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Block 10 week 4 > Liver I-usera > Flashcards

Liver I-usera Flashcards

1
Q

The (blank) is a location in the liver between a hepatocyte and a sinusoid. what is its function?
When can the function get impaired?

A

perisinusoidal space (or space of Disse)
allows for diffusion of nutrients
-in liver disease leading to obliteration of the space and decreased nutrient uptake and waste disposal by haptocytes.

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2
Q

What cells does the space of disse contain?
What do they do?
If you get a bunch of insults to these cells causing inflammation, what can result?

A

Hepatic stellate cells
Store fat or fat soluble vitamins (like Vit A)
Stellate cells transform into myofibroblasts resulting in collagen 1 and 3production, fibrosis and cirrhosis

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3
Q

What is a bile canalicuil?

A

how bile is connected throughout hepatocytes

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4
Q

What blood supply am I talking about:

Venous blood rich in nutrients from the alimentary tract (60-70%)

A

Portal Vein

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5
Q

What blood supply am I talking about:

Arterial blood rich in oxygen from the celiac axis (30-40%)

A

Hepatic artery

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6
Q

What does the right hepatic vein drain?
What does the left hepatic vein drain?
What does the middle hepatic vein drain?

A

Drains right lobe
Drains left lateral lobe
Drains middle, left lobe and right lobe

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7
Q

How does blood travel through the liver?

A

Portal vein-> central vein-> interlobular vein-> hepatic veins

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8
Q

What is the portal triad?

A

Hepatic artery, bile duct, portal vein

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9
Q 
What is a hepatic lobule?
What is this module for?
A

hexagonal unit oriented around central vein (hepatic vein) with portal vein around the periphery
-description of histopathology of the liver

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10
Q

What does centrilobular area indicate?

A

area of the liver closest to the hepatic vein

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11
Q

What does periportal area indicate?

A

area of the liver closest to the portal tract

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12
Q

What is an acinus?

What does an acinus

A

triangular unit with the apex situated near the hepatic vein and the base formed by portal vein tract

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13
Q

What do zones 1-3 indicate in an acinus?

A

zone 1 - closest to portal vein, most oxygenated
Zone 2 -middle
Zone 3- least oxygenated, closest to central vein

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14
Q

The liver is vulnerable to a wide variety of metabolic, toxic, microbial, circulatory, and neoplastic insults.
T or F

A

T

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15
Q

Liver disease is an insidious process in which clinical detection and symptoms of hepatic decompensation may occur (blank) afte the onset of injury

A

weeks to years

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16
Q

(blank) tests detect abnormal liver function help confirm the presence of liver disease but do not define the cause.

A

Biochemical

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17
Q

What tests detect hepatocyte integrity?

A

AST
ALT
Lactate dehydrogenase (LDH)

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18
Q

What tests detect biliary excretory function?

A
  • serum bilirubin (total, indirect, direct)
  • urine biliurbin
  • alkaline phosphatase
  • Gamma glutamyl transpeptidase (GGT)
  • 5-nucleotidase
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19
Q

What tests detect hepatocyte function?

A

Albumin
Prothrombin time (PT)
Ammonia

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20
Q

Indirect levels of bilirubin tell you about (blank).

Direct bilirubin tell you about (blank).

A

unconjugated bilirubin

conjugated bilirubin

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21
Q

What is the earliest sign of liver damage?

A

coagulopathy (PT will tell you this)

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22
Q

If you cant get ammonium you get (blank)

A

toxic encephalopathy

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23
Q

What are the patterns of liver injury?

A 
Inflammation (acute vs chronic)
Intracellular "things"
Necrosis
Regeneration
Fibrosis
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24
Q

SInce the liver responds to injury in only a few different ways, there are common clinical syndromes that occur as a consequence of many different diseases, what are these?

A

Hepatic failure
Cirrhosis
Portal HTN
Jaundice/Cholestasis

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25
Q

What is the most severe clinical consequence of liver disease?
This results from loss of (blank)% of hepatic functional capacity.

A

hepatic failure

80-90%

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26
Q

What is the end stage point of ALL LIVER pathology?

A

Cirrhosis

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27
Q

What are the three categoreis that hepatic failure can be grouped into?

A
  • acute liver failure
  • chronic liver disease
  • hepatic dysfunction without overt necrosis
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28
Q

What are examples of causes of acute liver failure?

A

Massive toxic overdose,
Massive infarct
Acute EBV w/ hepatic necrosis

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29
Q

What is the definition of chronic liver disease?

A

hepatic necrosis and inflammation are present for at least 6 months-> most common route with the endpoint as cirrhosis

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30
Q

What is the definition of hepatic dysfunction without overt necrosis? What are some examples of things that can cause this?

A

viable hepatocytes with an inability to perform metabolic function
-tetracycline toxicity, acute fatty liver of pregnancy

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31
Q

What is this:

Liver failure associated with encephalopathy within 6 months after diagnosis

A

Acute liver failure

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32
Q

What is this:

encephalopathy that develops within 2 weeks of jaundice

A

Fulminant acute liver failure

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33
Q

What is this

encephalopathy that develops within 3 months of jaundice

A

sub-fulminant liver failure

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34
Q

What are the causes of acute liver failure?

A

drugs
toxins
infections
autoimmune

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35
Q

What are the drugs that cause acute liver failure?

A

acetaminophen, rifampin, isoniazid, MAOIs, Halothane

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36
Q

What are the toxins that cause hepatic failure?

A 
carbone tetrachloride (used to be used in laundry mats)
mushroom poisoning (aflatoxin)
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37
Q

What are the infections associated with acute liver failure?

A

Hep A

Hep B

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38
Q

What are the clinical signs of hepatic dysfunction?

A 
jaundice
easy bruising (coagulopathy)
Hypoalbuminemia
Hyperammonemia
Hypoglycemia
Fetor hepatis (order of liver failure)
Hyperestrinism
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39
Q

What will hyperestrinism cause?

A 
hypogonadism
gynecomastia
spider angiomas
palmar erythema
muscle wasting (shoulder girdle atrophy)
40
Q

What are the complications of hepatic failure?

A

severe coagulopathy
encephelopathy
hepatorenal syndrome
multiple organ failure

41
Q

What are the complications of portal hypertension?

A

esophageal varices

42
Q

What are the compications of malignancy?

A

hepatocellular carcinoma

43
Q

Why does hepatic encephalopathy occur?

A

When your liver is broken it cant get rid of toxic metabolites so they go to your brain

44
Q

(blank) is due to poor renal perfusion and renal vasoconstriction. Is there intrinsic renal pathology?
What will your UA look like in hepatorenal syndrome?

A

hepatorenal syndrome
NO!
Urine is hyperosmolar, hyponatremic, no proteinuria

45
Q

What is a disorder of neurotransmission in the CNS and neuromuscular system associated with elevated levels of ammonia?

A

hepatic encephalopathy

46
Q

What are the signs and symptoms of hepatic encephalopathy?

A
  • subtle behavioral disturbances to confusion, stupor, coma and death
  • rigidity, hyper-refexia, asterixis
47
Q

What is this:

rena failure in patients with severe chronic liver disease with no intrinsic cause for renal failure.

A

Hepatorena syndrome

48
Q

What is hepatorenal syndrome due to?

A
  • Systemic vasodilation and decreased perfusion pressure
  • Activation of the renal sympathetic nervous system from vasoconstriction of afferent arterioles
  • Synthesis of renal vasoactive mediators
49
Q

What characterizes cirrhosis?

A

fibrosis (vascular disruption lead to hypoperfusion)
nodular regeneration
parenchyma/functiona diruption
greenish pigmentation (from trapped bile)

50
Q

WHy does fibrosis lead to cirrhosis?

A

because fibrosis blocks perfusion and leads to chronic ischemic state

51
Q

What is the most common cause of cirrhosis? Explain the MOA behind this?
Where does the fibrosis begin?

A

alcoholic liver disease
toxic metabolite from alcohol damages hepatic stellate cells and turns them into myofibroblasts which deposit collagen 1 and 3

Central vein and progresses towards sinusoids resuing in perisinusoid fibrosis

52
Q

What type of fibrosis is this:
deposition of types I and III colagen into spaces of Disse.
What is this faciliated by?
What is it due to?

A 
Bridging fibrosis 
Activation of stellate cells into myofibroblasts
-chronic inflammation 
-cytokine production
-disruption of the ECM
-direct stimulation by toxins
53
Q

What is this:
after injury, surviving hepatocytes regenerate as spherica nodules within the fibrous septa
What will this fibrous cause?

A

Parenchymal nodule formation

new vascular channels b/w portal vessels and hepatic veins

54
Q

In parenchymal nodule formation, the resultant fibrosis will cause new vascular channels b/w portal vessels and hepatic veins. This will cause what problem with the hepatocytes?

A
  • delivery of blood to hepatocytes will be compromised

- hepatocyte ability to secrete into plasma is compromised

55
Q

What is the result of architectura distortion?

A

diffuse parenchymal injury

diffuse fibrosis

56
Q

If you have distorted sinusoida architecture what will result?

A

increased resistance and portal HTN-> resulting in hepatosplenomegaly

57
Q

What is this:

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

A

Portal hypertension

58
Q

What are the prehepatic causes of portal HTN?

A

Obstructive thrombosis
Massive splenomegaly
Portal vein constriction

59
Q

What are the intrahepatic causes of portal hypertension?

A

Cirrhosis
Schistosomiasis (common in Africa)
Massive fatty change
Diffuse granulomatous disease (military TB etc)
Nodular regenerative hyperplasia (chronic insults)

60
Q

What are the posthepatic causes of portal hypertension?

A

Right sided heart failure
Constrictive pericarditis
Hepatic vein outflow obstruction

61
Q

Portal HTN occurs at the levels of the (Blank) caused by increased resistance. WHat are causes of this increased resistance?

A

sinusoid

  • Contraction of SMC
  • myofibroblasts
  • disruption of blood flow by scarring and formation of parenchymal nodules
62
Q

Portal HTN can occur due to increase flow by hyperdynamic circulation. What are the causes of this?

A

-arterial vasodilation in the splachnic circulation which leads to increase venous efflux in the portal system

63
Q

Why do you get ascites in portal HTN?

A

accumulation of serous fluid in the peritoneal cavity due to…

  • sinusoidal HTN
  • hypoalbuminemia
  • thoracic duct overflow
  • splachnic vasodilation and hyperdynamic circulation
64
Q

In portal HTN, you have some much blood backing up in your liver where does the blood go and why is this terrible?

A

goes to the esophagus creating esophageal varices-> prone to rupture
goes to rectum-> hemorrhoids
falciform ligament and umbilicus-> caput mudase (periumbilical vein engorgement)

65
Q

The rise in the portal system pressure leads to (blank) of blood flow.

A

reversal

(i.e. portal to system) by dilation of collateral vesses and development of new vessels

66
Q

A small fraction of unconjugated bilirubin is unbound and can cause (blank).
Is it soluble in water?
In high levels, what happens to the unconjugatd bilirubin?

A

toxic injury (kernicterus)

  • insoluble
  • it cannot be excreted in urine even when blood levels are high
67
Q

Unconjugated bilirubin makes a tight complex with (blank) in serum.

A

albumin

68
Q 
Is conjugated bilirubin...
(water soluble/ water insoluble)
(toxic/ non-toxic)
what is it bound to?
What happens to excess?
A

water soluble
non-toxic
albumin
excreted in urine

69
Q

Normal bilirubin levels are (blank).

Jaundice is noticable when bilirubin levels reach (blank)

A
  1. 3 – 1.2 mg/dL

2. 0- 2.5 mg/dL

70
Q

What is this:

when bili production exceeds hepatic clearance

A

jaundice

71
Q

What are the causes of unconjugated bilribubin induced jaundice?

A
  • overproduction (hemolysis)
  • Gilbert’ syndrome
  • Impaired conjugation (UGT1A1)
72
Q

How do you get excess production of unconjugated bilirubin resulting in jaundice?

A

high levels of Unconjugated Bilirubin overwhelm the conjugating ability of liver and then get hemolysed to cause jaundice

73
Q

What is gilberts syndrome?

When does this result in jaundice?

A
  • lack of glucuronyltransferase (which conjugates bilirubin) so build up of unconjugated bilirubin.
  • periods of prolonged fasting, chronic insults, stress
74
Q

What are the two disorders of unconjugated bilirubin that cause impaired conjugation (UGT)?

A 
Neonatal jaundice (babies doent make UGT for a little while)
Criglar-Najjar Types 1 and 2
75
Q

Which Criglar-Najjar syndrome is more severe, type 1 or type 2?

A

Type 1- AR, severe

Type 2- AD, less severe

76
Q

What are the 2 causes of jaundice causes by increased conjugated hyperbilirubinemia?

A
  • Rotor syndrome (AR)

- Dubin-Johnson Syndrome (AR)

77
Q

What is dubin johnson synrome?
What is the genetic problem?
Do you die from this?

A

defective secretion of bilirubin out of the liver-> results in black liver
absence of MRP-2 (transports bile out of the liver)
no

78
Q

What are the two types of neonatal jaundice?

A

Physiologic jaundice

Breast milk jaundice

79
Q

What is physiologic jaundice?

A

mild unconjugated hyperbilirubinemia due to immature hepatic conjugation and excretion system.

80
Q

What is breast milk jaundice?

A

bilirubin deconjugating enzymes in breast milk

81
Q

Crigler-Najjar syndrome type I is a (unconjugated/conjugated hyperbilirubinemia) problem. How is it inherited? What is the defect in bilirubin metabolism? What is the clinical course?

A
  • unconjugated hyperbilirubinemia
  • autosomal recessive
  • Absent UGT1A1 activity
  • Fatal in the neonatal period
82
Q

Crigler-Najjar syndrome type II is a (unconjugated/conjugated hyperbilirubinemia) problem. How is it inherited? What is the defect in bilirubin metabolism? What is the clinical course?

A
  • unconjugated hyperbilirubinemia
  • autosomal dominant with variable penetrance
  • decreased UGT1A1 activity
  • innocuous
83
Q

Gilbert syndrome is a (unconjugated/conjugated hyperbilirubinemia) problem. How is it inherited? What is the defect in bilirubin metabolism? What is the clinical course?

A

unconjugated
autosomal recessive
decreased UGT1A1
Innocuous

84
Q

Dubin-Johnson syndrome is a (unconjugated/conjugated hyperbilirubinemia) problem. How is it inherited? What is the defect in bilirubin metabolism? What is the clinical course?

A
  • conjugated
  • autosomal recessive
  • impaired excretion of bilirubin glucuronides due to mutation in MRP2
  • innocuous
85
Q

Rotor syndrome is a (unconjugated/conjugated hyperbilirubinemia) problem. How is it inherited? What is the defect in bilirubin metabolism? What is the clinical course?

A

conjugated

  • AR
  • decreased hepatic uptake and storage
  • innocuous
86
Q

What is this:
pathologic condition of impaired bile formation and bile flows that leads to the accumulation of bile pigment in hepatic parenchyma
What is it caused by?

A

Cholestasis

Extrahepatic or intrahepatic obstruction of bile channels
Defection in bile secretion

87
Q

Hepatocyte dysfunction or biliary obstruction results in (Blank)

A

cholestasis

88
Q

What are the signs of cholestasis?

A
  • Jaundice
  • Pruritis
  • xanthomas
  • “silver stool”
  • elevated alk phos
  • intestinal malabsorption (vit A, D, K)
89
Q

(blank) is defined as a decrease in bile flow due to impaired secretion by hepatocytes or to obstruction of bile flow through intra-or extrahepatic bile ducts.

A

Cholestasis

90
Q

What are the causes of neonatal cholestasis?

A
  • Bile duct obstruction
  • Neonatal infection
  • Toxic
  • Metabolic disease
  • Idiopathic neonatal hepatitis
91
Q

Neonatal cholestasis is a result of prolonged (unconjugated/conjugated) hyperbilirubinemia.

A

conjugated hyperbilirubinemia

92
Q

What bacterial infections can cause jaundice?

A 
Extrahepatic infections (sepsis)
Staphylococcus aureus
Salmonella typhi (typhoid fever)
Treponema pallidum
Ascending biliary infections (cholangitis)
93
Q

What parasitic infections can cause jaundice?

A 
Malaria
Schistosomiasis
Strongyloidiasis
Cryptosporidiosis
Leishmaniasis
Echinococcosis
Liver flukes
94
Q

What parasitic diseases can cause jaundice?

A 
Echinococcal cyst
Clonorchis sinensis
Fasciola hepatica
Schistosomiasis
Malaria
strongyloides
95
Q

(blank) is a parasitic disease of tapeworms of the Echinococcus type that infects the liver and causes jaundice.

A

echinococcal cyst

Block 10 week 4 (10 decks)

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