Cellular Pathology Flashcards
Pathology
study of disease
- external stimuli produce changes in the cells environment
- cell is challenged to maintain homeostasis
- to survive cells adapt
if cells are unable to adapt what happens?
cell death
cellular adaptions include?
- hyperplasia
- hypertrophy
- atrophy
- metaplasia
cellular adaption: hyperplasia
increase in the number of cells
physiologic hyperplasia
due to a normal stressor or initiator
- menstrual cycle
pathologic hyperplasia
due to abnormal stressor or initiator
- endometriosis
hypertrophy
increase in the size of the cell
physiologic hypertrophy
skeletal muscle hypertrophy with exercise
pathologic hypertrophy
left ventricle hypertrophy due to high BP
atrophy
decrease in the size of a cell that has at one time been of normal size
physiologic atrophy
decrease uterus size after pregnancy
pathologic atrophy
loss of stimulus to an organ or muscle; peripheral nerve damage
metaplasia
conversion of one cell type to another
- epithelium is normal in appearance but in an abnormal location
physiologic metaplasia
cervical ectopy; cellular replacement in presence of estrogen
pathologic metaplasia
conversion of columnar epithelial cells to squamous epithelial cells in airways of individuals who smoke
- can lead to cancer
cell injury
occurs when the cells cannot adapt to their new environment
causes:
- physical and chemical agents
- trauma
- infection
hypoxia
decreased oxygen
ischemia
decreased blood flow
what is vulnerable to cell injury?
- DNA
- cell membranes
- protein generation
- ATP production
two types of cellular injury
- reversible cellular injury
~ ex. low back pain and
patient learning better
posture - irreversible cellular injury
apoptosis
programmed cell death in response to damage to DNA or normal growth and development
apoptosis initiation
caspases is a catalyst of apoptosis
apoptosis execution
caspases causes cell death
does apoptosis cause an inflammatory response?
no, there is NO inflammatory response
necrosis
uncontrolled cell death
- causes an inflammatory response
liquefactive necrosis
transformation of tissue into a liquid viscous mass
- most often in high fat and low protein organs (brain) or high enzymatic content (pancreas)
- bacteria, virus, parasite
fat necrosis
inflammatory process which results in death of fat cells
- most common in breast tissue
avascular necrosis a.k.a osteonecrosis
death of bone tissue due to a lack of blood supply
- can lead to tiny breaks in bone
what causes avascular necrosis?
- joint or bone trauma
- fatty deposits in blood vessels
- sickle cells anemia
cellular accumulations
accumulation of substances in the cells as a result of damage to the cell (external factor) or genetic abnormality (internal factor)
substances:
- calcium
- protein
- iron
- fat
- cholesterol
- glycogen
- pigments
cellular accumulations of calcium
patients who have hypercalcemia have deposits of the calcium with normal or abnormal tissue
PT implications: should impingement
cellular accumulations: protein
neurofibrillary tangles seen in alzheimer disease
cellular accumulations: iron & its types
two types:
- hemosiderosis
- hemochromatosis
hemosiderosis
accumulation of iron in organs
- liver and pancreas
hemochromatosis
accumulation of iron in parenchymal cells
- CHF, diabetes, cirrhosis
most common cell of hemochromatosis?
parenchymal cells
fat accumulation
organs most commonly affected are the liver, kidney, heart and skeletal muscle
cholesterol accumulation
blood vessels
glycogen accumulation
liver and skeletal muscles
- typically due to a genetic disorder
pigment accumulation
exogenous (tattoo)
endogenous (jaundice)
cellular aging
the process of becoming older
- a process that is genetically determines and environmentally modulated
telomeres
protect the end of chromosomes with each cell division they shorten
- eventually DNA is interpreted as nonfunctional
what happens to telomeres as we age?
as we grow older, telomeres at the end of our chromosomes shrink
- new research suggests major depression is also linked to shorter telomeres as a sign of ‘accelerated aging’
werner syndrome
- autosome recessive
- rare, inherited disroder marked by rapid aging that begins in early adolescence or young adulthood and an increased risk of cancer
sign and symptoms:
- shorter than average height
- thinning and graying hair
- skin changes
- thin arms and legs
- voice changes
- unusual facial features
physical therapy implication: muscular atrophy
- therapeutic exercises
- strength training
- aquatic therapy
- standing programs
- respiratory management
- feeding
- skeletal and scoliosis management
- assistive devices
avascular necrosis PT treatment
- decrease load with assistive device
- maintain joint mobility
- strengthen muscles
- E-stim and US stimulating bone growth
