Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
78 Cards in this Set
- Front
- Back
The liver arises from what?
|
As the hepatic diverticulum from the endodermal lining of the foregut in the 3rd/4th week of gestation
|
|
Where is the youngest portion of the liver?
|
Outside, because grows inside out
|
|
Processes which interfere with post natal bile duct development will have their largest effect in what area of the liver?
|
Outside
|
|
What gives rise to the hepatocytes and bile ducts?
|
Common stem cell (vascular system from different process)
|
|
What process is normal in the fetal liver and continues until 34 weeks of gestation?
|
Extramedullary hematopoeisis
|
|
What is a bile duct hamartoma?
|
Benign solitary tumor of the liver, get multiple smaller veins in that triad
|
|
What is a congenital hepatic fibrosis?
|
Abnormality where EVERY portal tract has a bile duct hamartoma
Get increased portal hypertension due to increased resistance |
|
What is caroli's disease and polycystic liver disease?
|
Abnormality with a dilation in bile duct
Causes bile to become static in these areas and stones may arise |
|
What is the blood supply to the hepatocytes?
To the bile ducts? |
Hepatocytes: DUAL supply, hepatic artery and portal vein
Bile ducts: SINGLE supply, hepatic artery |
|
What is the clinical significant of the vascular supplies?
|
Easier to get ischemia to bile ducts because only one blood supply
|
|
Stellate cells in the space of disse store what?
|
Vitamin A
|
|
what are the macrophages associated with the fenestrated endothelium in the liver?
|
Kupffer cells
|
|
What is the overall purpose of the space of disse?
|
Hepatocytes need something to give structure.
Serves as framework/guide for hepatocyte regeneration But still just a MATRIX/GEL so allows for EXCHANGE |
|
Hepatic stellate cells (Ito cells) in the space of diss store Vitamin A and can transform into what?
|
Tranform into myofibroblasts and lay down mature collagen resulting in FIBROSIS
|
|
What does acute venous outflow obstruction cause in the liver?
|
Blood cannot leave liver, therefore get CONGESTION, especially in zone 3
|
|
What 2 conditions can cause ACUTE venous outflow obstruction?
|
1. Budd-Chiari
2. Cardiac Issues (ie congestive heart failure) |
|
What is a budd-chiari?
|
Blockage of ALL left, middle, and right hepatic veins
|
|
What are the 2 main causes of a budd-chaiai?
|
1. Hypercoaguability
2. Tumor invasion |
|
Grossly, what will a liver with acute outflow obstruction look like?
|
Nut-meg liver
|
|
Budd-chairi is more common in which sex?
|
Females
|
|
What is veno occlusive disease?
|
a condition in which central veins in the liver are obstructed due to central vein laying down collagen in response to prolonged injury
|
|
veno occlusive disease is a result of what?
|
Toxic injury - ex: CHEMO before a bone marrow transplant
|
|
If the injury in veno occlusive disease is chronic, what will be seen?
|
"Cardiac type fibrosis" - collagen layed down, space between hepatice cords decreased
|
|
Which lobe is NOT affected in budd-chiari?
|
Caudate because it has it's independent venous drainage into the IVC
|
|
What will become hypertrophied in chronic budd-chiari?
|
The caudate lobe due to its independent venous drainage into the IVC
|
|
What is pressure atrophy?
|
Hepatocyte degeneration in venous occlusion due to the decreased nutrients from decreased blood inflow
|
|
What can happen due to Vitamin A toxicity?
|
Stellate cells become swollen / have hyperplasia
|
|
What is the result of stellate cell swelling?
|
They can literally block or clog up the sinusoids
|
|
Overtime, Vit. A causes what?
|
Causes stellate cells to lay down collagen and may eventually lead to cirrhosis
cause increase portal hypertension eventually |
|
Is hepatic infarction common?
|
NO, due to the dual blood supply to the liver
|
|
What is seen histologically in a liver infarction?
|
Coagulative necrosis surrounded by a hyperemic ring
|
|
Does ischemia lead to fibrosis?
|
NO
|
|
When you see coagulative necrosis, what should you think?
|
ISCHEMIC INJURY!!
|
|
What is the effect of thrombosis of the portal vein?
|
NO acute effect
Overtime though, hypertension may occur and regeneration may be hurt due to decreased growth factors |
|
What happens to the portal vein in a portal triad in resonspe to chronic injury?
|
Collagen is laid down, Lumen becomes remodeled and made smaller (so almost can't see it)
Ex: Veno-occlusive disease |
|
What infection can cause chronic damage and portal tract venopathy?
|
Schistosoiasis
|
|
What are the 4 types of non-cirrhotic portal hypertension?
|
1. Portal vein thrombosis
2. Portal tract veinopathy / hepato-portal sclerosis 3. Nodular Regenerative hyperplasia 4. Infiltrative (Vit A, amyloid, fat) |
|
In nodular generative hyperplasia, what is seen wrt hepatocyte size?
|
Hepatocytes get smaller toward zone 3 due to nutrient and oxygen deprivation
|
|
The differential size of hepatocytes in response to different nutrient/oxygen supply gives what?
|
The impression of nodularity in "Nodular regenerative hyperplasia"
|
|
Is fibrosis seen in nodular regenerative hyperplasia?
|
NO
|
|
Are all endothelial cell in the liver the same, do they all respond the same way to different toxins?
|
NO
|
|
Are abnormal tests common in liver enzymes?
|
YES (however 1% prevelance of significant liver disease in all patients screened)
|
|
How could LFT's be elevated even in the liver is absolutely fine?
|
Could be indirect reaction to a systemic disease (ex: celiacs, hypothyroidism)
|
|
Which 2 enzymes are the "transaminases"?
|
AST and ALT
|
|
What type of enzyme is ALT?
It's elevation signifies what? |
Liver restricted enzyme, thus its elevation is indicative of a HEPATIC process
|
|
Where is AST found?
What does it's elevation mean? |
AST found is many tissues, thus its elevation may NOT be indicative of a hepatic process
|
|
What do the transaminases NOT reflect?
|
The synthetic function of the liver
|
|
What 2 proteins do give some correlation with synthetic ability?
|
Albumin and coagulation factors
|
|
Overal increase ALT usually means what?
Increased GGT? |
ALT = hepatic
GGT = infiltrative / blockage |
|
Generally, wrt to ALT, Alk Phos, and Bilirubin, what is seen in a hepatic cause?
|
Increased ALT, normal Alk Phos and Bilirubin
|
|
What is seen in cholestatic?
|
Normal ALT, increased Alk Phos, and somewhat increased Bili
|
|
What is seen in infiltrative?
|
Normal ALT, increased Alk Phos, and normal Bili
|
|
In the cell, where is AST located?
ALT? GGT? |
AST = mitochondria / and some cytoplasm
ALT = cytoplasm GGT = bile canaliculus membrane |
|
Hepatic forms of injury such as Hep C cause what?
|
Cause leakage of ALT and AST from hepatocytes
|
|
Usually, which is higher, ALT or AST?
|
ALT due to the relative subcellular distribution
|
|
Processes that hurt the mitchondira (ex: alcohol, some drugs, wilson's disease) cause what levels of AST?
|
More AST's in the blood than other hapatic injuries
ex: 2:1 ratio AST:ALT in alcoholic damage |
|
Why did the fish get kicked out of school?
|
Cause he was caught with seaweed.
Almost there!! Good job! |
|
GGT is elevated in what?
|
Cholestatic conditions
|
|
What causes increased Alk Phos?
|
Bile duct obstruction / irritation
|
|
What are the 4 main patterns of liver injury?
|
1. Hepatic
2. Steatotic 3. Cholestatic/Obstructive 4. Infiltrative |
|
What are the histologic features of hepatic pattern liver injury?
|
1. Lymphocytes in portal tracts
2. Apoptotic hepatocytes |
|
What are some common causes of hepatic damage?
|
HCV, auto-immune hepatitis
|
|
What is steatosis?
|
Injury in which the hepatocytes become engulfed in lipids
"Fatty Liver" |
|
What are some common causes of steatosis?
|
Obestiy, Diabetes, Alcohol Use
|
|
What are the enzyme levels in steatosis?
|
May have mild elevation of Alk Phos/GGT and/or mild elevation in AST/ALT
|
|
What is the main histologic sign of cholestatic damage?
|
Bile plugs - bilirubin "trapped" in the space between the hepatocytes
|
|
What enzyme levels are seen in cholestatic?
|
Extremely elevated Alk Phos/GGT
Elevated Bilirubin Minimally elevated AST/ALT |
|
What are some common causes of cholestatic damage?
|
Blockage of common bile duct by gall stone or tumor
|
|
Bilirubin is derived from what?
|
From hemaglobin in RBCs
|
|
Bilirubin is bound to what in the blood?
|
Albumin
|
|
Bilirubin is actively taken up by hepatocytes and conjugated with glucoronide to do what?
|
make it water soluble
|
|
What happens to the conjugated bilirubin?
|
Actively secreted out of the hepatocyte into the "bile"
|
|
What are the 3 types of bilirubin?
|
1. Conjugated
2. Unconjugated 3. Delta bilirubin (measured indirectly) |
|
What is cholestasis?
|
any condition in which the flow of bile from the liver is blocked.
|
|
What is normal bilirubin?
|
<1.1, 70% unconjugated
|
|
The accumulation of bile salts in cholestatic injury leads to what type of hepatocyte degeneration?
|
"Feathery Degeneration"
|
|
If the liver is seen to have "pink infiltrate" in the space of diss, but no elevation of LFT's, what could be the cause?
|
Amyloidosis
|
|
What do you call a woman with one leg?
|
- Ilene
BOOM BABY! YOUR DONE! |