Handout 5 Flashcards

1
Q

Reasons for fatty changes (5)

A
  • 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
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2
Q

Where else can fatty change occur?

A
  • cardiac muscle: hypoxia, results from decreased oxidation of fatty acids by mitochondria
  • lungs
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3
Q

Foam cells

A
  • macrophages that phagocytize large amts of lipid debris
  • look foamy
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4
Q

Intracellular protein accumulation

A
  • 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
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5
Q

Russell bodies

A
  • 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
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6
Q

Cause of intracellular accumulation of excessive glycogen

A

Abnormality of glucose or glycogen metabolism

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7
Q

2 categories of intracellular accumulation of glycogen

A
  • glycogen infiltration
  • glycogen storage
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8
Q

What does glycogen look like in H&E stains

A
  • clear vacuoles
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9
Q

2 stains used for glycogen

A
  • PAS (periodic acid schiff)
  • Best’s Carmine
  • glycogen stains rose to violet
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10
Q

Glycogen infiltration

A
  • 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
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11
Q

Diabetes types

A
  • mellitus: too much glucose
  • insipidus: insulin receptors not working
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12
Q

Glycogen within leukocytes

A
  • when dead/dying cells in a necrotic area release glycogen into intercellular medium, which is phagocytized by invading leukocytes
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13
Q

Glycogenoses

A
  • 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
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14
Q

Von gierke’s disease

A
  • glycogen storage disease type 1
  • genetic lack of glucose-6-phosphatase in liver
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15
Q

Inclusion bodies can develop in _____ & ______

A
  • nucleus
  • cytoplasm
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16
Q

Stain for DNA inclusion bodies

A

Feulgen

17
Q

Stain for single vs. double stranded nuclei strands

A

Acridine-orange

18
Q

Fluorescent antibody and immunohistory techniques can be used for…

A

IDing inclusion bodies

19
Q

Protein-lattice inclusion bodies

A
  • found in viral infections, metabolic diseases, and nonspecific changes in degenerating cells
  • large, rhomboid shapes w/ fibers
  • repeating units
  • Huntington’s disease in humans
20
Q

Huntington’s disease

A
  • humans
  • Neuronal inclusions form @ axons and dendrites, prod. damaged neurons
21
Q

Metallic inclusion bodies

A
  • lead poisoning
  • inclusions are acid-fast
  • in renal tubular epith.
  • intranuclear protein matrices
22
Q

Chediak-Higashi Syndrome

A
  • autosomal recessive
  • large intracytoplasmic granules (inclusions)
  • not found in RBCs (b/c no nucleus!)
23
Q

Lafora’s syndrome

A
  • progressive neuronal myoclonus epilepsy
  • humans and dogs
  • autosomal recessive
  • large, PAS +ve intracytoplasmic inclusions in neurons, hepatocytes, and myocardial fibers
24
Q

Brick inclusions

A
  • crystalline protein inclusions
  • in normal cells of liver, kidneys, and gonads
  • can be free (nucleus or cytoplasm) or in organelles
  • unknown significance