APP Basis of Disease Flashcards
Cellular injury
1 of 3 factors of response You MAY be able to com back from this, but at some point of stress, cell will no longer return to normal
Cellular Death
1 of 3 factor of response
Atrophy
Cellular adaptation in response to stress, cells DECREASE in size or DECREASE in cell number decsrease functioning of enzymes, less oxygen consumption, decrease in organelles
Hypertrophy
ONLY increase in cell size increase amount of functioning tissue mass usually result of increase in workload increase in functioning components of cells, so increase in number of organelles, enzymes, and functioning tissue pathological situation: cardiomegally Physiological: donated kidney, breast tissue, endometrium
Hyperplasia
increase in NUMBER OF CELLS it is a very controlled response, when stimulus is removed, should be removed uncontrolled leads to CA pregnancy: breast tissue hyperplasia and uterine hyperplasia
Metaplasia
due to chronic irritant change from one cell type to another stay within cell line, ex epithelial cell to another epithelial cell ex: lung tissue and esophagus tissue lung epithelial cells ciliated columnar cells turn to squamous cells in smoking GERD causes esophageal cells change into cells that we see in the stomach
Dysplasia
Are reversible Cell types are changed, but derangement in cell growth so different cell sizes and shapes and appearance found in metaplastic squamous epithelium of the respiratory tract and uterine lining
Stress
Mechanical forces electrical injuries nutritional imbalances biological agents poisons
Hypoxia
ischemia causes irreversible cell damage Check out the chart in ppt
Extremes of Temperature
Heat Cold
Heat
accelerate cellular metabolism activate and inactivate temp sensitive emzymes cellular membranes disrupted to temp changes coag of blood vessels coag of tissue proteins causes DIRECT cellular injury
Cold
increase in blood viscosity ice crystal formation induces vasoconstriction …
Chemical Agents
EX: Lead poisoning, HIGH: mental retardation, convulsions, coma LOW levels: reduced IQ and attn span, behavioral efects, crosses the BBB AND damages BBB
Effects of Lead - Phsiology
Causes ROS, decrease in antioxidant systems glomerular fibrosis and proximal tubule mitochondrial damage crosses and damages BBB lead looks like calcium, and enters transportors and changes the channels and cells as a result
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depletion of ATP in cell free-radical formation disruption of intracellular calcium hpmeostasis
Depletion of ATP
decrease in oxygenation of the cell Na/K pump will fail, and we get membrane depolatization and increase in intracellular Ca and Na –> cellular swelling 2/2 Na influx and water flux that goes with it –> maybe lysing switch to anaerobic metabolism –> increae in lactic acid –> decrease in cellular pH –> lysing of lysosomes (which are full of degratory enzymes, and get released due to decrease in pH and these enzymes ARE unregulated so cause damage)
Lysosomal destruction
Enzymes released, so IRREVERSIBLE damage
ischemia reperfusion injury
EX: crushing injuries, stroke, MI which causes decrease in blood flow to an area so that we can keep blood flow to keep cells alive kidneys usually tested in the tissues because only 1 artery to worry about inflammatory response damages tissue
Free radical injury
Essential to the physiology of our body, seen in our body due to metabolism and inflammatory response is due to CONTROLLED free radical response When uncolntrolled, can cause a lot of damage to our bodies Caused by: due to UV light, polution, excessive sugar production, lead, anything can become a free radical 3 major effects: 1) Lipid peroxidation 2) oxidative modification of our proteins 3) DNA effects unpaired electron will search for extra electron will chase things that are essentially immobile and can easily take an electron
ROS and effects on MI
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Cell Death
When we get to irreversible place of cell injury we get apoptosis and necrosis
Necrosis
UNPROMGRAMMED cell death When cell needs to die, this is one of two pathways Blebs occur here too, but cell leaks its contents thru lysis and immune response started by cells around which are effected by the lysis of their sister cell
Apoptosis
DOES NOT illicit immune response you get blebs which are outpockets (like a star fish) then broken up into small pieces and eaten by macrophages thru phagocytosis CELL NEVER LYSES
Pathways of apoptosis
1) intrinsic pathway- ex: stress and viruses, if DNA too damaged beyond repair, etc 2)extrinsic pathway- ex: too many cells in the tissue , like webbed feet! ALL pathways are propagated thru degratory enzymes called CASPASES and ONLY involved in apoptosis response
Apoptosis in Physiology
removal of proliferating cell populations (ex: intestinal epithelial cells) death of host cells that have finished use embryogensis control of immune cell numbers hormone-dependent involution of endometrium
Apoptosis in Pathophysiology
Growth of CA, viral infections,
Necrosis
result of lysis of our lysosomes Cathepsin causes degradation of the cell and when cell lyses the Cathepsin is in the extracellular environment and will break down cells in the area and so much debris formed that it overwhelms the immune system –>leads to gangrene
Gangrene
DRY - associated with arterial supply depletion, you can generally see where oxygen depletion occurs, turns black bc hemoglobin gets acted upon by bacteria production to make hydrogen sulfide WET - enough blood but can’t get blood out; usually seen in heels of feet, but sacrum, coccyx where pressure is increased
Normal range of SG
High 1.032 Low 1.015 isoosmotic urine would be 1.010 Compared to density of water
Bilirubin
indicates Liver problems bc its not going to the GI tract Pathway of breakdown in reticoloendothelial system: membranes of RBCs get weaker, and burst, releasing hemoglobin heme gets oxidized by Heme oxidase to make biliverdin which then gets reduced by biliverdin reductase to make bilirubin bilirubin attaches to albumin to get to liver and goes thru a few more steps to be transported to GI system
Immune outcomes from HBV
1) HBsAG totally cleared = immune stage 2) inactive carrier stage = no injury or inflammation of hepatocytes but patient can suffer from acute flares 3) if virus cannot be cleared and replication continues for > 6 months = chronic hepatitis stress causes virus to flare-up and replicate
Inflammation
baseline cause of almost all chronic diseases
Acute inflammation
Endothelial injury infection trauma exposure to physical or chemical agents tissue necrosis foreign bodies hypersensitivity rxns
Inflammation - vascular rxn
increase in vascular permeability
Inflammation - cellular rxn
begins with activation of the endothelium leukocyte margination leukocyte rolling and pavementing leukocyte adhesion leukocyte emigration thru endothelium chemotaxis to site of injury like leukotriences, anaphalaxins,
Chronic Inflammation
continuous activation of T cells accumulation and activation of macrophages in the area –> ROS get produced and released into tissue release TNF-alpha which are proinflammatory molecules and fibroblasts gets activated via TNF-alpha and proliferated fibroblasts lay down fibrous connective tissue in the area and lay down basement membrane –> THIS CAUSES FIBROSIS So fibrosis causes change in structure and therefore FUNCTION of the tissue
TNF=alpha
increase inflammatory cell recruitment and exacerbate IR increase in expression of MHC II tissue wasting …
HBsAG
Hepatitis B surface Antigen
Hepatitis B
DNA hepadenovirus transmitted via infected blood or by sexual contact present in saliva, semen, and vaginal secretions Most ppl with Hep B have been incarcerated
Pathophysiological Mechanisms
1) immune tolerance phase - no immune repsonse HBsAG is bound by hepatocyte surface receptors
Symptoms of Liver failiure
Fatigue bc of limited amount of energy in the body, and immune system uses most of that limited energy Hepatomegaly bc of swelling Arthralgias - Polyarthritis nodosa - effect on blood vessels due to hormonal changes Membranoproliferative glomerulonephritis Jaundice
Pathophysiology
structural and functional changes in disease states
