OBJ - Adaptation

Question 1

4 Common cellular inclusions

Answer 1

1) Abnormal metabolism (Fat/Protein)
i. e. Fats/lipid vacuoles in liver

2) Mutations causing alteration in protein folding

3) Deficiency in critical enzymes (leads to accumulation of endogenous materials)
i. e. glycogen stored in diabetics

4) Ingestion of indigestible materials (leads to accumulation of exogenous materials)
- carbon
- lipofuscin - wear & tear pigment (orange)
- melanin
- hemosiderin - yellow/green/brown (heme deposits from RBC) - use Prussian Blue stain (DARK blue)

Calcium - saponification/FA which are not phagocyted become calcified

• Dystrophic - normal Ca levels -> deposits on path tissue
• Metastic - due to hypercalcemia; Ca deposits on normal tissues

Myelin Figures - whorled phospholipid masses from damaged cell membranes

Question 2

Aging Process of Cells

Answer 2

1) Aging results from accumulation of cellular damage by FR
2) Reduced capacity to divide (telomere shortening)
3) Reduced ability to repair damaged DNA

Germ cells - don’t lose telomere length
Stem cells - lose very little
Somatic cells - telomeres shorten with each division
some cancer cells can increase their telomere length

Werner Syndrome - very rapid aging process

Question 3

Necrosis Vs Apoptosis

Answer 3

Necrosis:

• Larger cell size (swelling)
• Nucleus: Pyknosis, karyorrhexis, karyolysis
• Disrupted plasma membrane
• Enzymatic leakage
• INFLAMMATION
• generally pathological

Apoptosis: “falling off”/cellular suicide

• Smaller cell size
• Fragmented nucleus
• Intact plasma membrane
• intact cellular components
• NO INFLAMMATION
• generally physiologic programed cell death, can be pathologic

PICTURE

Question 4

Differences between:

Pyknosis, karyorrhexis, karyolysis

Answer 4

Pyknosis: nuclear shrinkage (pin point/tiny)

Karyorrhexis: nuclear fragmentation (break into pieces)

Karyolysis: nuclear dissolution

Question 5

Hypertrophy

Answer 5

increase in cell size

Phys: weight lifting
Path: BPH/ big LV

Question 6

Hyperplasia

Answer 6

Increase in cell number

Phys:
Path: BPH

Question 7

Atrophy

Answer 7

Decrease in number AND/OR size

Phys: bedrest/inactivity
Path:

Question 8

Metaplasia

Answer 8

change in cell type; reversible & protective

Path: lungs -> columnar with goblet cells to stratified squamous for protection

Question 9

Neoplasia

Answer 9

abnormal growth

Question 10

6 Types of Necrosis

Answer 10

1) Coagulative (heart)
2) Liquefactive (brain)
3) Gangrenous (wet or dry)
4) Caseous
5) Fat (pancreatic enzymes)
6) Fibrinoid

Question 11

Coagulatvie Necrosis

Answer 11

preservation of tissue architecture but dead cells/scar tissue

Eosinophillic - birght pink
Anucleate
Days-weeks

i.e. MI

Question 12

Liquefactive Necrosis

Answer 12

complete digestion of tissue transforming it into a liquid mass

characteristic of CNS/bacterial infections

Question 13

Gangrenous Necrosis

Answer 13

generally in an extremity
Coagulative necrosis of several layers of tissue

“Wet Gangrene” if infection with it as well (combo of Coag/Liqueficative)

DC Ulcer

Question 14

Caseous Necrosis

Answer 14

“cheese-like” - swiss - with holes
granular/chalky appearance

HALLMARK of TB

Question 15

Fat necrosis

Answer 15

peripancreatic tissue death from pancreatic lipase/enzyme leakage combine with Ca to produce chalky areas of fat saponification

Question 16

Fibrinoid Necrosis

Answer 16

**special form seen with Immune responses
THINK AUTOIMMUNE

Antigens/antibodies are deposited in vessels around/throughout organ organ

Question 17

Autophagy vs Heterophagy

Answer 17

Autophagy: cell digests its own organelle (i.e. nutrient deprivation)

Heterophage: cell digests substances outside the cell (i.e. macrophages)

Question 18

Principle of Cellular Injury

Answer 18

Cellular response to injury depends on:

• type
• duration
• severity of the injury

Consequence of injury depends on:

• type
• status
• adaptability
• genetic make up of the cell (hepatocyte vs neuron)

Question 19

Mechanism of Cell Injury

Answer 19

1) Mitochondrial damage (Depletion of ATP/increase in ROS)
- ATP deletion -> failure of energy dependent functions (Na/K pump)
- accumulation of ROS

2) Entry of Ca++ into the cell
- activates enzymes that damage cellular components/trigger apoptosis

3) Membrane Damage
- affect lysosomal, mitochondrial, plasma membranes

4) Protein misfolding/DNA damage
- accumulation triggers apoptosis

Question 20

Cellular responses to stress

Answer 20

Adaptations (hypertrophy, hyperplasia, metaplasia, atrophy)
-are reversible

Cell injury (can be reversible or irreversible -> necrosis/apoptosis)

Question 21

Mechanisms of Apoptosis

Answer 21

1) Mitochondrial Pathway (intrinsic)
Bcl2 deactivated (anti-apoptotic)/activates BAK/BAX (pro-apoptotic) which forms channels for Cytochrome C to leak out of Mito; activating initiator caspase -> executioner caspase -> triggering apoptosis

2) Death receptor Pathway (extrinsic)
FAS ligand/TNF receptor bind to “death domain” whcih recruit/activate initiator caspase -> executioner caspase -> triggering apoptosis