Transcript PREREQUISITE LEARNING - Welcome to Hansen Nursing

Disorders of the Gastrointestinal
System & Liver
University of San Francisco
Dr. M. Maag
©2003 Margaret Maag
Class 12 Objectives
• Upon completion of this lesson, the student
will be able to
– list the pathologies associated with GI motility.
– determine the infectious agents associated with GI
disorders.
– predict those at risk for GI bleeding and the S & S
these individuals could present.
– analyze the clinical manifestations of severe liver
impairment.
– state the normal clotting mechanisms and the role
vitamin K plays in blood clot formation.
– state the cause(s) of DIC and list the S&S.
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Pathologies of GI Motility
• Diarrhea
• Is an > in frequency, fluid and / or volume of
stool
– Osmotic: the presence of nonabsorbable
substances in the intestine causing water to be
drawn into the lumen by osmosis
• sorbitol-containing liquid medications; tube feedings
• lactose intolerance
– Secretory: excessive mucosal secretion of fluid
& electrolytes
• related to: gastroenteritis (E. Coli), rotavirus, laxative
abuse, hyponatremia, fecal impaction
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Pathologies of GI Motility
• Diarrhea
• Motile: > motility is d/t stimulation caused by
inflammation or obstruction
• resection of small intestine, fecal impaction, early
bowel obstruction (e.g. Bezor)
• Clinical Manifestations:
• crampy abdominal pain, > bowel sounds
• prolonged diarrhea leads to f & e imbalances and
dehydration
• infants & elderly are at risk: check hydration & f/e
status
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Case Study
• A 72 year-old woman, who lives alone, has a
history of laxative abuse. What type of
diarrhea is she at risk for? What type of fluid
imbalance is she at risk for?
• What would you expect her VS to be?
• Her electrolytes upon admission to the
hospital are: Na+ = 155; K+ = 3.5; Cl- = 116;
Hct = 45%
• Clinical manifestations? Treatment?
• Which acid-base disturbance is she at risk
for? Why?
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Pathologies of GI Motility
• Constipation
• Defined as infrequent or difficult defecation:
most frequently c/o digestive disorder
• Etiology : functional disorder of bowel
motility
• incidence is > in the elderly; diet poor in fiber &
fluids; anatomic lesions; drug therapy
• d/t poor neural stimulation of GI motility, abdominal
muscle weakness, bowel obstruction
• Mega colon, opiates, hypothyroidism, diabetic
neuropathy, sedentary lifestyle, low residue diet
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Pathologies of GI Motility
• GERD
• Reflux of gastric contents into lower esophagus resulting
in clinical symptoms or structural alterations in the
esophageal tissues (reflux esophagitis)
• 94% of the individuals have hiatal hernias
• a protrusion of some part of the upper portion of
stomach through esophageal hiatus and then into
the thorasic cavity
• Delayed gastric emptying is seen primarily in:
• diabetics, cigarette smoking, and ETOH abuse
• dysphagia, eructation, heartburn, GI bleeding,
abdominal discomfort when lying down, dyspnea
may be present
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• Heartburn, ulcerations, precancerous lesions
Fecal Incontinence
• Inadequate control of defecation in an adult
due to weak pelvic floor muscles and / or
weakness of the external anal sphincter
• Common causes:
• Clostridium difficile responsible for nosocomial
diarrhea
• Impaction, laxative abuse, hyperosmolar tube
feedings
• Risk factors: older persons in long-term
care institutions (Bliss, et al., 2000)
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Intestinal Obstructions
• Large Bowel
• A large bowel obstruction is an emergency
condition that requires early & prompt
surgical intervention
• Etiology:
• infectious / inflammatory, neoplastic, or mechanical
pathology (colorectal cancer)
• Rotation or twisting of the cecum or sigmoid
colon will cause abrupt onset of symptoms
• Immediate abdominal distention
– Decreases the ability to absorb F & E
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Intestinal Obstructions
• Sigmoid volvulus usually seen in the older
individual with a hx of straining at stool
• Symptoms: abdominal distention, nausea,
vomiting, and crampy abdominal pain; check
history of flatus and BMs
• Abrupt onset is indicative of an acute obstruction
– Sudden onset due to torsion or hernia
• A chronic hx of constipation is related to a dx of
diverticulitis or carcinoma
• Obstipation (no flatus or BM) & loss of weight =
carcinoma
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Intestinal Obstructions
• Paralytic ileus or “silent bowel” is most often
seen after abdominal surgery & anesthesia
• bowel activity is < d/t lack of neural stimuli
(“functional”)
• this can lead to “mechanical” obstruction d/t
accumulation of feces
• Hernias: a loop of bowel protrudes through
abdominal wall
• inguinal canal, umbilicus, or incisional scar tissue
• caused by heavy lifting, straining, or coughing
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Disorders of GI Bleeding
• Upper: includes the esophagus, stomach,
duodenum
• peptic ulcer disease (PUD) or esophageal varices
• Lower: includes the jejunum, ileum, colon, rectum
• colorectal cancer, polyps, hemorrhoids, IBD
• Manifestations:
•
•
•
•
hematemesis
bright red blood in the stool (“hematochezia”)
black,dark, tarry stools (“melena”)
“occult” bleeding (invisible blood in the stool)
• Tx: find the underlying cause; fluid volume
replacement; endoscopy or colonoscopy; medical
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and /or surgical tx
Disorders of GI Bleeding
• Results
• Shock will ensue if massive (25% EBL
within hours) bleeding occurs
• Metabolic acidosis, prerenal failure,
bowel infarction will occur
• < coronary & cerebral blood flow
• Death
– See McCance, Figure 38-1, p. 1265
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Peptic Ulcer Disease
• An inflammatory disorder causing deep erosion of
stomach or duodenal mucosa by HCL & pepsin
• At risk: infection with H. pylori; > NSAIDS; >
secretion of HCL as seen in Zollinger-Ellison
syndrome
• Etiology: age, family hx
– > mucolytic enzymes; may lead to pyloric obstruction,
bowel perforation and ultimately peritonitis
• Sx: hallmark sign = upper gastric pain
– Emergency:hematemesis, melena, occult blood, shock
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Peptic Ulcer Disease
• Treatment includes:
– < stress
– < ETOH intake
– screen for H. pylori (C-urea breath test)
– frequent small meals
– avoid calcium based antacids d/t > gastrin
release
– H2 blockers (Tagamet & Zantac)
– Insert NG tube for severe bleeding and gastric
lavage
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Gastric, Duodenal, Stress Ulcers
• Gastric
– > cancer risk
– Lack of remission or exacerbation periods
• Duodenal
–
–
–
–
Younger age at onset
Strong familial history
Ulcerogenic drugs used
Nocturnal pain more prevalent
• Stress
– Systemic trauma, severe illness, neural injury
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Intestinal Bowel Disorders
• Ulcerative Colitis
– Inflammatory disorder with eventual
erosion of the colon
• Crohn’s Disease
– Effects any part of the GI (mouth to anus)
– Smoking, diet, and/or bacteria may influence
– Cytokine-mediated damage
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Gastric Cancer
• Adenocarcinoma is the primary malignant
neoplasm
• 8th leading cause of mortality r/t cancer in US
• Epidemiology: 55-60 year olds; 2 times greater
incidence in men vs. women
• Risk factors: H. pylori, < socioeconomic class,
consumption of pickled foods, improper food
storage, radiation exposure
• Etiology:chronic inflammation, dietary
influences, genetic & environmental
factors
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Gastric Cancer
• Sx: Vague early sx with weight loss;
indigestion; abdominal distention; mild pain
induced with or without food; chronic blood
loss leads to anemia; occult blood in stool
• Tx: reduce risk factors; total or partial
gastrectomy; lymph node resection;
chemotherapy & radiation
• 15% of cases lend a 5-year survival rate
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Peritonitis
• Etiology: Inflammation of peritoneal membrane
• sterile: rupture of biliary system; hemorrhagic
pancreatitis, endometriosis, surgical procedures
• infectious: bacteria from ruptured bowel or appendix;
introduction of bacteria from abdominal trauma or
invasive procedures (e.g. peritoneal dialysis)
• Sx: Circulatory volume collapse, septic shock
causing a high mortality rate, absent bowel sounds,
pain, abdominal distention & rigidity, > nausea &
vomiting, paralytic ileus
• Tx: antibiotics, NG tube, IV fluids, surgical repair of
etiology
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Colorectal Cancer
• “Patients with long-standing ulcerative colitis
have been shown to be at increased risk of
developing colorectal cancer” (Medscape, 1999)
• Involves a primary malignant tumor of the rectum
or colon
• 2nd leading cause of cancer death in US
• > incidence in 50 year olds
• > fat and poor fiber diet; > ETOH consumption;
cigarette smoking; obesity; sedentary life style
• Exact etiology unknown…> incidence with polyps
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Colorectal Cancer
• Symptoms:
– fecal occult blood or ulcerative lesions manifest
as anemia or rectal bleeding
• distention, abdominal pain, vomiting, constipation
– metastatic disease: weight loss, anorexia,
possible palpable mass
• Prevention: ASA may < risk; routine
monitoring for guaic (+)
• Tx: colostomy repair; permanent colostomy
for rectal tumors
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Liver Disorders
Portal Hypertension
• Fibrosis of the liver structures causes an
increased resistance to blood flow within the
liver, therefore an elevation in the portal
venous pressure
– This > in pressure can cause esophageal varices
and hemorrhoids and 3rd spacing of fluid into
peritoneal cavity (ascites)
• “Hepatic encephalopathy” can occur d/t the
toxic effects of altered metabolism
– cerebral edema & IICP can result from
severe cases
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Ascites
• A common feature of liver failure.
• Basic mechanisms include:
– an increase in portal hypertension
– sodium and water retention
– decreased blood oncotic pressure
secondary to a low serum albumin level
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Cirrhosis
• Focal or diffuse inflammation and liver cell
necrosis that causes severe changes in the
structure and function of liver cells
• Inflamed liver cells compress the liver lobule
and cause increased resistance to blood flow
and portal hypertension
– Liver tissue is regenerated, but not in the normal
fashion
– Fibrotic changes are irreversible, causing liver
dysfunction
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Cirrhosis
• Alcoholic: results from long-term alcohol abuse;
most common cause in the USA
• Biliary: caused by a < in bile flow; commonly
caused by long-term obstruction of bile ducts
• Cardiac: caused by long-term right-sided CHF
– results in < oxygenation of liver cells
• Postnecrotic: result from hepatoxins, chemicals,
or infection with Hepatitis B or C
– massive death of liver cells & associated with
cancer
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Viral Hepatitis
• Inflammation of the liver followed by the necrosis of
hepatic cells
– Caused by infection with one or more hepatoviurses
• Types: A, B, C, D, E & G
• Little is known about the blood-borne “G”
– Hepatic inflammation may occur d/t toxins,
autoimmunity, and metabolic disorders
• http://www.roche.com/pages/facets/5/hepatitis.h
tm
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Viral Hepatitis
• HAV is found primarily in contaminated food
and water
– Transmitted by the enteric route (oral-fecal)
– Poor hand washing or unsanitary food preparation
– During the viremic phase of acute infection it can
be spread via blood exposure (unusual)
– Virus infects the liver and is excreted via the feces
– Most contagious before presentation of S & S
– Prevalence of immunity to HAV has decreased to
< 25% of US adults (DiCarlo, 1999)
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Hepatitis A Virus
• Hepatitis A antibodies show up in the blood
2-6 weeks following exposure & remain
indefinitely in the blood
• Clinical manifestations: fever, chills, brown
urine, anorexia, irritability, clay-colored feces,
N&V, headache
• Liver function tests & coagulation tests are
abnormal
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Hepatitis B Virus
• HBV is transmitted via blood & body fluids
– “Infected adults have a 50% chance of
developing acute symptoms, but only a
10% chance of developing chronic
infection” (DiCarlo, 1999)
– In the US, 60% of hepatitis B virus
infections are sexually transmitted
• unprotected sex with multiple partners
– A vaccine has been available since 1982
• immunity develops in more than 90%
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Hepatitis B Virus
• Hepatitis antigen-antibody complexes can be
detected from 1-10 weeks after exposure to
the virus
• Incubation period for HBV can last from
6 weeks to 6 months; clinical S & S of the
acute phase are the same as HAV
• Patients have an > chance of “fulimant
hepatic failure”…a sudden degeneration of
the liver & loss of all normal liver functions
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Hepatitis C Virus
• HCV is a blood-borne type of hepatitis
– Formerly known as non-A, non-B hepatitis
– Common among hemophiliacs & IV drug
abusers
– 40% of the cases are idiopathic
– Incubation period of 6-7 weeks and acute
infection results in a 30-40% chance of
jaundice
– 70% will develop some form of chronic
hepatitis (DiCarlo, 1999)
– Sexual transmission accounts for 15-20%
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of the infections in the US (DiCarlo,1999)
Other Types of Viral Hepatitis
• HDV is also known as the “delta virus”
– It is a blood-borne virus that must coexist
with HBV in order to exert its viral activity
– This covirus heightens the course and
outcome of illness with HBV
• HEV is the “enteric” form of non-A, nonB hepatitis
– is generally seen in underdeveloped
countries
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Precautions
• Use of gloves while handling all items
contaminated with client’s body secretions
• Use of disposable patient care items, such as
thermometers, dishes, eating utensils
• Use of private bathroom and room for clients
who are incontinent of feces.
• Double bagging and labeling of linen or any
hospital equipment that is contaminated with
feces or blood (Hartshorn, 1997, p. 462)
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Clotting Factor Defects
• Review normal function of clotting factors
• Inherited disorders: deficiencies of clotting factors
– Hemophilia's
– Willebrand disease
• Acquired cases
– Deficient synthesis of clotting factors by liver
– Liver disease, dietary deficiency of Vitamin K
• Factor 7 is first to decline then factor 2 and 10
– Thrombocytopenia may occur due to
splenomegaly  liver disease and portal
hypertension
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Disseminated Intravascular
Coagulation
• Acquired complex clinical syndrome
– Due to > protease activity in the blood
caused by > release of thrombin
– Acute, severe,life-threatening process
– Massive hemorrhage and thrombosis
– Becomes a chronic, low-grade condition
• Minor lab abnormalities with sub acute
hemorrhage and microcirculatory thrombosis
• May involve many organs
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References
• Bliss, D. Z., Johnson, S., Savik, Clabots, C.
R., & Gerding, D. N. (2000). Fecal
incontinence in hospitalized patients who
are acutely ill. Nursing Research,
49(2),.101-108.
• Hansen, M. (1998). Pathophysiology:
Foundations of disease and clinical
intervention. Philadelphia: Saunders.
• http://www.medscape.com
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