respiratory symptoms due to aspiration of gastric content - coughing, wheezing, hoarseness

61
Q

what is heartburn?

A

retrosternal or epigastric pain that can radiate to the throat, shoulders, or back, often confused w angina.

62
Q

what are the chronic complications associated w GERD?

A

1 - esophageal stricture
2 - barrett’s esophagus
3 - hiatal hernia
4 - hemorrhage + ulcerations

63
Q

define esophageal stricture

A

narrowing of the esophagus caused by scar tissue formation, spasm, or edema

64
Q

define Barrett’s esophagus

A

replacement of the esophageal stratified squamous epithelium w simple columnar epithelium (so that it resembles the stomach and intestine)

65
Q

what percentage of pts Barrett’s esophagus develop esophageal cancer?

A

10%

66
Q

What is a hiatal hernia

A

herniation of a portion of the stomach into the esophagus through the opening (hiatus) of the diaphragm

67
Q

Identify the 2 types of hiatal hernia

A

sliding + rolling

68
Q

Describe sliding hiatal hernias

A

gastro-esophageal junction slides above the hiatus of the diaphragm and part of the stomach slides into the hiatal opening

69
Q

Describe rolling hiatal hernias

A

fundus of the stomach rolls up through the hiatus while the gastro-esophageal junction remains in place

70
Q

describe the treatent methods for GERD

A
  • avoid large meals and foods that relax the LES such as fat, caffeine, alcohol, nicotine; sitting upright; drinking fluids; antacids; inhibiting gastric acid production w H2 blockers or H+ pump inhibitors
  • surgery for severee or unresponsive cases
71
Q

identify the 3 disorders of the stomach + upper SI

A
  • gastritis (acute / chronic)
  • upper GI bleeding
  • peptic ulcer disease
72
Q

Describe the anatomical difference between peptic ulcer disease and gastritis

A

both bleed

  • gastritis has inflammation
  • peptic ulcer disease has ulcers
73
Q

Define peptic ulcer disease

A

ulcerative lesions caused by exposure of the GI mucosa to acid-pepsin secretions

74
Q

How do acid-peptic diseases (like peptic ulcer disease) occur?

A
  • the GI mucosa is normally protected from acid-pepsin secretion by mucus that contains HCO3- and mucin, a protective glycoprotein
  • acid-peptic disease develops when there is excessive acid secretion and / or diminished mucosal defense
75
Q

identify the 2 most common locations for a peptic ulcer to occur

A

stomach + duodenum

76
Q

identify the 2 most common causes of peptic ulcer formation

A
  • helicobacter pylori infection
  • NSAID use

b/c they both destroy the mucus barrier

77
Q

why is NSAID use a cause of peptic ulcer formation?

A

NSAIDs block the action of prostaglandins, which are used to tell cells to secrete protective mucus in the stomach

78
Q

identify the 5 contributing factors of peptic ulcer formation

A
  • diet
  • alcohol
  • smoking
  • stress
  • zollinger-ellison syndrome (gastrin secreting tumor)
79
Q

identify the 4 clinical manifestations of peptic ulcer disease

A

1) pain
2) hemorrhage
3) obstruction
4) perforation

80
Q

describe pain as a clinical manifestation of peptic ulcer disease

A

burning, gnawing, cramp-like epigastric pain between meals that can be relieved by foods or antacids - often called dyspepsia

feels like hunger pains; uncomfortable sensation between meals

81
Q

describe hemorrhage as a clinical manifestation of peptic ulcer disease

A

hematemesis, melena, or occult blood; anemia or hypovolemia can occur if severe

82
Q

describe obstruction as a clinical manifestation of peptic ulcer disease. what causes it?

A

caused by edema, spasm, or scar tissue which can prevent the passage of chyme through the pylorus; can result in vomiting undigested food if severe

83
Q

describe perforation as a manifestation of peptic ulcer disease

A

peptic ulcer erodes through the GI wall which allows gastric juice + air to enter the peritoneum

causes peritonitis and possibly pancreatitis

84
Q

which drug classes are used to treat peptic ulcer disease?

A

antisecretory drugs (H2 receptor blockers, proton pump inhibitors)

antisecretory + cytoprotective drugs

neutralizing drugs (antacids)

antibiotics for h pylori

tricyclic antidepressants

85
Q

what are the postoperative complications associated with surgical therapy for peptic ulcer disease?

A

dumping syndrome
postprandial hypoglycemia
bile reflux gastritis

86
Q

define gastritis. what does chronic gastritis increase the risk of?

A

inflamed stomach mucosa

chronic gastritis increases the risk of peptic ulcers + stomach cancer

87
Q

identify the 7 causes of gastritis

A 
alcoholism
nsaids
portal hypertension induced gastropathy
h pylori infection
crohn's disease
pernicious anemia (autoimmune destruction of intrinsic factor)
stress
88
Q

describe stress related gastritis. what are the major risk factors?

A

occurs commonly in critically-ill hospitalized pts

major risk factors:

  • trauma
  • burns
  • hypotension
  • sepsis
  • coagulopathy
  • hepatic or renal failure
  • mechanical ventilation
89
Q

what are the clinical manifestations of gastritis?

A

often asymptomatic
dyspepsia, n + v
hematemesis + GI bleeding

90
Q

identify and describe the 2 types of upper GI bleeding

A

OBVIOUS bleeding: hematemesis (bloody vomitus - either fresh bright red blood or “coffee ground” appearance) OR melena (black, tarry stools, foul odour)

OCCULT - small amt of blood in gastric secretions, vomitus, or stools NOT apparent by appearance (guiac test needed)

91
Q

identify the 3 classes of acid controlling drugs

A

antacids
h2 antagonists
proton pump inhibitors

92
Q

describe the MOA of antacids (aluminum salts, mg salts, calcium salts, sodium bicarbonate)

A

neutralize stomach acid + promote gastric mucosal defense mechanisms including the secretion of mucus, bicarbonate, + prostaglandins

93
Q

aluminum salts

A
  • have constipating effects
  • often used w magnesium to counteract constipation
  • often recommended for pts w renal disease bc it is more easily excreted

ex – aluminum carbonate (basaljel)
ex – hydroxide salt (amphojel)
ex – combination products (aluminum + magnesium): gaviscon, maalox, mylanta, di-gel

94
Q

magnesium salts

A

magnesium salts
• commonly cause diarrhea so usually used w other drugs to counteract
• dangerous when used w renal failure
o failing kidney cannot excrete extra magnesium resulting in accumulation

ex – hydroxide salt: magnesium hydroxide (milk of magnesia)
ex – carbonate salt: gaviscon (also a combo)
ex – combination products such as Maalox, mylanta (aluminum + magnesium)

95
Q

calcium salts

A

calcium salts
• many forms but carbonate is most common
• may cause constipation + kidney stones
• not recommended for pts w renal disease
• long duration of acid action – may cause hyperacidity rebound (increased gastric acid secretion); difficult to stop taking - body makes more acid and then you take more tums
• often advertised as an extra source of dietary calcium
ex – tums (calcium carbonate)

96
Q

histamine type 2 (h2) antagonists

A

• block histamine at the H2 receptod of acid-producing parietal cells; ∴ reduce acid secretion
• all available OTC in low doses
• most popular drugs for treatment of acid-related disorders
o cimetidine (tagamet)
o ranitidine (Zantac)
o famotidine (pepcid)
• smoking decreases effectiveness

97
Q

proton pump inhibitors

A

• irreversibly bind to H+/K+ ATPase enzyme
• ∴ prevents the mvmt of hydrogen ions from the parietal cell into the stomach
• results in achlorhydria (ALL gastric acid secretion is temporarily blocked until parietal cell synthesizes NEW H+/K+ ATPase)
• S/Es:
o safe for short-term; some approved for long-term
o increased risk of infection
o uncommon adverse effects
 occasional rebound gastrin prod.
ex – pantoprazole (protonix) (IV available)
ex – omeprazole (prilosec)
ex – lansoprazole (prevacid)
ex – rabeprazole (AcipHex)
ex – esomeprazole (Nexium)

98
Q

sucralfate (carafate)

A
  • cytoprotective
  • used for stress ulcers, peptic ulcer disease
  • attracted to + binds to the base of ulcers + erosions ∴ forming a protective barrier over these areas
  • protects these areas from pepsin which normally breaks down proteins + makes ulcers worse
99
Q

misoprostol (cytotec)

A

• synthetic prostaglandin analog
• prostaglandins have cytoprotective activity
o protect gastric mucosa from injury by enhancing local prod of mucus
o inhivits acid prod at higher doses
o promote local cell regeneration
o help to maintain mucosal blood flow
• used for prevention of NSAID-induced gastric ulcers
• doses that are therapeutic enough to treat duodenal ulcers often produce abdominal cramps + diarrhea

NURS 2514 (10 decks)

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