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Block 10 Week 4 > Usera: Liver 1 > Flashcards

Usera: Liver 1 Flashcards

1
Q

Describe the blood supply to the liver

A

portal vein: venous blood rich in nutrients from the alimentary tract
hepatic artery: arterial blood rich in oxygen from the celiac axis
hepatic veins: right drains the right lobe, left drains the left lateral lobe, middle drains the middle of the left lobe & some of the right lobe

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2
Q

What is included in the portal triad?

A

portal vein
bile duct
hepatic artery

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3
Q

Describe the structural unit of the liver

A

the lobule is a hexagonal unit that is oriented around a hepatic vein with portal tracts at the periphery
centrilobular = area closest to the hepatic vein
periorbital = area closest to the portal tract

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4
Q

Describe the acinus model with zones 1-3, which describes the physiologic relationship of hepatocytes & the blood supple

A

The acinus is a triangular unit, with the apex near the hepatic vein & the base formed by the vessels of the portal tract
Zone 1 is closest to the portal tracts, while zone 3 is closest to the hepatic vein

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5
Q

T/F: Liver disease is an insidious process in which clinical detection and symptoms of hepatic decompensation may occur weeks, months or many years after the onset of injury

A

True

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6
Q

What are three liver tests used to assess hepatocyte integrity?

A

AST
ALT
lactate dehydrogenase (LDH)

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7
Q

What are some liver tests used to assess biliary excretory function?

A

serum bilirubin (total & direct)
urine bilirubin
alkaline phosphatase

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8
Q

What are some liver tests used to assess hepatocyte function?

A

albumin
prothrombin time
ammonia

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9
Q

The most severe clinical consequence of liver disease

Results from loss of 80-90% of hepatic functional capacity

A

hepatic failure

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10
Q

What are the 3 categories of liver failure?

A

acute liver failure
chronic liver disease
hepatic dysfunction w/o overt necrosis

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11
Q

Hepatic necrosis and inflammation are present for at least 6 months
Most common route with the endpoint of cirrhosis

A

chronic liver disease

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12
Q

Viable hepatocytes with an inability to perform metabolic function
Tetracycline toxicity, acute fatty liver of pregnancy

A

hepatic dysfunction w/o overt necrosis

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13
Q

Liver disease associated with encephalopathy within 6 months after diagnosis

A

acute liver failure

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14
Q

Encephalopathy that develops within 2 weeks of jaundice

A

fulminant liver failure

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15
Q

Encephalopathy that develops within 3 months of jaundice

A

sub-fulminant liver failure

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16
Q

What drugs can cause acute liver failure?

A 
acetaminophen
rifampin
isoniazid
MAOIs
halothane
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17
Q

What toxins can cause acute liver failure? What about infections?

A

carbon tetrachloride or mushroom poisoning

hep A and B

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18
Q

What are the clinical signs of hepatic dysfunction?

A 
jaundice
easy bruising
hypoalbuminemia
hyperammonemia
hypoglycemia
fetor hepatis
hyperestrinism: hypogonadism, gynecomastia, spider angiomas, palmar erythema, muscle wasting (shoulder girdle atrophy)
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19
Q 
What are these symptoms collectively known as? What are they clinical signs of?
Hypogonadism
gynecomastia
Spider angiomas
Palmar erythema
Muscle wasting (shoulder girdle atrophy)
A

hyperestrinism; signs of hepatic dysfunction

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20
Q

What are some complications of hepatic dysfunction?

A

hepatic failure: severe coagulopathy (can’t clot), encephalopathy, hepatorenal syndrome, multiple organ failure

portal hypertension: esophageal varices (abnormally enlarged veins in the lower esophagus - highly associated w/ liver failure)

malignancy

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21
Q

Disorder of neurotransmission in the CNS and neuromuscular system associated with elevated levels of ammonia
Spectrum of disturbances of consciousness
Subtle behavioral disturbances to confusion, stupor, coma and death

A

hepatic encephalopathy

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22
Q

What are the neurological signs of hepatic encephalopathy?

A

rigidity
hyper-reflexia
asterixis (flapping tremor)

23
Q

Renal failure in patients with severe chronic liver disease with no intrinsic cause for renal failure
Due to
Systemic vasodilation and decreased perfusion pressure
Activation of the renal sympathetic nervous system from vasoconstriction of afferent arterioles
Synthesis of renal vasoactive mediators

A

hepatorenal syndrome

24
Q

Common end stage to many underlying diseases
Fibrosis
Vascular disruption results in hypoperfusion
Nodular regeneration
Parenchymal/functional disruption

A

cirrhosis

25
Q

What is the most common cause of cirrhosis of the liver?

A

alcoholic liver disease

26
Q

What happens to hepatic stellate cells, which usu store Vit A, in response to inflammation or toxin exposure?

A

they transform into myofibroblasts & deposit collagen leading to fibrosis

27
Q

What are 3 morphologic characteristics of cirrhosis?

A

bridging fibrosis: deposition of collagen (types 1 & 3) due to activation of stellate cells into myofibroblasts

parenchymal nodule formation: after injury, hepatocytes regenerate as spherical nodules w/i the fibrous septa

architectural distortion: diffuse parenchymal injury & fibrosis

28
Q

An increase in pressure in the portal vein due to arterial pressures being imposed on the portal system

A

portal hypertension

29
Q

What are some prehepatic causes of portal hypertension?

A

obstructive thrombosis
massive splenomegaly
portal vein constriction

30
Q

What are some intrahepatic causes of portal hypertension?

A

cirrhosis
schistosomiasis
massive fatty change
diffuse granulomatous disease

31
Q

What are some posthepatic causes of portal hypertension?

A

Right sided heart failure
Constrictive pericarditis
Hepatic vein outflow obstruction

32
Q

What are the two main factors in portal hypertension?

A

increased resistance at the level of the sinusoids & increased flow

33
Q

What causes the increased resistance in portal hypertension?

A

disruption of blood flow by scarring & formation of parenchymal nodules

34
Q

What causes the increased flow in portal hypertension?

A

arteries vasodilate in the splanchnic circulation, leading to increased venous efflux in the portal system

35
Q

Complication of portal hypertension involving accumulation of serous fluid in the peritoneal cavity

A

ascites

36
Q

What are some porto-systemic shunts (bypasses) that can emerge as a result of portal hypertension? Why do these develop?

A

esophageal varices
rectum –> hemorrhoids
falciform ligament & umbilicus –> caput medusae

**The rise in the portal system pressure leads to reversal of blood flow (portal to systemic) by dilation of collateral vessels and development of new vessels

37
Q

What are the differences b/w unconjugated & conjugated bilirubin?

A

unconjugated: insoluble in water, tight complex with albumin in serum, cannot be excreted in urine
conjugated: water soluble, non-toxic, loosely bound to albumin, excess can be excreted in urine

38
Q

What is jaundice?

A

occurs when bilirubin production exceeds hepatic clearance

39
Q

What are some ways in which you can have an elevated unconjugated bilirubin?

A

overproduction - hemolysis
defective uptake - Gilbert’s syndrome
impaired conjugation - neonatal jaundice, or Crigler-Najjar types 1 & 2

40
Q

What is Crigler Najjar syndrome? Which form is more severe, type 1 or 2?

A

very rare inherited disorder in which bilirubin cannot be broken down
1 is AR & severe
2 is AD & less severe

41
Q

What are some causes of conjugated hyperbilirubinemia?

A

Rotor syndrome
Dubin-Johnson syndrome - defective secretion, absence of MRP-2

**Dubin-Johnson syndrome is an inherited, relapsing, benign disorder of bilirubin metabolism. This rare autosomal recessive condition is characterized by conjugated hyperbilirubinemia

42
Q

What is Dubin-Johnson syndrome?

A

an inherited, relapsing, benign disorder of bilirubin metabolism due to absence of MRP-2

43
Q

What are two forms of neonatal jaundice?

A

physiologic jaundice: due to immature hepatic function & excretion system

breast milk jaundice: bilirubin deconjugating enzymes in breast milk

44
Q

Autosomal recessive disorder due to absent UGT1A1
Characterized by unconjucated hyperbilirubinemia
Fatal in neonatal period

A

Crigler-Najjar type 1

45
Q

Autosomal dominant disorder due to decreased UGT1A1 activity
Characterized by unconjugated bilirubinemia
Mild symptoms

A

Crigler-Najjar type 2 or Gilbert syndrome

46
Q

Autosomal recessive disorder due to mutation in MRP2, leading to impaired excretion of bilirubin glucuronides
Characterized by conjugated hyperbilirubinemia

A

Dubin-Johnson syndrome

47
Q

Autosomal recessive disorder due to decreased hepatic uptake & storage
Leads to conjugated hyperbilirubinemia

A

Rotor syndrome

48
Q

Pathologic condition of impaired bile formation and bile flow that leads to the accumulation of bile pigment in hepatic parenchyma

A

cholestasis

49
Q

What causes cholestasis?

A

Obstruction of bile channels

Defection in bile secretion

50
Q

Signs & symptoms of cholestasis?

A 
jaundice
pruritis
xanthomas
silver stool
elevated alkaline phosphate
intestinal malabsorption
51
Q

Prolonged conjugated hyperbilrubinemia

Not a specific entity or necessarily inflammatory

A

neonatal cholestasis

52
Q

What are some causes of neonatal cholestasis?

A 
Bile duct obstruction
Neonatal infection
Toxic 
Metabolic disease
Idiopathic neonatal hepatitis
53
Q

What are some parasitic disease of the liver?

A 
echinococcal (hydatid) cyst
clonorchis sinensis
fasciola hepatica
schistosomiasis
malaria
strongyloides
54
Q

T/F: You can also get bacterial or amoebic abscesses in the liver

A

True

Block 10 Week 4 (8 decks)

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