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• Accessory Organs ○ Types of stones

○ Julie Mann, NP • Cholesterol (about 80%)


○ N145 • calcium salts with bilirubin
• Patient #1 • mixed compositions
○ Mrs. Miller is a 21 year old morbidly obese • Who’s at risk?
married female. She develops acute  "Fair, fat, female, and over forty.
abdominal pain in the epigastric area with 4f's"
nausea and vomiting. She calls the HMO  obesity
nurse helpline to report her symptoms and  women
get advice.  multiple pregnancies
• Questions  oral contraceptives
○ What might be going on with Mrs. Miller? • Increased estrogen interferes
• MI, GERDs, appendicitis (referred pain), with bile action.
intestinal blockage, gallstones. Billiary  Native Americans
colic. • Cholecystitis
○ What advice would you expect her to
receive?
• BRAT diet (bananas, rice, apple sauce,
toast)

• Cholelithiasis • Cholecystitis
○ Contributing factors ○ inflammation of the gallbladder d/t
• abnormal composition of the bile obstruction of the gallbladder outlet
• stasis of bile (obstruction) • Stone stuck in collecting duct.
• inflammation of the gall bladder
○Most cases associated with cholelithiasis • Infex (fever), possible rupture.
(gallstones) ○ As an urgent care nurse, what orders would
• mucus membrane is rendered you anticipate for the care of Mrs. Miller?
vulnerable to action of bile salts, • Septic --> emergency care.
further inflammatory condition.
○ Other cause is acalculous cholecystitis (no
stone present, can be trauma/infex) r/t
sepsis (huge infectious process in blood,
metabolic needs increase greatly), trauma,
or infection of the gallbladder
• damage from ischemia to the
gallbladder
• can lead to gangrene and perforation
○ May be acute - one big attack.
○ Chronic - multiple stones - colicky pain =
achy pain.
• Case Study
○ Mrs. Miller follows the advice she is given
and the pain persists and increases in
intensity. 2 days later...She rates her pain a
9/10 and states it has moved from the
epigastric area to her right upper quadrant ○ Pancreas does not take stress very well.
and to her back. She can’t eat and • Acute Pancreatitis
continues her n/v. She calls the nurse ○ reversible inflammatory process r/t
helpline again...
premature activation of pancreatic
○ Mrs. Miller again follows the directions of
enzymes
the nurse helpline. For 2 more days she has ○ Causes autodigestion of pancreatic tissue
persistent pain, anorexia, n/v. She develops
(pancreatic enzymes activate in pancreas)
a fever and pallor. Her family persuades her ○ inflammatory process may lead to systemic
to go to the urgent care.
inflammation and multiorgan system failure
○ At the urgent care her VS are T: 102.5, BP:
○ common causes
85/56 (RBCs are lysed, decreases Blood
1. Chronic alcohol ETOH: may stimulate
volume, or septic shock), HR 122, RR 36
pancreatic secretions, may obstruct the
and severe abdominal tenderness.
○ What might be going on with Mrs Miller?
sphincter of the pancreatic duct
i.Alcohol may stimulates secretion of
pancreatic enzymes.
1. cholelithiasis: obstruction leads to
activation of enzymes
• Case Study
○ Mrs. Miller is rushed to her local hospital
and discovered to have cholecystitis, acute
pancreatitis, and sepsis. She develops
acute respiratory distress and is intubated.
She takes an air ambulance to UCLA
Medical Center. She is immediately taken
into the OR.
○ What could have happened to Mrs. Miller?
• Actue pancreatitis, cholestitis (sp?)
○ What do you think they found in the OR?
• A Mess, ischemic inflamed necrotic
gallbladder broken apart, ischemic
pancreas inflamed necrotic, peritonitis
○ What further complications does she face?
• Liver - excess bile synthesis, bile sits,
expands size of liver, failure.
• Cirrhosis
○ liver tissue replaced with fibrous tissue and
nodules
○ fibrous tissue disrupts flow in vasculature
and biliary ducts
• Vasculature of liver becomes
obstructed, further exacerbates the
situation.
○ Assoc. with alcoholism, viral hepatitis, toxic
drugs, and biliary obstruction
○ Predisposes to portal hypertension and liver
failure
○ Under 20% of liver functioning --> start to
show signs of liver failure.

• Clinical Signs of Cirrhosis


○ Muscle wasting, ascites, hemorrhoids (inc
resistence against venous system),
ecchymose easily, purpura
(extremeties/abd), spleen enlarged (backup
in circ), awful breath (fetor hepaticus),
spider veins telangiectetas,
encephalopathy (high amonia in blood) -->
confusion, restlessness; jaundice, edema,
esophageal varices (backup in circ up to
esophagus, bleed in esophagus)
• Liver Failure (see book for pic)

• Jaundice
○ yellow discoloration of the skin and deep
tissues
• Ascites • First seen in sclera, elastic tissue.
○ Late stage cirrhosis. ○ high bilirubin level
○ excess fluid in the peritoneal space ○ Babies (particularly premi babies) overturn
○ occurs in late stage cirrhosis and portal RBCs at rapid pace, unable to eliminate
hypertension bilirubin at adult rate (feces) d/t immature
○ causes: GI tract.
• Treat by getting them to eat/poop.
• increased capillary pressure and
Possibly photolight therapy.
obstruction of venous flow in the liver,
○ 4 causes
hard to take deep breaths, dyspnea
particular at night. • excessive destruction of RBC’s
○ abdominal discomfort, dyspnea, & insomnia i. Usually only with Blood cell
○ Treatment transfusion. Sometimes genetic
• Paracentesis- take out fluid. Watch condition.
• impaired uptake of bilirubin by the liver
electrolytes!
• decreased conjugation of bilirubin
• Diuretics
• Obstruction/backup of bile flow
○Icterus period
• follows prodromal period by 5-10 days
• jaundice (except in HCV), severe
pruritis (buildup of bilirubin in skin) and
liver tenderness (inflamed)
○ Convalescent period
• increased feeling of well-being,
disappearance of jaundice, appetite
returns
• Hepatitis A
○ self limiting disease (happens and goes
• Viral Hepatitis away on own), rarely causing liver failure
○ All cause Inflammation of the liver and death
○ fecal-oral transmission (Get Hep A vaccine
○ HAV, HBV, HDV, HCV, HEV
for travel, unsanitary food prep)
○ Differ in the mode of transmission,
• Children, unsanitary food prep, day
incubation period, mechanism and degree
care centers, raw oysters, etc.
of liver damage, and presence of carrier
○ brief incubation period (15 to 50 days)
states
○ Modes of injury: • Transmitted to other people before
• direct cellular injury symptoms present.
○ virus replicates in liver, excreted from liver
• immune response to viral antigens
in bile, shed in stool
○ Amount of injury depends on immune
○ fecal shedding 2 weeks before symptoms
response
○ abrupt onset of fever, malaise, nausea,
• Chronic vs acute.
anorexia, abdominal discomfort (liver
○ Clinical course varies
inflammation), dark urine, & jaundice
• Acute Viral Hepatitis ○ IgM anti-HAV antibodies appear early and
○ Prodromal (preicteral/prejaundice) period
IgG antibodies lasts for years
• general malaise, myalgia, arthralgias, ○ immunization available (CDC recommends
easy fatigability, severe anorexia, n/v/d for all children)
may occur. Abdominal pain on R side
• Hepatitis B
• can be abrupt or insidious onset ○ can cause acute hepatitis, chronic hepatitis
• Period length determines on type of after acute episode, progression to
virus acquired cirrhosis, & fulminant hepatitis
(aggressive/rapid progression of disease
process)with massive hepatic necrosis.
○ virus found in most body secretions and in
blood.
○ Longer incubation period.
○ carrier state - some ppl asymptomatic but
spread continually.
○ can be transmitted by oral, sexual contact,
and blood secretions (needle stick).
○ immunization available (recommended for
Health Care workers, Children for school)
• Hepatitis C
○ most common cause of chronic hepatitis,
cirrhosis, and hepatocellular cancer
○ virus transmitted in blood & by sexual
contact with blood present, blood secretion.
○ carrier state (not everybody develops state)
○ usually asymptomatic or have a nonspecific
course (fatigue, malaise, anorexia, &
weight loss, may not remember) for 2 to 12
weeks
○ incubation period from 2 to 26 weeks
○ Most people will develop chronic hepatitis,
permanent liver damage, cancerous cells.