Cirrhosis, Hepatitis, and Tuberculosis

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91 Terms

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  1. WBCs

  2. C reactive protein

  3. Erythrocyte sedimentation rate

Lab values that indicate inflammation: [3]

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 Glucose metabolism & regulation

 Converts ammonia into urea

 Protein metabolism

 Fat metabolism

 Vitamin & iron storage

Bile formation

Bilirubin excretion

Drug metabolism

clotting factors

functions of the liver:

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Liver can regenerate if disease is caught in early stages and can stop disease progression. Cannot repair cirrhosis.

when ca liver disease progression be stopped?

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Cirrhosis

chronic inflammation of the liver leads to scarring and liver cannot repair itself

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  • nonalcoholic fatty liver siease and nonalcoholic steatohepatitis

  • alcohol and drug hepatitis

  • autoimmune and genetic liver disease

Causes of liver disease:

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Steatosis, can include Nonalcoholic fatty liver disease

Fat distributed at liver but no actual inflammation happening

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Fat leads to impaired function of the liver, can lead to severe scarring

How can steatosis lead to cirrhosis?

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If they start exercising and healthy eating

how can someone with nonalcoholic fatty liver disease see an improvement in liver function tests?

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Directed at reduction of risk factors

  • treating diabetes

  • reduction in body weight

  • elimination of harmful medicaions

Treatment for nonalcoholic fatty alcoholic liver disease: [3]

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replaced with fibrotic tissue, which does not function the same as normal, healthy tissue

in cirrhosis, normally functioning tissue is replaced with what?

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Liver transplant

only treatment for liver cirrhosis

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Chronic liver disease

Cirrhosis is the final stage of what?

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  • alcoholic cirrhosis

  • post-ecrotic cirrhosis

  • biliary cirrhosis

Three types of cirrhosis

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alcoholic cirrhosis

most common type of cirrhosis, buildup of scar tissue around hepatic portal system related to chronic alcoholism

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Post-necrotic cirrhosis

Cirrhosis associated with acute hepatitis, profuse scar tissue

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Biliary cirrhosis

Cirrhosis associated with chronic biliary obstruction (gallstones)

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Compensated cirrhosis

When cirrhosis is asymptomatic or has non-specific symptoms. All liver values are normal. Scar tissue is forming but functioning parts are able to pick up and meet the body’s needs

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  • albumin

  • bilirubin

  • PTT

Liver function tests: [3]

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if they give up alcohol or treat infection

How can patients compensate cirrhosis for years? [2]

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Decompensated cirrhosis

Advanced cirrhosis when body can no longer compensate. See abnormal liver function values. and lots of symptoms and one or more complications

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  • dull RUQ abdominal pain

  • anorexia

  • dyspepsia

  • N+V

  • weakness

  • Muscle loss

  • fatigue

  • slight weight loss

  • hepatomegaly

  • splenomegaly

Clinical manifestations of cirrhosis (pretty nonspecific) [10]

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  • jaundice

  • skin lesions

  • hematological conditions

  • endocrine disturbances

  • peripheral neuropathy

Manifestations of decompensated cirrhosis

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Jaundice

Buildup of bilirubin that can see in skin, eyes, top of nose

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Spider angioma

Circle spot on body, tiny capillaries extended from dilated blood vessels

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women: amenorrhea or bleeding

men: can develop breast tissue due to increase in estrogen and impotence

endocrine disturbances associated with decompensated cirrhosis

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associated with b12 deficiency because it is processed in the liver

why can decompensated cirrhosis case peripheral neuropathy

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  • thrombocytopenia

  • anemia (not able to absorb folic acid)

  • leukopenia

  • coagulation disorders (clotting factors)

Hematological conidtions associated with decompensated cirrhosis: [4]

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  • spider angioma

  • palmar erythema

skin lesions associated wiht decompensated cirrhosis [2]

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  • portal hypertension and esophageal& gastric varices

  • peripheral edema and ascites

  • hepatic encephalopathy

  • hepato-renal syndrome

complications where if patent has one of these, know cirrhosis is decompensated [4]

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Portal vein

vein carries blood from digestive organs to liver

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Portal hypertension

backflow of blood in the portal vein because there is a issue with the liver

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Varices

little swollen areas from pressure on vessel wall that can rupture and bleed

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in stomach and esophagus

Blood can back up further with portal hypertension and can see varicies where?

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Bleeding esophageal varices

most life-threatening complication of cirrhosis

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Blood backs up in portal vein due to issue with liver, can back up into spleen

why see enlarged spleen with decompensated cirrhosis?

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fluid is not circulating where it is supposed to be, shifting and collecting in abdomen

Why do patients with decompensated cirrhosis have ascites

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can before, during, or after ascites. happens from buildup of fluid.

decreased albumin production by liver, less pressure keeping fluid in the capillaries and so it leaks where its not supposed to do.

Why do patients with decompensated cirrhosis have peripheral edema

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hypokalemia

from fluid shift and dehydation with cirrhosis patients are at risk for which imbalance?

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Hepatic encephalopathy

Neuropsychiatric manifestation of advanced liver disease. Change in neurostatus and mental responsiveness caused by build up of waste products (amonia) in the blood and brain

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Asterixis

Flapping tremor. Push back on the person’s hands, tremor when they are released, brain is not working properly and hepatic encephalopathy is emergent. note how long.

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  1. writing impairments (get to draw a shape)

  2. asterixis

  3. hyperventillation

  4. hypothermia

  5. grimacing

  6. grasping reflex

clinical manifestations of hepatic encephalopathy:

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Hepato-renal syndrome

Complication of decompensated cirrhosis. Patient develops kidney failure with azotemia, oliguria, and ascites

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  • diuretics (isk for AKi)

  • hemorrhage

  • paracentesis (fluid shfted off and patient gets dehydrated)

hepato-renal syndrome commonly follows what?

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  1. Increased AST, ALT, ALP

  2. decreased protein, albumin

  3. increased serum bilirubin

  4. prolonged PTT

Lab values that indicate liver disease: [4]

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Blood takes longer to clot, has to do with liver producing clotting factors

Why do patients with decompensated cirrhosis have prolonged PTT?

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Decreased PTT, longer clotting so bleeding risk

Why might it not be a great idea for some patients to get a liver biopsy?

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treat symptoms and stop progression

goal for liver disease

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  1. alcohol

  2. sedatievs

  3. NSAIDs

drugs processed through the liver so patients with failure should avoid:

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Paracentesis

putting a sterile needle inside a cavity to drain fluid

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 Transjugular Intrahepatic Portosystemic Shunt (TIPS) procedure

Stent put in to connect portal vein to hepatic vein to decrease and shift pressure, done to prevent bleeding

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  1. airway management

  2. IV fluid and blood products (IV ACCESS!)

  3. Drugs

  4. endoscopic scleropathy or band ligation

  5. balloon tamponade

Interprofessional care if bleeding occurs: [5]

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Balloon tamponade

during endoscopy, a balloon is expanded to stop bleeding. very temporary, last resort

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  1. octreotide

  2. vasopressin

Drugs that slow blood to the portal vein [2]

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to get rid of ammonia. Want to have increased bowel movements.

why is lactulose given in hepatic encephalopathy?

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Some bacteria produce ammonia. Decrease the bacteria, decrease the ammonia

why are antibiotics given in hepatic encephalopathy?

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  1. high calorie, high carb, moderate to low fat

  2. only restrict protein after severe flare of symptoms

  3. Low sodium when ascites and edema are present

  4. no alcohol

nutritional therapy for liver disease: [4]

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Cholestyramine

med that removes bile acid

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Bile salts deposited in skin and bilirubin not getting excreted.

Why do patients with liver disease have dark urine and light stool

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  1. monitor I+O

  2. daily weight

  3. skin care, turn and position q2h

  4. support abdomen, elevate limbs

Nursing management for edema and ascites:

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: Level of responsiveness,

sensory and motor abnormalities

, fluid and electrolyte imbalances,

acid-base imbalances

, effect of treatment measures.

assessments for hepatic encephalopathy: [5]

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CAGE questionnaire (cut down, Annoyed, guilty, eye-opener)

questionnaire for alcohol withdrawl

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viral infection

most common cause of hepatitis

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  1. general malaise

  2. anorexia

  3. N+V

  4. headache

  5. low grade fever

  6. skin rashes

  7. RUQ pain

  8. jaundice

    1. (icteric: jaundice)

    2. Anicteric: no jaundice)

clinical manifestations in acute phase of hepatitis: [8]

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  1. cirrhosis

  2. cancer

  3. liver failure

untreated chronic hepatitis can lead to: [3]

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  • AST

  • ALT

two elevated lab tests mean liver cell injury

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  1. ALP

  2. GGT

two elevated lab tests mean bile duct injury

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  1. antibodies

  2. liver function tests

Diagnostics for hepatitis: [1]

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fecal-oral

  1. contaminated food or water

  2. poor hygiene

  3. poor sanitary condiions

sources of hepatits A (low incidence) [3]

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Universal precautions

precautions when you suspect to come into contact with bodily fluids

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  • mother to infant

  • through skin (needle stick)

  • sexually

  • permucosal exposure to infectious blood

Hepatitis B transmission

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Spontaneously resolves

How does acute hepatitis B treat?

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§Interferon

§Nucleos(t)ide analogues

 Medications For Chronic Hepatitis B (suppress   viral load & slow disease progression) [2]

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cirrhosis and end stage liver failure

Chronic hep B results in:

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percutaneous

high-risk sexual behaviour

blood transfusion before 1992

hemodialysis

Hep C risks [4]

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  1. Spontaneous clearance

  2. Chronic: manage with meds (direct-acting antiviral therapy)

treatment for Hep C [2]

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needs Hep B, can get same time or later. percutaneous infection

How can Hep D live?

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Hep E

Self-limiting heatitis from fecal oral route

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  • recent travel?
    high risk behaviours?

  • liver enzymes

  • Liver function tests

assessment for Hepatitis:

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  • well balanced diet

  • vitamins

  • rest

  • avoid alcohol

  • avoid tylenol

treatment for most hepatitis: [5]

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Airborne droplet

n95 mask and full PPE.

patient in private, negative pressure room

Precautions for TB

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in active stage

when is TB contageous?

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 Fatigue

 Malaise

 Anorexia

 Weight loss

 Low-grade fever

  Night sweats

 Cough – frequent, productive

 Chest pain – dull or tight

 Hemoptysis (advanced cases)

Active TB clinical manifestations: [9]

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  1. miliary TB

  2. pleural effusion

  3. empyema

  4. TB pneumonia

  5. meningitis

  6. bone and joint issues

complications of TB

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  • chest xray

  • TB skin test

  •  Acid-fast bacilli (AFB) smear: only true way to diagnose

    • ­Three consecutive sputum samples

  • Nucleic acid amplification (NAA)

  • QuantiFERON-TB Gold In-Tube

TB diagnosis:

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Reaction from protein dirivative of TB. Positive? Chest Xray and sputum sample

What does TB skin test look for?

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at home, want to irraticate it

Where is TB typically treated?

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  1. full drug course

  2. monitor sputum weekly (2-3 weeks)

  3. 3 negative tests

When is some one with TB no longer considered contageous?

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liver, meds are hard on liver

what function tests are important to monitor with TB?

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  1. wear mask

  2. open windows

  3. education

  4. med adherence is huge

home treatment for TB: [4]