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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

(53 cards)

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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

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A

Mummified tissue

23
Q

Where is gangrenous necrosis seen?

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A

Ischemia of lower limb and GI tract

24
Q

Caseous necrosis

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A

Like liquefactive necrosis where fungi or TB are present

Soft-friable necrotic tissue with cottage-cheese like appearance

25
Fat necrosis
Chalky-white appearance d/t deposition of calcium leading to saponification
26
Dystrophic vs metastatic calcification
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
In what conditions is metastatic calcification seen
Hyperparathyroidism leading to nephrocalcinosis
28
Fibrinoid necrosis
Necrotic damage to blood vessel wall
29
In what conditions is fibrinoid necrosis seen?
Malignant hypertension (PE leading to necrosis of placental vessels) Vasculitis
30
Function of bcl2
Bcl2 stabilizes the mitochondrial membrane preventing leakage of cytochrome c, which can activate caspases and apoptosis cascade
31
Describe extrinsic receptor-ligand pathway leading to apoptosis
1. FAS ligand binds FAS death receptor (CD95) 2. TNF binds TNF receptor on target cell Both lead to caspase activation
32
Describe CD8+ T Cell mediated apoptosis pathway
Perforins secreted from CD8+ cells = pores created in target cell Granzyme from CD8+ enters pores and activates caspases
33
Most damaging free radical
(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
What causes underlying damage seen in hemochromatosis and Wilson's disease?
Fe and Cu metals respectively induce free radicals
35
Type of damage free radicals cause
- Peroxidation of lipids | - Oxidation of DNA and proteins
36
Elimination of free radicals
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
Type of damage caused by CCl4
Free radicals generated by P450 system in hepatocytes = cell swelling of RER = impaired protein synthesis = reduced apolipoproteins = fatty changes
38
What types of shape are amyloid proteins?
Beta-pleated
39
Amyloid in plasma cell dyscrasias such as multiple myeloma
AL amyloid Derived from Ig light chain This is primary amyloidosis
40
Amyloid seen in secondary amyloidosis
AA amyloid derived from SAA, an acute phase reactant
41
Causes of secondary amyloidosis
Any chronic inflammatory state including lupus, RA, Crohns, UC, chronic osteomyelitis, malignancy
42
Familial Mediterranean Fever (FMF). What is it? SSx?
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
Classic clinical findings for systemic amyloidosis
1. Nephrotic syndrome 2. Restrictive cardiomyopathy or arrhythmia 3. Tongue enlargement, malabsorption, HSM
44
Most common organ involved in systemic amyloidosis
Kidney
45
Can amyloid be removed from tissue
No
46
How is amyloidosis diagnosed?
Tissue biopsy (abdominal fat pad and rectum)
47
Senile cardiac amyloidosis vs Familial amyloid cardiomyopathy. Describe presentation and type of amyloid
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
Amyloid seen in type II diabetics
Amylin (derived from insulin) in islet cells
49
Amyloid in AD
alpha beta amyloid
50
Where is alpha-beta amyloid derived?
Beta-amyloid precursor protein. Gene is on c/s 21.
51
Why do DS patients develop early onset AD?
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
Amyloid seen in dialysis-associated amyloidosis
Beta-2 microglobulin from MHC1
53
Tumor cells in an amyloid backgroun
Medullary carcinoma of the thyroid. This is calcitonin deposits within the tumor.

Step 1 USMLE/COMLEX (4 decks)

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