Abnormal accumulations & calcifications Flashcards
Intracellular accumulation:
Type 1
Normal endogenous products are made at normal or increased rates & metabolism is not fast enough to remove it
Intracellular accumulation:
Type 2
Abnormal accumulation of endogenous product because of defects in protein folding & transport or the cell can’t degrade the protein
Intracellular accumulation:
Type 3
A normal endogenous substance accumulates because of inherited defects in enzymes that are needed for metabolism of the substance
Intracellular accumulation:
Type 4
Build-up and deposition of an abnormal exogenous substance when the cell doesn’t have enzymatic machinery to degrade the substance or the ability to move it to other sites
What type of Intracellular accumulation type explains hepatic steatosis (fatty liver)
Type 1
Alpha1 antitrypsin deficiency is what kind of intracellular accumulation type?
Type 2
Tay Sachs & Gauchers disease are both what type of intracellular accumulation
type 3
Accumulation of carbon, silica, or asbestos are examples of what type of intracellular accumulation?
Type 4
Describe steatosis (fatty change)
An abnormal accumulation of triglycerides in the parenchyma of the liver, heart, muscle, or kidneys
Common causes are:
- alcoholism
- obesity
-diabetes
Alcohol induced fatty liver:
Describe the process
- Alcohol dehydrogenase & acetaldehyde dehydrogenase switch to shunting normal substrates to lipid synthesis (more NADH)
- More peripheral fat catabolism by activated hormone sensitive lipase (high blood LDLs)
- Impaired assembly and secretion of lipoproteins
The H&E and Oil red O staining show what condition?
Hepatic steatosis
Top of the histo slide shows _______
Bottom shows ________
diabetic/obesity induced intramyocardial lipid accumulation
The following histo slide shows what kind on intracellular body
Alcoholic hyaline (aka Mallory bodies) an accumulation fo cytoskeletal proteins in the liver cells common in alcoholic hepatitis
Describe the histo slide details
Xanthomas, an accumulation of cholesterol filled macrophages (foam cells) in subendothelial tissue and connective tissue because of hereditary hyperlipidemic states
Describe LDL catabolism without the presence of PCSK9
- When there’s no PCSK9, LDLR are made/inserted on hepatocytes membrane where it binds circulating LDL.
- LDLR-LDL complex enters the hepatocyte and disassociates in an endosome, so LDL can enter the lysosomal pathway (degraded) while LDLR is recycled
Describe LDL catabolism with the presence of PCSK9
- When PCSK9 is there it interacts with hepatocytes to blocks LDLR by entering the endosome and stopping LDLR-LDL dissociation