Cirrhosis Flashcards

1
Q

What is Liver Cirrhosis

A

Liver cells attempt to regenerate but the process is disorganized
- abnormal blood vessel and bile duct formation
- overgrowth of new fibrous connective tissue distorts liver’s normal structure, impedes blood flow
- irregular regeneration and disorganized regeneration, poor cellular nutrition and hypoxia d/t inadequate blood flow and scar tissue result in decreased liver functioning
Cirrhosis is the final stage of chronic liver disease

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2
Q

Etiology of Cirrhosis

A
  • insidious, prolonged course
  • eleventh leading cause of death in Canada
  • twice as common in men
  • highest in ages 40-60
  • Treatment focuses on trying to reduce complications and are aimed at stopping or delaying disease progression, minimizing liver cell damage and reducing complications.
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3
Q

Factors that can lead to cirrhosis (5)

A
  • Chronic alcohol use disorder (excessive alcohol ingestion is the single most common cause of cirrhosis, alcohol has a direct hepatotoxic effect)
  • Nonalcohol fatty liver disease (NAFLD)
  • Cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity
  • Patient with Hepatitis B and C
  • Environmental factors, as well as a genetic predisposition
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4
Q

Biliary Cirrhosis

A

Associated with chronic biliary obstruction
Diffuse fibrosis of liver with jaundice

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5
Q

Cardiac Cirrhosis

A

From longstanding severe right-sided heart failure

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6
Q

Common Assessment Findings for Hepatic Disorder (9)

A
  1. GI issues (clay coloured stool, no bile, anorexia, NV, constipation)
  2. Jaundice, dark urine from bilirubin, icterus, pruritis
  3. Energy deficits (d/t carb, lipid, and protein metabolism being effected. absorption is impacted. Not getting nutrients or from anemia from bleeding)
  4. Petechiae or bruising or bleeding from decreased VK absorption
  5. Peripheral or pulmonary edema
  6. Ascites
  7. Altered mental state, confusion r/t liver disease and build up of toxins
  8. Cachectic, so much fluid in interstitial space
  9. Look dired, dilated abdominal veins, protruding abdomen
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7
Q

Common laboratory findings indicating decreased liver function (5)

A

Elevated liver enzymes: ALT, AST, LDH, Alk Phos, GGT
Decreased serum albumin levels (normal 3.5-5)
Prolonged prothrombin time
Increased unconjugated bilirubin (fat soluble, indirect) - too much bilirubin in the blood
Increased Conjugated bilirubin (water soluble, direct) - impaired excretion

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8
Q

Collaborative Care

A
  • Rest
  • Avoidance of alcohol, Aspirin, acetaminophen, and NSAIDS
  • Management of ascites
  • Prevention and management of esophageal variceal bleeding
  • Management of encephalopathy
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9
Q

What causes Jaundice?

A

Bilirubin is formed when hemoglobin is broken down as part of the normal processes of recycling older damaged RBC. Unconjugaed bilirubin – carried in blood stream by albumin because it is insoluble, to the liver where it binds with bile and becomes conjugated. Bilirubin is then moved into the digestive tract to be eliminated from the body through the stool or urine.
If bilirubin cannot be moved through the liver it builds up in the blood and bile salts are deposited under the skin the result is jaundice and pruritis.
Many people with jaundice have dark urine and light coloured stool. Occur when a blockage or other problem prevents the bilirubin from being eliminated in the stool.
Often jaundice presents first in the scelra of the eyes

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9
Q

Skin Lesions (2) and what causes them?

A
  • Spider angioma occurs on the nose, cheeks, upper trunk, neck and shoulders
  • Palmar Erythema a red area that blanches with pressure appears on the palms of the hands
  • Both of these are caused by low levels of circulating estrogen as a result of the liver’s inability to metabolize steroid hormones
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10
Q

Peripheral Neuropathy
- what is it and what causes it

A

Found in alcoholic cirrhosis, probably caused by a deficiency in thiamine, folic acid, and vitamin B12
- damage to nerves outside of the brain and spinal cord. weakness, numbness or pain. stabbing, burning, tingling

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11
Q

Endocrine Disorders: Hypogonadism
- can cause: (4)

A

a decrease in male sex hormones can cause:
- gynecomastia
- loss of axillary and pubic hair
- testicular atrophy
- impotence +/- loss of libido

In women - amenorrhea, in older women - vaginal bleeding
Hypoaldosteronism: Na+ an water retention and potassium loss

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12
Q

Hematological Problems (4)

A

Thrombocytopenia - decreased platelets. strongest indicator of cirrhosis
Leukopenia - presence of a reduced volume of WBC
Anemia - reduced volume of RBC
Decreased prothrombin - results from the livers inability to produce prothrombin and other clotting factors. Manifested with gingival bleeding, epistaxis, purpura, petechiae, heavy menstrual bleeding

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13
Q

What causes hematological problems?

A
  • splenomegaly which results from the backup of blood from the portal vein into the spleen. Overactivity results in increased removal of blood cells especially platelets from circulation.
  • Anemia can be due to inadequate blood cell production and survival and also be due to esophageal varicies or bleeding
    Reasons: alcoholic bone marrow suppression, sepsis, lack of folate, platelets sequestering in the spleen, decreased thrombopoieten
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14
Q

Portal Hypertension

A

Portal hypertension is an increase in BP within the system of veins called the portal venous system. 2/3 of blood supply to the liver.
Veins coming from stomach, intestines, spleen and pancreas merge into the portal vein which then branches into smaller vessels and travels through the liver. If vessels are blocked due to liver damage, blood cannot flow properly - leads to high pressure in the portal system. May lead to development of varices in the esophagus, stomach, rectum or umbilical area
Varices can rupture and bleed resulting in potentially life-threatening complications

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15
Q

What are Esophageal Varices?

A

Result of portal hypertension. Tortuous veins. trying to offset the pressure in the portal vein through developing collateral circulation. Very fragile veins, tolerate high pressure poorly. Bleed easily

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16
Q

Signs and Symptoms of Esophageal Varices

A

Do a GI assessment. Look for risk of bleeding – easy bruising, petechiae, gingival bleeding, normal hemoglobin, anemic, RBC level. CBC.
Subjective assessment questions: if they have been vomiting – what did it look like. Blood that has been sitting in the stomach – looks like coffee grounds.
Stool – abnormal colour, does it look black (melina)
VS – any indication of alteration.
Evidence of hypovolemic shock

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17
Q

Diagnosis of Esophageal Varices

A

Endoscopy is indicated. Gastroscopy or upper gastrointestinal endoscopy. Preferred for diagnosis or screening for varices. Doctor is looking for dilated veins. Any red streaks or red spots. Treatment can be performed during exams.

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18
Q

Treatment of Esophageal Varices

A

Treatments – urgent hospital admission. IV fluids and transfusion of RBC. Transfusion of platelets and/or clotting factors may be necessary. Octreotide – reduces pressure in the portal venous system. Ligation with elastic bands to stop bleeding
Slow oozing ones can become abruptly gushing ones. Right around the connection between the esophagus and stomach. Be careful with NG tube.
Transjugular intrahepatic portosystemic shunt (TIPS) - may be done to reduce portal hypertension d

19
Q

Esophageal Varices: Supportive measures for acute bleeding (6)

A
  • fresh-frozen plasma
  • Packed RBCs
  • vitamin K
  • proton pump inhibitors
  • octreotide
  • octaplex (in severe cases)
20
Q

Ascites

A

Accumulation of serous fluid in the peritoneal or abdominal cavity d/t elevation of portal pressure. Increased pressure in portal vessels may cause proteins to shift from the blood vessels.
Usually proteins cant get through the capillary beds but the increased pressure in the vein and larger pores in the sinusoids which are the capillaries in the liver. Proteins can shift into lymph space. Third spacing. Fluid is stuck there. Taken out by paracentesis

21
Q

Peripheral Edema

A

Decreased colloidal oncotic pressure due to impaired liver synthesis of albumin and due to increased portal cable pressure d/t increased portal tension.
Pedal, presacral edema

22
Q

Clinical Manifestations of Ascites(6)

A

Abdominal distention +/- umbilical eversion
Weight gain – sitting of fluid that can’t go anywhere
Abdominal striae
Decreased urine output
Signs of dehydration – look to be fluid overloaded but intravascularly they are dehydrated
Hypokalemia – hyperaldosteronism and diuretics that are given to treat ascites.

23
Q

Collaborative Care of Ascites (3)

A
  1. Focused on sodium restriction, diuretics, and fluid removal
  2. Diuretics
  3. Paracentesis
24
Q

Paracentesis (5)

A
  • Removes fluid from abdominal cavity
  • Temporary measure
  • Continuous reinfusion of ascitic fluid from the abdomen to the vena cava
  • Not first-line therapy
  • Relief provided is only temporary
25
Q

Hepatic Encephalopathy

A

Hepatic encephalopathy is a neuropsychiatric manifestation of advanced liver disease. When blood is shunted past the liver via the collateral anastomoses, or when the liver is unable to convert ammonia to urea, ammonia levels in the systemic circulation rise. The ammonia crosses the blood-brain barrier and produces neurotoxic manifestations,
Liver normally converts the ammonia into urea which is eliminated in the urine. Ammonia levels in the blood rise when the liver cannot convert it to urea because it crosses the blood brain barrier it can be neurotoxic.

26
Q

Goal for Hepatic Encephalopathy

A

decrease protein in diet and eliminate the ammonia from the intestine quickly by giving lactulos and neomycin

27
Q

Wernicke’s Encephalopathy: primary cause

A

Alcoholic cirrhosis - helps make sense of the CIWA protocol
Malnutrition or starvation often associated with chronic drinking

28
Q

Clinical manifestations of Wernicke’s Encephalopathy
- is onset slow or abrupt?

A

altered mental status, ataxia (widened gait), diplopia, alterations in vision, nystagmus - horizontal CLASSIC
Occurs progressively - hepatic encephalopathy can occur slowly or abruptly

29
Q

Wernicke’s Encephalopathy: Treatment

A

Thiamine Administration
Prompt recognition to prevent Korakovs syndrome

30
Q

Clinical Manifestations of Hepatic Encephalopathy

A

CNS clinical manifestations - acute alterations in mental status, progressive confusion, stuporous, impaired thinking & judgement, neuromuscular disturbances - asterixis (liver flap_
- hyperreflexia

31
Q

What is Wernickes Encephalopathy

A

Complication of chronic alcohol abuse.
inflammatory, hemorrhagic, degenerative condition of the brain. Caused by a thiamine deficiency resulting from poor diet and alcohol-induced suppression of thiamine absorption. untreated or progessive Wernicke’s encephalopathy may lead to Korsakoff syndrome, an irreversible form of amnesia characteried by loss of short term memory and an inability to learn

32
Q

Diagnostics: LFTs

A
  • increased liver enzymes: ALT, AST, LDH, Alk Phos, GGT (ALT in particular). GGT often spikes with binge drinking
  • Decreased serum albumin levels (normal 3.5-5)
  • Increased prothrombin time/PT (normal 11-15 sec); INR trends similar to the PT
  • Unconjugated bilirubin (Fat soluble, indirect, pre-hepatic) - too much bilirubin in the blood
  • Conjugated bilirubin (water soluble, direct) - impaired excretion
33
Q

Lactulose for Hepatic Encephalopathy

A

Goal is reduction of ammonia formation
- lactulose (pulling ammonia out in the stool)
- antibiotics (reduces ammonia-producing enteric bacteria) -
- treatment of precipitating cause (controlling GI hemorrhage to decrease protein in the GI tract)
- liver transplant

34
Q

Drugs and Liver function: Avoid (2)

A

Avoid hepatotoxic drugs like Acetaminophen and ASA

35
Q

Drugs and Liver Function: First pass Effect

A
  • concentration of the drug after intestinal and hepatic alteration after absorption. oral drugs only
    they should be given in smaller doses because they end up having an increased effect or longer effect in patients with liver disease
    use caution in administering medications in patients with advanced liver disease
  • patients that drink have a higher tolerance for certain medications - particularly opioids
36
Q

Collaborative Care for Liver cirrhosis (5)

A
  • Rest
  • Avoidance of alcohol, Aspirin (clotting) acetaminophen (hepatotoxic) and NSAIDS (GI bleeding)
  • Prevention and management of esophageal variceal bleeding
  • management of ascites
  • management of encephalopathy (Wernickes, hepatic)
37
Q

Collaborative Care: Esophageal Varices. Prevention

A
  • All patients with cirrhosis have a screening UGI endoscopy
  • avoidance of alcohol ASA, NSAIDS
  • In non-bleeding varices present, take non-selective beta blockers (propranolol) - to reduce hepatic venous pressure
38
Q

Esophageal Varices - Acute Bleeding: Drug Therapy & Supportive Measures (6)

A
  • Fresh-frozen plasma
  • Packed RBC
  • Vitamin K
  • Proton pump inhibitors
  • Octreotide (decreases the inflow of blood to portal system by constricting the splanchnic arterioles and significantly reduces intravariceal pressure)
  • Octaplex (in severe cases) (belongs to a group of medicines called clotting factors. It contains the human vitamin K dependent blood coagulation factors. Octaplex is used to treat and prevent bleeding:
39
Q

Esophageal varices - Acute Bleeding - endoscopic

A

Endoscopic evaluation of the bleed: sclerotherapy, ligation

40
Q

Nursing Implications Liver Cirrhosis (7)

A
  • Health promotion
  • Acute interventions
  • Energy conservation
  • Symptom control
  • Intake and output monitoring
  • Strong Assessment and advocacy when complications occur
  • Patent IV access on patient’s with varices
41
Q

What is hepatitis?

A

inflammation of the liver. most common cause is a viral infection
Hepatitis A, B, C (primarily)

42
Q

Which hepatitis is fecal oral route?

A

Hepatitis A is contracting by consuming food or water contaminated by feces

43
Q

As a RN you must be immunized for hep?

A

Hepatitis B

44
Q

How is Hep C contracted?

A

Hepatitis C is contracted by direct contact with contaminated blood and bodily fluids.