Altered cellular and tissue biology Flashcards
cellular adaption definition
the cell’s response to escape and protect itself from injury
Adaptive changes in cells
atrophy = DEC cell size
hypertrophy = INC cell size
hyperplasia = INC cell number
metaplasia = reversible replacement of one mature cell type by another less mature cell type
dysplasia = deranged cellular growth; not a true cellular adaption (atypical hyperplasia)
Atrophy physiologic
occurs in early development; thymus shrink in childhood
Atrophy pathologic
results from DEC in workload, use, pressure, blood supply, nutrition, hormonal stimulation, nervous stimulation
Atrophy disuse
bedridden
Hypertrophy
caused by INC work demand or hormones
Hypertrophy physiologic
pregnancy
Hypertrophy pathologic
HTN, Heart valve dysfunction
Hyperplasia
INC rate of cellular division
Hyperplasia physiologic
compensatory = allows organs to regenerate (LIVER)
hormonal = replaces lost tissue or supports new growth (uterus/breast)
Hyperplasia pathologic
endometrium/BPH
Dysplasia
abnormal changes in size, shape, and organization of mature cells
atypical hyperplasia
does NOT indicate CA
Metaplasia
reversible replacement of one mature cell by another less mature cell
ex: replacement of normal bronchial columnar ciliated epithelial cells by stratified squamous epithelial cells
reprogramming of stem cells
Cellular injury
leads to injury of tissues and organs, determining structural patterns of disease
REVERSIBLE = injured cells recover
IRREVERSIBLE = injured cells die
causes cell stress
acute vs chronic and reversible vs irreversible
can involve necrosis, apoptosis, accumulation, pathologic calcification
Cellular injury CAUSES
1) lack of oxygen
2) free radicals
3) toxic chemicals
4) infectious agents
5) physical and mechanical factors
6) immunologic reactions
7) genetic factors
8) nutritional imbalances
9) physical trauma
Cellular injury BIOCHEMICAL mechanisms
1) ATP depletion
2) mitochondrial damage
3) accumulation of O2 and O2-derived free radicals
4) membrane damage (ATP depletion)
5) protein folding defects
6) DNA damage defects
7) calcium level alterations
Cellular injury can lead to CELL DEATH by…
1) DEC ATP production
2) failure to activate transport mechanism
3) cellular swelling
4) detachment of ribosomes from ER
5) cessation of protein synthesis
6) mitochondrial swelling from calcium accumulation
7) vacuolation
8) leakage of digestive enzymes from lysosomes, autodigestion of intracellular structures
9) lysis of plasma membrane
10) death
CI: Ischemia-Reperfusion Injury
DUE to:
1) oxidative stress
2) radicals that cause membrane damage and mitochondrial calcium overload
3) mitochondrial permeability transition pore
MECHANISM of injury in:
1) tissue transplantation
2) ischemic syndromes: myocardial, hepatic, intestinal, cerebral, renal, stroke
CI: Free radicals and ROS - oxidative stress
INC of different reactive species
Detrimental oxidation of:
1) lipids
2) proteins
3) nucleic acids
Mitochondrial effects: dysfunction caused by ROS, inefficient antioxidants
CI: Chemical Injury
direct toxicity to the cell = damage to or destruction of plasma membrane
reactive free radicals and lipid peroxidation
EX: lead, CO, ethyl alcohol, mercury, social or street drugs
CI: Carbon Monoxide
colorless and odorless
produces hypoxic injury
CO’s affinity for Hgb is much greater than that of oxygen; if quickly binds w/ the Hgb, preventing oxygen molecules from doing so
CI: Lead
exposure in children = learning/behavior problems, speech/hearing problems, brain/nervous system damage, slowed growth/development
common source: paint in old homes
PREVENTION is key
CI: Ethanol (alcohol)
folate deficiency
metabolized by liver
protective effect w/ the cardiovascular system
acute alcoholism affects CNS
chronic alcoholism affects liver and stomach
CI: Mercury
major sources: fish & healthcare
AVOID in pregnant women, nursing mothers, young children
in street drugs