Pathology S1 cells

categories of atrophy

disuse, denervation, loss of endocrine stim, inadequate nutrition, ischemia

common sites of atrophy

heart, secondary sex organs, brain, muscles

physiologic hypertrophy

skeletal muscle, reversible athletic left ventricle hypertrophy

pathologic hypertrophy

compensatory hypertrophy (kidney), adaptive (high blood pressure cardiomegaly)

cause of hypertrophy

increased demand

physiologic hyperplasia

hormonal (pregnancy)

non-physiologic hyperplasia

Excessive hormones, growth factors (ex: benign prostatic hyperplasia, warts

cause of hyperplasia

hormones

cause of metaplasia

chronic irritation, inflammation

is metaplasia cancer?

no

dysplasia commonly seen in

squamous epithelium (respiratory tract, cervix)

is dysplasia cancer?

no, but it is likely a precursor

dysplasia

strange changes in the organization, shape, and size of mature cell types.

metaplasia

when the cell is replaced by less mature cell type

Anaplasia, neoplasia

the growth of many new cells into abnormal tissue. No coordination or regulation of growth. Cancer.

Most common type of cell injury

hypoxia, ischemia

Categories of cell injury

hypoxic, oxidative, physical, chemical, infectious, immunological, genetic, nutritional

acute mountain sickness

hyperventhilation, polycythemia, brain vasodilation, cerebral edema because this overwhelms BBB, lung capillary vasoconstriction, pulmonary edema because this causes excess pressure in capillaries that leak.

decompression sickness

nitrogen is forced into body fluids at high pressure, then expand with depressurization

dystrophic calcification

dead or dying tissues accumulate calcium, hardening of tissues. Atherosclerosis, ductal carcinoma, aortic stenosis

metastatic calcification

in healthy tissues, calcification occurs due to hypercalcemia. D/t hyperparathyroidism, paget disease

cellular accumulation manifestations

LOA, fatigue, pyrexia, tachycardia, leukocytosis

physiologic apoptosis

development, remodeling, replacement, immune function

pathologic apoptosis

cancer, autoimmune diseases, neurodegenerative diseases

coagulative necrosis

when cell death denatures proteins (lysozomal enzymes) necessary to disassemble things, cell matter becomes a clump

gas gangrene

clostridium infection, bubbles form

first line of defense

innate, native immunity, physical barriers, from surfaces of the body. includes acidic secretions, epithelial chemicals (antimicrobial peptides), natural flora protects from new pathogens

second line of defense

innate, nonspecific, occur if surfaces are breached. Response to tissue damage, invasion. Acute or chronic. Inflammation

cardinal signs of inflammation

redness, warmth, swelling, pain, LOF

major components of inflammatory response

vascular response, activation of cells, activation of plasma protein systems

capillary permeability molecule

bradykinin

1st step of vascular response in acute inflammation

momentary vasoconstriction

2nd step of vascular response in acute inflammation

vasodilation

3rd step of vascular response in acute inflammation

increased capillary permeability

vasodilation in acute inflammation causes

heat and redness

toxic defense molecule

nitric oxide

components that enter area to defend during vasodilation

neutrophils, macrophages, mast cells, platelets, leukocytes - some of which make nitric oxide

histamine and bradykinin contribute to

swelling, itching, LOF

First phase of acute inflammation

vascular response

Second phase of acute inflammation

cellular response

What limits and controls the inflammatory process?

plasma protein systems, plasma cells

first responders when WBCs arrive to inflammation?

neutrophils

Steps of WBCs to get to invaders

Adhesion and Margination, Transmigration, Chemotaxis

When WBCs migrate through endothelial junctions

Transmigration (diapedesis)

enhances binding to antigens

opsonization

release of signals from immune cells

degranulation

granules released from immune cells

histamines, cytokines, chemotactic factors

cell mediators of inflammation

leukocytes like neutrophils, baasophils, eosinophils. Mast Cells make histamine

Granules that are dispersed in inflammatory response

histamine, chemotactic factors, cytokines.

lipid-derived inflammatory mediators

leukotrines, prostaglandins, platelet activating factor

Acute phase inflammation response

Increased ESR and C reactive protein

3 Phases of Repair

Acute inflammation, Reconstructive proliferation phase, and remodeling and maturation phase