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MedSurg 2 > Dysfunctions of Liver, Biliary Tract, and Pancreas > Flashcards

Dysfunctions of Liver, Biliary Tract, and Pancreas Flashcards

1
Q

Functions of the Liver

A 
blood clotting
carb metabolism
detoxification
fat metabolism
protein metabolism
bile production
bilirubin
blood filtration
blood reservoir
storage
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2
Q

Hepatitis

A

inflammation of the liver

causes:

  • viral (most common), 5 types (CMV, EBV = mono)
  • alcohol
  • medications (esp. ibuprofen)
  • chemicals
  • autoimmune diseases
  • metabolic problems
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3
Q

Hepatitis A Virus (HAV)

A
  • ranges from mild to acute liver failure
  • not chronic
  • vaccination available (get when 1 YO, adults at risk)
  • RNA virus transmitted via fecal-oral route
  • contaminated food or drinking water
  • post-exposure prophylaxis with HAV vaccine and immune globulin (IG)
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4
Q

Hepatitis B Virus (HBV)

A
  • acute or chronic disease
  • vaccination available
  • DNA virus transmitted:
  • perinatally
  • percutaneously (needle sticks)
  • via small cuts on mucosal surfaces and exposure to infectious blood, blood products, or other body fluids
  • post-exposure prophylaxis: vaccine and hepatitis B immune globulin (HBIG)
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5
Q

HBV: RF

A
  • household contact of chronically infected
  • patients on hemodialysis
  • health care and public safety workers
  • IV drug uses
  • recipients of blood products
  • higher risk sexual practices
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6
Q

Hepatitis C Virus (HCV)

A
  • acute: asymptomatic
  • chronic: liver damage
  • RNA virus transmitted percutaneously
  • IV drug use
  • higher-risk sexual behaviors
  • occupational exposure
  • perinatal exposure
  • blood transfusion before 1992 (before screening process)

no vaccine
no post-exposure prophylaxis

most common cause of liver transplant in US

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7
Q

Hepatitis Pathophysiology

A

acute infection:

  • large numbers of hepatocytes are destroyed
  • liver cells can regenerate in normal form after resolution of infection

chronic infection: can cause fibrosis and progress to cirrhosis

  • chronic HBV is more likely to develop in infants and those under age 5
  • HCV infection is more likely than HBV to become chronic
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8
Q

Hepatitis: S/Sx (general)

A

classified as acute or chronic

many pts are asymptomatic

sx: intermittent or ongoing
- anorexia
- malaise, fatigue, lethargy
- myalgias/arthralgia
- RUQ tenderness d/t liver inflammation

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9
Q

Hepatitis: S/Sx (acute phase)

A

maximal infectivity; lasts 1-6 months
sx during incubation OR no symptoms

  • n/v
  • RUQ tenderness
  • reduced sense of smell
  • find food repugnant
  • distate for cigarettes
  • hepatomegaly
  • lymphadenopathy
  • splenomegaly

icteric (jaundice) or anicteric

if icteric, pt can also have:

  • dark urine
  • light or clay-colored stools
  • pruritus
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10
Q

Hepatitis: S/Sx (convalescent phase)

A
  • begins as jaundice is disappearing
  • lasts weeks to months
  • major problems = malaise, easily fatigued
  • hepatomegaly persists
  • splenomegaly subsides
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11
Q

Hepatitis Recovery

A

most pts recover completely with no complications

most cases of acute hepatitis A resolve

some HBV and most HCV result in chronic hepatitis

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12
Q

Hepatitis Complications: Acute Live Failure

A

fulminant hepatic failure (severe and sudden onset)

manifestations include:

  • encephalopathy
  • GI bleeding
  • fever w/ leukocytosis
  • renal manifestations (oliguria, azotemia)

liver transplant is usually the cure

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13
Q

Hepatitis Complications: Cirrhosis

A

RF:

  • male gender
  • alcohol use
  • associated fatty liver disease
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14
Q

Hepatitis Complications: Hepatic Encephalopathy

A

potentially life-threatening spectrum of neurologic, psychiatric, and motor disturbances

results from liver’s inability to remove toxins (especially ammonia)

reduce ammonia formation:

  • lactulose (Cephulac), which traps ammonia in gut
  • Rifaximin (Xifaxan), antibiotic
  • prevent constipation

tx of precipitating cause:

  • lower dietary protein intake
  • control GI bleeding
  • remove blood from GI tract
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15
Q

Hepatitis Complications: Ascites

A

accumulation of excess fluid in peritoneal cavity
d/t reduced protein levels in blood, which reduces the plasma oncotic pressure

(fluid can become infected > peritonitis)

(portal HTN, hypoalbuminemia, hyperaldosteronism d/t low perfusion in kidney)

  • sodium restriction
  • diuretics, fluid removal
  • albumin
  • Tovaptan (Samsca)
  • Paracentesis
  • Transjugular intrahepatic protosystemic shunt (TIPS) - shunt blood around liver
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16
Q

Hepatitis Complications:

A
  • acute liver failure
  • cirrhosis
  • hepatic encephalopathy
  • ascites
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17
Q

Hepatitis: Dx

A
  • specific antigen and/or antibody for each type of viral hepatitis
  • liver function tests
  • viral genotype testing
  • physical assessment findings
  • liver biopsy
  • FibroScan (special u/s for liver that allows you to see how much scarring/fibrosis is in liver)
  • FibroSure (FibroTest)
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18
Q

Hepatitis: Tx - Medications

A

acute HAV infection: no specific meds

acute HBV infection: only if severe

acute and chronic HCV infection:

  • DAAs (direct-acting antivirals): block proteins needed for replication
  • 12wk oral regiment (>95% chronic HCV cure)

supportive drug therapy:

  • antihistamines for pruritus
  • antiemetics
  • Promethazine (Phenergan)
  • Ondansetron (Zofran)
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19
Q

Chronic Hepatitis B: Drug Therapy

A

Interferon:

  • naturally occurring immune protein
  • antiviral, anti-proliferative, and immune-modulating effects
  • pegylated interferon (PegIntron, Pegasys) given subcutaneously
  • SE = flu like symptoms, depression
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20
Q

Hepatitis Nutritional Therapy

A
  • check albumin levels
  • weight weekly at minimum
  • small meals w/ snacks (largest meal in AM)
  • vitamin supplements (liver damage may limit absorption and metabolism of fat-soluble vitamins A, D, E, and K)
  • limit sodium if edema or ascites occurs
  • antiemetics for n/v
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21
Q

Hepatitis: Nursing Assessment (Objective Data)

A 
low grade fever
jaundice
rash
hepatomegaly
splenomegaly
abnormal lab values
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22
Q

Cirrhosis

A
  • end-stage of liver disease, irreversible
  • extensive degeneration and destruction of liver cells
  • results in replacement of liver tissue by fibrous and regenerative nodules
  • usually happens after decades of chronic liver disease
  • most common causes in US are chronic hepatitis C and alcohol-induced liver disease

other causes:

  • right sided heart failure
  • extrememe dieting, malabsorption, obesity
  • environmental factors
  • genetic predisposition
23
Q

Cirrhosis: S/Sx

A

few sx in early-stage disease:

  • fatigue and enlarged liver may be early sx
  • blood tests may be normal (for compensated cirrhosis)

late manifestations:

  • result from liver failure and portal hypertension (jaundice, peripheral edema, ascites)
  • other: skin lesions, hematologic problems, endocrine problems, and peripheral neuropathies
  • liver becomes smaller, nodular
24
Q

Cirrhosis: Complications

A
  • PORTAL HTN
  • PERIPHERAL EDEMA: decreased colloidal oncotic pressure form impaired liver synthesis of albumin
  • ASCITES: accumulation of serous fluid in peritoneal cavity
  • ESOPHAGEAL VARICIES (most threatening complication)
  • HEPATIC ENCEPHALOPATHY
  • ASTERIXIS
  • IMPAIRED IN WRITING: difficulty in moving pen left to right
  • FETOR HEPATICUS (musty, sweet odor of patient’s breath)
25
Q

Esophageal Varicies

A

prevent bleeding/hemorrhage

  • avoid alcohol, aspirin, and NSAIDs
  • screen for presence w/ endoscopy w/ possible ligation
  • balloon tamonade
  • nonselective beta-blockers

If bleeding occurs, stabilize patient, manage airway, start IV therapy and blood products

drug therapy (restrict blood flow into portal):

  • Octreotide (Sandostatin)
  • Vasopressin

supportive measures for acute bleed

  • fresh frozen plasma
  • packed RBCs
  • Vitamin K
  • proton pump inhibitors
  • Lactulose (Cephulac) - enema that causes diarrhea, and rifaximin (Xifaxan)
26
Q

Cirrhosis: Dx

A
  • liver enzyme tests (alkaline phosphatase, AST, ALT, GGT)
  • total protein, albumin levels
  • serum bilirubin, globulin levels
  • cholesterol levels
  • prothrombin time
  • u/s elastography (Fibroscan)
  • MRI
  • Liver bx
27
Q

Cirrhosis: Nutritional Therapy

A

diet for pt w/o complications:

  • high calories (3000 cal/day)
  • high carb
  • moderate to low fat
  • between-meal snacks
  • protein restriction rarely needed

protein supplements for protein-calorie malnutrition

low-sodium diet for patient w/ ascites and edema
-seasonings to make food more palatable

oral hygiene
offer preferred foods
explanation of dietary restrictions
collaborate w/ dietician

28
Q

Cirrhosis: Measures to Relieve Pruritis

A
  • cholestyramine or hydroxyzine
  • baking soda or Alpha Keri baths
  • lotions, soft or old linen
  • antihistamines
  • temp control
  • short nails; rub with knuckles
  • monitor color of urine and stool
29
Q

Pancreatitis

A

acute inflammation ranging from mild edema to severe hemorrhagic necrosis

pancreas produces trypsinogen which is released into small intestine where it is activated to trypsin for digestion
-problem: d/t injury of the pancreas the activated trypsin refluxes back into pancreas causing auto-digestion and bleeding of the pancreas

prognosis: complete recovery > recurring attacks > chronic

can be life-threatening: severe pancreatitis can result in organ failure, sepsis, 25% mortality rate (pancreatic necrosis)

chronic: constant inflammation results in replacement of active tissue w/ fibrous scar tissue

30
Q

Pancreatitis: Causes

A

anything that causes injury to pancreas:

  • most common cause: gallbladder disease (stones) and then alcoholism
  • biliary sludge increases risk
  • hypertriglyceridemia (>1000 mg/dL)
  • less common: trauma, viral infections, penetrating Duodenal ulcer, & abscesses
31
Q

Acute Pancreatitis: S/Sx

A

abdominal pain predominant:

  • LUQ or mid epigastric
  • radiates to back
  • sudden onset
  • eating worsens pain
  • starts when recumbent
  • not relieved with vomiting

low-grade fever
leukocytosis
hypotension, tachycardia
jaundice

decreased or absent bowel sounds
crackles or lungs
abdominal skin discoloration (Grey Turner’s spots or signs - bluish flank discoloration, Cullen’s sign - bluish periumbilical discoloration)
shock

32
Q

Pancreatitis: Complications

A

Pseudocyst: a cavity surrounding outside of pancreas where necrotic products, enzymes, exudates leak into. May resolve on own or may perforate causing peritonitis. Tx w/ prolonged antibiotics and may require draining - surgical procedure,

Abscess: fluid filled cavity w/in pancreas d/t necrosis of pancreas. May become infected or perforate. Requires surgical drainage to prevent sepsis

33
Q

Acute Pancreatitis: Dx

A 
abdominal u/s
x-ray
contrast-enhanced CT scan
ERCP - endoscopic retrograde cholangiopancreatography
EUS - endoscopic ultrasonography
MRCP - magnetic resonance cholangeiopancreatography
angiography
chest x-ray
34
Q

Acute Pancreatitis: Conservative Care

A

shock: plasma or plasma volume expanders (dextran or albumin)

fluid/electrolyte problems:

  • lactated ringers solution
  • central venous pressure readings

ongoing hypotension: vasoactive drugs (dopamine)

prevent infection:

  • enteral nutrition
  • antibiotics
  • endoscoptically or CT guided percutaneous aspiration

supportive care:

  • aggressive hydration
  • pain management (IV opioid analgesics, antispasmodic agent)
  • management of metabolic complications (O2, glucose levels)
  • minimizing pancreatic stimulation (NPO status, NG suction, decreased acid secretion, enteral nutrition if needed)
35
Q

Acute Pancreatitis: Surgical Therapy

A

for gallstones:

  • ERCP plus endoscopic sphincterotomy
  • laparoscopic cholecystectomy
36
Q

Acute Pancreatitis: Drug Therapy

A 
IV morphine
antispasmodics
antacids
proton pump inhibitors
carbonic anhydrase inhibitors
37
Q

Acute Pancreatitis: Nutritional Therapy

A

-NPO status initially
-enteral versus parenteral nutrition
-monitor triglycerides if IV lipids given
small, frequent feeding when able (high-carb, low-fat)
-no alcohol
-supplemental fat-soluble vitamins

38
Q

Chronic Pancreatitis

A

continuous, prolonged, inflammatory, and fibrosing process of the pancreas

acute exacerbations (frequent attacks intervals of months or years)

39
Q

Chronic Pancreatitis: Tx

A

no smoking, no alcohol, no caffeine

meds:
- pancreatic enzyme replacement-enteric coated, fat-soluble vitamins
- PPI
- analgesics for pain relief (morphine or fentanyl patch [Duragesics])

diet:
- bland, low-fat
- small, frequent meals
- high carb die (unless diabetic then moderate and cover with insulin)

if DM develops, insulin or oral diabetic meds

40
Q

Chronic Pancreatitis: S/Sx

A

abdominal pain

  • located in same area as in acute pancreatitis
  • heavy, gnawing feeling; burning and cramp-like
  • more frequent w/ weight loss

constipaion
mild jaundice w/ dark urine
steatorhea
DM

41
Q

Pancreatic Cancer

A

cause unknown

RF: chronic pancreatitis, smoking, high fat die, DM, and certain chemical exposures

Dx: at later stage when metastasis has already occurred via CT, u/s, ERCP, MRI

prognosis: die w/in 5-12 months of dx

Sx: same as chronic pancreatitis

Tx: surgery (whipple’s procedure), radiation, chemo

42
Q

Gallbladder Disease

A

Cholelithiasis:

  • most common disorder of biliary system
  • stones in gallbladder
  • RF: female, pregnancy, obesity
Cholecystitis-
inflammation of gallbladder:
-confined to mucous lining or entire wall
-gallbladder is edematous
-may be distended with bile or pus
-cystic duct may become occluded
-scarring and fibrosis after attack

usually associated with gallstones

43
Q

Cholelithiasis: Etiology and Pathophysiology

A

-stasis of bile leads to super saturation and changes in composition of bile (biliary sludge)
-immobility, pregnancy, and inflammatory or obstructive lesions in biliary system, decreased bile flow
-develop when balance that keeps cholesterol, bile sales, and calcium in solution is changed, leading to precipitation
-stones may stay in gallbladder or may migrate to cystic or common bile ducts
(may lodge in ducts and cause an obstruction)

44
Q

Gallbladder Disease: S/Sx

A

vary from severe to none at all

pain more severe when stones moving or obstructing:

  • steady, excruciating
  • tachycardia, diaphoresis
  • residual tenderness in RUQ
  • occur 3-6 hours after high-fat meal or when patient lies down

when total obstruction occurs:

  • dark amber urine - more bilirubin eliminated in urine
  • clay-colored stools - no bilirubin moved to small intestines
  • pruitis
  • intolerance to fatty foods
  • bleeding tendencies: d/t lack or decreased absorption of Vitamin K resulting in decreased production of prothrombin
  • steatorrhea

in addition to pain:

  • indigestion
  • fever, chills
  • jaundice
45
Q

Gallbladder Disease: Dx

A 
u/s
ERCP
Percutaneous transhepatic cholangiography
Lab tests: 
-increased WBC
-increased serum bilirubin level
-increased urinary bilirubin level
-increased liver enzyme levels
-increased serum amylase level
46
Q

Cholelithiasis: Tx

A

dependent on sage of disease

oral dissolution therapy:

  • Ursodeozycholic acid (Ursodiol)
  • Chenodeozycholic acid (Chenodiol)

Extracorporeal shock-wave lithotripsy (ESWL):

  • if stones cannot be removed via endoscope
  • high energy shock waves disintegrate gallstones
  • takes 1 to 2 hours
  • used in conjunction with bile acids
47
Q

Cholecysitis: Tx

A

control possible infection:

  • antibiotic treatment
  • NG tube for severe n/v

cholecystotomy:
-opioids for pain control

anticholinergics:

  • decrease GI secretions
  • counteract smooth muscle spasm
48
Q

Gallbladder Disease: Meds

A

most common:

  • analgesics (morphine)
  • anticholinergics (atropine)
  • fat-soluble vitamins (A, D, E, K)
  • bile salts
49
Q

Gallbladder Disease: Nutritional Therapy

A
  • small, frequent meals with some fat
  • diet low in saturated fat
  • high in fiber and calcium
  • reduced-calorie diet if pt is obese
  • avoidance of rapid weight loss
50
Q

Gallbladder Disease: Acute Care

A

pain management: give drugs as needed before pain becomes severe, observe for SEs

comfort measures: positioning, oral care

manage n/v:

  • NG tube, gastric decompression
  • oral hygiene, care of nares
  • accurate I&O
  • maintaining suctioning
  • antiemetics
  • comfort measures

Pruritus relief measures:

  • antihistamines
  • baking soda or Alpha Keri baths
  • lotions
  • soft linen
  • control temps
  • short, clean nails
  • scratch with knuckles
  • Cholestyramine
51
Q

Gallbladder Disease: Surgical Therapy

A

laparoscopic cholecystectomy:

  • tx of choice
  • removal of gallbladder through 1 to 4 puncture holes
  • minimal postoperative pain
  • resume normal activities, including work, within 1 week
  • few complications

Incision (open) cholecystectomy:

  • removal of gallbladder through right subcostal incision
  • T-tube inserted into common bile duct (ensures patency of duct, allows excess bile to drain)
52
Q

Transhepatic Biliary Catheter

A
  • preoperative or palliative (when endoscopic drainage fails)
  • inserted percutaneously and attached to drainage bag
  • replace fluids lost w/ electrolyte-rich drinks
  • skin care important
53
Q

Gallbladder Disease: Postoperative Care

A

laparoscopic cholecystectomy:

  • monitor for complications
  • patient comfort (referred pain to shoulder from CO2, Sims position, deep breathing, ambulation, analgesia)
  • clear liquids
  • discharged same day

open-incision cholecystectomy:

  • monitor for post-op complications
  • T-tube or JP drain maintenance
54
Q

Gallbladder Disease: Ambulatory Care

A

laparoscopic cholecystectomy:

  • remove bandages day after surgery and then can shower
  • report sx of infection
  • gradually resume activities
  • return to work in 1 wk
  • may need low-fat diet for several weeks

open-incision cholecystectomy:

  • no heavy lifting for 4-6 wks
  • usual activities when feeling ready
  • may need low-fat diet for 4-6 wks

MedSurg 2 (18 decks)

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