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.
2
Q
Define elimination
A
elimination: excretion of waste products primarily through the urinary + GI system
3
Q
Identify the 4 histological layers of the GI tract (from inside –> outside)
A
- mucosa
- submucosa
- muscularis externa
- serosa
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
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
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
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
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
9
Q
Which part of our body controls n + v?
A
The emetic center of the medulla
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
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
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]
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
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
15
Q
Which nerve / pathway is stimulated to result in vomiting in the digestive tract?
A
vagus nerve / serotonin-based pathway is stimulated
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
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
18
Q
Which 4 drug classes produce N + V as a side effect?
A
- chemotherapy
- alcohol
- opioids
- SSRIs
19
Q
Why is aspiration a potential complication of vomiting?
A
Vomiting can lead to the passage of gastric contents into airways
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
21
Q
What is alkaline tide?
A
loss of Hcl, K+, and increased production of HCO3- by gastric mucosa
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
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
24
Q
Provide an example of an anticholinergic drug.
A
Scopolamine (buscopan)
25
Describe the MOA of antihistamines (H1 receptor blockers) as antiemetic + antinausea drugs
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
26
Provide 2 examples of antihistamine drugs
dimenhydrinate (Dramamine, Gravol)
| diphenhydramine (Benadryl)
27
Describe the MOA of serotonin blockers as antinausea and antiemetic drugs
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
28
Provide 2 examples of serotonin blockers
dolasetron (Anzemet)
| ondansetron (Zofran)
29
What is the MOA of glucocorticoids as antinausea + antiemetic drugs?
used to treat N + V associated w some chemo drugs
increases antiemetic effect of serotonin blockers like ondansetron
can be combined w
30
What is the MOA of tetracannabinoids?
- used for n + v associated w chemo + anorexia associated w weight loss in aids pts
- increase appetite
31
provide an example of a tetracannabinoid
ex - cannabidoil (Sativex)
32
how can ginger (a herbal product) help treat n + v? what are some potential adverse effects? drug interactions?
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
33
What is diarrhea?
Having 3+ loose or liquid stools per day; having more stools than normal
34
What does diarrhea result from?
- 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)
35
Why does diarrhea lead to metabolic acidosis and hyperkalemia?
b/c GI secretions are rich in HCO3- and K+
36
What are the causes of diarrhea?
- 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
37
What are the 2 potential risks associated w diarrhea?
rapid dehydration + hypovolemic shock
38
describe the MOA of adsorbent drugs and provide an example
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
39
Describe the side effects of Bismuth subsalicylate (Pepto-Bismol)
- 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
40
provide 2 examples of antimotility drugs
anticholinergics + opioids
41
Describe anticholinergics as antimotility drugs and provide an example
- 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
Describe opiates as antimotility drugs and provide 2 examples
- 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
define constipation
infrequent or hard-to-pass bowel mvmts
44
what is obstipation?
failure to pass stools or gas
45
describe severe constipation
includes onstipation and fecal impaction, which can progress to bowel obtruction and become life threatening
46
what is primary / functional constipation?
idiopathic; ongoing symptoms of constipation > 6 mo w no other cause
47
which medication classes can cause constipation (7)?
1) antidepressants
2) anticonvulsants
3) antihistamines
4) diuretics
5) aluminum / calcium antacids
6) calcium channel blockers
7) opioids
48
identify the 6 metabolic + muscular causes of constipation
1) hypercalcemia
2) hypothyroidism
3) dm
4) cystic fibrosis
5) celiac disease
6) mucular dystrophy
49
identify the 5 structural + functional abnormalities that can result in constipation
1) spinal cord lesions
2) parkinson's
3) colon cancer
4) anal fissures
5) paralytic ileus
50
What is a common side effect across all 6 classes of laxatives?
electrolyte imbalances
51
describe the MOA of bulk forming laxatives and provide 2 examples
- high fiber
- absorb water to increase bulk
- distend bowel to initiate reflex bowel activity
- psyllium (Metamucil)
- methylcellulose (Citrucel)
52
describe the MOA of emollient laxatives and provide 2 examples
- 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
describe the moa of hyperosmotic drugs and provide 3 examples
- 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
describe the moa of saline drugs and provide an example
- 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
describe the moa of stimulant drugs and provide 2 examples
increases peristalsis via intestinal nerve stimulation
ex - senna
ex - bisacodyl (Dulcolax)
56
describe the MOA of peripherally acting opioid antagonists and provide 2 examples
- 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
identify 3 esophageal disorders
GERD
hiatal hernia
esophageal cancer
58
define GERD
condition where gastric contents move into the esophagus creating the sensation of heartburn and / or esophagitis
59
identify the potential causes of GERD
- 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
identify the clinical manifestations of GERD
- heartburn
| - respiratory symptoms due to aspiration of gastric content - coughing, wheezing, hoarseness
61
what is heartburn?
retrosternal or epigastric pain that can radiate to the throat, shoulders, or back, often confused w angina.
62
what are the chronic complications associated w GERD?
1 - esophageal stricture
2 - barrett's esophagus
3 - hiatal hernia
4 - hemorrhage + ulcerations
63
define esophageal stricture
narrowing of the esophagus caused by scar tissue formation, spasm, or edema
64
define Barrett's esophagus
replacement of the esophageal stratified squamous epithelium w simple columnar epithelium (so that it resembles the stomach and intestine)
65
what percentage of pts Barrett's esophagus develop esophageal cancer?
10%
66
What is a hiatal hernia
herniation of a portion of the stomach into the esophagus through the opening (hiatus) of the diaphragm
67
Identify the 2 types of hiatal hernia
sliding + rolling
68
Describe sliding hiatal hernias
gastro-esophageal junction slides above the hiatus of the diaphragm and part of the stomach slides into the hiatal opening
69
Describe rolling hiatal hernias
fundus of the stomach rolls up through the hiatus while the gastro-esophageal junction remains in place
70
describe the treatent methods for GERD
- 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
identify the 3 disorders of the stomach + upper SI
- gastritis (acute / chronic)
- upper GI bleeding
- peptic ulcer disease
72
Describe the anatomical difference between peptic ulcer disease and gastritis
both bleed
- gastritis has inflammation
- peptic ulcer disease has ulcers
73
Define peptic ulcer disease
ulcerative lesions caused by exposure of the GI mucosa to acid-pepsin secretions
74
How do acid-peptic diseases (like peptic ulcer disease) occur?
- 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
identify the 2 most common locations for a peptic ulcer to occur
stomach + duodenum
76
identify the 2 most common causes of peptic ulcer formation
- helicobacter pylori infection
- NSAID use
b/c they both destroy the mucus barrier
77
why is NSAID use a cause of peptic ulcer formation?
NSAIDs block the action of prostaglandins, which are used to tell cells to secrete protective mucus in the stomach
78
identify the 5 contributing factors of peptic ulcer formation
- diet
- alcohol
- smoking
- stress
- zollinger-ellison syndrome (gastrin secreting tumor)
79
identify the 4 clinical manifestations of peptic ulcer disease
1) pain
2) hemorrhage
3) obstruction
4) perforation
80
describe pain as a clinical manifestation of peptic ulcer disease
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
describe hemorrhage as a clinical manifestation of peptic ulcer disease
hematemesis, melena, or occult blood; anemia or hypovolemia can occur if severe
82
describe obstruction as a clinical manifestation of peptic ulcer disease. what causes it?
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
describe perforation as a manifestation of peptic ulcer disease
peptic ulcer erodes through the GI wall which allows gastric juice + air to enter the peritoneum
causes peritonitis and possibly pancreatitis
84
which drug classes are used to treat peptic ulcer disease?
antisecretory drugs (H2 receptor blockers, proton pump inhibitors)
antisecretory + cytoprotective drugs
neutralizing drugs (antacids)
antibiotics for h pylori
tricyclic antidepressants
85
what are the postoperative complications associated with surgical therapy for peptic ulcer disease?
dumping syndrome
postprandial hypoglycemia
bile reflux gastritis
86
define gastritis. what does chronic gastritis increase the risk of?
inflamed stomach mucosa
chronic gastritis increases the risk of peptic ulcers + stomach cancer
87
identify the 7 causes of gastritis
```
alcoholism
nsaids
portal hypertension induced gastropathy
h pylori infection
crohn's disease
pernicious anemia (autoimmune destruction of intrinsic factor)
stress
```
88
describe stress related gastritis. what are the major risk factors?
occurs commonly in critically-ill hospitalized pts
major risk factors:
- trauma
- burns
- hypotension
- sepsis
- coagulopathy
- hepatic or renal failure
- mechanical ventilation
89
what are the clinical manifestations of gastritis?
often asymptomatic
dyspepsia, n + v
hematemesis + GI bleeding
90
identify and describe the 2 types of upper GI bleeding
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
identify the 3 classes of acid controlling drugs
antacids
h2 antagonists
proton pump inhibitors
92
describe the MOA of antacids (aluminum salts, mg salts, calcium salts, sodium bicarbonate)
neutralize stomach acid + promote gastric mucosal defense mechanisms including the secretion of mucus, bicarbonate, + prostaglandins
93
aluminum salts
* 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
magnesium salts
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
calcium salts
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
histamine type 2 (h2) antagonists
• 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
proton pump inhibitors
• 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
sucralfate (carafate)
* 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
misoprostol (cytotec)
• 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
