Alterations of Digestive Function Flashcards
anorexia
- loss of appetite
- lack of desire to eat, despite physiological stimuli that would normally produce hunger
vomiting
forceful emptying of the stomach and intestinal contents through the mouth
vomiting center
medulla oblongata
vomiting can lead to
fluid, electrolyte, and acid-base disturbances, hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis b/c of loss of stomach acids
retching
vomiting without expulsion of vomitus
common symptoms of nausea
hypersalivation & tachycardia
projectile vomiting
spontaneous vomiting that does not follow nausea or retching
normal transit (functional) constipation
normal rate of stool passage but difficulty with stool evacuation from low-residue, low-fluid diet
slow-transit constipation
impaired colonic motor activity with infrequent bowel movements and straining
pelvic floor dysfunction (pelvic floor dyssynergia or animus)
failure of the pelvic floor muscles to the anal sphincter to relax with defecation
clinical manifestations of constipation
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
fecal impaction
hard, dry stool retained in rectum
normal bower movements occur how often
2 or 3 per day to 1 per week
treatment of constipation
- bowel retraining
- moderate exercise
- increased fluid and fiber intake
- enemas (should not be habitually used)
- dyssynergic defecation: “biofeedback”
drugs to treat constipation
- colonic secretagogues lubiprostone
- plecanatide
- 5-HT4 agonist
- prucalopride
- methylnaltrexone: for opioid-induced constipation in individuals who are terminally ill
- stool softeners and laxatives
Diarrhea is defined as having increased frequency of bowel movements; ___ or more per day
3
___ volume, ____, weight of feces
increased; fluidity
3 types of diarrhea
osmotic, secretory, motility
osmotic diarrhea
nonabsorbable substance in the intestine draws water into the lumen by osmosis, causing large-volume diarrhea
exp. lactose intolerance
secretory diarrhea
form of large-volume diarrhea caused by excessive mucosal secretion of chloride or bicarbonate-rich fluid or the inhibition of net sodium absorption
motility diarrhea
excessive motility decreases transit time, mucosal surface contact, and opportunities for fluid absorption
clinical manifestations fo diarrhea
dehydration, electrolyte imbalance (hyponatremia, hypokalemia), metabolic acidosis, and weight loss
Treatment fo diarrhea
- 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
manifestations of acute bacterial or viral infection r/t diarrhea
fever with or without cramping
manifestations of malabsorption syndromes r/t diarrhea
steatorrhea (fat in the stools) and diarrhea
manifestations of inflammatory bowel dx r/t diarrhea
fever, cramping pain, bloody stools
abdominal pain
symptom of a number of GI disorders
from stretching, inflammation, or ischemia
parietal (somatic) pain
in the peritoneum
visceral pain
in the organs themselves
referred pain
felt in another area, usually the back
biochemical mediators of the ___ response (histamins, ___, and serotonin) stimulate ___ nerve endings, producing abdominal pain
inflammatory; bradykinin; pain
upper GI bleeding
- from the esophagus, stomach, or duodenum
- frank, bright red bleeding in emesis or digested blood (“coffee grounds”) in stool
lower Gi bleeding
from the jejunum, ileum, colon, or rectum
treatment of GI bleeding
blood products!!
hematemsis
bloody vomit
melena
black, tarry stools
hematochezia
bloody stools
occult bleeding
not visible form the outside
dyphagia
difficulty swallowing
types of dyphagia
- mechanical obstructions of the esophagus
- functional obstruction of esophageal motility
Achalasia (lack of LES)
- denervation of SM in the esophagus and lack of LES relaxation
-propensity for esophageal cancer
treatment of achalasia
dilation or surgical myotomy of the LES, helps with LES relexation
clinical manifestations of upper esophageal obstruction
discomfort 2-4 seconds after swallowing
clinical manifestations of lower esophageal obstruction
discomfort occurring 10-15 seconds after swallowing
all types of clinical manifestations of dysphagia
retrosternal pain, regurgitation of undigested food, unpleasant taste, vomiting, and weight loss* very common clinical manifestation
dysphagia treatment:
- 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
GERD
- 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
clinical manifestations fo GERD
heartburn from acid regurgitation, chronic cough, laryngitis, upper abd pain within 1 hour of eating
evaluation of GERD
biopsy: dysplastic changes (Barrett esophagus)
changes in the epithelial cells of the esophagus d/t reflux
treatment of GERD
- PPIs: most effective
- Histamine H2 antagonists, prokinetic agents, and antacids; pain meds
- elevate HOB 6 inches; reduce weight; stop smoking
- surgery: laparoscopic fundoplication
Hiatal hernia
protrusion (herniation) of the upper part of the stomach through the diaphragm and into the throax
pyloric (gastric outlet) obstruction
blocking or narrowing of the opening between the stomach and duodenum
effects gastric emptying
intestinal obstruction
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
small intestine obstruction
most common: fibrous adhesions
large bowel obstruction
- 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
Gatritis
- inflammatory disorder of the gastric mucosa
- acute gastritis: associated with helicobacter pylori, NSAIDs, drugs, chemicals
chronic fundal gastritis
- immune reactions
- type A
- associated with autoantibodies to parietal cells and intrinsic factor, resulting in gastric atrophy and pernicious anemia
chronic antral gastritis
- nonimmune
- type B
- associated with H. pylori and NSAIDs
Peptic ulcer disease
break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum
acute vs. chronic ulcers
superficial erosions vs. deep
risk factors of PUD
- 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
what is the most common of the peptic ulcers?
duodenal*
developmental factors of duodenal ulcers
- increased # of parietal cells
- high gastrin levels
- rapid gastric emptying –> acidic chyme into the duodenum
- acid production cause by cigarette smoking
clinical manifestations of duodenal ulcers
- 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
treatment of duodenal ulcers
- 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
risk of duodenal ulcer may be reduced with a diet high in
vitamin A and fiber
gastric ulcer
tends to develop in the antral region of the stomach, adjacent to the acid-secreting mucous of the body
pathophys of gastric ulcer
- frequent cause: H. pylori
- primary defect: increased mucosal permeability to hydrogen ions (making a whole ulcer)
- gastric secretion: normal or less than normal
clinical manifestations of gastric ulcer
pain occurs immediately after eating
tends to be chronic
anorexia, vomiting, and weight loss
treatment of gastric ulcer
same as duodenal ulcer
Malabsorption syndrome
interfere with nutrient absorption
maldigestion: failure of the chemical processes of digestion
malabsorption: failure of the intestinal mucosa to absorb (transport) the digested nutrients
pancreatic insufficiency
insufficient pancreatic enzyme production: lipase, amylase, trypsin, or chymotrypsin
causes of pancreatic insufficiency
pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis
primary problem of pancreatic insufficiency
fat maldigestion
most common signs of pancreatic insufficiency
fatty stools (steatorrhea) weight loss
Treatment of pancreatic insufficiency
lipase supplements
lactase deficiency
- 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
treatment of lactase deficiency
- avoidance of milk products; adherence to a lactose-free diet
- maintenance of adequate calcium intake to decrease risk of osteoporosis
bile salt deficiency
- 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)
treatment of bile salt deficiency
- increase medium-chain triglycerides in the diet
- parenterally administer vitamins A, D, and K
Fat-soluble vitamin deficiences
A, D, K, E
Vitamin A deficiency is associated with
night blindness
Vitamin D deficiency is associated with
decreased calcium absorption, bone pain, osteoporosis, fractures
Vitamin K deficiency is associated with
prolonged prothrombin time, purpura, and petechiae
Vitamin E deficiency is associated with
testicular atrophy, neurological defects in children
inflammatory bowel diseases
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
ulcerative colitis
is a *chronic inflammatory disease that causes ulceration of the colonic mucosa (sigmoid colon and rectum)
UC is common in those of what age and what descent?
20 to 40 years old
jewish
suggested causes of UC
infectious, immunologic (anti-colon antibodies), dietary, genetics
pathophys of UC
lesions are continuous with NO skipped lesions, are limited to the mucosa, and are NOT transmural
clinicla manifestaions of UC
- diarrhea (10 to 20 BMs per day), bloody stools, cramps
- remission and exacberations
treatment of UC
- 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
Crohn disease
- 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
Crohn dx causes __ lesions
“skip”
Crohn dx ulcerations are __ and __ inflammatory fissures extend into lymphoid tissue
longitudinal; transverse
produce a “cobblestone” appearence
clinical manifestations of Crohn’s
- 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
treatment of Crohn’s
- 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
what supplies blood to the stomach and intestine?
celiac artery, SMA, IMA
intestinal vascular insufficiency
- mesenteric venous thrombosis
- chronic mesenteric insufficiency
- acute mesenteric ischemia
clinical manifestations of intestinal vascular insufficiency
- abd pain, fever, bloody diarrhea, hypovolemia, and shock
treatment of intestinal vascular insufficiency
- abx, anticoagulation, vasodilators, and inhibitors of reperfusion injury, surgery
