GLOSSARY SECTION I PART B Flashcards
impaired outflow of venous blood-venous stasis (passive process)
caused by microscopic hemorrhaging-produces blue red color in effected area
congestion
labile cells divide continuously, proliferate throughout life, continuous replacement
continuously
control entry and progression thought the cell cycle
complex with and activate cyclin dependent kinases
function in DNA replication, depolymerization of nuclear lamina, formation of mitotic spindles
cyclins
important for cell signaling (IL-1, TNF)
can change cytoskeleton, be acted on to recruit WBC, cause chemotaxis
cytokines
due to albumin loss like renal disease
decreased albumin synthesis like liver disease
decreased plasma oncotic pressure
Coombs test
detects presence of immunoglobulin and or complement cascade components coating the surface of RBCs
direct antiglobin test
fluid accumulates under the skin usually in areas below the heart
dependent edema
CHF, constrictive pericarditis, cirrhosis
generalized edema
venous obstruction, thrombosis, external compression, inactivity
pulmonary edema
systemic thromboembolism
80% from heart and 20% from aortic aneurysm, plaques, valve vegetation
end up in brain 10% and lower extremity 75%
arterial emboli
pulmonary embolism
95% originiate in deep leg veins
saddle emboli or small multiple emboli
venous emboli
air that enters circulation, can coalesce and cause obstruction in flow like ischemia
occurs from obstetric procedure, chest wall injury, iatrogenic, decompression sickness
air embolus
uncommon complication
mortality 80%
amniotic fluid embolus
microscopic fat globules in circulation
occurs after the fracture of long bones
fat embolism syndrome 1-3 days after injury
fat embolus
comes from lipofuscin, melanin, and hemosiderin
endogenous glucose accumulation
endothelial cells are exposed to histamine and endothelial cells contract and leads to gap formation and stuff leaks out
contraction of endothelial cell with gap formation
endothelial cells are exposed to toxins, burns and chemicals
takes days to reverse
direct injury of endothelial cell (necrosis and detachment)
in lab-mitogenic for epithelial cells and fibroblast
in body causes hepatic cell division
epidermal growth factor basic
chemical species with a. single unpaired electron in outer orbital
highly reactive and unstable that initiates autocatalytic reactions
final common pathway of cell injury
free radicals
the hallmark of healing
has a granular and pink appearance
3 properties angiogenesis, fibroblast proliferation, edema
granulation tissue
pulmonary edema
left sided heart failure
extremity edema
right sided heart failure
iron
one of the ways endogenous glycogen can accumulate
hemosiderin
in mast cells, basophils, platelets
vasodilators arterioles, increases vascular permeability, primary cause of edema
histamine
alteration within cells or extracellular space that gives homogenous pink appearances with H&E
hyaline change
increased levels are caused by local and systemic things
can local or systemic
hydrostatic pressure
excess calcium in the blod
paraneoplastic mechanism (author that produces PTH)
non paraneoplastic mechanism
hypercalcemia
altered state of blood requiring less than normal clot promotion activities that produce a thrombus
causes:leiden mutation, prothrombin mutation, antithrombin III deficiency, protein C or S deficiency, fibrinolysis defects
hypercoagulability
increased blood flow due to arteriolar dilation (active process)
produces redness
hyperemia
increase in number of cells leading to increase in the size of an organ
physiologic or pathologic
hyperplasia
increase in size of the cell resulting in an increase in the size of an organ
due to limited capacity to divide, increased demand or increased growth factor
physiologic or pathologic
hypertrophy
found in endothelial cells for adherence
ICAM-1
binding of IgE to mast cells causes release of the following mediators: vasoactive, chemotactic, neutral proteases, lipid mediators and cytokines
causes seasonal allergies
anaphylaxis
IgE
opsonin
activates the classical pathway (2nd time infection with memory cells)
IgG