Cell Injury Flashcards
common causes of cell injury
- hypoxia and anoxia (primary cause)
- free radicals
- toxins
- infection
- immunologic or inflammatory responses
- genetic and metabolic disturbances
- traumatic injury
time course of cell injury:
1) homeostasis
2) cell injury
3) reversible changes:
- _____
- _____
- _____
4) cell death
5) irreversible changes:
- _____
- _____
- _____
ATP depletion;
biochemical dysfunction;
early ultrastructural changes: cytoplasmic swelling, vacuolation;
late ultrastructural changes;
early light microscopic changes: pyknosis;
late light microscopic changes: karyorrhexis, karyolysis
hypoxic injury and cellular swelling
reduces oxygen delivery to the cell –> inhibits cell’s ability to create adequate ATP –> water moves into cell (bc pumps aren’t working w/o ATP) –> swelling and vacuolation; can be reversible if oxygen delivery is restored
ischemic hypoxia
decreased blood flow therefore decreased oxygen (ex: pinched blood vessel); most common
ischemic anoxia
no blood flow (ex: blocked blood vessel)
anemic hypoxia
red blood cells can’t deliver sufficient oxygen to cells (ex: sickle cell anemia, carbon monoxide poisoning)
reactive oxygen species:
____ and _____ generated
internally; externally
normal metabolic processes (e.g., mitochondrial electron transport chain) and immune responses generate ___
free radicals
free radicals can cause damage to molecules by ____ through oxidation (called oxidative damage)
stealing their electrons
a free radical is an atom or group of atoms that have ____, making them extremely ___
1 or more unpaired electrons; reactive
___ and ___ forms of reactive oxygen species
radical; non-radical
ROS’s are typically neutralized by ____
internally produced anti-oxidants
ROS’s are produced in larger amounts with ____
injury and aging (oxidative stress)
ROS’s can break ____
covalent bonds in molecules
radical forms have an ____
unpaired electron- donates to or acquires electron from cellular molecules
ROS associated injury
- lipid peroxidation
- protein degradation
- DNA damage
ROS sources
- mitochondria
- inflammation
- exercise
- cigarette smoke
- pollution
- certain drugs, pesticides
- solvents
- reperfusion
direct toxic injury and examples
disrupt cellular function;
lead: CNS toxicity;
mercury: CNS toxicity;
carbon monoxide: anemic hypoxia
indirect toxic injury and examples
toxic after metabolism;
ethanol: CNS and liver toxicity (can also have direct toxicity);
ethambutol (TB drug): toxic optic neuropathy;
cyclosporine: renal toxicity
infectious injury direct cellular damage
ex: virus targets cell and causes cell to rupture; bacteria releases toxin that damages the cell
infectious injury indirect cellular damage via immune response
collateral damage that comes along with the immune response to an infection; typically normal
genetic and metabolic injury can be ___ or ____; they disrupt normal cell function; examples?
acquired; congenital;
sickle cell anemia, fatty liver disease, hepatolenticular degeneration, type 2 diabetes mellitus
traumatic injury examples in the eye
- blunt force trauma
- sharp force trauma
- penetrating trauma
- ionizing radiation
____ is a response to stress
adaptation
adaptation attempts to restore ____; result of altered ____; type depends on cell and stressor
homeostasis; gene expression
atrophy
decreased cell size; can be result of injury/decreased use
hypertrophy
increased cell size; can be result of exercise, pregnancy; left ventricular hypertrophy caused by obesity/hypertension
hyperplasia
increased cell number; ex: calluses form due to mechanical irritation, pregnancy
metaplasia
conversion of one cell type to another; in ectropion the exposed conj. may begin to keratinize due to exposure to external environment
dysplasia
disorderly growth; not an adaptation but rather damage; a precursor to cancer
intracellular and extracellular accumulations as adaptation
- water
- lipids
- cholesterol
- calcium
- pigments
- ex: bilirubin, lipofuscin
primary theories of aging
- accumulation of injurious events
- genetically controlled program
- likely a combination of both
as we age, our cells produce less ____ and more ____, which further reduces the ability to produce ____
ATP; free radicals; ATP
necrosis
initiated by (external) cell injury, leads to inflammation; group of cells; type of necrosis that occurs depends on the type of tissue in which it occurs
apoptosis
programmed cell death; initiated by suicide gene activation; single cell; orderly and non-inflammatory; body can recycle materials; developmentally necessary; ordered cell turnover; can also result from injury
coagulative necrosis
- kidneys, heart, adrenal glands
- begins with ischemia, leads to protein denaturation, cellular lysis, and clotting
liquefactive necrosis
- neurons and glial cells of the brain
- cells release hydrolytic enzymes which digest tissues into a wet/runny wound
- may form abscess or cysts
caseous necrosis
- cheese-like
- tuberculosis pulmonary infection
- combination of coagulative and liquefactive necrosis
gangrenous necrosis
clinical term; large area of affected tissue
dry gangrene
large area with coagulative necrosis
wet gangrene
large area with liquefactive necrosis
gas gangrene
associated with anaerobic bacteria that produce gas
fat necrosis
- breast, pancreas, and other abdominal organs
- action of lipases may cause saponification (changing of tissue into soapy texture)
somatic death
sufficient death of cells/tissues of vital organs: heart, brain, kidneys;
occurs when the death of the tissue exceeds the body’s ability for normal life processes
postmortem changes; useful for investigating unobserved deaths
- algor mortis: cooling of the body
- livor mortis: pooling of the blood
- rigor mortis: muscle contraction
- postmortem autolysis (endogenous) and putrefaction (exogenous)
