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NU 360 > Ch. 50 & 51 > Flashcards

Ch. 50 & 51 Flashcards

1
Q

hepatitis is

A

widespread viral inflammation of liver cells
- we are focusing on viral hepatitis: inflammation of liver caused by a virus
- other causes include: alcohol, chemicals (nice to know, not need to know)

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2
Q

which types of hepatitis are uncommon

A

hepatitis F and G

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3
Q

types of hepatitis that come from the bowel

A
  • A & E
  • fecal-oral: ingesting poop/contaminated food (A), contaminated water (E -rare)
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4
Q

hepatitis A

A
  • similar to that of a typical viral syndrome; often goes unrecognized
  • spread via the fecal-oral route
  • really hard to kill, stays alive on surfaces and hands
  • not horrible in healthy people: flu-like illness
  • muscle aches, myalgia, some people are asymptomatic
  • typically not life-threatening
  • healthy person, usually doesn’t leave liver damage
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5
Q

health promotion: hep A

A
  • handwashing
  • vaccination
  • avoid contaminated food and water
  • immune globulin within 14 days if exposed
  • if traveling: get hep A vaccine, wash fruits/vegs/hands
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6
Q

hepatitis B

A
  • spread via blood
  • needle-sticks, mom to baby, blood transfusions (not rly now), blood to blood exposure, unprotected sex
  • symptoms occur in 25 to 180 days after exposure, don’t know exposed and not understand your symptoms
  • sx can be vague: fever, crummy, fatigue, myalgia
  • sx could be more severe: dark urine, N/V, abdominal pain
  • pt can have immune response and be asymptomatic, in acute phase- not realize that they still have the disease
  • hepatitis carriers can infect others, even if they are without symptoms
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7
Q

health promotion: hep B

A
  • vaccine
  • standard precautions: gloves, eye protection, careful handing of blood and bodily fluid products
  • treat every patient as if they are a carrier
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8
Q

hepatitis C

A
  • spread to blood to blood
  • needle-sticks, sharing contaminated needles, sexually (not as easily as hep b): men who have unprotected sex with men, pt with multiple sexual problems
  • incubation period is 21 to 140 days
  • most individuals are asymptomatic
  • damage occurs over decades: chronic
  • scarring on liver leads to cirrhosis and can lead to liver cancer
  • new treatment now allow for complete cure: oral therapy- take it for a long time, weeks to months
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9
Q

clinical manifestations of hepatitis:
CNS, GU, Skin, MS, GI, Labs

A
  • CNS: encephalopathy- confusion, change in mental status
  • GU: dark concentrated urine (brownish)
  • MS: myalgia, muscle pain, joint pain, fatigue
  • GI: nausea, abdominal pain, anorexia (loss of appetite), light colored stools (clay color* flag of liver disease)
  • skin: jaundice (bile, yellow skin), dryness, pruritus/itchy
  • labs: increase in liver fx test: LFTs, antibody tests (this dx the type of hepatitis)
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10
Q

hepatitis lab assessment

A
  • liver enzymes
  • blood tests specific to hepatitis type
  • the antibody test will tell you what type of hepatitis the patient has
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11
Q

diagnostic assessment for hepatitis

A
  • liver biopsy
  • labs: liver enzymes, blood tests: antibody test to ID type of hepatitis
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12
Q

hepatitis patient problems

A
  • weight loss d/t complications associated with inflammation of the liver
  • fatigue d/t decreased metabolic production
  • potential for infection r/t state of immunocompromised
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13
Q

nonsurgical management of hepatitis

A
  • physical rest: take rest (plan activity around rest times)
  • psychological rest
  • diet therapy: frequent small meals, drink water, eat appealing foods
  • drug therapy includes: antiemetic to help with nausea, antiviral medications, be careful with drugs bc they hurt the liver
  • patient is immunocompromised so make sure patient takes precautions: handwashing, avoid crowds, avoid sick people
  • consult doctor
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14
Q

acute cholecystitis is

A
  • inflammation of the gallbladder
  • cholelithiasis (gallstones) usually accompanies cholecystitis
  • usually caused by gallstones causing a blockage which causes build up of bile resulting in inflammation
  • can have complications
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15
Q

acalculous cholecystitis is

A

inflammation in the absence of gallstones
- biliary stasis: bile is not moving in the duct

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16
Q

calculous cholecystitis is

A

the obstruction of the cystic duct by a stone, which creates an inflammatory response
- gallstones can cause a back up of bile into the liver and pancreas, bile and pancreatic enzymes needed to break down food in the duodenum

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17
Q

chronic cholecystitis

A
  • repeated episodes of cystic duct obstruction result in chronic inflammation
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18
Q

sx of chronic cholecystitis

A
  • jaundice: build up of bilirubin in the skin b/c bile cant get to duodenum to be excreted via stool
  • icterus: jaundice in the sclera: yellow sclera/eyes
  • pruritus: itchy skin from buildup of bilirubin and waste products in the blood; scratches on skin
  • stool change: gray stools d/t absence of bile- bile gives stool brown color; fatty stools- aka steatorrhea
  • urine change: dark amber, foamy/frothy appearance
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19
Q

cholecystitis: etiology/genetic risk

A
  • familial: lifestyle and diet- influenced by how a person was raised
  • lifestyle: sedentary
  • diet: high-fat, low-fiber, processed carbs
  • obesity
  • age: older at higher risk; females: 20-60 yo
  • medications: hormone replacement therapy
  • type 2 DM

4 F’s risk factors
female
forty
fat
fertile: hormonal changes/pregnancy

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20
Q

chronic cholecystitis: clinical manifestations

A
  • Abdominal pain: upper R quadrant radiates to R shoulder blade/scapula, comes and goes, worse after eating foods high in fat
  • Flatulence, indigestion, belching, anorexia (not eating b/c of association with pain), nausea and vomiting
  • Biliary colic: when stone moves through duct, causes spasms in the duct- acute pain that comes and goes
  • Murphy’s sign- deep palpation of liver, inspiratory arrest: gallbladder inflammation
  • Blumberg’s sign- rebound tenderness: pain on release = peritoneal inflammation
  • Steatorrhea: fatty stools
  • elevated temp, dehydration
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21
Q

cholecystitis: diagnostic tests

A
  • Differential diagnosis: b/c considering all options
  • Laboratory tests: high WBC, high bilirubin, LFTs: ALT/AST/LDH (liver), amylase/lipase (pancreas)
  • Abdominal x-ray: will only see calcified stones
  • Ultrasound of gallbladder: best, most common, slightly painful, non-invasive and quick
  • HIDA scan: requires pt to have chemical tracer injected via IV, evaluates patency of biliary duct system
  • ERCP: more invasive, contrast dye, ID blockages, can open blockage and restore flow in ducts
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22
Q

priority problems for patients with cholecystitis

A
  • weight loss d/t decreased intake due to pain, nausea, and anorexia
  • acute pain d/t gallbladder inflammation and/or gallstones
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23
Q

cholecystitis: nonsurgical management

A
  • diet therapy: low-fat, IF going to surgery: NPO
  • drug therapy: antiemetics, IVFs for dehydration, ABT w/ s/ of infection/sepsis, prophylactic ABT before surgery, can give meds that dissolve gallstones
  • percutaneous transhepatic biliary catheter insertion: catheter inserted to drain bile outside the body so it is not building up in the gallbladder
  • could also do an internal drain: gallbladder to duodenum (bypass the ducts)
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24
Q

cholecystitis surgical management: laparoscopic cholecystectomy, post-op care

A
  • minimally invasive, in and out same day- less risk of infection, less pain
  • Free air pain result of carbon dioxide retention in the abdomen
  • first 12 hours lay low
  • Ambulation: walk around more can help alleviate pockets of CO2
  • Return to activities in 1 to 3 weeks
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25
Q

cholecystitis surgical management: traditional cholecystectomy

A
  • open the abdomen, more extensive, more pain, longer recovery, longer hospital stay
  • Opioids via PCA pump d/t pain control
  • T-tube (and care of): drains bile externally to allow healing, temporary thing
  • Antiemetics d/t N/V
  • Wound care & JP drain: s/ infection, dressing changes- surgeon does 1st change
  • NPO- ensure passing gas/has had BM before giving food
  • Nutrition therapy: IVF
  • ice to site for pain
  • pt teaching
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26
Q

acute pancreatitis is

A

Serious and possibly life-threatening inflammatory process of the pancreas
- pancreatic enzymes attack the pancreas

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27
Q

Necrotizing hemorrhagic pancreatitis

A
  • when inflammation or fluid collection spreads to a nearby artery, causing it to erode and bleed
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28
Q

acute pancreatitis process

A
  • Lipolysis: lipase becomes active and attacks the pancreas
  • Proteolysis: splitting of proteins in the pancreas- breakdown of tissue
  • Necrosis of the Blood Vessels: elastase is activated, breaks down the blood vessels, causing them to dissolve and bleed/hemorrhage
  • Inflammation: of the pancreas itself, increased WBCs
  • abscesses form
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29
Q

acute pancreatitis can be caused by

A
  • alcoholism
  • gallstones
  • drug use: cocaine
  • infection
  • other unknown causes
  • operative manipulation and trauma
  • blunt abdominal trauma
  • biliary tract disease
  • post-ERCP: complication of ERCP
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30
Q

autodigestion refers to when

A

the enzymes the pancreas produces become active and eat (digest) itself

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31
Q

acute pancreatitis: clinical manifestations

A
  • skin: jaundice
  • pulmonary: L lung pneumonia, L pleural effusion- resp distress, dyspnea, lung sounds, O2 sat
  • endocrine: hyperglycemia/increaed glucose d/t no/decreased insulin production
  • cellular
  • abdominal: mid-epigastric/L upper Q pain radiates to L flank/shldr, “boring”/intense pain; cullen’s sign, turner’s sign
  • paralytic ileus: absent/decreased bowel sounds
  • elevated temp, tachycardia, low BP
  • at risk for hypovolemic/septic shock
32
Q

cullen’s sign

A

bruising or swelling around the UMBILICUS
- gray/blue discoloration to abdomen
- sign of intraperitoneal bleeding (acute pancreatitis)

33
Q

turner’s sign

A

ecchymosis or bruising on the lower abdomen or FLANK
- gray/blue discoloration to abdomen
- rare sign of internal bleeding in the abdomen
- usually indicative of severe acute pancreatitis (severe acute necrotizing pancreatitis)

34
Q

acute pancreatitis: labs and diagnostic tests

A
  • amylase/trypsin (elevated w/in 12 hrs, then drops)
  • lipase/elastase (stays elevated for longer)
  • glucose: increased
  • bilirubin: increased
  • WBC: increased
  • calcium and magnesium: decreased
  • CT scan ** gold standard for pancreas
  • ultrasound if gallbladder involved
  • chest x-ray if resp concerns
35
Q

priority collaborative problems for patients with acute pancreatitis

A
  • acute pain d/t pancreatic inflammation and enzyme leakage around pancreas
  • weight loss d/t inability to ingest food and absorb nutrients
36
Q

complications of acute pancreatitis

A
  • Hypovolemia: d/t dehydration, blood loss
  • Hemorrhage: of blood vessels
  • Acute renal failure
  • Paralytic ileus: frozen intestines/no digestion
  • Hypovolemic or septic shock
  • Pleural effusion, ARDS, pneumonia
  • Diabetes: long-term chronic effects
37
Q

acute pancreatitis: medical management

A
  • NPO during acute phase to allow pancreas to rest
  • medications
  • IVFs

procedures:
- NGT: severely ill pt
- Endoscopic retrograde cholangiopancreatography: for gallstones causing pancreatitis

38
Q

acute pancreatitis meds

A
  • analgesics: PCA, opioids- takes a few days to get pain under control
  • antiemetics: N/V
  • histamine2 receptor antagonists/PPIs: to reduce gastric acid secretion
  • antibiotics: for infection/sepsis, abscess
  • IVFs
39
Q

Endoscopic retrograde cholangiopancreatography (use/purpose)

A
  • dx use: to identify location of gallstones
  • therapeutic use: to assist with removal of gallstones
40
Q

acute pancreatitis surgical management: pre-op

A

NGT may be inserted

41
Q

acute pancreatitis surgical management: operative procedures

A
  • surgically drain the abscess
  • acute pancreatitis typically does not need surgery- unless r/t gallstones
42
Q

acute pancreatitis surgical management: post-op

A
  • monitor drainage tubes and record output from drain (like JP drain)
  • provide meticulous skin care and dressing changes
  • maintain skin integrity
43
Q

chronic pancreatitis is

A

Progressive destructive disease of the pancreas, characterized by remissions and exacerbations
- long-term, repeated exacerbations and remissions
- over time, pancreas is damaged more and more over time

44
Q

chronic pancreatitis assessment: s/sx

A
  • Abdominal pain
  • Ascites: fluid accumulates in abdomen, protruding abdomen
  • Respiratory compromise
  • Steatorrhea
  • Weight loss, protein malabsorption
  • edema in legs/feet/hands
  • Jaundice
  • Dark urine
  • Polyuria, polydipsia, polyphagia: s/ of DM
  • elevated bilirubin, amylase, glucose
45
Q

chronic pancreatitis treatment: nonsurgical

A
  • Analgesic administration: opioids/non-opioids
  • Enzyme replacement (PERT): PANCREALIPASE (Pancrease), taken with meals/snacks to aid in digestion of food since pancreas is not making enzymes. NO CHEWING, wipe mouth after taking
  • Insulin therapy: if diabetic as result (hyperglycemia)
  • Diet therapy: high protein, moderate-high carb, high calorie, limit fats
  • avoid alcohol, caffeine, nicotine
  • TPN possible with pt on bowel rest (NPO)
46
Q

Most serious complication of pancreatitis/necrotizing pancreatitis

A

pancreatic abscess
- always fatal if untreated (sepsis)

47
Q

pancreatic abscess: what is it and what will you see

A
  • Most serious complication of pancreatitis; always fatal if untreated (sepsis)
  • High fever: up to like 104
  • puss
  • Blood cultures
48
Q

treatment of pancreatic abscess

A
  • Drainage via the percutaneous method (drain or tube) or laparoscopy (sugery); may need to be done multiple times
    *Antibiotic treatment alone does not resolve abscess
49
Q

cirrhosis is

A
  • extensive scarring of the liver 2nd to chronic irreversible reaction to hepatic inflammation and necrosis
  • characterized by widespread fibrotic (scarred) bands of connective tissue
  • this changed the liver’s normal makeup and its associated cellular regulation
  • inflammation destroys hepatocytes
  • liver becomes nodular; blood and lymph flow are impaired- resistance to blood flow, blood backs up- portal HTN
50
Q

cirrhosis patho: early v. late

A
  • early: liver is enlarged, firm, hard (palpable)
  • late: liver shrinks, nodular (not palpable)

changes from early to late progress over years

51
Q

causes of cirrhosis

A
  • Alcohol* chronic alcoholism, years
  • Hepatitis- viral & autoimmune hepatitis
  • Drugs and toxins
  • Biliary disease
  • Nonalcoholic fatty liver disease
  • Metabolic/Genetic causes
  • Cardiovascular disease
52
Q

prevalence of cirrhosis: chronic liver disease and cirrhosis are major causes of ___

A

Combined, incidence of chronic liver disease and cirrhosis are a major common cause of death

53
Q

cirrhosis assessment

A
  • assess for exposure to alcohol and drugs, herbs, chemicals
  • risk of hepatitis: determine if there has ever been a needle-stick injury, tattoo placement, imprisonment, or employment as a healthcare worker, firefighter, or police officer
  • risk of hepatitis: assess sexual history and orientation
  • inquire about family history
  • collect previous medical history of pt: recent exposure to hepatitis, jaundice, have a hepatitis episode
54
Q

early sx of cirrhosis

A

vague symptoms
- fatigue
- significant change in weight: wt loss
- GI sx: anorexia, vomiting
- abdominal pain and liver tenderness
- liver enlarged early stages of cirrhosis/palpable (hepatomegaly: liver enlargement)

55
Q

late sx of cirrhosis

A
  • skin: jaundice, pruritis, rashes, petechiae, ecchymoses, palmar erythema: red palms, dry skin
  • vascular lesions: spider angiomas on skin r/t hormonal changes associated with liver disease
  • neuro: changes in mental responsiveness & memory
  • CNS: confusion, altered mental status, coma
  • CV: fluid overload, peripheral edema, fluid shifting
  • abdominal:
    -caput medusae: dilated abdominal veins
    -ascites: 3rd spacing fluid in the abdomen
  • asterixis: tremor- flapping of the hand, dorsiflexion of wrist
  • hematemesis, melena
  • female: amenoria
  • male: gynecomastia
56
Q

cirrhosis labs

A
  • AST/ALT/LDH: elevated, ESLD may be normal levels
  • serum bilirubin: elevated
  • albumin/protein levels: decreased albumin
    -causes ascites, edema
  • ammonia: hepatic encephalopathy, elevated
    -causes neurologic effects
  • PT/INR: prolonged/elevated- no bile= no absorption of vit K- unable to make clotting factors
    -bleeding risk
  • CBC- wbc/hgb/hct/plts: decreased
    -spleen impacted: decreased WBC/plt
    -anemic, thrombocytopenia
57
Q

cirrhosis patient problems

A
  • Fluid overload d/t third spacing of abdominal and peripheral fluid (ascites)
  • Potential for hemorrhage d/t portal hypertension
  • Acute confusion and other cognitive changes d/t increased serum ammonia levels and/or alcohol withdrawal
  • Pruritis d/t increased serum bilirubin and jaundice
58
Q

cirrhosis management\ patient problems

A

fluid and electrolyte imbalance
- low sodium diet
- vitamins, supplements, folate, thiamine, multivitamins through the IV/banana bag for hospitalized pt
- medications: diuretics
- daily weights, measure I&Os

high risk for bleeding
- propanolol (BB slows HR and decreases pressure)

high risk for portal-systemic (hepatic) encephalopathy

59
Q

complications of end stage liver disease

A
  • Portal hypertension: b/c blood is not flowing through easily, build up of pressure
  • Ascites
  • Bleeding esophageal varices
  • Coagulation defects: clotting issues
  • Jaundice
  • Portal-systemic encephalopathy with hepatic coma
  • Hepatorenal syndrome
  • Spontaneous bacterial peritonitis
60
Q

portal HTN is

A

Persistent increase in pressure within the portal vein
- Blood flows back to spleen: enlarged spleen (splenomegaly)
- Esophageal, stomach, intestines, abdominal and rectal veins dilate: increased pressure in the veins causes dilation

61
Q

treatment of portal HTN

A
  • propranolol
  • decrease HR and pressure to reduce risk of bleeding
62
Q

ascites is

A

Accumulation of free fluid in peritoneal cavity 2nd to portal htn leaking fluid
- Triggers renal vasoconstriction
- Increases NA and H2O retention

63
Q

ascites treatment

A
  • Diet: low sodium
  • Diuretics to get rid of extra fluid
  • Paracentesis: draining fluid out of abdomen
  • Albumin IV: after paracentesis may need infusion to keep fluid in vascular space/prevent fluid shift

*risk for peritonitis

64
Q

paracentesis

A
  • to drain fluid out of the peritoneal cavity
    *at risk for peritonitis b/c now there is an entry point for bacteria
  • can have resp distress
  • position of comfort: sit up right
  • uncomfortable
  • tell pt what to expect/answer question, weigh before, VS, void before procedure, position w/ HOB elevated
  • monitor VS during, monitor outflow amt- may culture
  • monitor dressing: leakages, drainages, s/ of infection
  • weigh after
  • monitor BP for hypotension, hypovolemia (this is when they may get albumin)
65
Q

esophageal varices

A

esophageal vessels distend from increase pressure
- at risk for rupturing and bleeding
- vomiting blood
- portal hypertension
- not a lot you can do to control it
- seen in chronic alcoholics
- give vasopressin to decrease pressure in vessels
- octeotride specifically for upper GI bleeding
- o-bands to decrease blood supply to varice/cut off blood flow
- blakemore tube
- airway concern

66
Q

blakemore tube

A

aka SBT tube
- used to control bleeding in the upper GI tract (esophageal varices)
- inserted through nose and mouth as temporary fix for bleeding esophageal and gastric varices
- balloon inflated in stomach and along sides of esophagus, to put pressure on the bleed to clot it
- pt is usually intubated; monitor airway

67
Q

coagulation defects with ESLD

A
  • decreased synthesis of bile
  • blood backs up to spleen
  • thrombocytopenia (decreased WBC)
68
Q

treatment of coagulation defects r/t ESLD**

A

??
- blood transfusion
- FFP

69
Q

portal-systemic (hepatic) encephalopathy is

A
  • enlarged liver
  • Toxic substances unable to be broken down in intestines – metabolic imbalances
  • PSE = hepatic encephalopathy = hepatic coma
70
Q

s/sx of portal-systemic (hepatic) encephalopathy

A
  • increased blood ammonia in liver
  • personality changes: combative, confused
  • changes in LOC
  • progressive confusion
  • stuporous, coma
  • impaired thinking & judgement
  • neuromuscular disturbances
  • asterixis “liver flap”
  • hyperreflexia
71
Q

treatment of portal-systemic (hepatic) encephalopathy

A
  • lactulose to get ammonia level down; results in lots of loose stool- this is NORMAL, 2-3/day
  • metronidazole
  • rifaximin: ABT used to decrease normal flora in intestine, which decreases ammonia production, not used long-term
  • decrease/restrict protein in diet
72
Q

portal-systemic (hepatic) encephalopathy is caused/precipitated by

A
  • increased protein
  • infection
  • hypovolemia (low BV, hypotension)
  • hypokalemia (low potassium)
  • GI bleeding
73
Q

hepatitis b carriers are at risk for

A

liver cirrhosis
- cirrhosis leads to liver cancer

74
Q

hepatitis is a ____ virus

A

oncogenic virus
- meaning it sets the body up to develop cancer

75
Q

what disease is the leading cause for ESLD in the world?

A
  • hep C
  • hep C is the leading indication for liver transplantation in the US
76
Q

hep C health promotion

A

if sharing a household with a positive hep C individual:
- don’t share razors
- don’t share toothbrushes
- don’t share pierced earrings

basically dont share anything that could have any blood on it

77
Q

cirrhosis dx tests

A
  • ultrasound of liver
  • biopsy of liver
  • labs

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