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Etiology; pathogenesis; morphologic changes; clinical significance

Homeostasis for normal stress

Adaptations due to severe stress (preserve viability, modulate function)

Hyperplasia = number of cells

Hypertrophy= size of cells

Atrophy= decrease size

Past this results in cell injury

Sometimes reversible, other times irreversible (point of no return)

Necrosis and apoptosis are possibilities

Form, color are indicators

Subcellular alterations usually due to chronic mild injury

Hypertrophy- no new cells, just bigger (more structural components not swelling)

Most common in non-dividing cells (myocardial cells, neurons)

Might have more dna (due to interruption in mitosis cycle)

Increased workload is most common cause (weight lifting)

Hyperplasia- increase in number of cells disrupting organ

Can partner with hypertrophy

Hormonal- puberty increases epithelium

Compensatory- increase tissue mass after damage

Increased growth factor production; increased receptors, intracellular signal pathways (or

combo)

Pathoologic: excessive hormonal stimulation; growth factors

Endometrial is hornmoe classic example; benign prostatic hyperplasia (can be reversed if

hormones are stopped)

Makes it easier for cancerous hyperplasia

Also occurs in wound healing by connective tissue

Atrophy- shrinkage, adaptiona that can lead to death, can affect organ size

Due to : decrease of use; loss of innervation, diminished blood, inadequate nutrition, agiing,

pressure

Physiologic: notochord and thyroglossal duct, uterus after birth

Pathology: local or generalized

Metaplasia- replacing of one cell with another type

Can be adaptive due to stress

Usually columnar to squamous

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Often reversible if stress is removed (stop smoking soon)

Vitamin a defiency squamous in respiratory epithelium

Vitamin A excess no keratinzation

Affects thpe of carcinoma

Barret esophagus is squamous to columnar due to refluxed acid- glandular adenocarcinomas

Hypoxia- defiency of oxygen reducing aerobic respiration

Not ischemia- blood supply loss from impeded arterial flow or reduced venous drainage

Affects not only oxygen levels but nutrient levels

Chemical agents- most common is glucose

Also salt and electrolyte imbalances

Oxygen in high amounts

Poisons, and environmental toxins

Recreational drugs

Infections and autoimmune

Genetics

Nutritional imbalance- protein calorie defiencies. Vvitamin defiency, anorexia, excess, metabnolic

disease

Physical agents- burns trauma

Aging-telomeres no longer functioning

Irreversible- inability to reverse mitochondrial dysfunction (lack of atp or phosphorylation); profound

membrance distrubences

Cellular swelling, fatty change (architecture changes)

Necrosis = never normal always abnormal stress and always pathologic!!!!!!

Nuclear changes= pyknosis (darken chromatin); karyorhexis (fragment nucleus); karyiolysis

(destroy nuclear particles)

Apoptosis- programmed cell death, phagocytized as compared to enzymatic

Coagulative necrosis- dead but architecture is preserved

Hard due to structural proteins and enzymes being blocked

Eventuallty removed by inflammation and hystiocites

Liquefactive necrosis- cells, tissue, and architecture dead/liquefied

Infections, bacterial, fungal promote inflammation that is then liquefied by enzymes

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Gangrenous- clinical not pathologic

Limbs that have lost circulation with coagulative necrosis

Wet-gangrene = liquefication due to bacterial infection secondary

Caseous necrosis- tuberculosis infection

Found in foci, cheese like appearance

Fragmented or lysed cells with granular appearance

Granulomas collection of epitheloid histiocytes/macrophages

Fat necrosis- adipose destruction- usually by enzymes.

Pancreatic leading to saponification fat cells by calcium salts

Fibrinoid- necrosis- immune rxn with blood vessels

Antibody and antigen in blood vessels

Deposits with leaking leads to pink color

Subcellular response

mechanisms

ischemia

Tegrity

Ischemia is most common cause of injury, faster than hypoxia

Reperfusion inflammation with ischemia

Apoptosis- tightly regulated, cells dna is degraded, membrane remains intact, structure is altered (blebs)

Rapidly cleared and does not elicit inflammatory response

Eliminate cells that are no longer needed (endometrium during menstrual cycle, ovarian

follicular atresia in menopause, regression of lactating breast, prostatic atrophy, )

Maikntains steady state; bby cyto t cells,

Due to dna damamge, misfolded proteins, infection, atrophy, tumors

Tegrtiy pathways

Cell chrinks, chromatin condenses, blebs,

Intracellular accumulation-

Normal in excess, abnormal, or pigments

Can be toxic, transient or in cytoplasm/nucleus

Some carbon pigment lines miami lungs and coal miner lungs

Fatty acid ccumulation

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Accumulation of protein less frequent

Anzyme defiencies or accumulation/overproduction (excessive albumin release nephrotic syndrome;

abnormal folding)

Mallory hyaline- alcoholic hyaline (aggregated intermediate filaments)

Glycogen accumulation (diabetes)

Pigments anthracosis (black lung)

Lipofuscin- insoluble, lipochrome wear and tear, gaining pigment

Lipids and phospholipids with proteins, not damaging (grainy reddish in pink tissue)

Hemosiderin- iron accumulation (local or systemic)

Local is due to hemorrhageing

Hemosiderosis (systemic) increase absorption, impaired use, hemolytic anemia, transfusions

Tiny spots on histo pictures

Calcification deposits

Dystrophic dying tissues

Metastatic- normal tissue usually hypercalcemia