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nurs 216 > elimination > Flashcards

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
Q

ranitidine

A

does not cross BBB; no CNS effects

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26
Q

cimetidine, famotidine

A

will cross BBB; CNS side effects

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27
Q

proton pump inhibitors

A

“ole”; binds to enzymes to inhibit proton pump preventing HCL acid secretion

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28
Q

omeprazole (losec), lansoprazole (prevacid), pantoprazole (pantoloc)

A

proton pump inhibitors; higher efficacy than H2, longer half life, chronic relief, long onset of action

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29
Q

antacids

A

alkaline agents that increase stomach pH, symptom relief only, 2hrs post/pre other PO meds

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30
Q

aluminium hydroxide (amphojel)

A

may cause constipation

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31
Q

magnesium hydroxide (milk of magnesia)

A

may cause diarrhea

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32
Q

calcium carbonate (tums)

A

eventually will cause high calcium levels in bloodstream

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33
Q

pepto bismol

A

antidiarrheal; bismuth subsalicylate; belongs to same drug class as ASA meaning it can cause platelet inhibition

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34
Q

PUD 1st line therapy

A

amoxicillin (penicillin), clarithromycin (macrolide) but if allergic then tetracycline, metronidazole + PPI (omeprazole)

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35
Q

bismuth therapy for PUD

A

antibiotics + pepto bismol; helps inhibit bacterial growth and mucosal adhesion

36
Q

small intestine

A

20ft long; duodenum (top), jejunum (middle), ileum (bottom); absorption of nutrients

37
Q

large intestine

A

5ft long; ascending colon, transverse colon, descending colon, sigmoid colon; re-absorption of water through simple columnar cells

38
Q

host flora in LI

A

vitamin B and K synthesis; not diet acquired

39
Q

protein absorption

A

gastric pepsin breaks down proteins; pancreatic enzymes

40
Q

carbohydrate absorption

A

amylase in saliva; pancreatic enzymes + brush border enzymes (convert glucose, galactose, and fructose)

41
Q

fat absorption

A

digested by lingual lipase, bile, pancreatic lipase; turn to fatty acids

42
Q

ANS bowel innervation

A

through sympathetic and parasympathetic; affects motility

43
Q

enteric nervous system innervation

A

mechanoreceptors for stretch in GI, chemoreceptors for food presence

44
Q

diarrhea

A

a symptom; acute or chronic

45
Q

acute diarrhea

A

less than 2 weeks;more likely to be caused by infection

46
Q

noninflammatory acute diarrhea

A

disruption of normal absorption or secretion; cramps, bloating, nausea, vomiting

47
Q

inflammatory acute diarrhea

A

infectious; predominantly affect colon; fever, bloody, LLQ cramps, urgency, dehydration

48
Q

chronic diarrhea

A

more likely to be caused by disease

49
Q

complications of diarrhea

A

electrolyte imbalance, dehydration, malabsorption

50
Q

IBS

A

caused by unknown physical markers, CNS dysregulation of normal motility

51
Q

IBD diarrhea MOA

A

autoimmune disease; inflammation causes vasodilation which decreases absorption leading to watery stool

52
Q

travelers diarrhea treatment

A

ciprofloxacin

53
Q

ciprofloxacin

A

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
Q

C.diff treatment

A

metronidazole as first line and vancomycin (glycopeptide) as second line

55
Q

probiotics

A

destroys bacteria by secreting toxic hydrogen peroxide; restores and protects normal flora

56
Q

antidiarrheals

A

target Mu2 receptor in GI; opioids + atropine

57
Q

antidiarrheal side effects

A

depression of ventilation, constipation

58
Q

atropine

A

anticholinergic; blocks PNS causing less activity

59
Q

Lomotil (diphenoxylate), Imodium, meperidine

A

antidiarrheals

60
Q

hirschsprung disease

A

constipative disease; PNS ganglion cells in wall of large intestine do not develop before birth

61
Q

bulk forming laxatives

A

pull water into stool and add bulk; most PO some PR

62
Q

softener laxatives

A

pulls water and fat into stool; main use for post myocardial infarction or post surgery

63
Q

saline and osmotic laxatives

A

pull water into stool

64
Q

stimulant laxatives

A

increase peristalsis

65
Q

miscellaneous laxatives

A

lubricating; should be used as an adjunct

66
Q

Enema

A

fluid into intestine to expand bowel and evacuate contents; PR administration with patient lying on left side

67
Q

metamucil (psyllium)

A

bulk forming laxative; prophylactic best, 1-2 days for effect, important to increase water intake

68
Q

colace (docusate sodium)

A

softener laxative; PO or PR with local effects beginning after 1-3 days; prophylactic, decreased straining, need good renal function for excretion

69
Q

milk of magnesia

A

saline & osmotic laxative; pre-procedural, potent, fast acting, renally excreted

70
Q

lactulose

A

saline & osmotic laxative; decreases amount of ammonia in blood; also used for treatment and prevention of liver disease, slow onset

71
Q

dulcolax, castor oil

A

stimulant laxative; side effects include N&V and cramping; not first choice in constipation

72
Q

bloating

A

response to lack of enzymes; usually lack of digestion of polysaccharides

73
Q

Gasex

A

treatment for bloating; enzymes to increase carbohydrate digestion

74
Q

vomiting centre

A

in medulla outside of BBB; receives sensory pathway signals from all over body

75
Q

drug as stimulus for vomiting

A

located in chemoreceptor trigger zone; targets D2 (dopamine) and 5HT (serotonin) receptors

76
Q

motion/position as stimulus for vomiting

A

located in vestibular area; targets M (muscarinic) and H1 (histamine) receptors

77
Q

visceral as stimulus for vomiting

A

located in organs; targets D2 and 5HT receptors

78
Q

non-specific as stimulus for vomiting

A

located in CNS; targets CB1 (cannabinoid) receptors

79
Q

dimenhydrinate, meclizine, diclectin

A

H1 antagonists as treatment for motion/morning N&V

80
Q

ginger gravol

A

herbal therapy; increases intestinal peristalsis

81
Q

antimuscarinic anticholinergics

A

N&V treatment with some affinity to H1 receptors; reduce vestibular excitation

82
Q

scopolamine (hyoscine)

A

antimuscarinic anticholinergic; N&V treatment, transdermal, IV, PO

83
Q

ondansetron

A

Zofran;serotonin antagonist as treatment for drug induced N&V; PO, IV

84
Q

metoclopramide (maxeran), prochlorperazine (stemetil)

A

phenothiazine (stimulate GI motility); dopamine receptor antagonist as treatment for GI pain induced N&V; PO or IV, may cause sedation

85
Q

dronabinol

A

CB1 & 2 agonists for chemotherapy induced N&V; cannabinoids, stimulation of GABA

nurs 216 (8 decks)

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