GI system

Anorexia

loss of appetite or desire for food

Nausea

subjective, unpleasant sensation that precede V, caused by distention anywhere in the GI tract or stimulated by higher brain center

vomiting

reflex mediated by vomiting center in medulla, in response to excessive distention or irritation of the stomach or duodenum, chemical stimulation, or pain. Projectile vomiting happens with increase ICP

acute diarrhea

frequent passage of loose stools persisting 3-5 days that are not bloody, purulent, or greasy. Lasts less than 2 weeks

Secretory diarrhea

secretory processes of the bowel are increased, more acute infectious diarrhea

osmotic diarrhea

water is pulled into the bowel by the hyperosmotic nature of its content

constipation

stools less than once every 3 days, caused by dehydration, delayed gastric motility, sedentary lifestyle, hypothyroidism, low fiber diet, psychogenic, drug side effect

Parietal pain

caused by stimulation of pain receptors in parietal peritoneum, pain is localized, sharp, intense, and lateralized

Visceral pain

caused by stimulation of abdominal organs, pain is vague, diffuse, and dull

Referred pain

felt at a distance from the affected tissue, localized at some point along the afferent nerve pathway of tissue

Hematochezia

bright red stools

Melena

black or tarry stools, foul-smelling caused by digestion of blood in GI tract

Hematemesis

bloody vomit, either fresh, bright red blood or dark grainy digested blood with “coffee ground” appearance

Occult bleeding

trace amounts of blood in normal-appearing stools or gastric secretions, detectable only with positive fecal occult test

Dysphagia

difficulty swallowing

Achalasia

loss of inhibitory neurons in the myenteric plexus with smooth muscle atrophy in the middle and lower portions of the esophagus

(7) s/s of dysphagia

stabbing pain at level of obstruction, discomfort after swallowing, regurgitation of undigested food, unpleasant taste sensation, vomiting, aspiration, weight loss

(4) physiologic factors of GERD

decreased lower esophageal sphincter tone, esophageal mucosal irritation from HCL acid and pepsin, delayed esophageal peristalsis, delayed gastric emptying

(7) s/s of GERD

heartburn (pyrosis), regurgitation of fluid/food particles, retrosternal aching or burning occurring 30-60 min after eating, chest heaviness, pressure radiating to neck, jaw, or shoulders, chronic cough, laryngitis

Hiatal Hernia

stomach protrudes through the diaphragm into the thorax

(2) s/s of Hiatal Hernia

asymptomatic or cause GERD symptoms

(5) complications of hiatal hernia

GERD, esophagitis, gastritis, ulcer formation, strangulation

Gastroparesis

delayed gastric emptying in the absence of a mechanical gastric outlet obstruction

mechanical intestinal obstruction

Mechanical is caused by anything that affects lumen of bowel, tumor, adhesion, and severe constipation. Severe cases can lead to ischemia of bowel, acidosis, perforation, shock, sepsis, and death.

nonmechanical intestinal obstruction

Nonmechanical is ileus. Ileus is the non-mechanical block of small and large intestine. It can be caused by surgery, disruption to blood supply to abdomen, and meds.  

(8) s/s of intestinal obstructional

pain, distention of bowel, N/V, anorexia, diarrhea, reduced bowel sounds, abdominal tenderness, fever

herniation intestinal obstruction

adhesions intestinal obstruction

valvulus intestinal obstruction

intussusception intestinal obstruction

what causes actue gastritis

caused by injury of the protective mucosal barrier

what are types of chronic gastritis

type A – chronic fundal gastritis  (immune) and type B – chronic antral gastritis (nonimmune)

(4) risk factors of peptic ulcer disease

advancing age, use for warfarin and NSAIDS, corticosteroid use, and smoking

patho of peptic ulcer disease

excessive acid leads to ulceration in the mucosa of stomach or duodenum -> break allows mucosa to be subjected to acidic or alkaline environment -> autodigestion occurs

Duodenal ulcer

happens in pt 25-75 y, epigastric burning 2-3 hr post meal, relief with food, awakening at 1-2am is common w/ symptoms, has periods of feeling well

Gastric ulcer

more common in NSAID users, 55-65 yrs, pain reported w/ or immediately after meals, N/V and weight loss are common

(6) s/s of peptic ulcer disease

dyspepsia, pain depending on ulcer type, hematemesis, melena, severe cases lead to perforation and hemorrhage

patho of dumping syndrome

too rapid movement of stomach contents and acid into duodenum overwhelms protective layer -> causes fluid shift from intravascular compartment into lumen into small intestine -> sudden loss of intravascular volume triggers set of vasomotor responses that include hypotension, tachycardia, dizziness, sweating -> as intestine fills up, individual develops sensation of intestinal fullness accompanied by cramping, N/V, and diarrhea

(8) s/s of dumping syndrome

early (hypotension, tachycardia, dizziness, sweating) late (cramping, N/V/D)

ulcerative colitis patho

autoimmunity leads to inflammatory ulceration in large intestine with mucosal erythema, edema, and friability -> mucosal ulceration and edema lead to narrowing of colonic lumen, D, and hematochezia = Begins in rectum, goes up to colon without skipping parts of mucosa, higher risk of cancer

patho of Chrohn’s disease

same as UC but has skip lesions, ulcerations can produce fissures that extend into lymphatics

(5) s/s of ulcerative colitis

cramping, abdominal pain and dehydration, 10 to 20 stools per day, bleeding can cause anemia

(11) s/s of chron’s disease

N/V, farting, colicky pain in RLQ, malabsorption, 3-5 semisolid foul-smelling stools/day, mucosa in stools possible with pus, intermittent nonbloody diarrhea, urgency to defecate at night, weight loss, hypoalbuminemia, perianal abscesses and fistulas

patho of diverticulitis

asymptomatic presence of poopball, associated with increased intracolonic pressure and abdominal intestinal mobility

patho of Diverticulosis

increased intraluminal pressure causes poopball to rupture -> bacterial invasion of weakened area -> local ischemia

(6) s/s of diverticulitis

steady and severe abdominal pain in LLQ, abdominal guarding and rebound, constipation more usual than D, pain increased with pooping, lower grade fever

(8) s/s of appendicitis

periumbilical or epigastric pain that localizes to RLQ, anorexia, N/V, leukocytosis, tenderness at McBurney’s point (pressing on appendix point), Rovsing sign (RLQ pain when palpating LLQ), Psoas sign (pain with right thigh extension), Obturator sign (pain with internal rotation of flexed right thigh)

patho of Cholecystitis

Inflammation of the gallbladder occurring acutely or chronically, often secondary to previously asymptomatic gallstones

Cholelithiasis leading to Cholecystitis

·      when a stone becomes impacted in the cystic duct, inflammation develops behind the obstruction

·      if not relieved, pressure builds up in the gallbladder and leads to distention, ischemic changes, gangrene, and perforation with subsequent abscess formation and less frequently generalized peritonitis

Acute cholecystitis s/s (6)

·      abdominal pain (sudden onset, intense, in epigastrium or RUQ, radiates to back or shoulder), “biliary colic” (pain that starts out from mild to steadily increasing in intensity and is present for more than 20 min )

·      N/V, recurrent attacks following fatty meals 1-6 hrs later, local tenderness in epigastric and RUQ aras, positive Murphy’s sign (tenderness on palpating RUQ)

(4) s/s of common duct stone

jaundice, fever and chills, mild to marked hepatomegaly

(2) s/s of chronic cholecystitis

asymptomatic, mild dyspepsia following fatty meals

(3) types of pancreatitis

  acute, biliary tract obstructions, and alcohol abuse

(3) s/s of Pancreatitis

LUQ pain, N/V, Cullen’s sign (bruising around the belly button)

Pancreatitis dx

serum amylase and lipase and CT

cause of Peritonitis

perforation of gut/organ into perineal space

(6) s/s of peritonitis

pain (over inflamed area and rebound in nature), N/V, rigid abdomen, tachycardia, fever, increased WBC

Preicteric stage

first stage before jaundice, flu-like symptoms (malaise, fatigue), anorexia, N/V/D, pain (headaches, muscle aches, polyarthritis), serum. Bilirubin and enzymes levels are elevated

Icteric stage

includes appearance of jaundice, dark-or-tea colored urine, clay-colored stools, pruritus, decreased in preicteric phase symptoms

Posticteric stage

jaundice decreased, color of urine and stool goes to normal, energy levels increase, pain subsides, GI symptoms are minimal to absent, serum bilirubin and enzyme levels return to normal

mode of transmission of Hep A

fecal-contaminated drinking water and food

mode of transmission of Hep B

exchange of body fluids (Sexual contact, IVDU with needle sharing, occupational exposure in health care workers), course of illness is 2-3 weeks

mode of transmission of Hep C

·      exchange of blood and body fluids (sexual transmission is low, maternal-fetus transmission is uncommon and is limited to women with high circulation HCV levels

·      Incubation period is 6-7 weeks

Hep A prevention

vaccine to pt who reside or travel to areas where disease is endemic, food handles, day care and long-term care workers AND Prevent infection through water and food safety, immunization, and post exposure immune globulin use

Hep B prevention

universal precautions, clean needle exchange, immunizations, and safer sex, Hep B vaccine does not contain live virus (most develop HbsAb after 3 doses which means you have protection for the virus), HBsAb testing to confirm the development of HBV protection in those with high risk as well as those at risk for poor immune responses

Laennec’s Cirrhosis

alcohol-induced, nutrition, portal cirrhosis, cellular necrosis causes eventual widespread scar tissue with fibrotic infiltration of liver

Postnecrotic Cirrhosis

occurs after massive liver necrosis, results as a complication of acute viral hepatitis or exposure to hepatotoxins, scar tissue causes destruction of liver lobules and entire lobes

Biliary Cirrhosis

develops from chronic biliary obstruction, bile stasis, and inflammation resulting in severe obstructive jaundice

Cardiac cirrhosis

associated with severe, right-sided congestive heart failure and results in an enlarged, edematous, congested liver. The liver becomes anoxic, resulting in liver cell necrosis and fibrosis

patho of cirrhosis

cellular injury -> fibrosis (leukocyte infiltration, release of inflammatory mediators, activation of fibrotic processes) -> structural changes (altered biliary channels and blood flow, formation of shunts, disrupted regeneration process) -> liver architecture distortion (formation of fibrous bands and regenerating nodules, cobbly appearance of liver)

(13) s/s of cirrhosis

jaundice, abdominal pain/tenderness, ascites, peripheral edema, dry skin and rashes, petechiae or ecchymosis, spider angiomas on the nose, cheeks, upper thorax, and shoulders, hepatomegaly, protruding umbilicus, dilated abdominal veins, fetor hepaticus (fruity, musty breath odor of chronic liver disease), asterixis (course tremor characterized by rapid, nonrhythmic extension and flexions in the wrist and fingers, delirium (accumulate NH3)

hepatic encephalopathy early s/s (6)

subtle changes in personality, memory loss, irritability, disinhibition, lethargy, and sleep disturbances

(7) s/s of late hepatic encephalopathy

disorientation to time and space, flapping tremor of the hands, slow speech, bradykinesia, stupor, convulsions, and coma