Cellular Injury, Adaptations, Maladaptive Changes (PATHO #1)

prokaryotes

a cell structure

Cyanobacteria(blue-green algae), bacteria, rickettsia

have no organelles or nuclear membrane

eukaryotes

cells of higher animals and plants

Protein synthesis, transport outer cell membrane, enzyme conent

three components of a cell

plasma membrane (outer membrane of cell)

cytoplasm (fluid filling)

nucleus (organs of cell)

nucleus

lg membrane- bound organelle

cell division, genetic info (controls cell activity and stores DNA) deoxyribonuceluic acid)

cytoplasm organelles

cytoplasmic matrix

fills space btwn nucelus and plasma membrane, aqueous mass

plasma membrane

protect cell

cell to cel recognition

gates, channels and pump

consists of lipids and proteins

lipids

bilayer made of up phosoplipids (phosphate bound to lipid) and glycolipids (carbohydrate bound to lipid)

trasnferring of ions and moleculues into and out of cell

proteins

some proteins can pass thry the membrane and some cant

trasnportation of cell

passive vs active

passive transport

no energy required

osmosis

diffusion

active transport

requires energy when trasnporting particles across the plasma membrane

etiology

og cause of cell alteration or diease

etiologic agents

causes of cell alteration or diease e.g infection, trauma

disease etiology

characterstic changes w specific etiologic agents

e.g cold temp=frostbite

in response: cell may devolop adaptive compensatory or maladaptive changes

cell size change

atrophy, hypertrophy (physiological vs pathological)

atrophy

decrease in cell size

hypertrophy

increase in cell size

cell number/apperance change

hyperplasia, metapasia dysplasia

hyperplasia

increase in cell number

metaplasia

reversiable replacement of one mature cell type by another less mature cell type or chnage in phenotype

dysplasia

derranged cellular growth

atrophy explained

decrease in cell size, decrease organ size if enough cells shrink

physiologic (normal in normal in early development)

pathlogic (adverse from disease/injury)results from decrease in workload, pressure, use, blood supply, nurtrion e,g paralysis shrinks skeletal muscle

hypertrophy explained

increase in cell size, increase organ size

physiologic (results from increased demand, stimularion by hormones, growth factors)

pathologic (results from chronic hemodynamic overload) e.g cardiac hypertropgy or strength training

physiological hypertropphy

cell enlargemnt w adequate supporting tissues

e.g enlargemnet of cardiac cells w exersise traning

pathological hypertrophy

increase in cell size, w/o increase in support structures

e.g enlargemnt of heart tissue due to hypertension

hyperplasia explained

increase in number of cells

only in cells capable of mitosis

can result from hormonal stimulation

e.g estrogen stimulates growth of breast cellls in pregency

may evolce inro maladaptive compensation (cell number increases to much, e.g keloid formation)

hyperplsia keloid formation

metaplasia explained

reversible replacement of one mature cell type by another

associated w tissue damage, repair, regenration

reprogramming of stem cells or undifferentaied mesenchymal cells

metaplasia explained

replacemet of one cell type w another r

genetic reprogramming (ensure cell survival e.g GERD)

metaplasia in GERD

lower esophageal cells, squamous epithliam transition to comulmnar stomack like

dysplasia explained

abnormal changes in size, shape, orgninization of mature cells

may b reversible if triggering stimulis is removed

tissue appears disorderly but is not cancer

(if changes penetrate basemnt membrane: invasive neoplasm) deranged cellular growth (often a result of chronic inflammation or precancerous condition.)

cells vary in size, shape, orgnization comparted w normal e.g cervical dysplasia detetced by PAP

neoplasia

new growth (disorganized, uncoordinated, uncontrolled)

cancerous

often interchanged with term tumor

neoplasms may b bengign or malignant

benign neoplasm

cells resemble normal cells

well differentated cells

do not metastasize

well defined boarders

maligant neoplasm

cells appear differet from healthy cells

poorly differentiated cells

increased likelihood of metastatiss

poorly defined boarders

cellular injury

oxidative stress and free radicals

an imbalence of free radicals and antioxidants in your body that leads to cell damage

exposure of cells to reactive oxygen specisis (ROS)— free radicals—cause cellular damage and targets DNA

clincal e.g heart disease, diabetes, cancer

antioxidants—-vitamin E—-reduce oxidative stress fror many diease processes

TIPS

T- toxins (endogenous (within body) exogenous (external enviorment e.g all)

I-infections

P-phsyical injury

S-serum deficit injury

toxins: cellular injury mechanisms

chemical or toxic injury (xeobiotics-toxic, mutagentic, carcinogenic)

lead, carbon monoxide, ethonal, mercury, social street drugs

chemical agenets of toxins cellular injury mech

over the counter and prescrived drugs, opiod abuse, leading cause of child posing is medications

toxins cellular injury mech (enviormental, heavy metals, ethanol)

emviormental- air pollution

heavy metals-lead cadmium arsenic mercury

ethonal-fetal alcohol syndrome, detal alcohol specturm disorders

infectious injury

pathogenecity of microorganism

bacterial or viral

disease prodcuing potential (invasion and destructuion, toxin production, production of hypersensitivry reactions)

physical unitential and intential injuries

blunt force injuries (result of application of mechanical force to body) results in tearinf shearing crushing of tissues e.g motor vechiles accidents and falls)

contusions, lacerations, fractures

unintetial and intentional injuries

sharp force injuries (stab wounds)

gunshot wounds

asphyxial injuries (suffocation, drowning)

s-serum deficit injury: cellular injury mechanism: hypoxia

hypoxic injury (single most common cause of cellualr injury)

results from ischemia (reduced supply of blood)

reduced oxygen conent in ambient air

loss of hemoglobin

decrease production of rbc

diseases of the respiratory and cadiovascular systems

posiinning of the oxidative enzymes (cytochromes) within the cells)

anozia0total lack of o2 caused by obstruction

ischemia

ischemia reperfusion injury

cell injury and death caused by rstoration of blood flow and oxygen

mechanism: oxidative stress, increase intracellualr calcium concentration, inflammation

apoptosis

programmed cellular death

normal part of aging

necrosis

associated w inflmmation and related to cellular injury

cell degeneration: necrosis

cell death due to injury

irreversaible process (membrane disintregrates, lysomal activation and autolysis

initatieates inflmmatory reaction

infarction

ischemic nercosis: death of tossue results from prolonged ischemia e.g MI cell contents cardiac proteins released into circulation

gangrene

prolonged ischemia, infaraction and necrosis

closttridum perfrigens (emits indefitable gas as it destory tissues, gas gangrene)

necrosis

gangeronous necrosis (death of tossue from severe hypoxic injury

dry: skin becomes dry shrivled brown/black

wet: arease become cold, swollen, black (Gas gangrene caused by clostridium

barrettes esophogus

metaplastic changes in GERD

may lead to cancer

endothilium could b consider body larget organ, active tissue is bulnarable to injury

ceullular injury

wellness and disease are reflected in cells, injury to a cell or its componements can lead to illness (biochemical lesion froms on the cell at the point of injury, a. chnages the chemistry of metabolic reaactions within cell e.g chronic alcoholism)

aging and altered cellular and tissue biology

aging—lose structure adn function—decrease—decrease in size or waste away

Aging and Altered Cellular and Tissue Biology- FRATLITY

weakness, decrease staminia, functional decline in older adults

increase vulnarability to falls, disability, disease, death

somatic death= death of entire body