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Pathoma > Chapter 1 - Cell Growth, Injury, and Death > Flashcards

Chapter 1 - Cell Growth, Injury, and Death Flashcards

1
Q

Does apocrine metaplasia of the breast (fibrous cystic change in breast) increase the risk for neoplasm?

A

NO

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2
Q

What is myositis ossificans?

A

Muscle tissue becomes metaplastic and changes to bone following trauma.

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3
Q

Is dysplasia (disordered cellular growth) reversible?

A

YES

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4
Q

What results from Budd-Chiari syndrome?

A

Ischemia of the liver parenchyma that can lead to infarction.

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5
Q

FIve causes of hypoxia???

A
  1. Altitude
  2. Hypoventilation
  3. V/Q mismatch
  4. Shunt
  5. Diffusion defect.
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6
Q

What is methemoglobinemia and what is the classic finding?

A

Oxidized heme iron (Fe3+), which cannot bind O2.

See cyanosis with chocolate-colored blood.

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7
Q

What happens to the structure of a cell with low ATP?

A

It swells, due to Na and H2O build up within the cell from impaired Na/K ATPase.

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8
Q

Hallmark of reversible cellular injury?

A

Swelling.

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9
Q

Hallmark of irreversible cellular injury?

A

Membrane damage

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10
Q

Pyknosis?

A

Nuclear condensation

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11
Q

Karyorrhexis?

A

Nuclear fragmentation

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12
Q

Karyolysis?

A

Nuclear dissolution

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13
Q

What is fat necrosis?

A

Saponification from released FA combining with Ca2+.

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14
Q

What is fibrinoid necrosis and when do you see it?

A

Necrotic damage to blood vessel walls. See with malignant hypertension and vasculitis.

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15
Q

what type of proteins mediate apoptosis?

A

Caspases

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16
Q

How are caspases activated (3)?

A
  1. Intrinsic- cell injury/loss of stimulation leads to inactivation of Bcl2, allowing cytochrome c to lead into cytoplasm and activate them.
  2. Extrinsic- FAS ligand binds to FAS death receptor or TNF binds TNF receptor.
  3. Cytotoxic CD8+ cells release perforins and granzymes….
17
Q

What is the most damaging free radical?

A

hydroxyl radicals (‘OH)

18
Q

What is the oxidative burst?

A

O2 –> ‘O2 via NADPH oxidase. Seen in neutrophils

19
Q

How do we get rid of free radicals (3 steps)?

A
  1. Superoxide dismutase: Superoxide (‘O2-) –> H2O2
  2. Glutathione peroxidase: GSH + free radical –> GSSH and H20
  3. Catalase: H2O2 –> O2 + H2O
20
Q

What clinical symptoms do you see from Carbon tetrachloride toxicity? (used in dry cleaning)

A

Fatty change in the liver due to decreased apolipoproteins from cellular swelling and decreased protein synthesis.

21
Q

What type of stains is used for AMYLOID

A

Congo red staining and apple-green birefringence under polarized light.

22
Q

What is primary amyloidosis and what is deposited?

A

Systemic deposition of AL amyloid derived from Ig light chain (often seen with MM, etc.).

23
Q

What is secondary amyloidosis and what is deposited?

A

Systemic deposition of AA amyloid derived from serum amyloid-associated protein (see in Familial Mediterranean fever, chronic inflammatory states, and malignancy)

24
Q

Most common clinical symptom of systemic amyloidosis?

A

Nephrotic syndrome

25
Q

What is senile cardiac amyloidosis?

A

Deposition of non-mutated serum transthyretin in the heart. Usually asymptomatic.

26
Q

What is familial amyloid cardiomyopathy?

A

Deposition of mutated serum transthyretin in the heart leading to restrictive cardiomyopathy.

27
Q

What type of amyloid is seen in Type II DM?

A

Amylin (derived from insulin) in islets of pancreas

28
Q

What type of amyloid is seen in Alzheimer’s?

A

Ab amyloid in brain

29
Q

What gene is beta-amyloid precursor protein found on?

A

Chromosome 21 (think Down Syndrome!)

30
Q

What type of amyloid is seen with dialysis?

A

B2-microglobulin in joints (from MHC class 1 that is not filtered well in dialysis).

31
Q

What type of amyloid is seen with Medullary carcinoma?

A

Calcitonin from C cells of the thyroid deposits within the tumor (tumor cells in an amyloid background found on FNA).

Pathoma (15 decks)

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