Pathophys objective flash cards.txt

Oxygen deprivation, Chemical Agents, Infectious agents, Immunologic reactions, genetic defects, genetic imbalances, physical agents, aging

ATP-dependent sodium efflux pump cannot function, ATP dependent Calcium cation efflux transport cannot function, anaerobic glycolysis increases as an attempt to restore the ATP levels

increased intracellular sodium cations, decreased potassium ion concentration, influx of water, cellular swelling, decreased protein synthesis

activation of ATPases, phospholipases, proteases, endonucleases

decreased glycogen stores, decreased pH level in the cell, decreased activity of cellular enzymes, detachment of ribosomes

functions as oxidizing agents

Incomplete reduction of O2 during respiration, Accepting or donating of electrons by transition metals, Absorption of X-rays, Detoxification or metabolism of chemicals in liver, Enzymes involved in inflammatory processes

Fatty Acids, Proteins, DNA

SOD, Glutathione peroxidases, catalase

depravation of hormones or GF (menstruation), irreparable DNA damage, accumulation of misfolded proteins (alzheimer's), Immune system development, Embryogenesis (loss of vestigial tail)

increase in cell size but not number caused by increase work load, occurs by increased protein synthesis

increase in cell number but not size (breast growth)

decrease in cell size but not number caused by decreased work load, proteins degrade and protein synthesis decreases

one adult cell type is replaced by another

hepatocytes

ethanol consumption and diabetes

decreased liver function

Damage due to ROS or OFR which indicates aging

break down of hemoglobin at sites of localized injury or hemmorrhage; associated with systemic overload of iron

rheumatic heart disease, heart valve becomes sticky causing leakage

accumulation of Ca associated with necrotic cells

pathologic bone reabsorption

metastatic cancer

death of cells of the vasculature, kidneys, lungs, and gastric mucosa

accumulation of damage (lipofuscin, incorrectly folded proteins/ cross-linked proteins, protein glycosylation, free radical damage), incomplete replication of protein ends by telomerase, reduced regenerative capacity of stem cells

Heat, redness, swelling, pain, loss of function

Vasodilation, increased viscosity, margination

endothelial cell contraction which leads to gaps that leak fluids, direct injury to endothelial cells, leukocyte-dependent endothelial cell damage, increased fluid flow through endothelial cells, leakage from new blood vessels that form at the site of injury

release of transudate, release of exudate, edema

WBC flow along the inner wall of blood cells due to changes in blood flow

leukocytes tumble along the wall

leukocyte squeezes through the gaps in edothelial cells

Selectins

Integrin

leukocytes follow a chemoattractant gradient composed of bacterial peptides, complement components, and cytokines to the site of an infection

7-transmembrane G-protein coupled receptor

opsonins

phagocytic vacuole containing foreign bodies

fusing with a lysosome which contains an oxidative burst

complement proteins, kinins, and coagulation factors

cleavage

mast cells, basophils, and platelets

physical injury, immune reactions, complement binding, neuropeptides, and cytokines

arteriolar dialation, increased vascular permeability, endothelial cell contraction; this results in swelling, edema, and congestion

Prostaglandins

leukotrienes and lipoxins

vasodilation and edema; pain and fever

NSAIDS

vasoconstriction and increased vascular permeability; airway constriction

counteract the activity of leukotrienes

HMWK

Kinin system, Complement system

triggers assembly of MAC

trigger histamine release

chemoattractant for WBC

obsonin which aids in phagocytosis

restoration to pre-injury state, scaring or fibrosis, chronic inflammation

infiltration by macrophages, lymphocytes and plasma cells, continuous tissue destruction by inflammatory cells, extensive tissue repair including angiogenesis and fibrosis

viral infections, persistent microbial infections, prolonged exposure to toxic agents, autoimmune diseases

release proteases, ROS, factors that release and promote inflammation, angiogenesis factors, growth factors stimulating infiltration and fibrosis

produce mediators which activate macrophages

Produce antibodies

produce major basic protein which is toxic

produce histamine and AA metabolites which play a role in anaphylactic shock and allergic reactions

permanently dividing and capable of regeneration (skin and GI tract)

normally nondividing but can divide in response to injury and regenerate themselves (liver, kidney, pancrease, fibroblastic connective tissue cells, endothelial cells)

Non dividing cells that are not capable of regeneration (nerves)

cyclins binding to CDK which then become active and phorphorylate proteins to begin the cell cycle

targets the same cell that produced the factor

targets adjacent cells

specialized form of paracrine signaling

hormone functions at a site distant

EGF--> EGFR-->RAS-->MAP Kinase Cascade-->cyclin transcription

amorphous gel between connective tissue

collagen, elastin, and proteoglycans

sits beneath epithelium to provide support

type IV collagen, laminin, other adhesive glycoproteins and proteoglycans

to define the cell orientation

• �Angiogenesis- Formation of new blood vessels at the site of injury (neovascularization)
• �Migration and proliferation of finroblass to the site of injury
• �Deposition of ECM by the fibroblasts
• �Maturation and remodeling of the fibrosis tissues by macrophages

• �Dilation and increased permeability of the preexisting blood vessel at the site of angiogenesis
• �Proteolysis of ECM to break down the basement membrane
• �Migration of endothelial cells toward a chemoattractant angiogenic stimulus a the site of injury
• �Endothelial cell proliferation just behind the leading edge of migrating cells
• �Once enough cells are present proliferation stops, lumen formation occurs and the endothelial cells self organize into tubes
• �Recruitment and organization of accessory cells to complete the mature vessel

Fibroblast growth factors, vascular endothelial growth factor

• �Emigration and proliferation of fibroblasts at site of injury
• �Deposition of ECM components by fibroblast at site of injury

PDGF, FGF, TGF beta

• �Induction of acute inflammatory response by injury
• �Parenchymal cell regeneration
• �Migration and proliferation of parencymal (epithelial) and connective tissue cells
• �Synthesis of ECM proteins
• �Remodeling of parenchymal elements to restore tissue function
• �Remodeling of connective tissue to restore wound strength

• �Incision fills with clotted blood which forms a fibrin clot and scab
• �Neutrophils migrate to clotted blood
• oThey produce factors the stimulate epithelial cell proliferation at the wound
• oEpithelial cells advance towards eachother and secrete basement membrane componants to pinch of the clot
• oEpithelial cells meet beneath a surface of scab and form a thin layer of epithelium
• �Macrophages replace neutrophils in stromal (subcutaneous) space
• oResolve inner scab and produce factors that promote neovascularization, fibroblast migration, and ECM deposition which leads to restoration of interstitial volume
• �Epithelium (epidermal cells) proliferate and epidermis recovers its normal thickness. Surface scab falls off.
• �Inner scab is resolved and replaced by a fibrous union. Inflammatory processes are resolved.