P2 - Cellular Injury Adaptation and Death Flashcards
consequences of cell membrane injury (3 things)
- loss of Na ion pump -> cell swelling
- abnormal Ca influx -> decrease ATP production and apoptosis
- injury to rough ER -> inhibition of protein synthesis
Free radicals (3)
- O2
- H2O2
- OH
list the antioxidants used a defense mechanism against oxidative stress (5)
- superoxide dismutase (SOD)
- catalase
- glutathione preoxidase
- vitamin E
- selenium
acute oxidative injury can cause (3 things)
- nutritional myopathy
- nutritional deficiency to vitamin E &/or selenium
- demonstrates importance of antioxidative mechanisms
chronic oxidative injury can cause (3 things)
- organ failure
- accelerate aging
- carcinogenesis and neoplastic disease
main functions of mitochondria (3 things)
- fatty acid oxidation
- citric acid cycle (Krebs cycle)
- oxidatie phosphorylation
vulnerabilities of mitochondria
- diminished ATP -> cell death
- leakage fo Ca -> apoptosis
main functions on nucleus (3 things)
- storage of genetic information
- maintenance of genetic information
- transmission of genetic information
nuclear envelope can be damaged by
oxidative stress
DNA damage can occur by (4 things)
- reactive oxygen and carbonyl species
- chemical, drugs, radiation
- random mutation and replication errors
- DNA repair malfunction
causes of cell injury (9 things)
- hypoxia
- physical agents
- infectious agents
- nutritional deficiencies and imbalances
- genetic derangement
- workload imbalance
- chemical, drugs, toxins
- immunologic dysfunction
- aging
inadequate tissue oxygenation (hypoxia) causes
- reduced blood flow
- reduced oxygen saturation of blood
cell types that are most susceptible to hypoxic injury
- have high metabolic demands
- have poor bloody supply
pathogenesis of hypoxia
- lack of O2 inhibits oxidative phosphorylation -> reduction of ATP -> loss of Na/K pump -> influx of Ca, H2O, Na and efflux of K -> cell swelling
physical agents causing cell injury (6 things)
- trauma
- extreme cold
- extreme heat
- electricity
- ionizing radiation
- radiation
types of cellular response to injury (2 types)
- reversible
- irreversible
hydropic degeneration (cell swelling) occurs with (2 things)
- hypoxia
- cell membrane injury
pathogenesis of hydropic degeneration
- injury -> hypoxia -> decreased ATP -> Na and H20 influx & K efflux -> osmotic pressure increases (push in) -> H2O moves into cell -> extensive vacuolation
hydropic degeneration is a ____ cellular response to injury
- reversible
ballooning degeneration
- severe cell swelling in epidermis
- indication of viral infection
cytotoxic edema
- severe cell swelling that occurs in CNS
Necrosis is a _____ cellular response to injury
- irreverisble
apoptosis is a _____ cellular response to injury
- irreversible
oncotic necrosis
- cell swelling beyond point of no return
pathogenesis of oncotic necrosis
- inadequate ATP production -> cytosolic influx of Ca -> activation of destructive enzymatic cascade (proteases and phospholipase) -> self destruct
nuclear changes of necrosis (3 things)
- pyknosis
- karyolysis
- karyorrhexis
pyknosis nuclear change
- shrinkage
karyolysis nuclear change
- lysis of nucleus
karyorrhexis nuclear change
- fragmentation of nucleus
cytoplasmic changes of necrosis
- increased eosinophilia and homogeneity
- loss of cell boundaries - rupture
- loss of cell adhesion
types of necrosis (4 types)
- coagulation
- caseation
- liquefactive
- gangrenous
types of injury that typically result in coagulation necrosis
- sudden loss of blood supply resulting in severe acute hypoxic injury
is coagulation necrosis acute or chronic
- acute
morphologic features of coagulation necrosis
- histologically - retention of cell outlines
- color change is white models surrounded by rim of red hemorrhage
types of injury that typically result in caseation (caseous) necrosis
- bacterial infection (intracellular)
is caseation (caseous) necrosis acute or chronic
- chronic
morphologic features of caseation (caseous) necrosis
- histologically - loss of cell outlines
- mass of granular material (friable and can be pulled apart)
type of necrosis that occurs in tissues of CNS
- liquefactive
malacia
- formation of gelatinous cavities
encephalomalacia
- gelatinous cavities in brain caused by liquefactive necrosis
myelomaicia
- gelatinous cavities in spinal cord caused by liquefactive necrosis
is liquefactive necrosis (encephalomalacia) acute or chronic
- acute
liquefactive necrosis (suppurative inflammation) caused by
- bacterial infection
morphologic features of liquefactive necrosis (suppurative inflammation)
- neutrophils resulting in pus
liquefactive necrosis (suppurative inflammation) acute form
- abscess
liquefactive necrosis (suppurative inflammation) chronic form
- inspissated with caseous texture
types of liquefactive necrosis (2 types)
- encephalomalacia - brain and spinal cord
- suppurative inflammation - everywhere else
types of gangrenous necrosis (3 types)
- dry
- moist
- gas
gangrenous necrosis with no bacterial involvement
- dry form
are all gangrenous necrosis acute or chronic
- chronic
features of dry gangrenous necrosis
- coagulation necrosis followed by mummification
gangrenous necrosis with bacterial putrefaction
- moist
features of moist gangrenous necrosis
- combination of coagulation and liquefactive necrosis
gangrenous necrosis with hemorrhagic exudate with bubbles
- gas
features of gas gangrenous necrosis
- necrosis followed by proliferation of anaerobic bacteria with gas production
common pathogen of gas gangrenous necrosis
- clostridium spp.
programed cell death with cellular shrinkage and without inflammation
- apoptosis
apoptotic bodies
- fragmentation of cell into small membrane-bound segments
embryogenesis apoptosis
- fetal development and remodeling
immunology apoptosis
- immune tolerance
- regulation of inflammatory responses to minimize associated tissue damage
pathological apoptosis
- hypoxia
- withdrawal of growth factors or hormones
- cell-mediated immune responses (cytokines and T-cells)
- chemicals and cytotoxic drugs
initiation phases of apoptosis (2 ways)
- intrinsic (mitochondrial)
- extrinsic (death receptor-initiated)
activation phase of apoptosis
- caspase enzyme cascade
chronic injury and cellular adaptation (6 things)
- autophagocytosis
- changes in cell size, number or appearance
- pathological calcification
- intracellular accumulations
- extracellular accumulations
- pigment accumulation
autophagocytosis (autophagy) purpose
- self digestion (removing junk in cell that isn’t needed)
- can be triggered by fasting
autophagocytosis (autophagy) pathogenesis
- damaged organelles enveloped by cell membrane to form autophagosomes that expelled by exocytosis or degraded by lysosomal fusion
- some vacuoles may persist in cell forming residual bodies filled with ceroid lipofuscin
atrophy
- decrease in size of amount of cell, tissue or organ after normal growth
hypertrophy
- increase in tissue mass due to increase in individual cell size
types of hypertrophy (2 types)
- functional
- hormonal
hyperplasia
- increase in tissue mass due to increase in number of cells
types of hyperplasia
- physiologic
- pathologic
- idiopathic
metaplasia
- adaptive change from one adult cell type to another usually due to a chronic stimulus
dysplasia
- abnormal growth
anaplasia
- dedifferentiation
types of pathological calcification (2 types)
- dystrophic
- metastatic
dystrophic pathological calcification
- Ca deposition occurs locally at site of injury and necrosis
metastatic pathological calcification
- Ca deposition occurs in normal tissue and is secondary to hypercalcemia
6 causes of hypercalcemia in vet med
- renal failure leading to secondary hyperparathyroidism
- primary hyperparathyroidism
- paraneoplastic - PTH-related protein
- Vit D toxicosis
- destructive bone tumor
- severe granulomatous disease
serum calcium concentration in dystrophic calcification
- normal
serum calcium concentration in metastatic calcification
- elevated
