1. Cell Adaptations, Injury, and Death

Question 1

cellular adaptation

Answer 1

changes that the tissues makes in response to a variety of stressors/signals without dying in the process

Question 2

hyperplasia

Answer 2

increase in cell #

depends on ability to synth DNA and divide

physiologic eg: increase capacity PRN like a gravid uterus or following loss of tissue mass like a liver or kidney

pathologic eg: excess stimulation (can regress if corrected) but risk of uncontrolled proliferation (cancer) like endometrial cancer

Question 3

mechanisms of hyperplasia

Answer 3

1. increased GFs and GFRs (combine to make an increased signal to the nucleus) and lead to increased proliferation
2. may involve development of differentiated cells from stem cells (less common/impt)

Question 4

hypertrophy

Answer 4

increase in cell size

**occurs in cells w/a limited capacity for division

physiologic eg: skeletal muscle/cardiac muscle in athletes

pathologic eg: constantly increased workload (HTTN and heart disease)…results in comprimise of long term function

stimulated by: increased functional demand or increased hormonal stimulation

occurs via increased synthesis of cellular machinergy (increased mitoch. and DNA content)

Question 5

atrophy

Answer 5

decrease in cell size

reduction in cell size (decreased nutritional demand) causes increased protein degradation and autophagy of organelles and may result in cell death

physiologic eg: early dev to make fingers out of paddles

pathologic eg: disused, diminished blood supply/nutrition, loss of stimulation, aging, chronic pressure

Question 6

metaplasia

Answer 6

change in cell type (to better withstand stress)

reprogramming of stem/progenitor cells

pro: preservation of cell pop
con: LOF of lost cell type & predisposition to malignancy

Question 7

general causes of cell injury and death

Answer 7

hypoxia
nutritional imbalances
physical stress
chemical agent
infectious agent
immunological process
genetic cause

Question 8

hypoxia

Answer 8

• reduced O2 availability
• injury: through loss of ox/phos (can adapt if abrupt but not if gradual)
• ischemia/reperfusion injury is worsening of injury due to restpred blood flow causing hemorrhagic effect

due to:

• ischemia (reduced blood flow, mechanical or hypotensive…worse kind)
• reduced oxygenation of blood (resp failure)
• decreased O2-carrying capacity of blood (CO poisoning)

Question 9

nutritional imbalances and cell injury/death

Answer 9

deficiency or excess

Question 10

physical stress and cell injury/death

Answer 10

heat, cold, electrocution, radiation, pressure, trauma

Question 11

chemical agent and cell injury/death

Answer 11

directly toxic to cell or metabolite may be toxic to cell (usu affects metabolizing organ - the liver) eg acetaminophen or alcohol

Question 12

infectious agent and cell injury/death

Answer 12

directly or via immune response (eg fungus invading BV)

Question 13

immune response and cell injury/death

Answer 13

host response to infection (eg HCV in the liver) or autoimmune with no external trigger

Question 14

genetic causes of cell injury/death

Answer 14

inherited, acquired (most)

cause cell death via apoptosis, LOF due to mutation, or accumulation of abn materials

Question 15

cell injury: aerobic respiration

Answer 15

poisoning (cyanide) causes injury to mitochondria, which causes depletion of oxygen/nutrients

some tissues are more resilient due to relatively greater capacity for glycolysis or lower metab demands

reduced ATP: dysfunction of PM, pH, ca++ homeostasis, protein synthesis, etc

result: cell death (necrosis)

Question 16

reversible vs irreversible injury

Answer 16

it is a continuum

irreversible: sufficient mito injury that ox/phos not able to restore or DAMAGE TO PM
reversible: fatty change (fat metab cells) or cellular swelling (due to PM function impairment and energy-dependent ion exchange failure)

depends on injury severity and cell type (eg liver is more resilient)

Question 17

necrosis: cell size, nucleus, PM, cellular contents, adjacent inflamm, physiologic or pathologic?

Answer 17

cell size: enlarged
nucleus: pyknosis -> karyorrhexus -> karyolysis
PM: disrupted
Cell contents: leaking out
Adjacent inflamm: frequent
physiologic or patholog? always pathologic

Question 18

apoptosis: ell size, nucleus, PM, cellular contents, adjacent inflamm, physiologic or pathologic?

Answer 18

cell size: reduced
nucleus: fragmentation
PM: intact
Cell contents: controlled, contained disposal
Adjacent inflamm: rare
physiologic or patholog? may be either

Question 19

necrosis hallmarks

Answer 19

unregulated traumatic cell death

• increased eosinophilia (basophillic RNA/DNA is lost and red is dead)
• nuclear change: pyknosis (condensation - shrink and dark) -> karyorrhexis (fragmentation of pyknotic nuclei) -> karyolysis (dissolution - light nuclei)
• confluent necrosis
• changes develop over time

Question 20

coagulative necrosis

Answer 20

hypoxic injury usu

outlines of cells persist, mummified, slow degradation

Question 21

liquefactive necrosis

Answer 21

bacterial infection (fungal sometimes, less often)

• necrosis associated with inflammation

Question 22

caseous necrosis

Answer 22

TB

cheesy material with loss of structure, amorphous debris with granulomatous reaction

Question 23

fat necrosis

Answer 23

pancreatic injury

outlines of cells with inflammatory reaction

Question 24

subcellular injury

Answer 24

inclusions (excess of normal substance or accum of abn substance)
- lipids, proteins, glycogen, lipofuscin, virous (not all pathologic)

cellular aging

• decline in capacity for prolif/repair
• regulated process
• structural changes
• replicative senescence