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D&T 4, Exam 3 (Liver) > Limjoco - Introduction to Liver > Flashcards

Limjoco - Introduction to Liver Flashcards

1
Q

What organ?

  • Largest organ, 1400-1600 gm
  • Crossroads between gastrointestinal tract and rest of body
  • Dual blood supply:
    • 2/3 via _______ (from GI tract)
    • 1/3 via _______ (from rest of body)
  • Blood drainage via hepatic veins –> IVC
A

The Liver

Portal vein

Hepatic artery

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2
Q

In the liver, blood from both the _______ and the ________ flows into the low-pressure sinusoids. (Sinusoids have Kupffer cells.)

  • Deoxygenated portal venous blood is rich in nutrients.
  • Arterial blood provides oxygen to the surrounding liver cells.

Blood then flows from the sinusoids into the central vein, then hepatic veins to return to the heart.

A

Portal vein, hepatic artery

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3
Q

Where is Bile produced?

Bonus: How does the flow of bile compare to vascular flow?

A

Bile is produced in hepatocytes

Flows from canaliculi into portal tract - opposite direction of flow from circulation

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4
Q

Where does exchange of nutrients and oxygen occur?

A

Sinusoids

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5
Q

Facts: Cells to know

  • Hepatocytes (liver parenchymal cells)
  • Bile duct cells
  • Endothelial cells (line sinusoids)
  • Kupffer cells (histiocytes, macrophages)
  • Ito stellate cells (line sinusoids, store fat and vitamin A)
A
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6
Q

What are Kuffper cells?

A

The histiocytes, or macrophages of the liver

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7
Q

What does this histo image show?

A
  • Sinusoids are lined by endothelial cells and Kupffer cells
  • Stellate (Ito) cells are present in the space of Disse.
  • Clear glycogenated nuclei and lipofuscin pigment are also present.
  • Hepatocytes show steatosis, with accumulation of small and large droplets of fat.
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8
Q

What do Stellate cells store?

*Stellate cells are very important in the fibrotic reaction of the liver

A

Fat and Vitamin A

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9
Q

What can cause pathology in the liver?

A
  • Infections (mainly hepatitis viruses)
  • Alcohol, Drugs
  • Metabolic derangements
  • Autoimmune diseases
  • Congenital diseases
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10
Q

What are the functions of the liver?

A
  • Metabolism (carbohydrates, lipids, amino acids)
  • Synthesis (albumin, clotting factors I, II, V, VII - XIII, lipoproteins VLDL, LDL, HDL, cholesterol, glycogen)
  • Catabolism (removes ammonia ->urea, hormones, detoxifies foreign compounds/drugs/chemicals)
  • Storage (glycogen, triglycerides, Fe++, Cu++, fat-soluble vitamins)
  • Excretion (bile, endogenous waste products)
  • Blood reservoir (can hold and release 10-15% of total blood volume)
  • Endocrine (modifies hormone action vit D to 25(OH)D, removes circulating hormones glucagon, etc.)

** mnemonic: My Skinny Cat Sees Every Bird Enter

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11
Q

What are the substances that the lab looks for in liver disease?

A
  • Serum transaminases
    • AST (SGOT) - aspartate aminotransferase
    • ALT (SGPT) - alanine aminotransferase
  • ALP - Alkaline phosphatase
  • GGT - Gamma glutamyl transpeptidase
  • Albumin
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12
Q

What enzyme that is elevated in liver dysfunction?

  • Removes PO4 groups
  • In liver, bone, intestine as different isoenzymes
  • In cell membrane bordering bile canaliculi cells, but also found in placenta and bone
  • Elevated in cholestatic disorders
A

Alkaline phosphatase

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13
Q

What enzyme?

  • Enzyme found in bile canaliculus
  • Involved in glutathione metabolism, drug detoxification
  • Most sensitive indicator of liver disease BUT not very specific
  • Therefore, if elevated together with ALP –> hepatobiliary disease

*** Also important in alcoholic liver disease

A

GGT - Gamma glutamyl transpeptidase

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14
Q

What marker?

  • Protein produced by liver
  • Maintains normal oncotic pressure
  • Decreased in liver disease (but level does not correlate with severity of disease)
A

Albumin

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15
Q

Etiologies of what disease?

Etiologies - myriad

  • VIRUSES (72%)
  • Excessive alcohol consumption
  • Acetaminophen overdose
  • Idiosyncratic response to medications
  • Autoimmune diseases (Autoimmune hepatitis)
  • Metabolic disorders (Reye syndrome, Acute fatty liver of pregnancy)
  • Circulatory disorders (Budd-Chiari syndrome, right-sided heart failure)
A

Acute Hepatitis

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16
Q

What is the brown pigment called? Is it normal?

A

Lipofuscin - “wear and tear” pigment

  • Normally found in liver with aging
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17
Q

What can been seen in this histology slide of a liver with hepatitis?

A
  • Spotty/lytic necrosis
  • Clusters of inflammatory cells (neutrophils/lymphocytes)
  • Ballooning edematous liver cells - loss of polygonal shape
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18
Q

What is interface hepatitis?

A

Inflammatory cells spill over past the limiting plate between the edge of the portal tract and hepatic parenchyma into the lobule

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19
Q

What are the necrotic areas between portal and central venous areas?

  • e.g. portal to portal, or venous to venous areas
A

Bridging necrosis

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20
Q

What are apoptotic cells called in the liver?

DNA fragmentation, cell shrinkage, degraded to apoptotic bodies that are phagocytosed by ______

  • Alternate pathway of death in hepatitis
  • Histology: individual cells with densely eosinophilic cytoplasm + fragmented nuclear remnants
A

Acidophil bodies

Kupffer cells

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21
Q

These are the clinical manifestations of what disorder - severe cases?

  • Acute encephalopathy
  • Coagulopathy
  • Acute renal failure
  • Gastrointestinal bleeding
  • Infection, sepsis
  • Respiratory failure
  • Cardiovascular collapse
A

Acute hepatitis

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22
Q

Outcomes of what disease?

  • Resolve spontaneously with supportive therapy
  • Proceed to Acute Liver Failure
  • Develop into Chronic Hepatitis
A

Acute hepatitis

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23
Q

True or False: liver has a large regenerative capacity?

A

True

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24
Q
  • __________ divide even in presence of confluent necrosis or chronic injury.
    • Can regenerate from 25% of normal tissue - but need intact normal framework
A
  • Mature hepatocytes
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25
Q

What is the clinical syndrome that results from 80-90% reduction of liver’s functional capacity – either due to diminished cell number or impaired function?

ACUTE
DECOMPENSATED
- from compensated chronic disease with sudden flare of activity (acute-on-chronic liver failure) = as patient with underlying cirrhosis

A

Acute hepatic failure

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26
Q

What disease state?

  • Coagulopathy (INR >1.5 –> prolonged clotting), hepatic encephalopathy, developing within 26 weeks of first insult, in a patient without preexisting disease or cirrhosis
  • In patients with chronic liver disease/cirrhosis, may also develop acute liver failure if disease recognized <26 weeks, with sudden flare of activity precipitatedd by insult (bleeding, infection, drug)
A

Acute Hepatic Failure

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27
Q

Pathology of what disease?

  • Acute massive hepatic necrosis (80-90% of liver function lost)
  • Non-necrotic liver failure (acute fatty liver of pregnancy/tetracycline toxicity/Reye syndrome)
  • Chronic liver disease/cirrhosis - most common route to hepatic failure (e.g., undiagnosed Wilson’s disease, autoimmune or B viral hepatitis, severe alcoholic hepatitis)
A

Acute Hepatic Failure

28
Q

Clinical manifestations of what disease?

  • Jaundice
    • Due to retention of bilirubin – not excreted from body, accumulates in fatty tissues
    • Yellow skin, sclerae, mucous membranes
  • Nausea, vomiting - toxins
A

Acute hepatic failure

29
Q

What manifestiation of acute hepatic failure?

  • Neuropsychiatric abnormalities
  • Potentially reversible
  • Altered metabolic milieu due to: shunting of blood from portal to systemic circulation, bypassing liver
    • Hyperammonemia main cause
    • Rigidity, hyperreflexia (asterixis),EEG changes
    • Behavioral abnormalities, personality changes
A

Hepatic encephalopathy

30
Q

What manifestation of acute hepatic failure?

  • Bleeding diathesis (decreased production of clotting factors)
  • Increased prothrombin time (decreased Factor VII)
  • Thrombocytopenia (hypersplenism, marrow suppression)
  • Disseminated intravascular coagulation (liver fails to clear activated factors from circulation)
A

Coagulopathy

31
Q

What does this histology slide of acute hepatic failure show?

A
  • Microvesicular steatosis/fatty change
  • Swollen hepatocytes with foamy-looking cytoplasm
  • small lipid vesicles (less than 1 μm in diameter) may or may not be visible.
  • Typically centrally located nucleus
32
Q

Laboratory Findings of what disease?

  • Markedly elevated serum AST, ALT
  • Hypoalbuminemia
  • Hyperammonemia
A

Acute Hepatic Failure

33
Q

Mnemonic - Causes of Acute Hepatic Failure:

A

B

C

D

E

F

A
  • A Acetaminophen, Hep A, autoimmune hepatitis
  • B Hep B
  • C Hep C, cryptogenic
  • D Drugs, toxins, Hep D
  • E Hep E, esoteric causes (Wilson’s dis, Budd-Chiari)
  • F Fatty change of microvesicular type (fatty liver of pregnancy, valproate, tetracycline, Reye syndrome)
34
Q

What can be associated with acute hepatic failure?

  • Kidney failure
  • Due to decreased renal perfusion in cirrhotic patients
  • Portal HTN –> systemic vasodilatation –> compensatory renal vasoconstriction
  • Decreased vasodilators, increased vasoconstrictors on renal circulation
  • Pulmonary failure
  • Due to pulmonary vasodilatation causing ventilation-perfusion mismatch –> hypoxia, shortness of breath

*Function normalizes with renal transplant

A
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
35
Q

What disease? (Associated with acute hepatic failure)

  • 1/16,000 - rare, potentially fatal cx in 3rd trimester or early post-partum
  • Microvesicular steatosis (liver biopsy rarely needed)
  • Due to abnormal fatty acid metabolism – accumulation of toxic products from placenta and fetus in mother
A

Acute Fatty Liver of Pregnancy

36
Q

Manifestations and treatment of what disease?

Clinical Manifestations

  • Malaise, N/V, RUQ pain, jaundice, fever, pruritus
  • Resemble preeclampsia, HELLP (Hemolysis, Elevated Liver tests, Low Platelets) syndrome – but with higher liver enzyme levels, more severe hypoglycemia

Treatment

  • Supportive care, fluids, mx of complications, delivery of baby
A

Acute Fatty Liver of Pregnancy

37
Q

What disorder? (Associated with acute hepatic failure)

  • First described in 1963; last reported cases in 1997
  • Acute metabolic encephalopathy in babies and children following acute respiratory viral illness + associated with salicylate (esp. aspirin) intake.
  • Due to abnormal fatty acid and carnitine metabolism
  • Affects primarily the liver and brain, and presents with certain biochemical and anatomic features
A

Reye syndrome

38
Q

What disorder?

Clinical Manifestations

  • Acute encephalopathy, pernicious vomiting, evidence of liver dysfunction especially in <2 yr old

Liver Biopsy

  • Microvesicular steatosis
  • Need to test for Inborn Errors of Metabolism ( ___ syndrome-like conditions)

Treatment

  • Supportive measures, especially maintaining normal blood glucose levels
A

Reye Syndrome

39
Q

What disease?

  • Various liver diseases + abnormal tests lasting longer than 6 months/26 weeks associated with progressive fibrosis
  • Ultimately leads to CIRRHOSIS
A

Chronic Liver Disease

40
Q

Etiologies of what disease?

  • NAFLD (Non-Alcoholic Fatty Liver Disease)
  • Hepatitis B, C
  • Alcoholic Liver Disease
  • Hereditary Hemochromatosis (abnormal retention of iron in liver, iron toxic to cells - treat with phlebotomy)
  • Alpha-1 Antitrypsin Deficiency
  • Wilson’s Disease
  • PBC, PSC
  • Autoimmune hepatitis
A

Chronic Liver Disease

41
Q

FACT:

A
42
Q

Pathology of what disorder?

  • Fibrosis c/o delicate bands or broad scars surrounding multiple adjacent regenerative lobules
  • Entire liver architecturally disrupted by interconnecting fibrous scar = bridging portal-portal, portal-central, central-central fibrosis
A

Liver Cirrhosis

43
Q

Pathology of liver cirrhosis - form –>

  • _______________: Micro (<3mm) and macro (> 3 mm) nodules from regeneration of liver cells in canals of Hering (progenitors of parenchymal and bile duct cells)
A

Regenerative Nodules

44
Q

Pathogenesis of Liver Cirrhosis:

Stimulation of _____________ by reactive oxygen species, growth factors, tumor necrosis factors, IL-1 produced by damaged hepatocyte

  • Becomes __________: produces smooth muscle actin, GFAP
  • Collagen deposited >>> fibrosis >>> cirrhosis
A

Perisinusoidal Stellate Cells (Ito Cells)

myofibroblast-like

45
Q

What stain picks up the reticulin framework (fibers that support the framework of the liver)?

A

Silver stain

46
Q

What is the most important change in liver cirrhosis?

A

Alterations in microvasculature architecture!

47
Q

Pathology of what disorder?

  • ALTERATIONS IN MICROVASCULATURE ARCHITECTURE – very important consequence!
  • Loss of sinusoidal cell fenestrations
  • Shunt development - bypasses the liver microcirculation
  • High-pressure, fast-flowing vessels WITHOUT solute exchange

–> Loss of functional integrity!

A

Liver cirrhosis

48
Q

Manifestations of what disorder?

  • Can be silent
  • Can have nonspecific symptoms - Weakness, anorexia, weight loss
  • Can lead to advanced disease: Progressive liver failure
  • Can lead to portal HTN - Ascites, portosystemic venous shunts, congestive splenomegaly, hepatic encephalopathy
A

Liver cirrhosis

49
Q

ADVANCED Liver cirrhosis leads to what manifestations?

A
  • Encephalopathy
  • Hyperreflexia, asterixis (flapping tremor), confusion, clonus, drowsiness, poor memory and alertness
  • Impaired metabolism of estrogenic compounds
  • Gynecomastia, spider angiomas
50
Q

Symmary of portal HTN from cirrhosis picture

A
51
Q

When cirrhosis is inactive for years, histology may show well-defined septal margins and incomplete septa. _______ may occur, but abnormal microvasculature and dysfunction remain.

A

Regression of cirrhosis

52
Q

Bile is:

  • A complex fluid of ______ and _______, produced by liver
  • Flows through biliary tract into the small intestine, where bile acids are reabsorbed and returned to the liver and re-secreted
  • 500 – 600 mls produced daily!
A
  • BIle acids and bilirubin
53
Q

What are some functions of bile acids?

A
  • Emulsification and micelle formation for absorption of dietary fat in the gut
  • Provides bicarbonate for neutralizing gastric acid
  • Helps eliminate cholesterol, highly protein-bound organic molecules, heavy metals, lipophilic drug metabolites that the kidney cannot filter
  • Protects gut from infection – excretes IgA, cytokines
54
Q

Structure of bile?

A
  • Hydrophobic and hydrophilic side, forms mycelles and facilitates absorption of fat from diet
55
Q

Bile salts are __________ (catabolic products of ________) that are conjugated with taurine or glycine

  • Are detergents - solubilize water-insoluble lipids
  • Cholic acid, chenodeoxycholic acid are two main bile acids
  • 95% bile acids/salts reabsorbed from intestine and returned to liver
A
  • Bile acids
  • Cholesterol
56
Q

What are 2 main bile acids?

A

Cholic acid, chenodeoxycholic acid

57
Q

What is the other component of bile (Besides bile salts)?

  • Comprises only 2% of bile
  • Breakdown product of heme (from senescent red blood cells) formed in SPLEEN; no real function
  • Accounts for yellow color in bruises, jaundice
  • UNCONJUGATED form - water insoluble, toxic to cells – so is bound to albumin, travels in blood
  • CONJUGATED form - water soluble, occurs in liver, is nontoxic, secreted in bile ducts
A

Bilirubin

58
Q

What is urobilinogen?

  • how is it excreted?
A

In the GUT, bacteria convert bilirubin into

UROBILINOGEN

  • excreted as stercobilinogen (stool)
  • reabsorbed in gut, recirculated, metabolized in liver or excreted via kidneys in urine
59
Q
  • The tiny bile canaliculi between hepatocytes become _________, then _______, then larger _________.
  • Beyond the porta hepatis, the main hepatic duct merges with the ________to become the _______, which goes to the duodenum.
A
  • ductules, interlobular bile ducts, larger hepatic ducts.
  • gallbladder’s cystic duct, common bile duct
60
Q

What is the name for decreased bile flow accompanied by accumulation of substances normally excreted in bile (bilirubin, bile acids, cholesterol)?

Bonus: will present with what physical finding?

A

Cholestasis

  • Jaundice (occurs when 2-3x excess of normal levels of bilirubin)
  • Prehepatic:
    • Hemolysis
  • Hepatic:
    • Hepatitis (viral, drug-induced, autoimmune)
    • Cirrhosis (decompensated)
    • Malignancy
    • Defect in bilirubin metabolism
  • Posthepatic:
    • Gallstones
    • Tumors, strictures
    • Compression by tumor (pancreatic head cancer)
61
Q

What step?

  • senescent RBCs, hemoproteins

Pathology:

  • Prehepatic
  • Unconjugated hyperbilirubinemia
  • hemolytic anemia, hematoma/internal hm’ge, ineffective erythropoiesis (PA, thalassemia)
A

Bilirubin Production

62
Q

What step?

  • Bilirubin-albumin complex transported across cell membrane, taken up by protein carrier

Pathology:

  • Intrahepatic
  • Unconjugated hyperbilirubinemia
  • Impaired uptake/binding
    • hepatocellular injury
    • drugs (interfere with membrane carrier system)
    • physiologic jaundice of NB – immature system
    • Gilbert’s syndrome
A

Uptake/binding

63
Q

What step?

  • Conjugated bilirubin diffuses through cell to bile canaliculus, excreted into bile

Pathology:

  • Intrahepatic or posthepatic
  • Predominantly conjugated
  • Dubin-Johnson, Rotor (deficiency of canalicular membrane transporter)
  • Autoimmune (IgG4) cholangiopathy
  • Duct obstruction
A

Excretion

64
Q

Summary:

  • Bile excreted into ________
  • Bilirubin hydrolyzed to free bilirubin by gut bacteria (by their _________)
  • Degraded to mix of pyrroles + urobilinogen
  • Urobilinogen mostly excreted in feces
  • 20% reabsorbed in ______ and goes back to liver (enterohepatic circulation), then re-excreted in bile or in urine
A
  • Small bowel
  • beta-glucuronidases
  • Ileum
65
Q

Micrograph of what?

A

Cholestasis in the liver

  • Feathery degeneration, clear cytoplasm, wispy cytoplasmic threads due to retained bile acids
66
Q

Clinical manisestations of what disorders?

  • Increased serum bilirubin: _____
  • Serum bile acids: ______
  • Malabsorption of fats: _______
  • Malabsorption of vitamins A D K: ____________
  • Increased serum cholesterol: _____________
A
  • Jaundice
  • Pruritis
  • Steatorrhea
  • Hemorrhagic, clotting disorders
  • Xanthomas

D&T 4, Exam 3 (Liver) (19 decks)

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