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Step 1 USMLE/COMLEX > Pathoma Chapter 1: Growth Adaptations, Cellular Injury & Cell Death > Flashcards

Pathoma Chapter 1: Growth Adaptations, Cellular Injury & Cell Death Flashcards

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USMLE® Step 1 flashcards
1
Q

Cells that can only undergo hypertrophy, not hyperplasia

A

Nerve, cardiac muscle and skeletal muscle

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2
Q

Exception to pathologic hyperplasia

A

BPH does not progress to dysplasia and increased risk of prostate cancer

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3
Q

Barrett’s esophagus

A

Non-keratinized squamous epithelium => non-ciliated columnar epithelium with mucin (goblet cells)

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4
Q

Metaplasia can progress to dysplasia and cancer, with exception of:

A

Apocrine metaplasia of breast (seen w/fibrocystic changes of breast), which carries no increased risk for cancer

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5
Q

Myositis ossificans

A

CT within muscle changes to bone during healing after trauma. Type of metaplasia.

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6
Q

Metaplasia vs Dysplasia. Which is reversible?

A

Metaplasia: change in cell type d/t stress

Dysplasia: disorganized cell growth

Both reversible. If dysplasia progresses to carcinoma, that is irreversible.

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7
Q

Budd-Chiari syndrome

A

Thrombosis of hepatic vein leading to liver infarction

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8
Q

Most common cause of Budd-Chiari syndrome

A

Polycythemia vera

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9
Q

Describe PaO2 and SaO2 in anemia, CO poisoning and methemoglobinemia

A

Anemia: Pao2 normal, Sao2 normal

CO poisoning: Pao2 normal, Sao2 decreased

Methemoglobinemia: Pao2 normal, Sao2 decreased

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10
Q

CO poisoning SSx? Most common early sign? Pathogenesis?

A

SSx: cherry-red appearance of skin, headache, confusion leading to coma, death

Most common early sign = headache

Path: CO has 100 x more affinity to Hb than o2

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11
Q

Methemoglobinemia SSx? When is this seen? Pathogenesis?

A

SSx: cyanosis w/chocolate-colored blood

Seen with oxidant stress: sulfa-drugs, nitrates. Also seen in newborns who have poorly developed mechanisms to deal with oxidative stress.

Path: Fe2+ in heme is oxidized to Fe3+, which doesn’t bind o2. Mnemonic = Fe two binds o2.

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12
Q

Tx for methemoglobinemia? MOA?

A

Tx = methylene blue

MOA = reduces Fe3+ back to Fe2+

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13
Q

Hallmark sign of reversible injury to cell

A

Cellular swelling. Note: this includes membrane blebbing

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14
Q

Hallmark sign of irreversible injury to cell

A

Membrane damage

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15
Q

What cellular functions are disrupted with low ATP

A
  1. Na-K pump resulting in increased intracellular Na
  2. Ca2+ pump resulting in Ca buildup in cell
  3. Aerobic glycolysis resulting in decreased pH in cell
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16
Q

Morphologic hallmark of cell death

A

Ultimately loss of nucleus, which occurs in various stages:

  1. Pyknosis: condensing of nuclear material
  2. Karyorrhexis: fragmentation of nuclear material
  3. Karyolysis: dissolution of nuclear material
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17
Q

Which type of cell death is followed by acute inflammation?

A

Necrosis only. Not apoptosis.

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18
Q

Coagulative necrosis

A

Necrotic tissue that is firm. Cell-shape and organ structure preserved, w/nuclear disappeared.

Happens in ischemic infarction

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19
Q

In what tissues is coagulative necrosis seen?

A

All except brain (undergoes liquefactive necrosis)

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20
Q

Liquefactive necrosis

A

Necrosis tissue that becomes liquified. Enzymes lyse cells and protein.

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21
Q

Where is liquefactive necrosis seen?

A

Brain infarct (d/t microglial cells, which are macrophages of brain)

Abscess

Pancreatitis (to pancreatic parenchyma, not surrounding fat)

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22
Q

Gangrenous necrosis

A

Mummified tissue

23
Q

Where is gangrenous necrosis seen?

A

Ischemia of lower limb and GI tract

24
Q

Caseous necrosis

A

Like liquefactive necrosis where fungi or TB are present

Soft-friable necrotic tissue with cottage-cheese like appearance

25
Q

Fat necrosis

A

Chalky-white appearance d/t deposition of calcium leading to saponification

26
Q

Dystrophic vs metastatic calcification

A

Dystrophic calcification = calcium deposits on dead tissues in setting of normal serum calcium and phosphate

Metastatic calcification = calcium deposition in normal tissue in setting of high serum calcium and phosphate

27
Q

In what conditions is metastatic calcification seen

A

Hyperparathyroidism leading to nephrocalcinosis

28
Q

Fibrinoid necrosis

A

Necrotic damage to blood vessel wall

29
Q

In what conditions is fibrinoid necrosis seen?

A

Malignant hypertension (PE leading to necrosis of placental vessels)

Vasculitis

30
Q

Function of bcl2

A

Bcl2 stabilizes the mitochondrial membrane preventing leakage of cytochrome c, which can activate caspases and apoptosis cascade

31
Q

Describe extrinsic receptor-ligand pathway leading to apoptosis

A
  1. FAS ligand binds FAS death receptor (CD95)
  2. TNF binds TNF receptor on target cell

Both lead to caspase activation

32
Q

Describe CD8+ T Cell mediated apoptosis pathway

A

Perforins secreted from CD8+ cells = pores created in target cell

Granzyme from CD8+ enters pores and activates caspases

33
Q

Most damaging free radical

A

(dot)OH

This is the hydroxyl radical. It is o2 with three electrons and requires a 4th desperately to become water.

Progression (with 1 electron added each time) = O2 -> O2(dot)- -> H2O2 -> dot(OH) -> H2O

34
Q

What causes underlying damage seen in hemochromatosis and Wilson’s disease?

A

Fe and Cu metals respectively induce free radicals

35
Q

Type of damage free radicals cause

A
  • Peroxidation of lipids

- Oxidation of DNA and proteins

36
Q

Elimination of free radicals

A

Antioxidants (glutathione, Vitamins A C E)

Enzymes

a. SOD (mito): superoxide (o2dot- -> h2o2)
b. Catalase (in peroxisomes): h2o2 -> o2 + h2o
c. Glutathione peroxidase (mito): 2GSH + free radical (typically hydroxyl) -> GS-SG + h2o

Metal carrier proteins

37
Q

Type of damage caused by CCl4

A

Free radicals generated by P450 system in hepatocytes = cell swelling of RER = impaired protein synthesis = reduced apolipoproteins = fatty changes

38
Q

What types of shape are amyloid proteins?

A

Beta-pleated

39
Q

Amyloid in plasma cell dyscrasias such as multiple myeloma

A

AL amyloid

Derived from Ig light chain

This is primary amyloidosis

40
Q

Amyloid seen in secondary amyloidosis

A

AA amyloid derived from SAA, an acute phase reactant

41
Q

Causes of secondary amyloidosis

A

Any chronic inflammatory state including lupus, RA, Crohns, UC, chronic osteomyelitis, malignancy

42
Q

Familial Mediterranean Fever (FMF). What is it? SSx?

A

AR dysfunction of neutrophils common seen in persons of Mediterranean decent

SSx: episodes of fever and serosal inflammation (mimicking appendicitis, arthritis, or MI). Find high SAA during attacks.

43
Q

Classic clinical findings for systemic amyloidosis

A
  1. Nephrotic syndrome
  2. Restrictive cardiomyopathy or arrhythmia
  3. Tongue enlargement, malabsorption, HSM
44
Q

Most common organ involved in systemic amyloidosis

A

Kidney

45
Q

Can amyloid be removed from tissue

A

No

46
Q

How is amyloidosis diagnosed?

A

Tissue biopsy (abdominal fat pad and rectum)

47
Q

Senile cardiac amyloidosis vs Familial amyloid cardiomyopathy.
Describe presentation and type of amyloid

A

Senile cardiac amyloid = non-mutated serum transthyretin deposits in heart.
Presentation: usually asymptomatic. Present in over 25% of individuals > 80.

Familial amyloid cardiomyopathy = mutated serum transthyretin deposits in heart leading to restrictive cardiomyopathy.
Presentation with restrictive cardiomyopathy. 5% of African Americans have mutated gene.

48
Q

Amyloid seen in type II diabetics

A

Amylin (derived from insulin) in islet cells

49
Q

Amyloid in AD

A

alpha beta amyloid

50
Q

Where is alpha-beta amyloid derived?

A

Beta-amyloid precursor protein. Gene is on c/s 21.

51
Q

Why do DS patients develop early onset AD?

A

Alpha beta amyloid plaque is derived from the Beta amyloid precursor protein, encoded by its gene on c/s 21. They have an extra copy therefore have more protein and earlier onset.

52
Q

Amyloid seen in dialysis-associated amyloidosis

A

Beta-2 microglobulin from MHC1

53
Q

Tumor cells in an amyloid backgroun

A

Medullary carcinoma of the thyroid. This is calcitonin deposits within the tumor.

Step 1 USMLE/COMLEX (4 decks)

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