Chapter 1

Question 1

What are the main types of cellular adaptations?

Answer 1

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

Question 2

What are the mechanisms behind hypertrophy?

Answer 2

Increased cytoskeletal proteins (e.g., actin, myosin)

Gene activation

Protein synthesis

Organelles increase in number and size

Question 3

Can hyperplasia and hypertrophy occur together? Provide an example.

Answer 3

Yes. For example, in the uterus during pregnancy:

Hyperplasia of smooth muscle cells

Hypertrophy due to increased hormonal stimulation

Question 4

Which types of cells cannot undergo hyperplasia and only undergo hypertrophy?

Answer 4

Permanent cells (e.g., cardiac muscle, skeletal muscle, neurons)

Question 5

Example of both hypertrophy and hyperplasia occurring together?

Answer 5

Uterine smooth muscle cells during pregnancy

Question 6

What is physiologic vs pathologic hyperplasia?

Answer 6

Physiologic: normal hormonal response (e.g., endometrium)
Pathologic: excessive stimulation (e.g., endometrial hyperplasia → risk of cancer)

Question 7

What are the causes of atrophy?

Answer 7

Decreased workload, denervation, decreased blood supply, malnutrition, loss of endocrine stimulation, aging

Question 8

Cellular mechanisms of atrophy?

Answer 8

Ubiquitin-proteasome degradation and autophagy

Question 9

What is metaplasia and give a classic example?

Answer 9

Reversible change in cell type due to stress; example: Barrett’s esophagus (squamous to columnar)

Question 10

Risk associated with metaplasia?

Answer 10

Increased risk of dysplasia and cancer (except apocrine metaplasia in breast)

Question 11

What factors determine the extent of cell injury?

Answer 11

Cell type, stress type, duration, and pre-existing condition

Question 12

Three main causes of hypoxia?

Answer 12

Ischemia, hypoxemia, decreased oxygen-carrying capacity

Question 13

How does hypoxia cause cell injury?

Answer 13

Decreased ATP → failure of Na+/K+ pump, Ca2+ influx, anaerobic glycolysis → cell swelling and death

Question 14

What lab marker indicates membrane damage in myocardial infarction?

Answer 14

Elevated troponin or CK-MB

Question 15

Key differences between necrosis and apoptosis?

Answer 15

Necrosis: uncontrolled, inflammatory, cell swelling
Apoptosis: programmed, non-inflammatory, cell shrinkage

Question 16

What are the types of necrosis and one example each?

Answer 16

Coagulative (heart infarct)

Liquefactive (brain infarct)

Caseous (TB)

Fat (pancreatitis, trauma)

Fibrinoid (vasculitis)

Gangrenous (dry/wet limb)

Question 17

What enzymes are central to apoptosis?

Answer 17

Caspases

Question 18

What triggers the intrinsic (mitochondrial) apoptotic pathway?

Answer 18

Cellular injury, DNA damage → Bcl-2 inhibition → cytochrome c release

Question 19

What triggers the extrinsic apoptotic pathway?

Answer 19

FasL binding Fas (e.g., thymic selection) or TNF-α receptor activation

Question 20

What does Bcl-2 do and what cancer is it associated with?

Answer 20

Stabilizes mitochondrial membrane, inhibits apoptosis; associated with follicular lymphoma (t(14;18))

Question 21

Major sources of reactive oxygen species (ROS)?

Answer 21

ETC leakage, inflammation (NADPH oxidase), Fenton reaction, drugs (e.g., acetaminophen)

Question 22

What protects cells against ROS damage?

Answer 22

SOD (superoxide dismutase), glutathione peroxidase, catalase, vitamins A/C/E

Question 23

What is reperfusion injury?

Answer 23

Restoration of blood flow after ischemia → ROS generation → further cell damage