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Patho463 Glossary
Patho463 WebCT Glossary
TERM | DEFINITION |
---|---|
Apoptosis | programmed, or orderly cell death. A normal part of the life hisotry of each cell in the body. Does not result in release of intracellular contents into the circulation. Is a part of the normal cellular maturation process. |
apoptosis - death ligands-initiators | see page 29 for good picture include FAS and TNF Cytotoxic T lymphocyte at level of CD recepors Injury Withdrawal of growth hormones |
Acidosis | The state of blood when the pH is below the expected range - it is an increase in hydrogen ions, for a variety of reasons. see Acidosis ct'd |
Acidosis ct'd | There are two main mechanisms for correction of acidosis - respiratory, ( blowing off CO2) and metabolic ( shift of HCO3 ) in the renal tubules . Both may be activated, respiratory is faster, metabolic takes more time. |
active oxygen species ( oxygen free radicals) | mediators of inflammation released by all leukocytes |
apoptosis mediators - intracellular | bcl-2 family cytochrome c p53 intracellular caspases granzyme B all leading to executioner caspase |
arachidonic acid metabolites | prostaglandins and leukotrienes - powerful, shortacting compounds derived from arachidonic acid, make by all cells that have various effects on other cells. |
Autosomal Recessive Trait | A genetic defect usually expressed only when there are two defective copies present. Hemachromatosis is an example |
basophil | a form of Polymorphonucleocyte with granules. rich in heparins and some vasoactive amines - similar to mast cells in the tissues. Origin is bone marrow, exact pathway a little cloudy. |
BMP | Basic metabolic panel A group of labroatory tests used to assess organ function ususally includes Glucose, BUN,Creatinine, Na,K,Cl, Calcium or Total Protein |
BUN | part of a metabolic panel. Nitrogen - in the form of ammonia is a by product of amino acid ( protein) catabolism). The ammonia is converted to Urea by an enzyme made by the liver. |
BUN ct'd 1 | The urea is for the most part eliminated by the kidney by passive filtration. |
BUN ct'd 2 | Therefore, the BUN can be used to asses both renal filtration rate and liver function. It is affected by dietary intake of protein and by degradation of protein within the body ( bleed into GI tract) |
CBC | Combination test assessing three different systems. Erythron( Red Cell mass), Coagulation ( Platelets and Immune ( WBC and differential) The following specific tests are included : WBC RBC HGB HCT MCH MCHC MCV PLT Neut Lymphs Monos Eosinophils Basophils |
cell injury causes | as listed in the book hypoxia - oxygen deprivation example terminal event in MI, terminal event in Septic shock. physical agents chemical agents Infectious agents - toxins, activations of inflammatory pathways example our patient in HUS, Septic Shock |
cell injury causes ct'd 1 | Immunological reactions - Antibody or T-cell damage - Islet cell destruction in Diabetes, Major systemic damage in Lupus. |
cell injury causes ct'd 2 | Genetic - Hemachromatosis is a good example. Lack of or malfuntioning enzyme as a result of a gene mutation. Sickle cell anemia is another. |
cell injury causes ct'd 3 | Nutritional imbalances - Pernicious anemia is an example.-DNA synthesis is blocked. |
cell injury mechanisms | Depletion of ATP Mitochondrial Damage Influx of Calcium Accumulation of Oxygen free radicals Defects in Membrane permeability |
chemokines | mediators that act as attractants - cells move along a gradient of these to the area of injury - The book metions 40, many of the intermediates and by products of the inflammatory process itself are also chemokines |
CKMB | CK is an intracellular enzyme, found in highest concentrations in muscle, heart and brain. |
CKMB ct'd | The source can be identified by looking at the relative proportions of MB (heart) MM (muscle) and BB(brain). In practice we look at the ration of MB to total CK for early detection of heart attacks. |
coagulation system | see big picture discussion |
complement system | see big picture discussion |
creatinine | part of a basic metabolic panel. Creatinine is made in muscle as a result of ATP utilization. It is made in proportion to the muscle mass, it is passively filtered through the kidneys and therefore can be used to assess renal filtration rate. |
creatinine ct'd | It is affected by muscle mass but not diet |
CRP | C-reactive protein - both a mediator of inflammatory response and an indicator of inflammation. May be one of the most important players in the development of cardiovascular disease. |
cytokines | mediators made in one cell but with effects on other cells, usually by receptro mediated pathways. TNF and Interleukins are prime examples |
DIC | Disseminated Intravaxcular Coagulation - simultanwous activation of the Coagulation and Fibrinolytic systems with consumption of platelets and fibrinogen. A compnent of many infectious and inflammatory states. |
endothelial cells | line the vasculature and dance a pas de deauz witht he platelets and the other cellular componenst of the blood. |
Enzymes (lab tests) | Intracellular enzymes present in all cells but varying in proportions. Release into the bloodstream indicates cellular damage, most likely necrosis or loss of membrane integrity. Location of injury can sometimes be deduced by looking at the pattern. |
Enzymes (lab tests) ct'd 1 | For example An elevated CKMB suggests heart damage while an elevated AST,ALT and ALP suggest liver damage. |
Enzymes (lab tests) ct'd 2 | The exact location can sometimes be pinpointed. For example, markedly elevated AST and ALT with a mild elevation of ALP suggests liver parenchyma. Mild elevation of AST,ALT but marked elevation of ALP suggest Biliary tract damage. |
eosinophil | a form of polymorphonuceocyte with vasoactive amines in its granules. Involved in certaiin inflammatory responses. Made in the bone marrow |
etiology | real cause of the disease or disorder - beginning point for your organization of each disease. THERE MAY BE MULTIPLE FACTORS |
fibrinolytic system | see big picture discussion |
fibroblast | part of connective tissue |
histamine | vasoactive amine - dilation of arterioles and opens up endothelial junctions - from mast cells, platelets basophils and eosinophils |
homeostasis | maintaining the status quo - applies to many systems |
HUS | microangiopathic hemolytic anemia precipitated by infection with Shiga Toxin producing E. coli and possibly other bacteria. Closely related to TTP ( Thrombotic, thrombocytopenic purpura) and DIC( Disseminated intravascular coagulation) |
hyperplasia | increase in number of individual cells as opposed to hypertrophy which is increase in size |
hypertrophy | increase in size of cell |
Ischemic vs hypoxic | Ischemic low perfusion and combines effects of low oxygen with lack of nutrients for anaerobic pathways, Hypoxic is low Oxygen availability. Ischemic is usually more severe than hypoxic |
kinin system | see big picture discussion |
lymphocyte - two kinds, B and T | The T cells organize and modulate the immune response as well as participate in direct dilling. The B cell produces antibodies. Both are from the bone marrow originally but mature in the peripheral lympatic system ( spleen and lymph nodes. |
lysosomal enzymes | proteolytic enzymes found in neutrophils and macrophages - mediators of inflammation - aggravators |
manifestations | What we see either in the patient, in the tissues we examine or the laboratory and other tests. |
Monocyte-macrophage | cell made in bone marrow travels in the blood, migrates to tissue - responsible for phagocytosis and also presents antigen to lymphocytes - active in inflammatory response |
myoglobin | the oxygen carrier in muscle and heart muscle ( similar in structure to hemoglobin and performs a similar function - makes muscle red - released from cells when damage occurs. Used as an early marker for cardiac damage - watch out for other muscle sources |
necrosis | disordered cell death - usually sudden, results in disruption and release of cell contents |
nitric oxide | mediator of inflammation that is release from macrophages - causes effects on vessel relacation |
pathogenesis | The development of the disease - sequence of events. In many cases involves the bodies own response to the original cell injury ( inflammation for example). kind of like the old spy vs. spy vs. spy vs. spy. |
pathogenesis ct'd | Nearly always fultifactoral, multiple processes. Sometimes resulting in morphological change - the bread and butter of traditional pathologists - but sometimes going directly to functional alterations and manifestations |
platelets | small anucleate cells that orchestrate the coagulation and inflammatory responses. |
platelets ct'd | Although they are unable to synthesize fprotein after release fromt he bone marrow, they contain a whole host of interesting mediators of inflammation adn growth factors and provide a platform for the development of a clot. |
PMN, neutrophil, seg | formed in the bone marrow, short lived. travels in the blood stream - moves to tissue in response to cytokines. Has lysosymal enzymes. |
protein c | Activated protein C - is a regulator of the coagulation, and fibrinolytic pathways directly and the kinin and complement pathways indirectly. Major role in the treatment of septic shock. |
resolution | What happens in the end - healing, repair, replacement, adapatation to functional changes or death. Also includes intervention and treatment. |
Reticulocyte Count | Very young ( up to 48 hours old red cells.) Can be used to distinguish a hemolytic anemia from a non-production ( aplastic ) anemia. It is also used to monitor response to therapy. |
serotonin | similar to histamine - richest in platelets |
Troponins | Several exist, these are part of the contractile apparatus in heart muscle. Appear in the ciruclation after damage to heart muscle. |