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NSG 470 - Exam 4 > Liver Disorders > Flashcards

Liver Disorders Flashcards

1
Q

what is the A/P of the liver? (location, func)

A

largest gland of the body

Right Upper Quad (RUQ)

very vascular

received blood from nutrient rich blood from GI tract via portal vein and O2 rich blood from hepatic artery

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2
Q

what are functions of the liver?

A

glucose metabolism + regulation
ammonia conversion –> urea
protein metabolism (albumin, globulins, clotting factors, lipoproteins) –> vit K needed to make prothrombin + other clotting factors
fat metabolism –> breaks down fatty acids for energy
vitamin/iron storage (A, B, D)
bile formation (water, electrolytes, bicarb, lecithin, fatty acids, cholesterol, bilirubin, bile salts)
bilirubin excretion –> gall bladder –> intestine
drug metabolism (first pass effect)

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3
Q

what important labs refer to the liver?

A

AST, ALT, GGT, LDH (ALT> AST - liver, AST>ALT - myocardial necrosis
protein/albumin
bilirubin
clotting factors (PT/INR, plts)
alkaline phosphatase (Alk phos, ALP, AP)
ammonia
lipids

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4
Q

what is the normal AST levels?

A

8 - 48

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5
Q

what is the normal ALT levels?

A

7 - 55

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6
Q

what is the normal ALP levels?

A

45 - 115

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7
Q

what is the normal bilirubin levels?

A

0.1 - 1.2

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8
Q

what is the normal total protein levels?

A

6.3 - 7.9

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9
Q

what is the normal albumin levels?

A

3.5 - 5.0

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10
Q

what are transaminases?

A

indicators of liver cells injury (detects hepatitis)

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11
Q

what do ALT levels indicate?

A

increased in liver disorders; used to monitor course of hepatitis, cirrhosis + effects of tx that are liver toxic

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12
Q

what do AST levels indicate?

A

not specific to liver diseases

may be inc in cirrhosis, hepatitis, and liver cancer

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13
Q

what do GGT levels indicate?

A

assoc w/ cholestasis; alcoholic liver disease

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14
Q

what are the liver diagnostics?

A

ultrasound
CT
MRI
ERCP (Endoscopic retrograde cholangiopancreatography)
Transient Liver Elastography – degree of cirrhosis (firm liver) - Stiffness of liver tissue
Liver biopsy

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15
Q

what health hx questions are asked?

A

if any exposure to hepatotoxic substances?
infections?
travel or substance abuse?
meds? inc OTC supplements?
family liver dx?

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16
Q

what are the manifestations of liver disease?

A

Cognitive changes
Altered sleep/wake pattern, irritability
Gastroesophageal bleeding–hematemesis, melena
Splenomegaly
Ascites
Jaundice
Petechiae, ecchymosis, nosebleeds
Palmar erythema
Spider
Dependent peripheral edema of extremities and sacrum
Asterixis –> coarse tremor characterized by rapid, nonrhythmic extension and flexion of the wrists and fingers
Fetor hepaticus (fruity or musty odor, possibly stool smell)

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17
Q

what are the hepatic dysfunction disorders?

A

fatty liver disease = (Nonalcoholic fatty liver disease (NAFLD), Nonalcoholic steatohepatitis (NASH))

infection = hepatitis

liver cirrhosis = compensated, decompensated

liver failure = acute or end stage LD

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18
Q

what are the complications of hepatic dysfunction?

A

jaundice
ascites
portal htn
hepatic encephalopathy/coma
varices
nutritional deficiencies

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19
Q

what is jaundice?

A

Yellow or greenish-yellow sclera and skin
Bilirubin level > 2 mg/dL
Types: Hemolytic, Hepatocellular, obstructive (Hereditary hyperbilirubinemia)

Hepatocellular + Obstructive are most associated with liver disease

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20
Q

what is hepatocellular jaundice?

A

damaged liver cells from infection, excessive alcohol use (cirrhosis), prolonged obstructive jaundice

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21
Q

what is obstructive jaundice?

A

extra-hepatic (gall stone, inflammatory process, tumor) or intra-hepatic (stasis, thickening of bile in canaliculi)

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22
Q

what is hemolytic jaundice?

A

due to RBC breakdown

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23
Q

what are the s/s of hepatocellular jaundice?

A

Mild or severely ill
Lack of appetite, nausea or vomiting, weight loss
Malaise, fatigue, weakness
Headache, chills, fever, infection

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24
Q

what are the s/s of obstructive jaundice?

A

Dark orange-brown urine, **clay-colored stools
Indigestion and intolerance of fats, impaired digestion
Pruritus
Skin excoriation from scratching

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25
Q

what is portal htn?

A

Obstructed blood flow through the liver results in increased pressure throughout the portal venous system

results = ascited + esophageal/gastric varices

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26
Q

what is ascites?

A

portal htn –> inc cap refill –> obstruction of venous blood flow through damaged liver

dec serum osmotic pressure w/ movement of albumin + fluid from intravascular space to extravascular space including peritoneal cav –> peripheral edema + ascites

*can also occur from cancer, kidney disease + HF

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27
Q

how do you assess for ascites?

A

record abdominal girth/weight DAILY

striae, distended veins, umbilical hernia

assess abdominal cavity for fluid; dyspnea, abdominal discomfort

monitor for potential fluid/electrolytes imbalances (sodium, potassium, renal function)

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28
Q

what is the treatment for ascites?

A

low sodium diet, fluid restriction
diuretics (spironolactone, furosemide)
bedrest
paracentesis
admin of salt - poor albumin
transjugular intrahepatic portosystemic shunt (TIPS)
other methods: peritoneal drains

29
Q

what is spironolactone?

A

potassium-sparing diuretic
blocks activity of aldosterone –> can secrete sodium + fluid –> dec overall fluid vol

dose: 50 mg - 400 mg

30
Q

what are the side effects of spironolactone?

A

mild: hyponatremia, hypomagnesemia, hypocalcemia, abd pain, N/V, fatigue, leg cramps, dizziness/lightheadedness, male gynecomastia

serious: hyperkalemia, Hypotension, Decreased kidney function, Anaphylaxis, Stevens-Johnson Syndrome, Toxic Epidermal Necrolysis (TENs)

31
Q

what are esophageal varices?

A

inc occurrence as liver disease progresses

dilated, tortuous veins of the esophagus + stomach that dev due to portal htn and obstruction of portal venous circulation

manifest: GI bleeding, hematemesis, melena, hemorrhagic shock

32
Q

how to prevent esophageal varices?

A

pt w/ cirrhosis should undergo screening endoscopy q 2-3 yrs to monitor for varices

33
Q

what is the treatment for bleeding esophageal varices?

A

ICU mgmt
tx hemorrhagic shock (ABCs)
O2, airway, possible mechanical vent
IV fluids, electrolyte replacement, volume expanders, blood prods
vasopressin, somatostatin, octreotide
nitroglycerin in combo w/ vasopressin to red coronary vasoconstriction
propranolol + nadolol (dec portal pressure)
balloon tamponade, saline lavage

34
Q

what are the surgical mgmt of varices?

A

Endoscopic sclerotherapy
Endoscopic variceal ligation (esophageal banding therapy)
Transjugular intrahepatic portosystemic shunt (TIPS)
Surgical management (Surgical bypass procedures, Devascularization and transection)

35
Q

what is hepatic encephalopathy?

A

life-threatening
2 abnorms:
hepatic insufficiency (inability of liver to detox toxic by products of metabolism

portosystemic shunting (collateral vessels dev allowing elements of the portal blood to enter systemic circulation

accumulation of ammonia levels in blood (mental status change + motor disturbances

36
Q

how to assess encephalopathy?

A

EEG
Changes in LOC and motor function
Potential seizures
Fetor hepaticus, asterixis
Monitor fluid, electrolyte, and ammonia levels
Stages: 1-4

37
Q

stage 1 encephalopathy s/s

A

norm LOC w/ periods of lethargy + euphoria; reversal of day-night patterns

impaired writing and ability to draw line figures, norm EEG

38
Q

stage 2 encephalopathy s/s

A

inc drowsiness; disorientation; inappropriate behavior, mood swings; agitation

asterixis, fetor hepaticus
abnorm EEG w/ generalized slowing

39
Q

stage 3 encephalopathy s/s

A

stuporous; diff to rouse, sleeps most of time; marked confusion; incoherent speech

asterixis, inc DTR, rigid of extremities, EEG abnorm

40
Q

stage 4 encephalopathy s/s

A

comatose; may not respond to painful stimuli

absence of asterixis + DTR; flaccid extremities, EEG marked abnormally

41
Q

what is the medical mgmt of hepatic encephalopathy?

A

reduce protein

reduce ammonia from systemic circulation/GI tract by gastric suction, lactulose, enema, oral antibiotics

discont sedatives, analgesics, tranquilizers; and other meds that can affect liver function

42
Q

what is fatty liver disease?

A

accumulation of lipids in hepatocytes
NASH more serious than NAFLD (damaged fibrotic changes in liver –> cirrhosis)

both assoc w/ obesity
combination of obesity + heavy drinking (severe liver damage) - can take 20-30 yrs to dev into ESLD

43
Q

what is viral hepatitis?

A

Viral hepatitis: most common

causes necrosis and inflammation of liver cells leading to liver enlargement and obstruction of blood flow to liver

Hep A, B, C, D, E, G

44
Q

what is nonviral hepatitis?

A

toxic + drug induced
alcohol, hepatotoxic chemicals, medications, botanical agents (Acetaminophen, mushrooms, carbon tetrachloride)

Anorexia, N/V, jaundice, hepatomegaly, bleeding, chills, fever, rash, pruritis

Recovery unlikely if prolonged period b/t exposure and symptoms

45
Q

type A hepatitis

A

source: feces
transmission: feces-oral
chronic: no
prevention: pre/post immunization

46
Q

type B hepatitis

A

source: blood/blood-derived body fluids
transmission: percutaneous permucosal
chronic: yes
prevention:pre/post immunization

47
Q

type C hepatitis

A

source: blood/blood-derived body fluids
transmission: percutaneous permucosal
chronic: yes
prevention: pre/post immunization; blood donor screening; risk behavior modification

48
Q

type D hepatitis

A

source: blood/blood-derived body fluids
transmission: percutaneous permucosal
chronic: yes
prevention: pre/post immunization; risk behavior modification

48
Q

type D hepatitis

A

source: blood/blood-derived body fluids
transmission: percutaneous permucosal
chronic: yes
prevention: pre/post immunization; risk behavior modification

49
Q

type E hepatitis

A

source: feces
transmission: fecal-oral
chronic: no
prevention: ensure safe drinking water

50
Q

what are common findings in hepatitis?

A

hx: exposure to infected blood, stool or body fluid

flu-like symptoms: fatigue, dec appetite, nausea, abdominal pain, joint pain

physical: fever, vomiting, dark colored urine, clay colored stool, jaundice

51
Q

hepatitis A (HAV)

A

poor hand hygiene/sanitation (fecal-oral) = contaminated food/water, contact w/ stool

anti-HAV = hep A infection

s/s: fatigue, mild flu-like symptoms, low-grade fever, anorexia, later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen

tx: bedrest (acute), supportive care

52
Q

what is prevention + mgmt of HAV?

A

hepatitis A immunization
immune globulin
good handwashing, safe water, proper sewage disposal

53
Q

hepatitis B (HBV)

A

transmission: blood, saliva, semen, vaginal secretion (sexually), infant @ birth

major cause of cirrhosis/liver cancer

risk factors: Unprotected sex, Infant born to infected mother, Contact with infected blood/body fluids (HCWs), Substance use disorder (injectable substances), Tattoos, Travel, Hemodialysis, Institutions (correctional facilities, LTC)

manifest: insidious and variable; similar to HAV, loss of appetite, dyspepsia, abdominal pain, generalized aching, malaise, and weakness, +/- Jaundice (light colored stools, dark urine)

54
Q

what is mgmt of HBV?

A

Acute infection: No meds; supportive care
Chronic infection: unable to clear virus
(Antivirals: tenofovir, adefovir dipivoxil, interferon alfa‑2b, peginterferon alfa‑2a, lamivudine, entecavir, and telbivudine)

Bedrest and nutritional support

55
Q

hepatitis C (HCV)

A

Transmission: blood
Cause of 1/3 cases of liver cancer and most common reason for liver transplant
Risk factors: same as HBV
Symptoms are usually mild if at all
Chronic carrier state frequently occurs

56
Q

what is the mgmt of HCV?

A

No benefit to rest, vitamins, diet

Direct Acting Antivirals (DAA): Protease inhibitors for HCV

Can be undetectable and cured after 8-12 weeks of completed Tx
(simeprevir, sofosbravir, paritaprevir, glecaprevir, grazoprevir)

Alcohol potentiates disease; meds that effect the liver should be avoided

57
Q

hepatitis D (HDV)

A

Only persons with hepatitis B are @ risk (Co-Infection)
Blood + sexual contact transmission, injection drugs, hemodialysis, and recipients of multiple blood transfusions

S/S similar to HBV, more likely to develop acute, fulminant liver failure or chronic active hepatitis and cirrhosis

High dose Interferon alfa x at least 1 year

58
Q

hepatitis E (HEV)

A

Transmitted by fecal–oral route, contaminated water

Resembles hepatitis A; self-limiting, abrupt onset, not chronic

No treatment except supportive care

59
Q

what is hepatic cirrhosis

A

Alcoholic: scar tissue surrounds the portal areas, most common

Post-necrotic: broad bands of scar tissue

Biliary: scarring occurs in the liver around the bile ducts, d/t chronic biliary obstruction

patho: replacement of normal liver tissue w/diffuse fibrosis

Manifestations: liver enlargement, portal obstruction, ascites, infection/peritonitis, varices, edema, vitamin deficiency, anemia, mental deterioration

60
Q

what are s/s of compensated cirrhosis?

A

ab pain, ankle edema, firm + enlarged liver, flatulent dyspepsia, intermittent mild fever, palmar erythema, splenomegaly, unexplaied epistaxis, vague morning indigestion, vascular spirers

61
Q

liver cancers

A

primary liver tumors = assoc w/ hep B + C, hepatocellular carcinoma (HCC)

liver metastasis = lung, breast, GI, tumor cells seed in liver thru circulation/lymphatics

62
Q

how to manage liver cancer?

A

surgery (lobectomy, liver transplant)
chemotherapy
percutaneous biliary drainage
cryoablation
radiofreq ablation
chemoembolization
arterial embolization

63
Q

what is acute liver failure?

A

Severe acute liver injury w/ encephalopathy and impaired PT/ INR of ≥1.5 in a patient without cirrhosis or preexisting liver disease

Viral/drug-induced hepatitis most common causes

S/S: = more severe b/c acute failure. Hepatic encephalopathy symptoms.

Hepatic encephalopathy + ALF ->high risk of life-threatening cerebral edema

64
Q

what is the tx for acute liver failure?

A

ICU, ABCs, mechanical ventilation, Tx underlying cause, potential liver transplant
Correct abnormal levels (coagulation, ammonia, electrolytes, mannitol if cerebral edema (ICP monitoring), sedation, plasmapheresis

Acetaminophen –> N-Acetylcysteine
Mushrooms –> Penicillin, Activated charcoal

65
Q

causes of acute liver failure (ABCs)

A

A - acetaminophen, hep A, autoimmune hep, adenovirus, mushroom poisoning
B - hep B, budd-chiari syndrome
C - cryptogenic, hep C, CMV
D - hep D, drugs, toxins
E - hep E, EBV
F - fatty infiltration (acute fatty liver of preg, Reye’s syndrome)
G - genetics, wilsons disease
H - hypoperfusion (ischemic hepatitis, SOS, sepsis) HELLP, HSV, heat stroke, hepatoectomy, hemophagocytic lymphohistiocytosis
I - infiltration by tumor

66
Q

drugs assoc w/ acute liver failure

A

acetaminophen, alcohol, carbon tetrachloride, cocaine, halothane, He Shou Wu, hebalife, hydroxycut, kava, Ma HUang, MDMA (ecstasy), methamphetamine, NSAIDs, poison mushrooms

67
Q

liver transplant

A

Stringent criteria if have primary liver cancer—small, early lesions (1 x < 5cm or 3 x < 3cm)

End-Stage Liver Disease (ESLD)—whole liver from deceased donor or partial liver (right lobe) from live donor

Immunosuppressants: Cyclosporine, Tacrolimus, Sirolimus, Everolimus, Mycophenolate - Corticosteroids used only when needed ex. induction immunosuppression or signs of rejection

Graft vs Host Disease—rejecting liver

68
Q

education and intervention for liver disease

A

viral hep: approp contact precautions, avoid sex until neg hep AB tes, proper hand hygiene, refer to substance abuse, avoid alc, needle/syringe program

resp: comfort measures, sit in case or elev bed to 30, O2, cough, deep breath

skin: reposition q 2 hrs, mon for skin breakdwon, gentle skincare, avoid soap, lotion, assess for excoriations, bruising/petechiae, jaundice

nutrition: high carb, high cal, mod fat, low sodium, small freq meals

fluids: mon for ab distention, peripheral edema

activity: bedrest during acute illness, planned exercise + rest pd (slow + gradual)

neuro: mon for asterixis + fetor hepaticus, lactulose if inc ammonia

GI: observe for bleeding, pain mgmt

NSG 470 - Exam 4 (4 decks)

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