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Pathophysiology Final > Liver Conditions > Flashcards

Liver Conditions Flashcards

1
Q

Location of Liver

A

RUQ
1.2-1.6 kg in most adults
R and L lobe

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2
Q

Lobules are the Functional Components of the Liver

A
  • composed of a plate of specialized hepatocytes arranged around a central vein
  • Capillaries are arranged between the plates of hepatocytes and are covered in cells that carry out phagocytic activity
  • Remove bacteria, parasites, fungi, and other bacteria from the blood
  • Hepatocytes release bile into the canaliculi and then into the gall bladder
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3
Q

The liver receives both arterial and venous blood

A
  • About a third of the blood comes from the hepatic artery which carries oxygenated blood. 2/3 of the livers blood supply comes from the portal vein which is fed by blood from the spleen, intestines, stomach, and pancreas. It is partially oxygenated. The portal vein carries absorbed products of digestion for example nutrients, metabolites, and toxins such as alcohol, directly to the liver where it comes in contact with each lobule which processes and detoxifies and/or assimilates those substances. The blood leaves the liver via the hepatic vein and enters the heart via the inferior vena cava
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4
Q

How much circulating blood exists in the GI system?

A

25-30%

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5
Q

Liver: Structure and Function

  • metabolic
  • Storage
  • Bile synthesis
  • Mononuclear phagocyte system
A
  • metabolic functions include carbohydrate, protein, and fat metabolism, detoxification of the blood, steroid metabolism
  • bile synthesis functions include bile production, excretion
  • Storage functions include glucose (in the form of glycogen); fat-soluble vitamins (ADEK); and water soluble vitamins (B1, B12, folic acid); minerals (iron), amino acids in the form of albumin and beta-globulins
  • Mononuclear phagocytes system (Kupffer cells) functions include: breakdown of old RBCs, WBCs, bacteria, etc. Breakdwon of Hgb into bilirubin and biliverdin.
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6
Q

Functions of the Liver (11)

A
  1. Bile production
  2. Absorbs and metabolizes Bilirubin
  3. Assists in creating blood clotting factors or coagulants
  4. Fat metabolism
  5. Carbohydrate metabolism
  6. Vitamin and mineral storage
  7. Protein metabolism
  8. Filters the blood
  9. Liver has immunological functions.
  10. Production of albumin
  11. Synthesis of antiotensinogen
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7
Q
  1. Bile Production
A

helps the small intestine break down and absorb fats, cholesterol, and some vitamins. Bile consists of bile salts, cholesterol, bilirubin, electrolyte, and water.

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8
Q
  1. Absorbs and metabolizes bilirubin.
A

Bilirubin is formed by the breakdown of hemoglobin. The iron released is stored in the liver or bone marrow and is used to make the next generation of RBCs.

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9
Q
  1. Assists in creating blood clotting factors or Coagulants.
A

Bile is essential for absorbing vitamin K which is necessary for blood clot.

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10
Q
  1. Carbohydrate metabolism.
A

Carbs are stored in the liver and siphoned into the blood stream to maintain normal blood glucose levels

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11
Q
  1. Vitamin and mineral storage.
A

Liver stores the fat-soluble vitamins A, D and K and B12. years worth of vitamins. iron from hemoglobin in the form of ferritin. Ready to make new RBCs. Also stores copper.

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12
Q
  1. Protein metabolism
A

Bile helps break down proteins

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13
Q
  1. Filters the blood
A

filters and removed compounds in the body such as estrogen and aldosterone. And compounds from outside the body like alcohol or drugs. Altered liver function is going to impact how a person is able to metabolize a drug.

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14
Q
  1. Liver has immunological functions
A

has a high number of immunologically active cells called the Kupffers cells that destroy any pathogens that may enter the liver via the gut.

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15
Q
  1. Production of albumin
A

most common protein in the blood. Transfers fatty acids and steroid hormones to help maintain the correct oncotic pressure and prevent blood vessels from becoming leaky.

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16
Q

Liver Cirrhosis

A
  • liver cells attempt to regenerate but the regenerative process is disorganized.
  • Abnormal blood vessels and bile duct formation.
  • Overgrowth of new fibrous connective tissue distorts liver’s normal structure, impeding blood flow
  • Irregular regeneration and disorganized regeneration, poor cellular nutrition and hypoxia due to inadequate blood flow and scar tissue results in decreased liver functioning
    Cirrhosis is the final stage of chronic liver disease
  • insidious, prolonged course
  • 10th leading cause of death in Canada
  • twice as common in men than women
  • highest in ages 40-60
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17
Q

Focus of treatment for liver cirrhosis

A
  • focuses on cause, remove and minimize risk factors and symptoms
  • patient must stop drinking
  • may be treated with antiviral if caused by hepatitis
  • drug therapy
  • bleeding - serious side effect, may prescribe beta-blockers
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18
Q

Etiology and Pathophysiology of Liver Cirrhosis (Factors that can lead to cirrhosis)

A
  • Chronic alcohol use disorder (excessive alcohol ingestion is the single and most common cause of cirrhosis. Alcohol has a direct hepatotoxic effect. Some controversy continues as to whether the cause of cirrhosis is alcohol or the protein malnutrition that frequently coexists with chronic ingestion of alcohol)
  • nonalcohol fatty liver disease
  • Cases of nutrition-related cirrhosis have resulted from extreme dieting, malabsorption, and obesity
  • patients with hepatitis B and C
  • Environmental factors as well as genetic disposition
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19
Q

Compensated

A

liver is able to function normally despite hepatic cell injury

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20
Q

Decompensated

A

one or more of the complications occur

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21
Q

Common Assessment Findings for Cirrhosis

A
  • GI issues
  • Light coloured stool
  • Anorexia, N&V, diarrhea
  • Jaundice
  • Icterus
  • Pruritis
  • Fatigue, energy deficits
  • Anemia - liver disease influences clotting factors
  • Petechia
  • Peripheral edema
  • Pulmonary edema
  • Ascites
  • Changes in patients mentation
  • Cachectic
  • Puffy
  • Dilated abdominal veins
  • Protruding abdomens
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22
Q

Clinical manifestations of Advanced Cirrhosis

A
  1. jaundice
  2. Skin lesions
  3. Hematological Problems
  4. Endocrine Disorders
  5. Peripheral neuropathy
  6. Portal hypertension
  7. Esophageal Varies
  8. Peripheral Edema & Ascites
  9. Hepatic Encephalopathy
  10. Wernicke’s Encephalopathy
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23
Q

What causes jaundice?

A
  • Bilirubin is formed when hemoglobin is broken down. Unconjugate bilirubin is carried in the blood stream usually attached to albumin. It is carried to the liver and then moved through the bile ducts and into the intestine so it can be eliminated from the body. If it cannot be moved through the bile ducts and into the intestine so it can be eliminated from the body. If it cannot be moved through the liver it builds up in the blood and bile salts are deposited under the skin. Can also cause pruritus, dark urine, and light stool
  • Occur when a blockage prevents the bilirubin from being eliminated the stool so more has to be eliminated in the urine.
  • seen first in the sclera of the eyes then in the skin.
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24
Q

Skin lesions

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) these are both caused by increased levels of circulating estrogen as a result of the livers inability to metabolize steroid hormones

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25
Q

Hematological Problems - Thrombocytopenia

A

due to alcoholic bone marrow suppression, sepsis, lack of folate, platelet sequestering in the spleen, decreased thrombopoietin
- decrease platelets

26
Q

HematologicL Problems - Leukopenia

A

Reduced production of WBC

27
Q

Hematological Problems - Anemia

A

Production or destruction issue

28
Q

Hematological Problems - Coagulopathies

A

Results from livers inability to produce prothrombin and other factors essential for clotting
Gingival bleeding, epistaxis, easy bruising, heavy menstrual cycles

29
Q

Endocrine Disorders: in men

A
  • gynecomastia
  • loss of axillary and pubic hair
  • testicular atrophy
  • impotence +/- loss of libido
30
Q

Endocrine Disorders: in women

A
  • Amenorrhea (younger women)

- Vaginal bleeding (older women)

31
Q

Endocrine Disorders: Hyperaldosteronism

A

Na+ and water retention and K+ loss

32
Q

Peripheral Neuropathy

A
  • found in alcoholic cirrhosis, probably caused by a deficiency in thiamine, folic acid, and vitamin b12
  • causes weakness, numbness, and pain, stabbing, burning, or tingling nerve pain, altered sensation
33
Q

Portal Hypertension

A
  • Increase in the blood pressure within the system of veins called the portal venous system,
  • Gets backed up because of blockage
  • May lead to the development of varices in the esophagus, abdomen, and umbilical areas. can rupture and bleed resulting in potentially life-threatening complications
34
Q

Esophageal Varices - very fragile. Most dangerous complication
- Clinical Manifestations and diagnosis

A
  • GI assessment, look for risk of bleeding. Easy bruising, petechia, are they bleeding from their gums, do they have normal Hgb, look at CBC.
  • Ask subjective questions: have they been vomiting? if they have been vomiting, what does it look like? Ask about stool, is it an abnormal color? Does it look black? Look at their vital signs to see if there are any indications of bleeding.
  • Evidence of hypovolemic shock
    Diagnosis: endoscopy, gastroscopy
35
Q

What is the greatest risk with esophageal varices?

A
  • bleeding to death
  • require urgent hospital admission
  • Give IV fluids, and transfusion of RBC, give plasma and clotting factors, IV meds to reduce pressure in portal venous system
  • Using elastic bands to close off bleeding veins is called ligation
  • Have poor outcome (not so much, poor oozing ones)
  • Be careful inserting NG tube into someone with severe liver disease
36
Q

Complication: Peripheral Edema & Ascites

A
  • Decreased colloidal oncotic pressure due to impaired liver synthesis of albumin and due to increased portal hypertension
  • Sinusoids
  • Manifests as:
    Pedal: in the feet
    And presacral: lower back
37
Q

Ascites - due to elevation of portal pressure

A
  • Gets stuck there so it has to be taken out with parathesis
38
Q

What does Ascites look like?

A
  • Abdominal distension +/- umbilical eversion
  • weight gain
  • Abdominal striae
  • decreased U/O
  • Signs of dehydration
  • Hypokalemia - due to hyperaldosteronism and diuretics diven to treat ascites
39
Q

3 main causes of peripheral edema and ascites

A
  1. Proteins leaking into the abdominal cavity related to the back pressure on the vessels due to the portal hypertension. Proteins leak into the lymph and then into the cavity
  2. Hypoalbuminemia: not enough albumin. oncotic pull pressure is decreased.
  3. Hyperaldosteronism: aldosterone is not metabolized in the liver and so there is excess aldosterone and therefore fluid and Na+ retention
40
Q

Hepatic Encephalopathy

A
  • High ammonia levels, can cross the blood-brain barrier
  • Reduce proteins, or eliminate the ammonia from the intestine quickly
  • acute onset of symptoms
  • measured through increase levels of ammonia in the blood although this is not always present. Do blood test.
41
Q

Clinical Manifestations of Hepatic Encephalopathy

A
  • Altered LOC

- Asterixis (classic hand tremor) UNIQUE TO HEPATIC ENCEPHALOPATHY

42
Q

Wernicke’s Encephalopathy

A
  • ataxia, nystagmus (lateral twitching of the eye), altered LOC
  • primary cause: malnutrition or starvation associated with alcholism
  • brain damage caused by a lack of vitamin B1
  • horizontal nystagmus
  • treatment: thiamine (vitamin b1 supplement)
43
Q

Difference between Wernicke’s encephalopathy and hepatic encephalopathy

A

Differentiate LOC with liver disease. Asterixis is specific to hepatic encephalopathy

44
Q

Third LOC

A
  • if patients come in drunk, they will have a high blood alcohol
  • if you get a low blood alcohol or a 0, their altered LOC is not related to alcohol intoxication
45
Q

Withdrawal

A
  • you can get altered LOC in acute alcohol withdrawal as well
46
Q

Diagnostics: Liver Function Tests

A
  • Common laboratory findings
  • increased liver enzymes: ALT (MAIN ONE), AST, LDH, Alk Phos (indicate liver damage), GGT (enzyme in the blood)
  • A drop in serum albumin levels
  • Increased prothrombin time; INR trends similar to the PT
  • increased Unconjugated bilirubin (fat-soluble, indirect, pre-hepatic) - too much bilirubin in the blood
  • increased Conjugated bilirubin (water-soluble, direct) - impaired excretion
47
Q

normal albumin levels

A

3.5-5 G/dl

48
Q

Normal PT

A

11-15 seconds

49
Q

Collaborative Care

A
  • rest
  • avoidance of alcohol, aspirin, acetaminophen, and NSAIDs
  • prevention and management of esophageal variceal bleeding
  • management of acites
  • management of encephalopathy
    wernickes
    hepatic
50
Q

Collaborative Care: Esophageal Varices

- Prevention of Varices

A
  • All patients with cirrhosis have a screening UGI endoscopy
  • Avoidance of alcohol, ASA, NSAIDs
  • If non-bleeding varices present, take non-selective beta blockers
51
Q

Collaborative Care: Esophageal Varices

- If acute bleeding begins:

A

Drug theary and supportive measures:
- Fresh-frozen plasma
- packed RBC
- Vitamin K
- Proton pump inhibitors
- Octreotide (inhibits acid and pepsin secretion)
- Octaplex (treatment s of bleeding in patients with deficiency of the prothrombin complex coagulation factors) - only given in severe cases
Endoscopic evaluation of the bleed
- Sclerotherapy (solution injected into the vein that makes the lining of the vessel stick together)
- ligation

52
Q

TIPS

A

Trans jugular intrahepatic protosystemic shunt

53
Q

Collaborative Care: Acites

A
  • focused on sodium restriction, diuretics, and fluid removal
  • diuretics
  • Paracentesis
    (removes fluid from abdominal cavity, temorary measure, not first-line therapy. Often done to increase comfort)
54
Q

Collaborative Care: Hepatic Encephalopathy

Goal: reduction of ammonia formation

A

Treatment:

  • Lactulose (Decrease intestinal absorption and production of ammonia)
  • Antibiotics (to reduce ammonia-producing enteric bacteria in patients with hepatic encephalopathy)
  • Treatment of precipitating cause (controlling GI hemorrhage to decrease protein in the GI tract)
  • Liver transplant
55
Q

Collaborative Care Wernicke’s Encephalopathy

A
  • prompt recognition

- Thiamine administration

56
Q

Nursing Implications

A
  • health promotion
  • acute interventions (energy conservation, symptom control, intake and output monitoring, strong assessment and advocacy when complications occur, patent IV access of patient with varices)
57
Q

Drugs and Liver Function

A
  • avoid hepatotoxic drugs like Acetaminophen and ASA
  • First pass effect (ORAL DRUGS ONLY)
  • This affects oral meds, and they should be given in smaller doses
  • Use caution in administering medications in patients with advanced liver disease
58
Q

Chronic alcoholism can cause…

A

a tolerance to medications

59
Q

Hepatitis

A
  • A, B, C (primarily)
  • contracted by consuming food or water contaminated by feces is hep A (vaccine is give to those who are going to other countries where they may be in contact with unclean cooking habits)
  • 1% of patietns can clear hep B on their won. if it does not clear, many can evelop incurable chornic hep B.
  • spread in blood and body fluids. (sexual contact)
  • A significant reason for patients going on to develop primary liver cancer. medication management reduces viral load and incidene of liver cancer.
  • Hep C is contracted by direct contact with contaminated blood and body fluids. This one is treatable. Can be eliminated through drugs. Can be cured.
60
Q

Liver Cancer

A
  • hepatocellular carcinoma
  • third most common cancer in the world
  • causes: Cirrhosis, chronic HCV or HBV, NAFLD)
  • clinical manifestations: similar to cirrhosis; minimal in early stages
  • treatment: surgical removal or palliation
  • focus of care: symptom managememt
61
Q

Liver Transplantation

  1. Living Donor
  2. Deceased Donor
A

Living donor transplant is possible because the human liver regenerates and returns to its normal size shortly after surgical removal of part of the organ

Pathophysiology Final (7 decks)

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