Handout 5 Flashcards
Reasons for fatty changes (5)
- too much fat entering liver
- decreased fatty acid oxidation by mitochondria
- protein and triglycerides not combining to form lipoproteins
- impaired apoprotein synthesis
- impaired excretion of lipoproteins
Where else can fatty change occur?
- cardiac muscle: hypoxia, results from decreased oxidation of fatty acids by mitochondria
- lungs
Foam cells
- macrophages that phagocytize large amts of lipid debris
- look foamy
Intracellular protein accumulation
- usually in epithelium of PCT in kidney and plasma cells
- usually albumin, but can be hemoglobin or myoglobin
- protein is pinocytosed into PCT epithelial cells which fuses w/ lysosomes, producing a phagolysosome
- look like hyaline granules in cytoplasm
Russell bodies
- plasma cells actively engaged w/ prod. of immunoglobulins that are overloaded w/ Igs and large eosinophilic inclusions
- membrane bound
- localized in dilated cisternae of ER
Cause of intracellular accumulation of excessive glycogen
Abnormality of glucose or glycogen metabolism
2 categories of intracellular accumulation of glycogen
- glycogen infiltration
- glycogen storage
What does glycogen look like in H&E stains
- clear vacuoles
2 stains used for glycogen
- PAS (periodic acid schiff)
- Best’s Carmine
- glycogen stains rose to violet
Glycogen infiltration
- glycogen accumulation due to hyperglycemia ( a lot glucose)
- diabetes mellitus
- tissues involved: epithelial cells of distal part of DCT, loop of henle, leukocytes in inflamed or necrotic tissue, liver, cardiac muscle
Diabetes types
- mellitus: too much glucose
- insipidus: insulin receptors not working
Glycogen within leukocytes
- when dead/dying cells in a necrotic area release glycogen into intercellular medium, which is phagocytized by invading leukocytes
Glycogenoses
- AKA Glycogen storage issues
- autosomal recessive genetic disorder
- defective catabolism of glycogen w/ accumulation in lysosomes
- Von Gierke’s disease, Pompe disease, Cori’s disease, McArdle’s Syndrome
Von gierke’s disease
- glycogen storage disease type 1
- genetic lack of glucose-6-phosphatase in liver
Inclusion bodies can develop in _____ & ______
- nucleus
- cytoplasm
Stain for DNA inclusion bodies
Feulgen
Stain for single vs. double stranded nuclei strands
Acridine-orange
Fluorescent antibody and immunohistory techniques can be used for…
IDing inclusion bodies
Protein-lattice inclusion bodies
- found in viral infections, metabolic diseases, and nonspecific changes in degenerating cells
- large, rhomboid shapes w/ fibers
- repeating units
- Huntington’s disease in humans
Huntington’s disease
- humans
- Neuronal inclusions form @ axons and dendrites, prod. damaged neurons
Metallic inclusion bodies
- lead poisoning
- inclusions are acid-fast
- in renal tubular epith.
- intranuclear protein matrices
Chediak-Higashi Syndrome
- autosomal recessive
- large intracytoplasmic granules (inclusions)
- not found in RBCs (b/c no nucleus!)
Lafora’s syndrome
- progressive neuronal myoclonus epilepsy
- humans and dogs
- autosomal recessive
- large, PAS +ve intracytoplasmic inclusions in neurons, hepatocytes, and myocardial fibers
Brick inclusions
- crystalline protein inclusions
- in normal cells of liver, kidneys, and gonads
- can be free (nucleus or cytoplasm) or in organelles
- unknown significance
