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Patho II > Alterations of Digestive Function > Flashcards

Alterations of Digestive Function Flashcards

1
Q

anorexia

A
  • loss of appetite
  • lack of desire to eat, despite physiological stimuli that would normally produce hunger
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2
Q

vomiting

A

forceful emptying of the stomach and intestinal contents through the mouth

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3
Q

vomiting center

A

medulla oblongata

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4
Q

vomiting can lead to

A

fluid, electrolyte, and acid-base disturbances, hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis b/c of loss of stomach acids

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5
Q

retching

A

vomiting without expulsion of vomitus

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5
Q

common symptoms of nausea

A

hypersalivation & tachycardia

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6
Q

projectile vomiting

A

spontaneous vomiting that does not follow nausea or retching

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7
Q

normal transit (functional) constipation

A

normal rate of stool passage but difficulty with stool evacuation from low-residue, low-fluid diet

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8
Q

slow-transit constipation

A

impaired colonic motor activity with infrequent bowel movements and straining

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9
Q

pelvic floor dysfunction (pelvic floor dyssynergia or animus)

A

failure of the pelvic floor muscles to the anal sphincter to relax with defecation

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10
Q

clinical manifestations of constipation

A

at least 2 of the following:
- straining with defecation at least 25% of the time
- lumpy or hard stools at least 25% of the time
- sensation of incomplete emptying at least 25% of the time
- manual maneuvers to facilitate stool evacuation for at least 25% of defecations
- fewer than 3 bowel movements per week

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11
Q

fecal impaction

A

hard, dry stool retained in rectum

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12
Q

normal bower movements occur how often

A

2 or 3 per day to 1 per week

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13
Q

treatment of constipation

A
  • bowel retraining
  • moderate exercise
  • increased fluid and fiber intake
  • enemas (should not be habitually used)
  • dyssynergic defecation: “biofeedback”
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14
Q

drugs to treat constipation

A
  • colonic secretagogues lubiprostone
  • plecanatide
  • 5-HT4 agonist
  • prucalopride
  • methylnaltrexone: for opioid-induced constipation in individuals who are terminally ill
  • stool softeners and laxatives
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15
Q

Diarrhea is defined as having increased frequency of bowel movements; ___ or more per day

A

3

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16
Q

___ volume, ____, weight of feces

A

increased; fluidity

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17
Q

3 types of diarrhea

A

osmotic, secretory, motility

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17
Q

osmotic diarrhea

A

nonabsorbable substance in the intestine draws water into the lumen by osmosis, causing large-volume diarrhea

exp. lactose intolerance

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18
Q

secretory diarrhea

A

form of large-volume diarrhea caused by excessive mucosal secretion of chloride or bicarbonate-rich fluid or the inhibition of net sodium absorption

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19
Q

motility diarrhea

A

excessive motility decreases transit time, mucosal surface contact, and opportunities for fluid absorption

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20
Q

clinical manifestations fo diarrhea

A

dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss

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21
Q

Treatment fo diarrhea

A
  • restore fluid and electrolyte balance
  • medications: anti-motility (loperamide, or atropine) and or water absorbent (attapulgite and polycarbophil)
  • mild diarrhea: natural bran and psyllium
  • C. Diff associated diarrhea: probiotics
  • fecal transplatation
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22
Q

manifestations of acute bacterial or viral infection r/t diarrhea

A

fever with or without cramping

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23
Q

manifestations of malabsorption syndromes r/t diarrhea

A

steatorrhea (fat in the stools) and diarrhea

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24
Q

manifestations of inflammatory bowel dx r/t diarrhea

A

fever, cramping pain, bloody stools

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25
Q

abdominal pain

A

symptom of a number of GI disorders
from stretching, inflammation, or ischemia

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26
Q

parietal (somatic) pain

A

in the peritoneum

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27
Q

visceral pain

A

in the organs themselves

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28
Q

referred pain

A

felt in another area, usually the back

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29
Q

biochemical mediators of the ___ response (histamins, ___, and serotonin) stimulate ___ nerve endings, producing abdominal pain

A

inflammatory; bradykinin; pain

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29
Q

upper GI bleeding

A
  • from the esophagus, stomach, or duodenum
  • frank, bright red bleeding in emesis or digested blood (“coffee grounds”) in stool
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30
Q

lower Gi bleeding

A

from the jejunum, ileum, colon, or rectum

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31
Q

treatment of GI bleeding

A

blood products!!

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31
Q

hematemsis

A

bloody vomit

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32
Q

melena

A

black, tarry stools

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33
Q

hematochezia

A

bloody stools

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34
Q

occult bleeding

A

not visible form the outside

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35
Q

dyphagia

A

difficulty swallowing

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36
Q

types of dyphagia

A
  • mechanical obstructions of the esophagus
  • functional obstruction of esophageal motility
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37
Q

Achalasia (lack of LES)

A
  • denervation of SM in the esophagus and lack of LES relaxation
    -propensity for esophageal cancer
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38
Q

treatment of achalasia

A

dilation or surgical myotomy of the LES, helps with LES relexation

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39
Q

clinical manifestations of upper esophageal obstruction

A

discomfort 2-4 seconds after swallowing

40
Q

clinical manifestations of lower esophageal obstruction

A

discomfort occurring 10-15 seconds after swallowing

41
Q

all types of clinical manifestations of dysphagia

A

retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, and weight loss* very common clinical manifestation

42
Q

dysphagia treatment:

A
  • eating slowly, eating small meals, taking fluid with meals, and sleeping with the head of the bed elevated
  • oral meds: may need to be formulated to facilitate swallowing
  • tube feeding, particularly after a stroke
  • anticholinergic drugs: may alleviate symptoms
  • mechanical dilation of the esophageal sphincter and surgical separation of the LE muscles with a longitudinal incision (myotomy) widening the passage into the stomach
43
Q

GERD

A
  • acid and pepsin refluxe from the stomach into the esophagus, causing esophagitis
  • resting tone of the LES tends to be lower than normal from either transient relaxation or weakness of the sphincter
  • conditions that increase abd pressure can contribute to GERD –> vomiting, coughing, lifting, bending, obesity
44
Q

clinical manifestations fo GERD

A

heartburn from acid regurgitation, chronic cough, laryngitis, upper abd pain within 1 hour of eating

45
Q

evaluation of GERD

A

biopsy: dysplastic changes (Barrett esophagus)

changes in the epithelial cells of the esophagus d/t reflux

45
Q

treatment of GERD

A
  • PPIs: most effective
  • Histamine H2 antagonists, prokinetic agents, and antacids; pain meds
  • elevate HOB 6 inches; reduce weight; stop smoking
  • surgery: laparoscopic fundoplication
46
Q

Hiatal hernia

A

protrusion (herniation) of the upper part of the stomach through the diaphragm and into the throax

47
Q

pyloric (gastric outlet) obstruction

A

blocking or narrowing of the opening between the stomach and duodenum

effects gastric emptying

48
Q

intestinal obstruction

A

any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion

49
Q

small intestine obstruction

A

most common: fibrous adhesions

50
Q

large bowel obstruction

A
  • most common: colorectal cancer, volvulus (twisting), and strictures r/t diverticulitis
  • acute colonic pseudo-obstruction (Ogilvie syndrome): massive dilation of the large bowel; patients who are critically ill and older adults who are immobilized
51
Q

Gatritis

A
  • inflammatory disorder of the gastric mucosa
  • acute gastritis: associated with helicobacter pylori, NSAIDs, drugs, chemicals
52
Q

chronic fundal gastritis

A
  • immune reactions
  • type A
  • associated with autoantibodies to parietal cells and intrinsic factor, resulting in gastric atrophy and pernicious anemia
53
Q

chronic antral gastritis

A
  • nonimmune
  • type B
  • associated with H. pylori and NSAIDs
54
Q

Peptic ulcer disease

A

break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum

acute vs. chronic ulcers

superficial erosions vs. deep

55
Q

risk factors of PUD

A
  • genetic predisposion
  • H. pylori infection
  • habitual use of NSAIDs
  • excessive use of alcohol, smoking, acute pancreatitis, COPD, obesity, cirrhosis, and over 65 years of age
56
Q

what is the most common of the peptic ulcers?

A

duodenal*

57
Q

developmental factors of duodenal ulcers

A
  • increased # of parietal cells
  • high gastrin levels
  • rapid gastric emptying –> acidic chyme into the duodenum
  • acid production cause by cigarette smoking
58
Q

clinical manifestations of duodenal ulcers

A
  • chronic intermittent pain in the epigastric area
  • pain begins 30 mins to 2 hours after eating when the stomach is empty
  • pain is relieved by food
59
Q

treatment of duodenal ulcers

A
  • antacids: to neutralize gastric contents, elevate pH, inactivate pepsin, and relieve pain
  • PPIs/anticholinergic drugs: to suppress acid secretion
  • Bismuth and combinations of abx, sump with vit C: to eradicate H. pylori
  • sucralfate and colloidal bismuth: to coat ulcer
  • surgical resection
60
Q

risk of duodenal ulcer may be reduced with a diet high in

A

vitamin A and fiber

61
Q

gastric ulcer

A

tends to develop in the antral region of the stomach, adjacent to the acid-secreting mucous of the body

62
Q

pathophys of gastric ulcer

A
  • frequent cause: H. pylori
  • primary defect: increased mucosal permeability to hydrogen ions (making a whole ulcer)
  • gastric secretion: normal or less than normal
63
Q

clinical manifestations of gastric ulcer

A

pain occurs immediately after eating
tends to be chronic
anorexia, vomiting, and weight loss

64
Q

treatment of gastric ulcer

A

same as duodenal ulcer

65
Q

Malabsorption syndrome

A

interfere with nutrient absorption
maldigestion: failure of the chemical processes of digestion
malabsorption: failure of the intestinal mucosa to absorb (transport) the digested nutrients

66
Q

pancreatic insufficiency

A

insufficient pancreatic enzyme production: lipase, amylase, trypsin, or chymotrypsin

67
Q

causes of pancreatic insufficiency

A

pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis

68
Q

primary problem of pancreatic insufficiency

A

fat maldigestion

69
Q

most common signs of pancreatic insufficiency

A

fatty stools (steatorrhea) weight loss

70
Q

Treatment of pancreatic insufficiency

A

lipase supplements

71
Q

lactase deficiency

A
  • congenital defet on the lactase gene
  • inability to breakdown lactose into monosaccharides and thus prevent lactose digestion and monosaccharide absorption
  • fermentation of lactose by bacteria, causing gas (cramping pain, flatulence) and osmotic diarrhea
72
Q

treatment of lactase deficiency

A
  • avoidance of milk products; adherence to a lactose-free diet
  • maintenance of adequate calcium intake to decrease risk of osteoporosis
72
Q

bile salt deficiency

A
  • conjugated bile salts are needed to emulsify and absorb fats and are synthesized from cholesterol in the liver
  • is the result of liver dx and bile obstructions
  • poor intestinal absorption of lipids causes fatty stools, diarrhea, and loss of fat-soluble vitamins (A, D, E, K)
73
Q

treatment of bile salt deficiency

A
  • increase medium-chain triglycerides in the diet
  • parenterally administer vitamins A, D, and K
74
Q

Fat-soluble vitamin deficiences

A

A, D, K, E

75
Q

Vitamin A deficiency is associated with

A

night blindness

76
Q

Vitamin D deficiency is associated with

A

decreased calcium absorption, bone pain, osteoporosis, fractures

76
Q

Vitamin K deficiency is associated with

A

prolonged prothrombin time, purpura, and petechiae

77
Q

Vitamin E deficiency is associated with

A

testicular atrophy, neurological defects in children

78
Q

inflammatory bowel diseases

A

chronic, relapsing inflammatory bowel disorders of “unknown” origin –> genetics, alterations of epithelial barrier functions, immune reactions to intestinal flora (bacteria), abnormal T-cell responses (immune)

exp. ulcerative colitis, chrons dx

79
Q

ulcerative colitis

A

is a *chronic inflammatory disease that causes ulceration of the colonic mucosa (sigmoid colon and rectum)

80
Q

UC is common in those of what age and what descent?

A

20 to 40 years old
jewish

81
Q

suggested causes of UC

A

infectious, immunologic (anti-colon antibodies), dietary, genetics

82
Q

pathophys of UC

A

lesions are continuous with NO skipped lesions, are limited to the mucosa, and are NOT transmural

83
Q

clinicla manifestaions of UC

A
  • diarrhea (10 to 20 BMs per day), bloody stools, cramps
  • remission and exacberations
84
Q

treatment of UC

A
  • first-line therapy: 5- aminosalicylic acid (mesalazine)
  • steroids and salicylate
  • immunosuppressive agents
  • broad spectrum abx
  • surgery: resection of the colon or a colostomy

increased risk for colon ca is demonstrated

85
Q

Crohn disease

A
  • granulomatous colitis, ileocolitis, or regional enteritis
  • idiopathic inflammatory disorder; affects any part of the digestive tract, from mouth to anus
  • difficult to differentiate from UC (similar risk factors and theories of causation)
  • strong association –> nucleotide-binding oligomerization domains (CARD15/NOD2) gene mutations
86
Q

Crohn dx causes __ lesions

A

“skip”

87
Q

Crohn dx ulcerations are __ and __ inflammatory fissures extend into lymphoid tissue

A

longitudinal; transverse

produce a “cobblestone” appearence

88
Q

clinical manifestations of Crohn’s

A
  • abd pain and diarrhea are the most common signs; more than 5 stools per day
  • anemia may develop as a result of malabsorption of vitamin B12 and folic acid
89
Q

treatment of Crohn’s

A
  • similar to UC
  • immunomodulatory agents
  • TNF- alpha-blocking agents: to treat fistulas and maintain remission
  • surgery: complication –> short bowel syndrome with malabsorption, diarrhea, and nutritional deficiencies
90
Q

what supplies blood to the stomach and intestine?

A

celiac artery, SMA, IMA

91
Q

intestinal vascular insufficiency

A
  • mesenteric venous thrombosis
  • chronic mesenteric insufficiency
  • acute mesenteric ischemia
92
Q

clinical manifestations of intestinal vascular insufficiency

A
  • abd pain, fever, bloody diarrhea, hypovolemia, and shock
93
Q

treatment of intestinal vascular insufficiency

A
  • abx, anticoagulation, vasodilators, and inhibitors of reperfusion injury, surgery
94
Q
A
94
Q
A
95
Q
A
96
Q
A
97
Q
A

Patho II (5 decks)

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