cpt 4: cell injury, aging and death Flashcards
cellular swelling and the accumulation of excess substance within the cell is frequently seen with what cell inury?
Reversible cellular injury
early stages of irreversible cellular injury
cellular adaption
generally reversible
may be detrimental to cell
results in changing structure or function of cell
Necrosis
type of irreversible cell injury leading to death of tissue
gangrene
type of necrosis that can be described as wet, dry, or gas
determination based upon location and appearance.
proteasomes
degrade intracellular proteins
telomeres
get shorter with each cell division, leading to cell aging
normal intracellular substances that accumulate in injured cells (4)
lipids
carbohydrate
glycogen
protein
adaption response: swim team student with increased skeletal muscle mass
beneficial hypertrophy
adaption response: cardiovascular pt with BLE hair loss and skin thinning
pathologic ischemic atrophy
adaption response: ETOH addiction and hepatomegaly
pathologic hypertrophy
adaption response: development of breast in puberty
beneficial hypertrophy
adaption response: increase in RBC when training in high altitude mountains
beneficial hyperplasia
adaption response: epithelium changes in bladder as a result of chronic cystitis
pathologic hyperplasia
adaption response: calluses on hands
pathologic hyperplasia
adaption response: cervical cells with abnormal variations in size, shape, and arrangement
pathologic dysplasia
adaption response: conversion of bronchial ciliated columnar epithelium to stratified squamous epithelium in smoking pt.
pathologic metaplasia
types of tissue necrosis with examples: 4
coagulative: MI
liquefactive: abscess
fat: cyst after breast surgery
caseous: damaged lung from TB
Common etiologies of cellular injury (5)
ischemia and hypoxic injury nutritional injury infectious and immunologic injury chemical injury physical and mechanical injury
Na/K pump failure to remove Na probable cause of
cellular swelling during early stages of cell injury
glandular tissues response to increased functional demand
hyperplasia
steps of coagulative necrosis (4)
- ischemic cellular injury
- plasma membrane unable to maintain electrochemical gradient
- influx of Ca and mitochondrial dysfunction
- degradation of plasma membrane and nuclear structures.
hypoxia due to ischemia results in (3)
lactic acidosis
hydropic swelling
reduced ATP production
hydropic swelling: malfunction of Na/K pump
accumulation of Na in cell, creating osmotic gradient for water.
pump needs ATP: decease ATP leads to dysfunction, leads to swelling
organ enlargement
swelling of cells in a particular organ
reasons for accumulation of normal substances inside cell (2)
faulty metabolism: excess storage
absent enzyme: no breakdown
lipid accumulation: location and causes
liver
excessive alcohol intake
genetic disorders: enzymes needed to metabolize lipids is impaired.
carbohydrate accumulation: cause
lysosomal enzyme degradation of these is impaired
glycogen accumulation
common with diabetes, excess sugar is stored.
accumulation of protein cause
denatured proteins due to cellular stress, may cause dysfunction and death.
chaperones will try to correct defect
ubiquitin
protein that binds with abnormal proteins creating a complex that enters a proteosome where proteins are digested into fragments.
accumulation of pigments and inorganic particles (2)
endogenous: produced by body: hemosiderin, bilirubin
exogenous: introduced form outside: tar, mineral dust.
atrophy
cells shrink and reduce their differentiated functions.
disuse: reasoning and leads to
bedrest, casting
leads to atrophy
denervation: reasoning and leads to
loss of nervous stimulation -> decrease muscle size
leads to atrophy
ischemia
loss of blood supply
leads to atrophy
nutrient starvation
poor intake, absorption, or distribution.
leads to atrophy
cells attempt to minimize its energy and nutrient consumption by decreasing number of intracellular organelles and other structures
atrophy
cells shrink
hypertrophy
increase in cell mass accompanied by an augmenting functional capacity
in response to increased physiologic or pathophysiologic demands
hyperplasia
increase in number of cells.
demand induced hyperplasia
increase in cells due to physiologic demand: increased RBC in high elevation
pathologic hyperplasia
dysregulation of hormones or growth factors: thyroid or prostate enlargement.
chronic irritation hyperplasia
calluses or corn
metaplasia
replacement of one differentiated cell with another.
fully reversible when stimulus is removed.
dysplasia
disorganized appearance of cells due to variations in size, shape, and arrangement.
carcinoma in situ
necrosis
consequence of ischemia or toxic injury characterized by cell rupturing, contents spilling into extracellular fluid, and inflammation.
indications of necrosis (7)
general inflammatory response malaise fever tachycardia increased WBC decreased appetite intracellular proteins in bloodstream determine location and extent of death.
gangrene
cellular death involving a large area of tissue
usually results from a major interruption of blood supply
dry gangrene
form of coagulative necrosis
blackened, dry, wrinkled tissue
generally on extremites
wet gangrene
form of liquefactive necrosis
typically found in organs
cold, black, and foul smelling
gas gangrene
characterized by formation of bubbles of gas in damaged tissue
result of infection of necrotic tissue by anaerobic bacteria clostridium.
apoptosis
organized cellular death
fas ligand
extracellular signal that binds to cell and triggers death cascade in apoptosis
internal activated apoptosis
mitochomial damage leaks cytochrome C in to cytoplasm with activates apoptosis pathway.
caspases
degrades intracellular structures in apoptosis
ischemia and hypoxic injury
insufficient amount of oxygen to produce ATP and survive
re-perfusion injury
occurs after ischemia/hypoxic injury.
cellular damage occurring after blood supply to tissue is restored.
re-perfusion injury cascade
calcium overload
formation of reactive oxygen molecules: free radicals
subsequent inflammation: free radicals stealing H atoms forming abnml molecular bonds causing more free radicals.
damage cell membrane, denature proteins, and disrupt chromosomes
increased inflammation
nutritional injury
excess or deficient nutrients:
lipids, proteins, carbs, vitamins and minerals.
infectious and immunologic injury
bacteria and viruses
bacteria affect on cell
from outside:
excrete digestive enzymes that digest cellular membrane and connective tissue
produce exotoxins which interfere with cellular functions
gram negative bacteria affect
endotoxins in cell wall. When bacteria is killed endotoxins release causing
fever, malaise, shock
infectious and immunologic injury from immune response
WBC secrete enzymes and chemicals meant to kill invading organism
normal body cells exposed
immune cells produce free radicals which can attack host cell membranes.
virus affect on cells
genetic material able to gain access to cell
uses host cell to replicate
can live in cell a long time or cause rapid lysis
chemical injury
chemicals, posions, toxins
can cause direct cell injury or become injurious when metabolized.
physical and mechanical injury
extreme temp abrupt changes in atmospheric pressure mechanical deformation electricity ionizing radiation
cellular basis of aging
progressive decline in the proliferative and reparative capacity of cells along with exposure to environmental factors.
programed senescence theory
aging is a result of an intrinsic genetic program
cells have a finite number of divisions
somatic death
death of an entire organism
no immunologic or inflammatory response
24-48 hours after death
tissue deterioration or putrefaction apparents
brain dead
unresponsive, flaccidity, absence of brain stem reflexes, no respiratory effort, absence of brain waves, lack of cerebral blood flow.
