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NURS 1650 - Here We Go Again > Pathophysiology of Liver Disease > Flashcards

Pathophysiology of Liver Disease Flashcards

1
Q

Describe the structure and role of sinusoids in the liver:

A

Sinusoids are hepatic capillaries

  • Have larger lumens than other types of capillaries
  • Have fenestrations (pores) that are larger than usual and large intracellular clefts –> allows unimpeded blood flow to bathe the hepatocytes
  • Gaps allow the products of the liver to leave the liver and enter the circulation by first entering the Space of Disse
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2
Q

What are Kupffer cells?

A

Resident macrophages in the lumen of the liver

  • Phagocytose bacteria
  • Activate other cell types (stellate cells)
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3
Q

What do stellate cells do?

A

Located the sinusoids

Usual function is to store Vitamin A

When activated, play a key role in liver scarring and fibrosis

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4
Q

What is the Space of Disse?

A

The space between the sinusoidal endothelium and hepatocytes

The plasma that collects here flows back toward portal triads, and collects in lymphatic ducts, forming a large portion of the body’s lymph

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5
Q

What role do microvilli of hepatocytes have in the Space of Disse?

A

Microvilli of hepatocytes extend into the Space of Disse, allowing proteins and other plasma components from the sinusoids to be absorbed by the hepatocytes

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6
Q

Describe the steps of the synthesis, metabolism, and excretion of bilirubin

A
  1. Old RBCs are broken down by macrophages. The heme portion of the RBC is converted first to biliverdin and then to bilirubin. This is unconjugated, “indirect” bilirubin.
  2. Bilirubin tightly binds to albumin; needs a carrier protein in plasma.
  3. Albumin-bound bilirubin is delivered to the liver.
  4. In the liver, bilirubin has glucuronides attached to it. This is conjugated, “direct” bilirubin. It is water-soluble, but usually travels in plasma loosely bound to albumin.
  5. Conjugated bilirubin is excreted into the bile, and works its way through the gut. Bacteria in the gut deconjugate the bilirubin and degrade it to urobilinogen and then stercobilin. Stercobilin is excreted in the feces. A small amount of urobilinogen is recirculated and then excreted in the urine.
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7
Q

Unconjugated vs. Conjugated Bilirubin:

A

Unconjugated bilirubin: hydrophobic, tightly-bound to albumin, toxic, indirect lab results

Conjugated: hydrophilic, loosely bound to albumin, has glucuronides, not toxic, direct lab results

Conjugation INCREASES water-solubility of bilirubin

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8
Q

What is jaundice? What is it a result of?

A

Jaundice is green-yellow staining of tissues

Caused by an excess of bilirubin

Common in liver disease (sign by which we quickly know something has gone wrong)

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9
Q

G6PD Deficiency is a _____ cause of jaundice

A

Prehaptic

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10
Q

Physiologic Jaundice of the Newborn is a _____ cause of jaundice

A

Hepatic

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11
Q

Cholestasis is a ______ cause of jaundice

A

Posthepatic

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12
Q

Describe the liver’s regeneration abilities

A

After damage or disease, the liver recovers, and hepatocytes regenerate via hyperplasia

This ability is not limitless, however

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13
Q

What is acute viral hepatitis?

A

Inflammation of the liver. Can be caused by many viruses

Hep A (HAV)

Hep B (HBV)

Hep C (HCV)

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14
Q

S/Sx if Hep A, B, and C:

A

Fever

Fatigue and malaise

A/N/V

Abdominal pain / RUQ pain

Dark urine

Jaundice

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15
Q

What kind of virus is Hep A? How is it spread?

A

RNA virus

Spread via fecal-oral route, mainly from contaminated food or water

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16
Q

Does Hep A have a vaccine available?

A

Yes

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17
Q

Can Hep A become chronic?

A

No

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18
Q

What kind of virus causes Hep B? How is it spread?

A

DNA virus

Spread primarily by parenteral contact with infected blood, semen, or other body fluids (mucous membranes, non-intact skin)

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19
Q

Who is at the highest risk of developing chronic HBV infection?

A

Infants and very young children

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20
Q

Is there a vaccine available for Hep B?

A

Yes

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21
Q

What causes the most damage in Hep B?

A

Cytotoxic T cells attacking infected cells

22
Q

What kind of virus causes Hep C? How is it spread?

A

RNA virus

Spread primarily through IV drug use or other blood exposure

23
Q

Is an acute HCV infection asymptomatic or symptomatic?

A

Often asymptomatic

24
Q

Can HCV become chronic?

A

Yes

25
Q

Is there a vaccine available for HCV?

A

No

26
Q

Describe fibrosis that occurs in HCV. What can it lead to?

A

The inflammatory response to viral infection activates the process of fibrosis

Fibrosis may progress slowly or rapidly to compensated cirrhosis and ultimately decompensated cirrhosis or liver cancer

27
Q

When are babies screened for HCV when born to an HCV-positive mother, why?

A

After 18 months

False positive can occur prior due to the maternal antibodies

28
Q

Patient teaching for patients with liver disease:

A
  • Avoid alcohol
  • Avoid acetaminophen
  • Avoid potentially hepatotoxic drugs
  • Avoid aspirin, and NSAIDs due to increased bleeding risk, as well as risk of kidney damage
  • Get vaccinated against Hep A and Hep B
29
Q

What is NAFLD?

A

Chronic Liver Disease // Nonalcoholic Fatty Liver Disease

Fat droplets accumulate in liver cells –> Enlarged fatty liver -> swelling and damage to the liver

30
Q

How does NAFLD progress? What causes this progression?

A

Obesity-related liver disease progression is the fastest-growing reason for NAFLD

Diet changes can reverse NAFLD

It can become NASH (non-alcoholic steatohepatitis) + inflammation

Fibrosis progressing to cirrhosis

Can lead to hepatocellular carcinoma

31
Q

What is cirrhosis? What does it result in? Describe the state of the liver in cirrhosis

A

Progressive, irreversible end stage of many different hepatic injuries – not a disease itself

The liver is fibrotic, scarred, and nodular

Results in permanent alteration in hepatic blood and bile flow and liver function

32
Q

Compensated vs. Uncompensated Cirrhosis

A

Compensated:
- Liver is scarred/fibrotic, but can still perform many important functions
- Few to no symptoms

Uncompensated:
- Liver is extensively scarred/fibrotic and can no longer perform important functions
- Jaundice, portal hypertension, ascites, edema, varices

33
Q

Describe the role of Kupffer cells, Stellate cells, and collagen in the path of cirrhosis

A

Chronic inflammatory process due to Kupffer cells, generating cytokines and other inflammatory mediators

Activation of Stellate cells by Kupffer cells increases the rate of deposition of extracellular matrix, including collagen in the Space of Disse –> FIBROSIS

Subendothelial collagen disrupts blood flow and impairs the movement of solutes between hepatocytes and plasma (ex. proteins)

34
Q

What happens to the hepatic microvilli and fenestrations in endothelial cells in cirrhosis?

A

Hepatic microvilli are lost/flattened

Fenestrations between endothelial cells are narrowed or closed

35
Q

What happens when blood flow is disrupted in cirrhosis?

A

Disruption of hepatic blood flow can cause:

  • Increased vascular resistance
  • Portal hypertension
  • Ascites
  • Hepatic encephalopathy
  • A large number of body system dysfunctions
36
Q

What are the general manifestations of chronic liver disease?

A

Abnormal storage and release of glucose

Inadequate protein metabolism

Impaired processing of endogenous steroid hormone: estrogen

Impaired clearance of exogenous drugs and toxins (conversion of ammonia to urea is impaired)

Portal hypertension

Hepatic encephalopathy

37
Q

What is portal hypertension? What causes it?

A

Increased pressure in the portal circulation
- Due in large part to scarring, fibrosis

The portal vein normally has low pressure and lacks the valves we see in other veins

The pressure will continue back up and engorge other veins

38
Q

What is hepatic encephalopathy? What causes it?

A

Complex neuropsychiatric syndrome [occurs in late-stage chronic liver disease]

Blood no longer passes through the liver for the removal of toxic substances. Results in more toxic substances and bacteria in the systemic circulation

Ex. The liver is unable to get rid of ammonia, which can cross the BBB and is toxic

39
Q

What can portal hypertension result in?

A

Alternate pathways of blood flow back to the vena cava –> esophageal, GI varices (engorged blood vessels)

Caput meduase (engorged superficial abdominal veins)

Splenomegaly (blood backs up into the spleen)

Hepatic encephalopathy

Ascites

40
Q

Why does ascites occur in chronic liver disease?

A

A shift in the Starling forces (movement out of the capillaries into the extravascular/interstitial space)

Increase in hepatic sinusoid/capillary hydrostatic pressure –> lymph fluid formation –> overwhelms the ability of thoracic duct to carry away the lymph –> increased hydrostatic pressure –> fluid moves out of the capillaries

Capillary oncotic pressure decreases –> fluid moves out of the capillaries

Extravascular/tissue oncotic pressure increases –? fluid moves out of the capillaries

41
Q

How does portal hypertension contribute to ascites?

A

Causes hemodynamic changes –> hypovolemia signal

Compensatory mechanisms activated –> RAAS

Increased vasopressin/ADH and aldosterone release

Lead to increased sodium retention –. increased water retention and eventually an increase in plasma volume that worsens the ascites

42
Q

How is ammonia converted to urea?

A

Liver forms urea by combining

Ammonia + CO2 = Urea + water

43
Q

Hepatic Encephalopathy S/Sx

A

Confusion, impaired cognition

Insomnia or hypersomnia

Psychotic symptoms

Asterixis (liver flap // spastic jerking of the hand)

Coma in severe cases

44
Q

How is serum ammonia level used to test the severity of hepatic encephalopathy?

A

It does not correlate well with the severity of encephalopathy

Is NOT used to determine encephalopathy severity or prognosis

45
Q

How does chronic alcohol abuse affect the liver?

A

Acetaldehyde (a breakdown product of alcohol) can directly injure hepatocytes and increase levels of ROS

Glutathione can be bound to it and unable to exert its effects

Endotoxins from the gut can be released and activate Kupffer cells –> cytokine release –> inflammation –> stellate cell activation –> liver fibrosis

46
Q

What is Hereditary Hemochromatosis (HH)?

A

Common autosomal recessive disorder that allows excessive and uncontrolled iron absorption

Iron deposits in numerous organs (liver, pancreas, heart)

Can progress to hepatocellular carcinoma

47
Q

Hereditary Hemochromatosis (HH) Clinical Manifestations:

A

Hepatomegaly

Elevated liver enzymes

DM, hyperpigmentation (bronzing) , polyarthritis, hypogonadism

Heart failure

48
Q

What is the treatment mainstay for Hereditary Hemochromatosis (HH)?

A

Routine phlebotomy

Avoid iron supplementation, minimize iron-rich foods

49
Q

How are AST and ALT used in liver function tests?

A

They are intracellular liver enzymes

Elevated serum levels of these enzymes indicate necrosis –> current liver injury

If acute, they will return to baseline approx. 2 weeks after an injury. Longer = chronic injury

50
Q

How is alkaline phosphatase or ALP used in liver function tests?

A

Elevated ALP points to cholestasis

Found in the bile duct epithelium

Bile salts can’t leave the liver –> release of AP into the bloodstream

51
Q

How is serum albumin used in LFTs?

A

Elevated urinary bilirubin may be a sign of liver dysfunction

Measured on a urine dipstick

NURS 1650 - Here We Go Again (20 decks)

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