Pathophysiology NUR 231 Questions with Complete Solutions 100% Solved| Grade A+
COX-1 cycloxigenase 1 - good, creates GI mucous, platelet formation/clot formation, platelet
aggregation
COX-2 cycloxigenase 2 - bad, causes inflammation, pain, bradykinnins
types of cell injury ischemia, physical injury, mechanical exposure(pressure ulcer), chemical
exposure, actions of microbs, abnormal metabolites, nutritional deficits, fluid/electrolyte
imbalance
exogenous created from outside
endogenous created from inside, metabolites
Stage I Cellular injury reversible, if cause if removed, cell will recover
Stage II Cellular injury irreversible, cell death
somatic death brain death (5 mins no oxygen)
histamine released in response to injury, causes inflammatory response, released from mast
cells
platelets aid in clotting
specific immune system humoral and cell-mediated
non -specific immune system physical,secretions, phagocytosis, inflammatory, interferron
,chemotactic factors attract leukocytes to area, chemical scent trail
kinins cause pain, proteins, chemotaxis, cause inflammation
cytokines influence other cells, released from T-cells, cause fever
leukotrienes mast cells made from arachidonic aced
prostaglandins mast cells made from arachidonic acid, inflammation, pain
granulocytes contain granulocytes, neutrophil, basophil, eosinophil
agranulocytes no granulocytes, lymphcytes (B/T), monocytes-macrophages
neutrophil granulocyte, most abundand phagocyte -70-75% WBC
basophil granulocyte, histamine releasing phagocyte (type I hypersensitivity anaphylaxis)
eosinophil granulocyte, phagocyte, involved in type I hypersensitivity reaction, release
histamine (food allergy etc)
lymphocyte agranulocyte, specific immune system, B cells - humoral, T cells - cell mediated
monocyte agranulocyte, diapedesis- macrophage, big eater cell
, leukocytosis elevated WBC - if increase in neutrophils - bacterial, if increase in lymphocytes -
viral/fungal
differential count proportion of WBC's altered, count # of each type of WBC
sed rate rate at which blood settles, if have inflammation then blood doesn't settle as
quickly - elevated sed rate
corticosteriods shut down inflammation response, block immune response - increase in
infection, increase in blood sugar, osteoporosis
resolution (cellular healing) minimal tissue damage, scraped knee, atrophy, hypertrophy,
hyperplasia, metaplasia
regeneration (cellular healing) tissue regenerated by new cells, occurs only if cells are able
to regenerate
replacement (cellular healing) original cells cannot regenerate - normal cells are replaced
with another cell type - connective tissue/scar. Burn - no cells left to regenerate
adheasion two areas that should move past one another don't due to scar tissue formation -
gut/intestines
ulceration continually irritated, does not heal
hypovolemia occurs in burn patient, swelling causing a drop in BP
parkland formula used to determine the amount of fluids needed for a burn patient
COX-1 cycloxigenase 1 - good, creates GI mucous, platelet formation/clot formation, platelet
aggregation
COX-2 cycloxigenase 2 - bad, causes inflammation, pain, bradykinnins
types of cell injury ischemia, physical injury, mechanical exposure(pressure ulcer), chemical
exposure, actions of microbs, abnormal metabolites, nutritional deficits, fluid/electrolyte
imbalance
exogenous created from outside
endogenous created from inside, metabolites
Stage I Cellular injury reversible, if cause if removed, cell will recover
Stage II Cellular injury irreversible, cell death
somatic death brain death (5 mins no oxygen)
histamine released in response to injury, causes inflammatory response, released from mast
cells
platelets aid in clotting
specific immune system humoral and cell-mediated
non -specific immune system physical,secretions, phagocytosis, inflammatory, interferron
,chemotactic factors attract leukocytes to area, chemical scent trail
kinins cause pain, proteins, chemotaxis, cause inflammation
cytokines influence other cells, released from T-cells, cause fever
leukotrienes mast cells made from arachidonic aced
prostaglandins mast cells made from arachidonic acid, inflammation, pain
granulocytes contain granulocytes, neutrophil, basophil, eosinophil
agranulocytes no granulocytes, lymphcytes (B/T), monocytes-macrophages
neutrophil granulocyte, most abundand phagocyte -70-75% WBC
basophil granulocyte, histamine releasing phagocyte (type I hypersensitivity anaphylaxis)
eosinophil granulocyte, phagocyte, involved in type I hypersensitivity reaction, release
histamine (food allergy etc)
lymphocyte agranulocyte, specific immune system, B cells - humoral, T cells - cell mediated
monocyte agranulocyte, diapedesis- macrophage, big eater cell
, leukocytosis elevated WBC - if increase in neutrophils - bacterial, if increase in lymphocytes -
viral/fungal
differential count proportion of WBC's altered, count # of each type of WBC
sed rate rate at which blood settles, if have inflammation then blood doesn't settle as
quickly - elevated sed rate
corticosteriods shut down inflammation response, block immune response - increase in
infection, increase in blood sugar, osteoporosis
resolution (cellular healing) minimal tissue damage, scraped knee, atrophy, hypertrophy,
hyperplasia, metaplasia
regeneration (cellular healing) tissue regenerated by new cells, occurs only if cells are able
to regenerate
replacement (cellular healing) original cells cannot regenerate - normal cells are replaced
with another cell type - connective tissue/scar. Burn - no cells left to regenerate
adheasion two areas that should move past one another don't due to scar tissue formation -
gut/intestines
ulceration continually irritated, does not heal
hypovolemia occurs in burn patient, swelling causing a drop in BP
parkland formula used to determine the amount of fluids needed for a burn patient
