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)
2
Q
which types of hepatitis are uncommon
A
hepatitis F and G
3
Q
types of hepatitis that come from the bowel
A
- A & E
- fecal-oral: ingesting poop/contaminated food (A), contaminated water (E -rare)
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
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
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
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
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
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)
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
11
Q
diagnostic assessment for hepatitis
A
- liver biopsy
- labs: liver enzymes, blood tests: antibody test to ID type of hepatitis
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
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
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
15
Q
acalculous cholecystitis is
A
inflammation in the absence of gallstones
- biliary stasis: bile is not moving in the duct
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
17
Q
chronic cholecystitis
A
- repeated episodes of cystic duct obstruction result in chronic inflammation
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
19
Q
cholecystitis: etiology/genetic risk (4 F’s)
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
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
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
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
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)
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
25
cholecystitis surgical management: traditional cholecystectomy
- 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
26
acute pancreatitis is
Serious and possibly life-threatening inflammatory process of the pancreas
- pancreatic enzymes attack the pancreas
27
Necrotizing hemorrhagic pancreatitis
- when inflammation or fluid collection spreads to a nearby artery, causing it to erode and bleed
28
acute pancreatitis process
- 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
29
acute pancreatitis can be caused by
- alcoholism
- gallstones
- drug use: cocaine
- infection
- other unknown causes
- operative manipulation and trauma
- blunt abdominal trauma
- biliary tract disease
- post-ERCP: complication of ERCP
30
autodigestion refers to when
the enzymes the pancreas produces become active and eat (digest) itself
31
acute pancreatitis: clinical manifestations
- skin: jaundice
- pulmonary: L lung pneumonia, L pleural effusion- resp distress, dyspnea, lung sounds, O2 sat
- endocrine: hyperglycemia/increased 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
cullen's sign
bruising or swelling around the UMBILICUS
- gray/blue discoloration to abdomen
- sign of intraperitoneal bleeding (acute pancreatitis)
33
turner's sign
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
acute pancreatitis: labs and diagnostic tests
- 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
priority collaborative problems for patients with acute pancreatitis
- acute pain d/t pancreatic inflammation and enzyme leakage around pancreas
- weight loss d/t inability to ingest food and absorb nutrients
36
complications of acute pancreatitis
- 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
acute pancreatitis: medical management
- NPO during acute phase to allow pancreas to rest
- medications
- IVFs
procedures:
- NGT: severely ill pt
- Endoscopic retrograde cholangiopancreatography: for gallstones causing pancreatitis
38
acute pancreatitis meds
- 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
Endoscopic retrograde cholangiopancreatography (use/purpose)
- dx use: to identify location of gallstones
- therapeutic use: to assist with removal of gallstones
40
acute pancreatitis surgical management: pre-op
NGT may be inserted
41
acute pancreatitis surgical management: operative procedures
- surgically drain the abscess
- acute pancreatitis typically does not need surgery- unless r/t gallstones
42
acute pancreatitis surgical management: post-op
- monitor drainage tubes and record output from drain (like JP drain)
- provide meticulous skin care and dressing changes
- maintain skin integrity
43
chronic pancreatitis is
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
chronic pancreatitis assessment: s/sx
- 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
chronic pancreatitis treatment: nonsurgical
- 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
Most serious complication of pancreatitis/necrotizing pancreatitis
pancreatic abscess
- always fatal if untreated (sepsis)
47
pancreatic abscess: what is it and what will you see
- Most serious complication of pancreatitis; always fatal if untreated (sepsis)
- High fever: up to like 104
- puss
- Blood cultures
48
treatment of pancreatic abscess
- 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
cirrhosis is
- 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
cirrhosis patho: early v. late
- early: liver is enlarged, firm, hard (palpable)
- late: liver shrinks, nodular (not palpable)
changes from early to late progress over years
51
causes of cirrhosis
- Alcohol* chronic alcoholism, years
- Hepatitis- viral & autoimmune hepatitis
- Drugs and toxins
- Biliary disease
- Nonalcoholic fatty liver disease
- Metabolic/Genetic causes
- Cardiovascular disease
52
prevalence of cirrhosis: chronic liver disease and cirrhosis are major causes of ___
Combined, incidence of chronic liver disease and cirrhosis are a major common cause of death
53
cirrhosis assessment
- 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
early sx of cirrhosis
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
late sx of cirrhosis
- 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
cirrhosis labs
- 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
cirrhosis patient problems
- 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
cirrhosis management\ patient problems
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
complications of end stage liver disease
- 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
portal HTN is
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
treatment of portal HTN
propranolol
- decrease HR and pressure to reduce risk of bleeding
62
ascites is
Accumulation of free fluid in peritoneal cavity 2nd to portal htn leaking fluid
- Triggers renal vasoconstriction
- Increases NA and H2O retention
63
ascites treatment
- 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
paracentesis
- 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
esophageal varices
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
blakemore tube
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
coagulation defects with ESLD
- decreased synthesis of bile
- blood backs up to spleen
- thrombocytopenia (decreased WBC)
68
treatment of coagulation defects r/t ESLD**
??
- blood transfusion
- FFP
69
portal-systemic (hepatic) encephalopathy is
- enlarged liver
- Toxic substances unable to be broken down in intestines – metabolic imbalances
- PSE = hepatic encephalopathy = hepatic coma
70
s/sx of portal-systemic (hepatic) encephalopathy
- 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
treatment of portal-systemic (hepatic) encephalopathy
- 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
portal-systemic (hepatic) encephalopathy is caused/precipitated by
- increased protein
- infection
- hypovolemia (low BV, hypotension)
- hypokalemia (low potassium)
- GI bleeding
73
hepatitis b carriers are at risk for
liver cirrhosis
- cirrhosis leads to liver cancer
74
hepatitis is a ____ virus
oncogenic virus
- meaning it sets the body up to develop cancer
75
what disease is the leading cause for ESLD in the world?
- hep C
- hep C is the leading indication for liver transplantation in the US
76
hep C health promotion
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
cirrhosis dx tests
- ultrasound of liver
- biopsy of liver
- labs
