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Nursing 332 > Hepatic Disorders > Flashcards

Hepatic Disorders Flashcards

1
Q

what is jaundice?

A

yellow discolouration of the skin and sclera d/t excess serum bilirubin (40umol/L, 3mg/dL)

not necessarily liver disease

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2
Q

what types of jaundice are there?

A

conjugated and unconjugated
obstructive and non-obstructive (clinical)
pre-hepatic, hepatic and post-hepatic

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3
Q

example of post hepatic jaundice

A

could be due to tumors or stones

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4
Q

what is pruritus caused by in jaundice?

A

cutaneous fat deposits d/t malabsorption

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5
Q

what class of meds is not admin in jaundice?

A

antihistamines bc you have a compromised liver

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6
Q

important teaching point with jaundice

A

keep skin clean and moisturized

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7
Q

obstructive jaundice

A

~biliary atresia; biliary disease or blockage d/t inflmtn
~gallstones - cholestatic meds can cause internal blockage of ducts
~bile can’t flow into intestines and backs up in liver and blood, staining skin, sclera, and urine bright orange and frothy
~stool is clay-coloured and skin is itchy
~intolerance of fatty foods; you will have fatty stools
~AST, ALT and GGT levels rise moderately, but alkaline phosphatase and bilirubin levels are elevated
~post hepatic (stones, tumors) - urine is high coloured

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8
Q

hepatocellular jaundice

A
  • viral, alcohol, toxins, drugs
  • liver damage is unconjugated
  • swelling, canicular obstruction is conjugated
  • liver unable to clear bilirubin d/t damage
  • can be d/t: infection, toxins, meds, alcohol, obesity
  • AST and ALT levels may be increased (indicates cell necrosis)
  • may be reversible unless cirrhosis develops
  • serum bilirubin and urobilinogen levels may be elevated
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9
Q

if cause of hepatocellular jaundice is infectious, what manifestations will occur in the pt?

A

headache, chills, fever

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10
Q

hemolytic jaundice

A
  • result of inc destruction of RBCs, effect of which is to flood plasma w/ bilirubin so rapidly that liver can’t excrete bilirubin as quickly as it is made
  • in pts with hemolytic transfusion rxns and hemolytic disorders
  • fecal and urine urobilinogen levels are inc, but urine is free of bilirubin
  • predisposes to formation of pigment stones and extremely severe jaundice
  • bilirubin levels >300-400umol/L causes brainstem damage
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11
Q

hereditary hyperbilirubinemia jaundice

A
  • serum bilirubin increases but LFT and liver histology remains normal
  • Gilbert’s syndrome : familial disorder characterized by increased level of unconjugated bilirubin
  • affects 3-8% of population (mainly males)
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12
Q

portal HTN

A
  • increased pressure throughout the portal venous system that results from obstruction of blood flow through the liver
  • associated with hepatic cirrhosis
  • changes in clotting increase risk of bleed
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13
Q

what is portal HTN caused by?

A
  • portosystemic shunts
  • ascites - d/t liver and kidney disease, CA, and heart failure
  • varices - risk for GI bleed (upper, rectal)
  • splenomegaly
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14
Q

portal HTN is a result from…

A

circulatory changes w/in diseased liver and produces severe GI hemorrhages and marked Na+/fluid retention

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15
Q

contributing factors of ascites

A

portal HTN and obstruction of venous blood flow to liver

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16
Q

patho of ascites

A 
movement of fluid from vascular system into peritoneal space is d/t:
 Na+/H2O retention 
 inc intravascular fluid vol
 inc lymphatic flow 
 dec synthesis of albumin
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17
Q

why do you have sodium and water retention?

A

liver can’t metabolize aldosterone, so kidneys retain these things

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18
Q

how much fluid accumulates in ascites?

A

15L of albumin-rich fluid accumulates in peritoneal cavity and if you increase portal pressure, you will have movement of fluid into peritoneal cavity

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19
Q

treatment of ascites

A
  • dietary modification (restrict Na and fluids)
  • diuretics (spironolactone and lasix)
  • bed rest (upright position to activate RAAS and SNS)
  • paracentesis (admin of albumin to shift fluid from IS to vascular space)
  • TIPS (Transjugular Intrahepatic Portosystemic Shunt)
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20
Q

things to remember about diuretics

A
  • when used with other diuretics, helps prevent potassium loss
  • long term use of oral diuretics can cause hyponatremia
  • daily weight loss should not exceed 1-2kg in pts with ascites and peripheral edema or 0.5-0.75kg in pts without edema
  • fluid restriction is not attempted unless serum sodium [ ] is very low
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21
Q

how would you go about making dietary modifications for someone with ascites and impaired renal fx?

A

avoid salt substitutes containing potassium

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22
Q

other methods of treating ascites?

A

insertion of peritoneovenous shunt to redirect ascitic fluid from peritoneal cavity into systemic circulation

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23
Q

pitting edema

A

hypoalbuminemia d/t dec hepatic production of albumin

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24
Q

nutritional deficiencies

A

inability of the damaged liver cells to metabolize certain vitamins leading to:

- Impaired fxing of the central and peripheral nervous system 
- Abnormal bleeding tendencies
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25
Q

Korsakoff syndrome

A
  • chronic, memory disorder and is caused by lack of thiamine (vitamin B1), which affects the brain and nervous system
  • most commonly caused by alcohol misuse, but certain other conditions can also cause it
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26
Q

what happens with people who drink lots of alcohol?

A
  • people who drink excessive amounts of alcohol are often thiamine deficient - bc many heavy drinkers have poor eating habits and their diet does not contain essential vitamins
  • alcohol can interfere with the conversion of thiamine into the active form of the vitamin
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27
Q

disadvantages of alcohol on the body

A
  • can inflame the stomach lining and cause frequent vomiting and make it difficult for the body to absorb key vitamins it receives
  • also makes it harder for the liver to store vitamins
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28
Q

decreased synthesis

A

Hepatic encephalopathy:

- d/t accumulation of ammonia in the serum d/t impaired protein metabolism

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29
Q

esophageal varices

A
  • develop in majority of pts with cirrhosis

- tortuous veins in the submucosa of the lower esophagus but can be in the higher esophagus and extend into the stomach

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30
Q

cause of esophageal varices

A
  • d/t portal HTN; variscosities that develop from increased pressure in veins that drain into portal system. increased obstruction of the portal vein causes venous blood to take alt route to the right atrium, inc pressure in vessels of submucosal layer
  • vessels are not elastic = fragile and will bleed easily
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31
Q

what happens if varices bleed?

A

life threatening - will cause hemorrhagic shock, leading to dec cerebral, renal and hepatic perfusion

32
Q

causes of bleeding varices

A

sneezing, coughing, lifting, straining, emesis reflux, esophagitis, irritation of vessels from poorly chewed foods, salicylates and meds that erode esophagus

33
Q

diagnosis of varices

A

endoscopy to find site and cause of bleed

CT, US, barium swallow, angiography

34
Q

manifestations of varices

A
  • hx of ETOH
  • hematemesis, melena, general deterioration in physical and mental status
  • s&s of shock
35
Q

goal of treatment for varices

A

to remove or alleviate underlying cause of cirrhosis, prevent further liver damage and prevent/treat complx

36
Q

when does LFT become abnormal?

A

when >70% of liver is damaged

37
Q

what does increased ALT indicate?

A

indicates liver disorders - used to monitor course of hep or cirrhosis, or effects of treatments toxic to the liver

38
Q

what does increased AST mean?

A

not specific to the liver; indicates high metabolic activity or damage to an organ

39
Q

what does increased GGT mean?

A

linked to cholestasis or alcohol liver disease

40
Q

what does albumin and PT-INR indicate?

A

impact on synthetic fx of liver; PT-INR provides index of liver’s ability to synthesize Vit K+ dependent clotting factors

41
Q

what does increased alkaline phosphatase mean?

A

increase in bile excretion

42
Q

best dx test to view liver damage?

A

abdominal US

43
Q

other diagnostic tests for liver disease

A
  1. CT and MRI
  2. Urinanalysis: R&M, C&S, bilirubin
  3. liver biopsy: risky d/t coagulation, risk for peritonitis
  4. CT of brain to assess level of atrophy
  5. abdominal paracentesis
  6. alpha-fetoprotein (serology)
  7. US most commonly done
  8. scope to visualize liver, pelvic structures, dx and stage CA
  9. ECRP (endoscopic retrograde cholangiopancreatogram)
44
Q

ECRP

A

biliary tree exam to detect blockages causing cholestasis

45
Q

alpha-fetoprotein

A

> 250ng/mL = hepatocellular CA

<= 100ng/mL = hepatic regeneration

46
Q

how should you treat pts with alcoholism?

A
  • ACCURATE I&O IS CRITICAL

- all pts with alcoholism should be given thiamine and multivitamins daily

47
Q

complx that can arise from use of diuretics

A

f/e disturbances and encephalopathy (may be precipitated by dehydration and hypovolemia

48
Q

treatment for varices

A
  • meds that cause selective GI vasoconstriction and slow motility
  • endoscopic sclerotherapy
  • surgical management
  • partial transplant from cadavers and living donors
  • TIPS
  • balloon tamponade
  • beta blockers to decrease portal HTN
49
Q

meds for varices

A
  • infections: spontaneous bacterial peritonitis treated w/ 3rd gen abx
  • H2 receptor blockers to prevent stress ulcers and GI bleed (pariet, pantoloc, ranitidine)
  • Ativan for withdrawal symptoms (less hepatotoxic)
  • lactulose to break down NH3 (inc d/t GI bacterial action)
  • Spironolactone and Lasix
  • metronidazole to dec bacteria and NH3
50
Q

functions of the liver

A
  1. metabolizes CHO, fats and proteins
  2. detoxifies blood
  3. ammonia -> urea for excretion
  4. synthesizes plasma proteins, nonessential a.a., Vit A, and essential nutrients such as iron, Vit D, B12
  5. secretes bile -> helps digest fats and absorb fatty acids, cholesterol, and lipids
  6. stores Vit A, B, B complex, D, iron, copper
  7. breaks down fatty acids into ketones
  8. uses Vit K to synthesize prothrombin and other clotting factors
  9. excretes bilirubin from breakdown of Hgb -eliminated in bile
51
Q

self protection of the liver

A
  • Regenerates itself be repairing or replacing injure tissue
  • Liver has many cell units responsible for same task. Therefore, if one area is injured, other cells will perform the functions of the injured section indefinitely
52
Q

liver disease

A
  • 11th most common cause of death in Canada (not including deaths d/t hepatitis and CA)
  • Twice the rate in men than women
  • Affects children
53
Q

what is the leading cause of liver disease in Canada?

A

NAFLD and then Hep C (but is decreasing)

54
Q

hepatitis

A

infltmn of the liver that can be caused by a virus inherited disorder, and sometimes by certain meds or toxins such as alcohol or drugs

55
Q

cirrhosis

A

consequence of chronic liver disease characterized by replacement of liver tissue by fibrosis (scar tissue in liver) and regenerative nodules that leads to loss of liver function

○ Common end result of many chronic liver disorders 
○ Diffuse scarring of liver - follows hepatocellular necrosis of hepatitis 
○ Inflmtn - healing with fibrosis - regenerating nodules 
○ Loss of normal architecture and fx
56
Q

non viral hepatitis

A

inflmtn of the liver that usually results from exposure to certain chemicals or drugs. Most pts recover from non-viral hepatitis; although some develop cirrhosis

57
Q

cause of non viral hepatitis

A

hepatotoxic chemicals such as carbon tetrachloride, trichloroethylene, vinyl chloride; Hepatotoxic drugs such as tylenol, poisonous mushrooms

58
Q

treatment of non viral hepatitis

A

Treatment: effective treatment aims to remove causative agent by lavage, catharsis, or hyperventilation

59
Q

viral hepatitis

A

the viral form of hepatitis is an - acute inflmtn of the liver marked by liver cell destruction, necrosis, and autolysis. In most pts, hepatic cells eventually regenerate with little or no damage

  • Complicated by age and underlying disorders which increase the likelihood of complx
  • Prognosis is poor in the presence of edema and hepatic encephalopathy
60
Q

hepatitis A

A
  • Accounts for 20-25% of cases of clinical hepatitis in developed countries
    • Caused by RNA virus of the enterovirus family
    • Persons at risk of HVA include travellers to HVA endemic countries, illicit drug users, men who have sex with men
    • Age-specific incidence is highest among those 5-9 years old
    • Transmitted primarily through the fecal-oral route, by the ingestion of food or liquids infected by the virus
    • More prevalent in countries with overcrowding and poor sanitation
    • Young child or adult acquires the infection at school through poor hygiene, hand to mouth contact, or close contact during play
    • Hep A can be transmitted during sexual activity
    • Incubation period is estimated between 2-6 weeks
    • Illness may be prolonged, lasting 4-8 weeks; usually lasts longer and is more severe in those older than 40 yrs of age
    • Most pts recover from Hep A
    • Mortality rate of Hep A is ~0.5% for those younger than 40 yrs of age and 1-2% for older people
61
Q

hepatitis B

A

○ STD
○ Caused by HBV and is spread by contact with infected blood, semen, and some other body fluids
○ Get it by:
- Unprotected sex with infected person
- Using a syringe that was previously used by an infected person
- Having your skin perforated with unsterilized needles, as might be the case when getting a tattoo
- Healthcare workers at risk from needlestick injuries
- Sharing personal items such as toothbrushes or razors with an infected person
- Being bitten by someone who is infected
- The liver of a person infected with hepatitis B swells. Pt can suffer serious liver damage due to infection, resulting in CA. For some pts the hepatitis becomes chronic. Donated blood is always tested for hep B

62
Q

hepatitis C

A

○ Spread through direct contact with blood of person who has hep C
○ Caused by HCV
○ Liver can swell and become damaged
○ Liver CA risk is only increased in people with cirrhosis and only 20% of hep C pts get cirrhosis
○ Feces is NEVER a route of transmission
○ Donated blood is also tested for hep C
○ Misuse of anesthesia can result in transmission of hep B and hep C viruses

63
Q

hepatitis D

A

○ Only a person infected with hep B can get hep D
○ Caused by HDV
○ Contact through infected blood, perforation of skin, unprotected sex
○ Your liver swells

64
Q

patient teaching for non viral hepatitis

A

○ Proper use of drugs

○ Proper handling of cleaning agents and solvents

65
Q

patient teaching for viral hepatitis

A

○ Regular medical check at least once a year
○ No alcohol
○ S&S of recurrence
○ Hepatitis carrier must be advised how to prevent exchange of body fluids during sexual relationships
○ Pts must avoid contact sports for as long as liver is enlarged
○ Abstain from alcohol
○ TIME TO REST!

66
Q

treatment of viral hepatitis

A

○ Rest in early stages of the illness
○ Small meals high in calories and protein
○ Chronic hep B w liver inflmtn is tx with interferon alpha-2b for 16 wks - monitoring blood counts essential
○ Lamivudine therapy to decrease viral load of Hep B
○ Hep C can be treated with interferon and ribavirin therapy
○ Decisions regarding treatment made after labs and biopsy results confirm infltmn early cirrhosis. Tx last 6-18 months

67
Q

how is diet affected in cirrhosis?

A

○ Fibrous tissue caused by cirrhosis prevents liver from functioning properly, including metabolizing and storing nutrients
○ One of the nutrients affected by cirrhosis is protein. Cirrhotic liver causes the body to breakdown proteins at a fast rate, quickly depleting stores and increased body needs
○ Some ppl with cirrhosis have high levels of ammonia, a by product of protein metabolism, in their blood and may need to restrict protein intake to prevent adverse effects

68
Q

what is common in pts with cirrhosis in relation to diet intake?

A

○ Malnutrition d/t to poor appetite and intake, malabsorption of nutrients and impaired nutrient metabolism
○ While protein breakdown is elevated with cirrhosis, synthesis is decreased, which causes muscle wasting and a decrease in blood essential to maintain adequate levels of protein and prevent further illness

69
Q

alcohol liver injury

A

○ Ethyl alcohol = common causes of acute/chronic liver disease
○ Alcoholic liver disease - patterns:
- Fatty change
- Acute hepatitis
- Chronic hepatitis with portal fibrosis
- Cirrhosis, chronic liver failure
All reversible except cirrhosis stage

70
Q

signs and symptoms of alcohol liver injury

A

○ NEURO: asterixis, LOC might drop; caused by brain bathing in ammonia, behavioural changes, paresthesias, sensory disturbances, cognitive changes
○ Ex) Wernicke’s syndrome
○ SKIN: spider angiomas, jaundice (dec hair prod, inc pigmentation), white nails, palmar erythema, pruritus, caput medusa, bruising

71
Q

CAGE

A

○ Critical to Diagnosis is the History and Physical Examination
○ Has the pt been traveling (inc risk of hepatitis infection?)
○ Has the pt been drinking alcohol? (ask the CAGE questions)

72
Q

CAGE questions

A
  • Have you ever felt the need to cut down?
  • Have you ever felt annoyed by criticism of your drinking?
  • Have you ever felt guilty about your drinking?
  • Have you ever had a drink to get you started in your day or to steady your nerves (eye-opener)?
73
Q

manifestations of hep A

A
  • Anicteric (without jaundice) and symptomless
    • When symptoms appear, they resemble those of a mild, flulike upper respiratory tract infection, with low grade fever
    • Anorexia, an early symptom, is often severe
    • Jaundice and dark urine become apparent later; indigestion is present in varying degrees, marked by vague epigastric distress, nausea, heartburn, and flatulence
    • Symptoms tend to clear as soon as the jaundice reaches its peak, perhaps 10 days after its initial appearance
    • Symptoms may be mild in children; in adults, they may be more severe and the course of the disease is prolonged
74
Q

assessment and diagnostic findings with Hep A

A
  • The liver and spleen are often moderately enlarged for a few days after onset; other than jaundice, there are few other physical signs
    • Hepatitis A antigen may be found in the stool 7-10 days before the illness and for 2 to 3 weeks after symptoms appear
    • HAV antibodies are detectable in the serum, but usually not until symptoms appear
    • Analysis of subclass of immunoglobulins can help determine whether the antibody represents acute or past infection
75
Q

prevention of hep A

A
  • handwashing, safe water supplies

- Vaccines - Havrix and Vaqta

76
Q

medical management of hep A

A

Family teaching on: diet, rest, follow-up blood work, and the importance of avoiding alcohol, as well as sanitation and hygienemeasures
-Specific teaching includes: good personal hygiene, stressing careful handwashing (after BM and before eating) and environmental sanitation

Nursing 332 (7 decks)

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