Chapter 1 - Cell Growth, Injury, and Death Flashcards
Does apocrine metaplasia of the breast (fibrous cystic change in breast) increase the risk for neoplasm?
NO
What is myositis ossificans?
Muscle tissue becomes metaplastic and changes to bone following trauma.
Is dysplasia (disordered cellular growth) reversible?
YES
What results from Budd-Chiari syndrome?
Ischemia of the liver parenchyma that can lead to infarction.
FIve causes of hypoxia???
- Altitude
- Hypoventilation
- V/Q mismatch
- Shunt
- Diffusion defect.
What is methemoglobinemia and what is the classic finding?
Oxidized heme iron (Fe3+), which cannot bind O2.
See cyanosis with chocolate-colored blood.
What happens to the structure of a cell with low ATP?
It swells, due to Na and H2O build up within the cell from impaired Na/K ATPase.
Hallmark of reversible cellular injury?
Swelling.
Hallmark of irreversible cellular injury?
Membrane damage
Pyknosis?
Nuclear condensation
Karyorrhexis?
Nuclear fragmentation
Karyolysis?
Nuclear dissolution
What is fat necrosis?
Saponification from released FA combining with Ca2+.
What is fibrinoid necrosis and when do you see it?
Necrotic damage to blood vessel walls. See with malignant hypertension and vasculitis.
what type of proteins mediate apoptosis?
Caspases
How are caspases activated (3)?
- Intrinsic- cell injury/loss of stimulation leads to inactivation of Bcl2, allowing cytochrome c to lead into cytoplasm and activate them.
- Extrinsic- FAS ligand binds to FAS death receptor or TNF binds TNF receptor.
- Cytotoxic CD8+ cells release perforins and granzymes….
What is the most damaging free radical?
hydroxyl radicals (‘OH)
What is the oxidative burst?
O2 –> ‘O2 via NADPH oxidase. Seen in neutrophils
How do we get rid of free radicals (3 steps)?
- Superoxide dismutase: Superoxide (‘O2-) –> H2O2
- Glutathione peroxidase: GSH + free radical –> GSSH and H20
- Catalase: H2O2 –> O2 + H2O
What clinical symptoms do you see from Carbon tetrachloride toxicity? (used in dry cleaning)
Fatty change in the liver due to decreased apolipoproteins from cellular swelling and decreased protein synthesis.
What type of stains is used for AMYLOID
Congo red staining and apple-green birefringence under polarized light.
What is primary amyloidosis and what is deposited?
Systemic deposition of AL amyloid derived from Ig light chain (often seen with MM, etc.).
What is secondary amyloidosis and what is deposited?
Systemic deposition of AA amyloid derived from serum amyloid-associated protein (see in Familial Mediterranean fever, chronic inflammatory states, and malignancy)
Most common clinical symptom of systemic amyloidosis?
Nephrotic syndrome
What is senile cardiac amyloidosis?
Deposition of non-mutated serum transthyretin in the heart. Usually asymptomatic.
What is familial amyloid cardiomyopathy?
Deposition of mutated serum transthyretin in the heart leading to restrictive cardiomyopathy.
What type of amyloid is seen in Type II DM?
Amylin (derived from insulin) in islets of pancreas
What type of amyloid is seen in Alzheimer’s?
Ab amyloid in brain
What gene is beta-amyloid precursor protein found on?
Chromosome 21 (think Down Syndrome!)
What type of amyloid is seen with dialysis?
B2-microglobulin in joints (from MHC class 1 that is not filtered well in dialysis).
What type of amyloid is seen with Medullary carcinoma?
Calcitonin from C cells of the thyroid deposits within the tumor (tumor cells in an amyloid background found on FNA).
