Cellular Adaptation/Injury/Death

Cellular Adaptation

cell adapts to maintain homeostasis to it’s best ability

failure to adapt→cellular injury+death

adaptation types:
size
number
type

cellular adaptation: size changes

Atrophy: decreased workload/adverse environmental factor→smaller size→more efficient

hypertrophy: increased workload→larger size+increased tissue mass→more efficient

cellular adaptation: number changes

hyperplasia: increased number of cells
only in cells capable of mitosis

metaplasia: chronic irritation/inflammation→one cell type replaces another
reversible
maybe precancerous

dysplasia: deranged cell growth→varied size/shape/organization
maybe reversible
strong precursor to cancer

normal→hyperplasia→dysplasia→cancer

cellular injury causes

physical agents:
injury/trauma
extreme temperature
electrical forces

radiation injury:
ionizing
ultraviolet (UV)
non-ionizing

chemical injury:
drugs
lead
mercury

biological agents:
viruses
parasites
bacteria

nutritional imbalances: excess and deficiencies

cellular injury classes

reversible: stressor removed→damage mild→cells survive

irreversible→cell death

apoptosis: normal
ex: menses
aging

necrosis: digestive enzymes remove dead cells after dead organism

pathological necrosis: cell death in an organ/tissue in a living organism

unregulated enzymatic destruction→loss of cell membrane integrity→inflammatory response

Intracellular Accumulations (General)

buildup of substances that the cell cannot immediately use or eliminate

usually in

• cytoplasm
  -lysosomes

• nucleus

• abnormal substances
  -endogenous
  -exogenous

transient or permanent/toxic or harmless

water accumulation

mechanism: ATP/pump/electrolyte issue→water moves into the cell

result:
cytoplasm degeneration
organ swelling
reversible or sublethal

manifestation:
fever
hypokalemia
infection

lipid accumulation

mechanism: metabolic disorders (obesity/diabetes)
protein malnutrition
toxins
anoxia (no O2 in tissues)

result: lipids accumulate in spleen/liver/CNS

manifestation:

CNS: neurologic deficits
intellectual impairment (Tay-Sach’s)

liver: steatosis (fatty liver)

protein accumulation

mechanism: genetic mutation

result: intracellular accumulation→release of enzymes/crowding of organelles→cell damage

manifestation: kidneys
plasma cells in immune system

pigment accumulation

mechanism:

endogenous:
melanin
hemoglobin

exogenous:
coal dust
tattoo dye

result: UV→stimulates synthesis of melanin+traps free radicals

manifestation:
melanoma
skin moles
albinism (absence of melanin)

calcium accumulation

mechanism: mitochondria+endoplasmic reticulum release calcium

result:
membrane damage
cytoskeleton damage
chromatin damage
phosphorylation damage
chromatin fragmentation

manifestation: cellular calcification

urate accumulation

mechanism: elevated serum urate levels

result: sodium urate crystals accumulate in tissues

manifestation: gout

cellular injury systemic manifestations

fatigue

malaise

loss of well-being

altered appetite

fever

leukocytosis (increase in WBC)

increased heart rate

pain

etc.

necrosis vs. apoptosis

necrosis:
induced by injury
surrounding inflammatory response
large areas of contiguous cells
pathological cellular response

apoptosis:
genetically triggered
little/no inflammation
only a few scattered cells involved
part of normal cellular relations

necrosis types

caseous:
E: tuberculosis pulmonary infection
coagulative+liquefactive necrosis combination
walled off cheese-looking substance

fat: action of lipases
E: breast
pancreas
other abdominal structures

gangrenous:
clinical term
dry vs. wet vs. gas gangrene

coagulative: protein denaturation+changes protein albumin
E: kidneys
heart
adrenal glands

liquefactive: hydrolytic enzymes→liquid-filled cysts/pus
E: neurons
glial cells

apoptosis

programmed cellular death

active process of cellular destruction

can be normal or pathologic

dysregulated apoptosis:
insufficient (too little) or excessive (too much)

P: cancer
autoimmune disorders
neurodegenerative disease
ischemic injury