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elimination Flashcards

1
Q

slow transition time

A

constipation

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2
Q

fast transition time

A

diarrhea

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3
Q

GI tract

A

oral cavity to rectum

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4
Q

accessory organs

A

salivary glands, liver, gallbladder, pancreas

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5
Q

digestion functions

A

transport through peristalsis, absorb through vili and water, digest through HCL and bile

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6
Q

gastric pits

A

indented depressions where food comes in first that are lined with mucous cells

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7
Q

HCL acid production

A

made in the parietal cells

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8
Q

pepsinogen

A

come from chief cells, inactive form of pepsin

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9
Q

HCL production

A

stimulus from endocrine cells at bottom of gastric pit for parietal cells –> secrete gastrin and histamine–> gastrin stimulates parietal to pump out HCL–> histamine binds to receptor on parietal and we get more HCL

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10
Q

G cells

A

secrete gastrin and histamine

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11
Q

mucous cells

A

protect from gastric juices; mucous and bicarbonate

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12
Q

bicarbonate layer

A

non-existent in duodenum

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13
Q

G cell HCL positive feedback

A

G cells secrete gastrin –> parietal cells and histamine stimulated –> HCL production from cells –> proton pump releases HCL into stomach

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14
Q

Histamine HCL positive feedback

A

histamine released from G cells –> binds to H2 on parietal cells –> increased HCL production

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15
Q

GERD

A

reflux of gastric contents into esophagus due to weak lower esophageal sphincter; may also be caused by delayed gastric emptying due to overeating; common in pregnant and obese patients due to high amounts of pressure

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16
Q

PUD

A

failure of mucous/bicarbonate layer causing mucosal erosion

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17
Q

gastric ulcer

A

increased pain with eating, anorexia, weight loss is common, hematemesis; pain is more persistent

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18
Q

duodenal ulcer

A

more common; pain relieved by eating and may also be nocturnal, normal appetite, weight gain is common, melena stool

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19
Q

H.pylori infection

A

gram -; present in 90% of duodenal ulcers and 75% of gastric; synthesization of urase which produces ammonia causing gastric mucosa damage, and the response is inflammation

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20
Q

ways to diagnose H.pylori

A

blood in stool, ammonia breath test

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21
Q

NSAID’s as a cause of PUD

A

COX-2 inhibition and sometimes COX-1 which are protective prostaglandins of GI mucosa

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22
Q

H2 receptor antagonism MOA

A

antagonize H2 receptors so histamine does not stimulate HCL production

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23
Q

H2 receptor antagonists

A

“ine”; for gastric histamine, decrease HCL production

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24
Q

ranitidine (zantac), cimetidine (tagamet), famotidine (pepcid)

A

H2 receptor antagonists; quick relief, acute treatment

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25
ranitidine
does not cross BBB; no CNS effects
26
cimetidine, famotidine
will cross BBB; CNS side effects
27
proton pump inhibitors
"ole"; binds to enzymes to inhibit proton pump preventing HCL acid secretion
28
omeprazole (losec), lansoprazole (prevacid), pantoprazole (pantoloc)
proton pump inhibitors; higher efficacy than H2, longer half life, chronic relief, long onset of action
29
antacids
alkaline agents that increase stomach pH, symptom relief only, 2hrs post/pre other PO meds
30
aluminium hydroxide (amphojel)
may cause constipation
31
magnesium hydroxide (milk of magnesia)
may cause diarrhea
32
calcium carbonate (tums)
eventually will cause high calcium levels in bloodstream
33
pepto bismol
antidiarrheal; bismuth subsalicylate; belongs to same drug class as ASA meaning it can cause platelet inhibition
34
PUD 1st line therapy
amoxicillin (penicillin), clarithromycin (macrolide) but if allergic then tetracycline, metronidazole + PPI (omeprazole)
35
bismuth therapy for PUD
antibiotics + pepto bismol; helps inhibit bacterial growth and mucosal adhesion
36
small intestine
20ft long; duodenum (top), jejunum (middle), ileum (bottom); absorption of nutrients
37
large intestine
5ft long; ascending colon, transverse colon, descending colon, sigmoid colon; re-absorption of water through simple columnar cells
38
host flora in LI
vitamin B and K synthesis; not diet acquired
39
protein absorption
gastric pepsin breaks down proteins; pancreatic enzymes
40
carbohydrate absorption
amylase in saliva; pancreatic enzymes + brush border enzymes (convert glucose, galactose, and fructose)
41
fat absorption
digested by lingual lipase, bile, pancreatic lipase; turn to fatty acids
42
ANS bowel innervation
through sympathetic and parasympathetic; affects motility
43
enteric nervous system innervation
mechanoreceptors for stretch in GI, chemoreceptors for food presence
44
diarrhea
a symptom; acute or chronic
45
acute diarrhea
less than 2 weeks;more likely to be caused by infection
46
noninflammatory acute diarrhea
disruption of normal absorption or secretion; cramps, bloating, nausea, vomiting
47
inflammatory acute diarrhea
infectious; predominantly affect colon; fever, bloody, LLQ cramps, urgency, dehydration
48
chronic diarrhea
more likely to be caused by disease
49
complications of diarrhea
electrolyte imbalance, dehydration, malabsorption
50
IBS
caused by unknown physical markers, CNS dysregulation of normal motility
51
IBD diarrhea MOA
autoimmune disease; inflammation causes vasodilation which decreases absorption leading to watery stool
52
travelers diarrhea treatment
ciprofloxacin
53
ciprofloxacin
fluoroquinolone; treats travelers diarrhea; 70% bioavailable, little 1st pass metabolism, direct binding of bacteria in GI, phase 1 metabolism, CYP inhibitor, half life is 4 hours
54
C.diff treatment
metronidazole as first line and vancomycin (glycopeptide) as second line
55
probiotics
destroys bacteria by secreting toxic hydrogen peroxide; restores and protects normal flora
56
antidiarrheals
target Mu2 receptor in GI; opioids + atropine
57
antidiarrheal side effects
depression of ventilation, constipation
58
atropine
anticholinergic; blocks PNS causing less activity
59
Lomotil (diphenoxylate), Imodium, meperidine
antidiarrheals
60
hirschsprung disease
constipative disease; PNS ganglion cells in wall of large intestine do not develop before birth
61
bulk forming laxatives
pull water into stool and add bulk; most PO some PR
62
softener laxatives
pulls water and fat into stool; main use for post myocardial infarction or post surgery
63
saline and osmotic laxatives
pull water into stool
64
stimulant laxatives
increase peristalsis
65
miscellaneous laxatives
lubricating; should be used as an adjunct
66
Enema
fluid into intestine to expand bowel and evacuate contents; PR administration with patient lying on left side
67
metamucil (psyllium)
bulk forming laxative; prophylactic best, 1-2 days for effect, important to increase water intake
68
colace (docusate sodium)
softener laxative; PO or PR with local effects beginning after 1-3 days; prophylactic, decreased straining, need good renal function for excretion
69
milk of magnesia
saline & osmotic laxative; pre-procedural, potent, fast acting, renally excreted
70
lactulose
saline & osmotic laxative; decreases amount of ammonia in blood; also used for treatment and prevention of liver disease, slow onset
71
dulcolax, castor oil
stimulant laxative; side effects include N&V and cramping; not first choice in constipation
72
bloating
response to lack of enzymes; usually lack of digestion of polysaccharides
73
Gasex
treatment for bloating; enzymes to increase carbohydrate digestion
74
vomiting centre
in medulla outside of BBB; receives sensory pathway signals from all over body
75
drug as stimulus for vomiting
located in chemoreceptor trigger zone; targets D2 (dopamine) and 5HT (serotonin) receptors
76
motion/position as stimulus for vomiting
located in vestibular area; targets M (muscarinic) and H1 (histamine) receptors
77
visceral as stimulus for vomiting
located in organs; targets D2 and 5HT receptors
78
non-specific as stimulus for vomiting
located in CNS; targets CB1 (cannabinoid) receptors
79
dimenhydrinate, meclizine, diclectin
H1 antagonists as treatment for motion/morning N&V
80
ginger gravol
herbal therapy; increases intestinal peristalsis
81
antimuscarinic anticholinergics
N&V treatment with some affinity to H1 receptors; reduce vestibular excitation
82
scopolamine (hyoscine)
antimuscarinic anticholinergic; N&V treatment, transdermal, IV, PO
83
ondansetron
Zofran;serotonin antagonist as treatment for drug induced N&V; PO, IV
84
metoclopramide (maxeran), prochlorperazine (stemetil)
phenothiazine (stimulate GI motility); dopamine receptor antagonist as treatment for GI pain induced N&V; PO or IV, may cause sedation
85
dronabinol
CB1 & 2 agonists for chemotherapy induced N&V; cannabinoids, stimulation of GABA

nurs 216 (8 decks)

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