GI Alterations Flashcards
lack of desire to eat despite physiologic stimuli that would normally produce hunger
nonspecific symptom that is often associated with nausea, abdominal pain, diarrhea, and psychologic distress
anorexia
_____ is a subjective experience, and associated symptoms are tachycardia and hypersalivation
nausea
metabolic consequences of vomiting
hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis
projectile vomiting is spontaneous vomiting that ____ follow nausea or retching and what is the cause?
does not follow nausea or retching
cause by direct stimulation of the vomiting center (medulla oblongata) by neurologic lesions – increased ICP, tumors, brain stem aneurysms – neuro problems
different types of constipation
normal transit (functional) constipation: normal function but decreased evacuation d/t low-residue (low fiber), low-fluid diet
slow-transit constipation: impaired colonic motor activity
pelvic floor dysfunction: failure of the pelvic floor muscles or anal sphincter to relax with defecation (pelvic floor dyssynergia or animus)
secondary: from an actual disease process, condition, or med
Diagnosis of constipation
Two of the following for at least 3 months
• 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 three bowel movements per week
large volume diarrhea cause
volume of feces is increased – caused by excessive amounts of water or secretions or both in the intestines
small volume diarrhea cause
volume of feces is not increased - result of increased intestinal motility
systemic effects of diarrhea
dehydration, electrolyte imbalance, metabolic acidosis (loss of sodium bicarb), and weight loss
_____ and ______ are common signs of malabsorption syndromes
diarrhea and steatorrhea (fat in stool)
types of diarrhea - osmotic, secretory, motility
osmotic draws water in by osmosis (non-absorbable substance like with lactose deficiency, magnesium sulfate, magnesium phosphate)
secretory forms large volume diarrhea caused by excessive mucosal secretion of chloride or bicarb-rich fluid or the inhibition of net sodium absorption (bacterial enterotoxins like E.coli)
motility - excessive motility decreases transit time, mucosal surface contact, and opportunities for fluid absorption (resection of SI, short bowel syndrome, abnormal fistula)
black, tarry stools could be d/t
upper GI bleed, pepto bismol intake, increased iron intake
frothy, fatty, pale (steatorrhea)
problems w/fat digestion, children w/CF, adults with pancreatic disease or cholecystitis – indicates loss of bile needed for fat digestion
remember that light or clay-colored stools due to decrease in conjugated bilirubin and bile (gallbladder or liver disease)
parietal (somatic) pain
in the peritoneum
localized, intense, sharp
mechanical obstruction of the esophagus
intrinsic - in wall of the esophageal lumen (tumors, strictures, diverticular herniations)
vs extrinsic - outside esophageal lumen and narrow esophagus by pressing inward (tumors)
clinical manifestations of dysphagia…difficulty beginning with both solids and liquids
neuromotor function loss
resting tone of the lower sphincter LES tends to be lower than normal from transient relaxation or weakness
GERD
risk factors for GERD
H.pylori, obesity
GERD that does not cause symptoms - LES relaxes and regurgitation of gastric contents into esophagus - acid is neutralized and cleared by peristaltic action in esophagus in 1-3 minutes
physiologic reflux
symptoms of reflux disease but no visible mucosal injury
nonerosive reflux (NERD)
combination of factors causes injury and inflammation
reflux esophagitis
clinical manifestations of GERD
heartburn, regurgitation of acidic chyme, and upper abdominal pain w/i 1 hour of eating
s/sx worse if person lies down or it intra-abd pressure is increased (vomiting, coughing)
association with GERD and:
laryngitis, asthma, and chronic cough
Acute gastritis associated with, and cause what symptoms?
H. pylori, NSAIDS, drugs, chemicals
vague abdominal discomfort, epigastric tenderness, and bleeding
Chronic gastritis: Fundal (upper) gastritis
Immune, type A
autoantibodies against parietal cells and intrinsic factor causes atrophy and pernicious anemia
chronic gastritis: antral (lower) gastritis
associated with?
nonimmune, type B
associated with H.pylori and NSAIDS (also w/acute)
2 basic causes of peptic ulcer disease (PUD)
- decreased mucosal protection (NSAIDS block prostaglandins which are involved in mucous production, stress ulcers, tobacco and EtOH)
- increased acid production - Zollinger-Ellison syndrome -gastroma – increases gastrin which increases acid secretion
Deep PUD
true ulcers extend through muscularis mucosae and damage blood vessels causing hemorrhage or perforate the GI wall
most common of PUDs and tends to develop in younger people d/t H.pylori infection
-cause chronic intermittent epigastric pain that begins 30 minutes to 2 hours after eating when stomach is empty - can occur during night and disappear by morning
relieved by ingestion of food or antacids - “pain-food-relief” pattern
duodenal ulcers
Gastric ulcers - location typically? causes? clinical manifestations?
tend to develop in the antral region (bottom of the stomach) where most of the acid secreting cells are
causes are often from H.pylori - primary defect is an increased mucosal permeability to hydrogen ions and gastric secretion tends to be normal or less than normal
similar to duodenal - pain-food-relief pattern - pain also occurs immediately after eating - tends to be chronic rather than intermittent
*causes more anorexia, n/v, and weight loss than duodenal ulcers
types of stress ulcers
ischemic: within hours of trauma, hemorrhage, sepsis, burns (curling ulcers)
Cushing: as a result of brain injury – decreased mucosal blood flow and hypersecretion of acid caused by overstimulation of the vagal nerve
Clinical manifestations of pyloric obstruction
epigastric pain, fullness, nausea
Succession SPLASH: sloshing sound in abdomen: at this stage vomiting is cardinal sign - copious and occurs several hours after eating - contains undigested food but NO bile (no way for bile to enter)
*with prolonged obstruction, malnutrition, dehydration, electrolyte abnormalities, and extreme dehydration can occur
Developmental factors of early dumping syndrome
loss of gastric capacity, emptying control, and feedback control by the duodenum when it’s removed
plasma volume decreases – vasomotor responses – tachycardia, hypotension, weakness, pallor, diaphoresis, dizziness – rapid distention of the intestine produces feeling of epigastric fullness, cramping, n/v/d
late dumping syndrome
occurs 1-3 hours after eating
higher concentration of conjugated bilirubin
this means that the liver is able to conjugate the bilirubin but has a problem with secretion into bile
this could occur with biliary obstruction, or hepatitis
higher concentration of unconjugated bilirubin
means breakdown of RBC before reaching liver releases bilirubin or inability of liver to conjugate
ex. missing enzyme (congenital), hemolytic anemia
upper GI bleeding location and what does it look like?
esophagus, stomach, or duodenum
causes include bleeding peptic ulcers
Frank? Bright red blood in emesis (hematemesis), or digested blood (coffee-grounds emesis)
Melena: dark, tarry stools
Lower GI bleeding location and what does it look like? Causes?
Below ligament of treitz, jejunum, ileum, colon, rectum – causes: polyps, diverticulosis, cancer, hemorrhoids
Hematochezia: bright red or burgundy blood from rectum
Occult bleeding: slow, non-obvious blood loss that results in iron-deficiency anemia
GI bleeding causes what?
accumulation of blood in the intestinal tract leads to irritation - increased peristalsis - diarrhea
BUN will increase if blood has been digested - breakdown of RBCs - proteins increase serum urea
hgb and hct are not good indicators of immediate blood loss
failure of the chemical processes of digestion
maldigestion
failure of the intestinal mucosa to absorb (transport) the digested nutrients. common causes?
malabsorption
*bile salt deficiencies, enzyme deficiencies, bacterial infections, disruption of mucosal lining, disturbed lymphatic and vascular circulation, loss of gastric or intestinal surface area
pancreatic insufficiency primary problem and most common signs? what causes?
insufficient enzyme production – lipase, amylase, typsin, chymotrypsin
lactase deficiency
- Congenital defect in the lactase gene
- Inability to break down lactose into monosaccharides and thus prevent lactose digestion and monosaccharide absorption
- Fermentation of lactose by bacteria, causing gas (cramping pain, flatulence) and osmotic diarrhea
bile salt deficiency results from? causes?
Conjugated bile salts are needed to emulsify
and absorb fats and are synthesized from
cholesterol in the liver.
• Is the result of liver disease and bile
obstructions.
• Poor intestinal absorption of lipids causes
fatty stools, diarrhea, and loss of fat-soluble
vitamins (A, D, E, K).
vitamin A deficiency
night blindness
vitamin D deficiency
decreased calcium absorption, bone pain, osteoporosis, fractures
vitamin K deficiency
prolonged PT time, purpura, petechiae
vitamin E deficiency
testicular atrophy, neuro defects in children
obstruction of the intestines - usually more common in the small intestine d/t narrower structure
ileus
small intestine obstruction (think blockage of chyme passage = intestinal obstruction) s/s
colicky pains caused by intestinal distention followed by n/v
large intestine obstruction s/s
s/s, consequences r/t?,
hypogastric pain and abdominal distention
consequences related to the competence of the ileocecal valve
acute colonic pseudo-obstruction - massive dilation of large bowel that occurs in critically ill patients and immobilized older adults - characterized by dilation of the cecum and absence of mechanical obstruction
Ogilvie syndrome
location of obstruction and vomit
pyloric, proximal SI, lower in SI
pyloric: early, profuse vomiting of clear gastric fluid
proximal SI: mild distension and vomiting of bile-stained fluid
lower SI: more pronounced distension bc a greater length of intestine is proximal to the obstruction; vomiting may or may not occur
chronic inflammatory disease that causes ulceration of the colonic mucosa of sigmoid colon and rectum
lesions are…
clinical manifestations
ulcerative colitis
lesions are continuous with NO SKIP lesions - limited to mucosa - not transmural
clinical manifestations: diarrhea 10-12 times/day, BLOODY stools, crampy lower abd pain relieved by defecation - remissions and exacerbations
idiopathy inflammatory disorder affecting any part of the digestive tract but most often affecting the SI and proximal colon
patho, clinical manifestations
Patho: SKIP lesions - inflammation affects some segments but not others – ulcerations produce longitudinal and transverse inflammatory fissures that extend into lymphoid tissue “cobblestone” - GRANULOMA
clinical manifestations: abd pain and diarrhea >5/day with passage of blood and mucus (not as much blood as UC), RLQ tenderness and wt loss
anemia may result from vit B12 and folic acid; bone disease from malabsorption of calcium; protein loss leads to hypoalbuminemia
functional gastrointestinal disorder with no specific structural or biochemical alterations characterized by recurrent abdominal pain and discomfort associated with altered bowel habits that present as diarrhea or constipation or both
symptoms relieved with?
IBS
*symptoms are relieved by defecation and do not interfere with sleep
overweight BMI
> 25
obese BMI
> 30
molecules that stimulate eating
orexins
(hypocretins [from the hypothalamus], a
peptide family that act as neurotransmitters for
stimulating eating)
molecules that inhibit eating
anorexins
visceral obesity
intra-abdominal, central, apple shaped obesity
peripheral obesity
gluteal-femoral, subcutaneous, pear shape
patho of appendicitis
obstruction by inflammatory process, foreign body, or neoplasm
normally polymicrobial process
obstruction of the lumen leads to increased pressure, ischemia, and inflammation of the appendix
formed in sterile environment and primarily composed of caclium bilirubinate polymer from hyperbilirubinbilia
black pigmented gallstone
associated with bacterial infection of the bile ducts with formation of stone that is composed of calcium soaps, unconjugated bilirubin, cholesterol, fatty acids, and mucin
brown stones gallstones
remember that if a gallstone gets lodged in the common bile duct this can cause what s/s
jaundice
gallstone complication
pancreatitis
clinical manifestations of cholecystitis
fever, leukocytosis, rebound tenderness, abdominal muscle guarding
pain increases after fatty meal when bile is trying to be secreted
acute pancreatitis resolves how? clinical manifestations?
spontaneously
epigastric or midabdominal pain, n/v, fever, leukocytosis
elevated amylase 3x normal (amylase P is more specific)
lipase elevated and remains high
clinical manifestations of chronic pancreatitis
continuous or intermittent pain associated with increased intraductal pressure, increased tissue pressure, ischemia, neuritis, ongoing injury, and changes in central pain perception
weight loss, steatorrhea, DM accompanies disease progression
patho of acute liver failure
leading cause?
occurs in the absence of liver disease or cirrhosis
leading cause is acetaminophen overdose
patho: hepatocytes become edematous - patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma - hepatic necrosis is irreversible
irreversible inflammatory fibrotic disease that disrupts liver function and structure
cirrhosis
causes of cirrhosis
viral hepatitis and alcohol abuse
patho of cirrhosis
fibrosis occurs and biliary channels become obstructed and cause portal HTN - portal HTN causes blood to be shunted away from the liver - hypoxic necrosis develops
alcoholic liver disease caused by and what does it cause?
oxidation of alcohol causing damage to hepatocytes
impairs the hepatocytes’ ability to oxidize fatty acids, synthesize enzymes and proteins, degrade hormones, and clear portal blood of ammonia and toxins
stages of alcoholic liver disease
Stages:
Steatosis (alcoholic fatty liver) Is the mildest form.
Is reversible if drinking is stopped.
Alcoholic hepatitis (steatohepatitis) •Is characterized by inflammation. •Degeneration and necrosis of the hepatocytes occur.
Alcoholic cirrhosis (fibrosis)
•Toxic effects of alcohol metabolism on the liver, immunologic alterations,
oxidative stress from lipid peroxidation, and malnutrition occur.
clinical manifestations of alcoholic liver disease
anorexia, nausea, fever, abdominal pain, jaundice
primary biliary cirrhosis vs secondary biliary cirrhosis
primary (autoimmune): t-lymph mediated and antibody mediated destruction of the small intrahepatic bile ducts
secondary biliary cirrhosis: common bile duct obstruction; resolved w/removal
portal hypertension regions affected
pre hepatic (portal vein): caused by thrombosis or narrowing of the portal vein
intrahepatic (within the liver): from vascular remodeling with intrahepatic shunts, thrombosis, inflammation, or fibrosis of the sinusoids
posthepatic (hepatic vein): occur from hepatic vein thrombosis or cardiac disorders (RHF or pericarditis) that impair pumping of R heart
most common clinical manifestation of splenomegaly from hepatic HTN
thrombocytopenia - increased tendency to bleed
jaundice from extra hepatic obstruction to bile flow
gallstones
intrahepatic obstruction - jaundice - from what?
from cirrhosis or hepatitis
prehepatic obstruction - jaundice
excessive production of bilirubin from excessive hemolysis of RBCs
stages of hepatitis
incubation
prodromal (pre-icteric): begins approx 2 weeks after exposure; ends with appearance of jaundice
-clinical manifestations: fever, malaise, anorexia, hepatomegaly, tenderness; HIGHLY TRANSMISSIBLE
icteric phase: actual phase of illness
-jaundice, hyperbilirubinemia, fatigue, abdominal pain, increased bilirubin in serum, PT prolonged
recovery phase: begins with resolution of jaundice
-symptoms resolve after several weeks - chronic or chronic active hepatitis may develop
