Exam 3 Flashcards
what does chron’s involve that UC doesn’t and what does that contribute to?
it involves the small intestine, contributing to malabsorption
IBD
chronic, recurrent inflammation of the intestinal tract that has periods of remission and exacerbation
types of IBD
UC and chron’s
is UC or chron’s autoimmune?
chron’s
clinical manifestations of IBD
- diarrhea
- bloody stool
- weight loss
- abdominal pain
- fever
- fatigue
complications of IBD
hemorrhage, strictures, perforation, fistulas, colonic dilation, colorectal cancer, liver failure, systemic problems
pattern of inflammation in chron’s
it involves all layers of the bowel wall that can occur anywhere in the GI tract
where is chron’s most commonly found?
the terminal ileum and colon
what is good way to recognize chron’s during a scope?
it will look like cobblestones
because inflammation in chron’s goes through the entire wall, what can happen?
- abscesses can form and peritonitis can result
- fistulas can develop
clinical manifestations of chron’s
- diarrhea
- crampy abdominal pain
- weight loss when the small intestine is involved
- rectal bleeding
- fever or other systemic symptoms
pattern of inflammation in UC
starts in rectum and moves up towards the cecum
what electrolyte is mostly lost when someone has diarrhea?
mostly potassium
clinical manifestations of UC
- bloody diarrhea
- abdominal pain
- fever
- rapid weight loss
- anemia
- tachycardia
- dehydration
what would you expect in lab results with UC?
low H and H and increased WBC
goal of drug treatment in IBD
to induce and maintain remission
what kind of ostomy is usually given with IBD?
ileostomy: going to be very dehydrated
gerontologic considerations with IBD
- second peak of disease in 60s
- diagnosis can be difficult ~ confused with c. diff
- distal colon is usually involved in UC
clinical manifestations of IBS
- abdominal pain
- diarrhea or constipation
- abdominal distention
- excessive flatulence
- bloating
- urgency
- sensation of incomplete evacuation
- fatigue
- sleep disturbances
what is loperamide (imodium) and when would you not recommend this drug?
it is used to treat diarrhea and it decreases the intestinal tract. you do not want to use it if F/E are out of balance
what is a huge factor of IBS?
stress
gastritis
inflammation of gastric mucosa that results in the breakdown of gastric mucosal barrier
in gastritis, what is the stomach tissue unprotected from?
autodigestion by HCl acid and pepsin
since the stomach is in LUQ, what can this be confused with?
heart problems
what problem results from gastritis?
tissue edema and disruption of capillary walls that can cause hemorrhage
what kind of drugs can cause gastritis?
NSAIDs, including aspirin and corticosteroids
what diet contributes to gastritis?
alcohol or spicy foods
what environmental factors contribute to gastritis?
radiation or smoking
how can an NG tube contribute to gastritis?
there is constant irritation on the stomach wall
autoimmune atrophic gastritis
- affects fundus and body of stomach
- associated with increased risk of gastric cancer
- may be linked to presence of H. pylori and development of chronic gastritis
clinical manifestations of acute gastritis
- anorexia
- N/V
- epigastric tenderness
- feeling of fullness
- hemorrhage
clinical manifestations of chronic gastritis
- similar to acute
- loss of intrinsic factor can occur when acid-secreting cells are lost or nonfunctioning
what is diagnosis of gastritis based on?
history of drug and alcohol abuse
why would we confirm presence of anemia with possible gastritis?
unfound anemia is almost always a GI bleed
what diagnostic studies can we do for gastritis?
- CBC
- occult blood test
- serum antibody tests
- tissue biopsy to rule out cancer
what might be needed in severe cases of gastritis?
an NG tube; observe for bleeding and lavage to flush precipitating agent from stomach
most common manifestations of GI diseases
nausea and vomiting
chemoreceptor trigger zone (CTZ)
- responds to chemical stimuli of drugs and toxins
- located in the brainstem
- site of action of drugs used to induce vomiting
- plays a role in vomiting cause by labyrinthine stimulation
parasympathetic stimulation of N/V
- relaxes lower esophageal sphincter
- increases gastric motility and salivation
what can vomiting result in?
- metabolic alkalosis: from loss of gastric HCl
- metabolic acidosis: from loss of bicarbonate if the contents from the small intestine are vomited
what might indicate a lower intestinal obstruction in throw up?
fecal odor and bile
what kind of complications would bright red blood in vomit indicate?
- mallory-weiss tear
- esophageal varices
- gastric or duodenal ulcer or neoplasm
what nutritional therapy would we start after N/V?
- IV fluids to replace fluids and electrolytes, glucose
- NG tube suction to decompress stomach
- clear liquids started first
why do we use gatorade and broth with caution after N/V
because of high salt intake
how can we avoid overdistention of the stomach?
take fluids between meals instead of with
GERD
- common problem
- chronic manifestation of mucosal damage
- caused by reflux of gastric contents
- not a disease, but a syndrome
who are GI issues more common in?
males
incompetent LES
- primary factor in GERD
- results in decreased pressure in distal portion of esophagus so gastric contents move from stomach to esophagus
- can be due to certain foods (caffeine, chocolate) and drugs (anticholingergics)
clinical manifestations of GERD
- heartburn (pyrosis): burning, tight sensation felt beneath the lower sternum and spreading upward to throat or jaw
- dyspepsia: pain of discomfort centered in upper abdomen
- regurgitation: hot, bitter, or sour liquid coming into throat or mouth
- respiratory symptoms: wheezing, coughing, dyspnea, nocturnal coughing with loss of sleep
- otolaryngologic symptoms: hoarseness, sore throat, lump in throat, choking
- GERD-related chest pain
what can esophagitis result in?
dysphagia
barrett’s esophagus (esophageal metaplasia)
- replacement of normal squamous epithelium with columnar epithelium
- precancerous lesion
- must be monitored every 2-3 years by endoscopy
what can GERD cause from acid reflux into mouth?
dental erosion
nutritional therapy in GERD
- decrease high-fat foods
- take fluids between rather than with meals
- avoid milk products at night
- avoid late-night snacking or meals
- avoid chocolate, peppermint, caffeine, tomato products, orange juice
- weight reduction therapy
- chewing gum and oral lozenges can increase saliva and help with mild symptoms
anytime we cut into GI tract, what is there a risk for?
a stricture
nursing management for GERD
- elevate HOB 30 degrees
- not lying down for 2-3 hours after eating
- avoid late night eating
- evaluate effectiveness of medications
- observe for side effects of medications
- avoid factors that cause reflux: smoking, alcohol, caffeine, acidic foods
- stress reduction techniques
- weight reduction
- small, frequent meals
hiatal hernia
- hernation of portion of stomach into esophagus through an opening or hiatus in diaphragm
- more common in older adults and women
two types of hiatal hernia
- sliding ~ most common
- paraesophageal or rolling
what factors increase risk of a hiatal hernia?
- weakening of muscles of diaphragm
- increased intraabdominal pressure: obesity, pregnancy, heavy lifting
- increasing age
- trauma
- poor nutrition
- forced recumbent position
- congenital weakness
clinical manifestations of hiatal hernia
- heartburn
- dysphagia
lifestyle modifications for hiatal hernia
- eliminate alcohol
- elevate HOB
- stop smoking
- avoid lifting/straining
- reduce weight
- use antisecretory agents (H2) and atacids
eosinophilic esophagitis
- swelling of esophagus cause by an infiltration of eosinophils
- personal or family history of other allergic diseases
most common food triggers in eosinophilic esophagitis
milk, egg, wheat, rye, and beef
clinical manifestations of eosinophilic esophagitis
- severe heartburn
- difficulty swallowing
- food impaction
- N/V
- weight loss
three main areas of esophageal diverticula
- zenker’s diverticulum: most common, above the upper esophageal sphincter
- traction diverticulum: near esophageal midpoint
- epiphrenic diverticulum: above the LES
clinical manifestations of esophageal diverticula
- dysphagia
- regurgitation
- chronic cough
- aspiration
- weight loss
how can we get rid of esophageal diverticula?
- apply pressure at a point on the neck to empty pocket of food
- diet limited to foods that are blenderized
most common cause of esophageal stricture
GERD
achalasia
- rare, chronic disorder
- in lower two third of esophagus, peristalsis is absent
- LES pressure increases
- obstruction occurs at/near diaphragm
- food and fluid accumulate in lower esophagus
result of achalasia
dilation of lower esophagus
clinical manifestations of achalasia
- dysphagia
- substernal chest pain
- halitosis
- inability to belch
- GERD
- regurgitation
- weight loss
types of peptic ulcers
acute and chronic
when do ulcers develop?
in the presence of an acid environment
the stomach is normally protected from autodigestion by what?
gastric mucosal barrier
how often is the surface mucosa of the stomach renewed
about every 3 days
what can pass through the gastric barrier?
water, electrolytes, and water-soluble substances
if the mucosal barrier is impaired, what can occur?
back diffusion of acid and pepsin
destroyers of mucosal barrier
- H. pylori
- aspirin and NSAIDs
- corticosteroids
- lifestyle factors
gastric ulcers
- occur in any portion of the stomach
- less common than duodenal
- prevalent in women, older adults
- peak incidence >50 years
duodenal ulcers
- occur at any age in anyone: increases between ages 35-45
- familial tendency
- associated with increased HCl acid secretion: alcohol and cigarette smoking
- H. pylori found in 90-95% of patients
clinical manifestations of gastric ulcers
- pain is high in epigastrium
- occurs 1-2 hours after meal
- “burning” or “gaseous”
- gastric ulcer pain doesn’t radiate around
clinical manifestations of duodenal ulcers
- midepigastric region beneath xiphoid process
- back pain if ulcer is located posteriorly
- 2-5 hours after meals
- “burning” or “cramplike”
- tendency to occur, then disappear, then occur again
three major complications of an ulcer
- hemorrhage
- perforation
- gastric outlet obstruction
most common complication of PUD
hemorrhage
most lethal complication of PUD
perforation
clinical manifestations of a perforation
- sudden, dramatic onset
- initial phase (0-2 hours after): severe upper abdominal pain that spreads, tachycardia, weak pulse, rigid boardlike abdominal muscles
- shallow, rapid RR
- bowel sounds absent, N/V
what can occur from a perforation?
bacterial peritonitis may occur within 6-12 hours
clinical manifestations of gastric outlet obstruction
- pain worsens toward end of day as stomach fills
- relief obtained by belching or vomiting
- constipation
- swelling: if stomach is grossly dilated, may be palpable
- loud peristalsis
what does medical regimen consist of with PUD
- adequate rest
- drug therapy
- elimination of smoking and alcohol
- dietary modification
- long-term follow-up care
- stress management
- reduce degree of gastric acidity
how long does ulcer healing take?
requires many weeks of therapy, pain disappears after 3-6 days
nutritional therapy for PUD
- bland diet
- six small meals
what is an acute exacerbation accompanied by?
bleeding, increased pain and discomfort, N/V
focus of treating a perforation
- stop spillage of gastric or duodenal contents into peritoneal cavity
- restore blood volume
- place NG tube on continuous suction
- indwelling catheter inserted and monitored hourly
what is done to treat a perforation?
- broad-spectrum antibiotics
- pain meds
- repair
with a perforation, what do you want to do until the HCP is notified?
stop all oral, NG feeds/drugs
HAV
- mild to acute liver failure
- not chronic
- incidence decreased with vaccination
- RNA virus transmitted via fecal-oral route
- contaminated food or drinking water
HBV
- acute or chronic disease
- incidence decreases with vaccination
- DNA virus transmitted perinataly, percutaneously, via mucosal exposure to blood, blood products, or other body fluids
at risk populations for HBV
- high-risk sexual activity
- household contact of chronically infected
- pts. undergoing hemodialysis
- health care and public safety workers
- transplant recipients
how long can HBV live on a dry surface?
7 days
HCV
- acute: asymptomatic
- chronic: liver damage
- RNA virus transmitted percutaneously
- it is curable
HDV
- cannot survive on its own
- requires HBV to replication
- transmitted percutaneously
- no vaccine
HEV
- RNA virus transmitted via fecal-oral route
- most common mode of transmission is drinking contaminated water
- occurs primarily in developing countries
- few cases in US
- acts like A, but out of country
acute infection of hepatitis
- liver damage: lysis of infected cells
- cholestasis
- liver cells can regenerate in normal form after resolution of infection
chronic infection of hepatitis
can cause fibrosis and progress to cirrhosis
systemic manifestations of hepatitis
- rash
- angioedema
- arthritis
- fever
- malaise
- cryoglobulinemia
- glomerulonephritis
- vasculitis
symptoms during incubation phase of hepatitis
- malaise
- anorexia
- weight loss
- fatigue
- N/V
- abdominal discomfort
- distaste for cigarettes
- dec. sense of smell
- headache
- low-grade fever
- arthralgias
- skin rashes
if a pt. is icteric, how would that present?
- dark urine
- light or clay-colored stools
- pruritus
clinical manifestations of convalescent phase
- begins as jaundice is disappearing
- lasts weeks to months
- major complaints are malaise and easy fatigability
- hepatomegaly persists
- splenomegaly subsides
recovery phase of hepatitis
- homologous immunity to HAV or HBV
- pt. can be reinfected with other types of viral hepatitis, as well as different strains of HCV
- most pts. recover completely with no complications
complications of hepatitis
- acute liver failure
- chronic hepatitis (some HBV and majority HCV)
- cirrhosis
- hepatocellular carcinoma
how do we screen for hepatitis
specific antigen and/or antibody for each type of viral hepatitis
collaborative care of acute and chronic hepatitis
- well-balanced diet (increased calorie and low fat if not tolerated_
- vitamin supplements
- rest
- avoid alcohol intake and drugs detoxified by the liver
- notify possible contacts and health dept.
what drug therapy do we give with acute hepatitis C
pegylated interferon to reduce progression to chronic infection
goal of chronic hepatitis B
to decrease viral load, liver enzyme levels, and rate of disease progression
who should receive a hepatitis vaccine?
- all children at 1 year of age
- adults at risk
is isolation required for hepatitis?
no, just infection control measures
which hepatitis is there no vaccine?
HCV; do general measures to prevent transmission
how do stones form in cholelithiasis?
through biliary sludge
cholecystitis
most commonly associated with obstruction from stones or sludge
what occurs from inflammation in cholecystitis?
- it is confined to mucous lining or entire wall
- gallbladder is edematous and hyperemic
- maybe distended with bile pus
- cystic duct may become occluded
- scarring and fibrosis after attack
clinical manifestations of cholecystitis
- steady, excruciating pain
- tachycardia, diaphoresis, prostration
- may be referred to shoulder/scapula
- residual tenderness in RUQ near liver
- occur 3-6 hours after high-fat meal or when patient lies down
- indigestion
- fever
- jaundice
- N/V
- restlessness
- diaphoresis
total obstruction symptoms
- jaundice
- dark amber urine
- clay-colored stools
- pruritus
- intolerance of fatty foods
- bleeding tendencies
- steatorrhea
complications of cholecystitis
- gallbladder rupture that can lead to peritonitis
- gangrenous cholecystitis
- subphrenic abscess
- pancreatitis
- cholangitis
- biliary cirrhosis
- fistulas
- choledocholithiasis
what would lab tests show with gallbladder problems?
- inc. WBC
- inc. serum bilirubin level
- inc. urinary bilirubin level
- inc. liver enzyme levels
- inc. serum amylase level
collaborative care with cholecysitis
- pain control
- control infection
- maintenance of F/E balance
surgical therapy treatment of choice for cholecystitis
laparoscopic cholecystectomy
what drug can be given for pruritus in cholecystitis?
cholestyramine (questran)
after a laparoscopic cholecystectomy, what would the nurse do to maintain pt. comfort?
- referred pain to shoulder from CO2
- sims’ position
- deep breathing, ambulation, analgesia
most common complication of a pressure ulcer
recurrence
inflammatory response
- neutralizes and dilutes inflammatory agent
- removes necrotic materials
- establishes an environment suitable for healing and repair
vascular response of inflammatory response
after cell injury, arterioles in area briefly undergo transient vasoconstriction - decrease bleeding
what do vasodilation chemical mediators do?
- endothelial cell retraction
- increased capillary permeability
- movement of fluid from capillaries into tissue spaces - causing edema
chemotaxis
mechanism for accumulating neutrophils and monocytes at site of injury
neutrophils
- first leukocytes to arrive at site of injury (6-12 hours)
- phagocytize bacteria, other foreign material, and damaged cells
- short life span (24-48 hours)
*high neutrophils = body thinks it’s infected
monocytes
- second type to migrate to site of injury
- arrive within 3-7 days after onset of inflammation
- on entering tissue space, monocytes transform into macrophages
- assist in phagocytosis of inflam. debris
- have long life span and can multiply
macrophage
- important in cleaning the area before healing can occur
- may stay in damaged tissues for weeks
lymphocytes
- arrive later at the site of injury
- primary role involves immunity
major functions of cellular response
- enhanced phagocytosis
- increased vascular permeability
- chemotaxis
- cellular lysis
what can chronic inflammation result from?
changes in immune system (like autoimmune disease)
