Block 1 Adaptation & Necrosis

Question 1

Causes of atrophy

Answer 1

Physiologic: thymus, tonsils
Pathologic: decreased workload, denervation, ischemia, inadequate nutrition, decreased endocrine stimulation, aging, pressure

Question 2

Causes of hypertrophy

Answer 2

Physiologic: hormones
Pathologic: increased workload, hormonal stimulation, growth factors, switch to adult gene/protein

Question 3

Causes of hyperplasia

Answer 3

Physiologic: hormonal, compensatory
Pathologic: increased hormonal stimulation, growth factors, viral infections (HPV)

Question 4

Causes of metaplasia

Answer 4

Cytokines, growth factors, ECM components, environmental

Question 5

Hallmark of reversible cell injury

Answer 5

decreased oxidative phosphorylation –> decreased ATP –> cell swelling & fatty change (lipid vacuoles)
Gross: pallor, turgor, weight, greasy, larger

Question 6

Hallmark of irreversible cell injury

Answer 6

Mito swelling, PM damage, lysosomal swelling

Question 7

Features of necrosis

Answer 7

Group of cells, inflammation, cytoplasm and mito swelling, loss of PM integrity, Ca2+ overload

Question 8

Coagulative necrosis

Answer 8

Infarcts, firm tissue, cell outlines preserved, general red appearance, inflammation, leuko lysosomes remove dead cells

Question 9

Liquefactive necrosis

Answer 9

Bacterial & fungal infections, brain infarcts; microbial cell, inflammatory cells, cell debris

Question 10

Caseous necrosis

Answer 10

TB; cheese-like, amorphous debris in granuloma with lympho border and macrophages

Question 11

Fat necrosis

Answer 11

Acute pancreatitis, white areas from new FFAs with Ca2+, shadowy outline of cells with bluish cast (Ca), b/c damaged cells release lipases

Question 12

Fibrinoid necrosis

Answer 12

Vasculitis, bright pink amorphous area around vessel, immune complexes in artery walls

Question 13

Gangrene

Answer 13

Loss of blood supply (DM) –> black decomposing skin
Dry: coagulative necrosis
Wet: liquefactive due to superimposed bacterial infection

Question 14

Apoptosis features

Answer 14

Singe cells, no inflam, shrinking cyto and mito, blebbing w/o loss of integrity, fragmented and hyperchromatic nuclei, ATP-dep

Question 15

Physiologic vs. pathologic apoptosis

Answer 15

Phy: embryogenesis, menses, lymphocyte selection
Path: DNA or protein damage, GF deprivation, infection, atrophy

Question 16

Intrinsic & extrinsic apoptosis pathway proteins

Answer 16

I: Bcl-2, Bax, Bak, Bcl-x, cyt C
E: Fas, TNF-R, caspases

Question 17

Bcl-2

Answer 17

Anti-apoptotic important in cancer, inhibit Bax and Bak from opening pore in mito –> apoptosis

Question 18

Bak, Bax

Answer 18

Pro-apoptotic, open pore in mito to release cyt C and pro-apoptotic proteins

Question 19

Substances accumulated intracellularly

Answer 19

Fat, cholesterol, protein, glycogen, pigment, calcification

Question 20

Foam cell

Answer 20

Oxidative LDL cholesterol ingested by MFs –> atherosclerotic plaque

Question 21

Protein accumulation

Answer 21

AD neurofibrillary tangles of hyper-P Tau

Question 22

Pigment accumulation

Answer 22

Carbon (pollution -> anthracosis), lipofuscin (ROS damage; heart, liver, brain), melanin, hemosiderin (excess iron)

Question 23

Anthracosis

Answer 23

Benign deposition of coal dust in lungs from inhalation of sooty air

Question 24

Calcifications

Answer 24

Ca salts, iron, Mg
Dystrophic: dying/dead cells secondary to injury/necrosis (heart valves) with normal serum Ca level
Metastatic: normal cells, hypercalcemia (PTH-sec tumor, Paget’s, vit D disorders, renal failure)

Question 25

Icterus

Answer 25

Yellow appearance (bilirubin)