NURS 334 EXAM QUESTIONS AND ANSWERS A
+ GRADED
inflammation
an immunologic defense against tissue injury
inflammatory response
sequential response to cell injury
neutralizes and dilutes inflammatory agent
removes necrotic materials
establishes an environment suitable for healing and repair
intensity of the inflammatory response depends on
extent and severity of injury & reactive capacity of injured person
inflammatory response stages (4)
vascular response
cellular response
formation of exudate
healing
vascular response - inflammation
cell injury -> brief vasoconstriction/release of chemical mediators (histamine, kinins,
prostaglandins) -> vasodilation -> increased blood flow to the site -> increased capillary
permeability -> fluid moves from the capillaries into tissue spaces -> inflammatory
exudate (contains plasma proteins, mainly albumin)
cellular response - inflammation
chemotaxis (WBC rushing to site) -> migration of leukocytes to the site of injury
(neutrophils, monocytes, and lymphocytes) -> macrophages -> phagocytosis (clean up
crew) -> exudate
leukocytes involved with cellular response to inflammation
neutrophils: 1st to show up (SEGS are mature, BANDS are immature) (shift to the left
means an increase # of BANDS)
monocytes: show up 3-7 days later
lymphocytes: show up late, a week later
the exact nature and amount of exudate depends on...
the type/severity of the injury
local clinical manifestations - inflammation
redness: due to vasodilation & increased capillary permeability
heat: due to increased metabolism at the site
pain: due to change in pH, nerve stimulation by chemicals, and pressure from fluid
exudate
swelling: caused by shift of fluid/exudate formation
loss of function: due to all the above responses
systemic clinical manifestations - inflammation
increased WBC count
malaise, fatigue, tired
nausea & anorexia
, VS changes (increased pulse, increased RR)
Fever
fever considerations
often a good sign, body is doing what it needs to do
often wait till a fever of 100.5 to step in
elderly are not as quick to run a fever due to their blunted response so may intervene
quicker
acute inflammation
healing occurs in 2 to 3 weeks, usually leaving no residual damage
neutrophils are predominant cell type at this site of inflammation
chronic inflammation
may last for years
injurious agent persists or repeats injury to site (keeps coming back or never clears)
predominant cell types involved are lymphocytes and macrophages
has lasting effects
primary prevention (health promotion) - inflammation
prevention of injury
adequate nutrition
early recognition of inflammation
immediate treatment
proper storage and preparation of food
secondary prevention - inflammation
no specific screenings
diagnostics for early identification
CBC
CRP, ESR = non specific inflammatory markers
MRI, CT, PET scans
tertiary intervention - inflammation
observation
vital signs
fever management
fever management
moderate: up to 103, uncomfortable but should not harm healthy person
severe: greater than 104 causes delirium, altered mental status, seizures, brain damage
risk factors for inflammation
age (young and old)
immunocompromised
uninsured/underinsured (don't go in till its BAD)
nursing and inter-professional management
drug therapy - inflammation
aspirin: blocks prostaglandin synthesis
acetaminophen: blocks prostaglandin synthesis, has effect on hypothalamus, does not
thin blood
NSAIDs: inhibits prostaglandin synthesis, SE: GI irritation and bleeding
Corticosteroids: antipyretic, prevents chemical mediators from being excretes,
immunosuppressive, used in short spurts for acute situations
+ GRADED
inflammation
an immunologic defense against tissue injury
inflammatory response
sequential response to cell injury
neutralizes and dilutes inflammatory agent
removes necrotic materials
establishes an environment suitable for healing and repair
intensity of the inflammatory response depends on
extent and severity of injury & reactive capacity of injured person
inflammatory response stages (4)
vascular response
cellular response
formation of exudate
healing
vascular response - inflammation
cell injury -> brief vasoconstriction/release of chemical mediators (histamine, kinins,
prostaglandins) -> vasodilation -> increased blood flow to the site -> increased capillary
permeability -> fluid moves from the capillaries into tissue spaces -> inflammatory
exudate (contains plasma proteins, mainly albumin)
cellular response - inflammation
chemotaxis (WBC rushing to site) -> migration of leukocytes to the site of injury
(neutrophils, monocytes, and lymphocytes) -> macrophages -> phagocytosis (clean up
crew) -> exudate
leukocytes involved with cellular response to inflammation
neutrophils: 1st to show up (SEGS are mature, BANDS are immature) (shift to the left
means an increase # of BANDS)
monocytes: show up 3-7 days later
lymphocytes: show up late, a week later
the exact nature and amount of exudate depends on...
the type/severity of the injury
local clinical manifestations - inflammation
redness: due to vasodilation & increased capillary permeability
heat: due to increased metabolism at the site
pain: due to change in pH, nerve stimulation by chemicals, and pressure from fluid
exudate
swelling: caused by shift of fluid/exudate formation
loss of function: due to all the above responses
systemic clinical manifestations - inflammation
increased WBC count
malaise, fatigue, tired
nausea & anorexia
, VS changes (increased pulse, increased RR)
Fever
fever considerations
often a good sign, body is doing what it needs to do
often wait till a fever of 100.5 to step in
elderly are not as quick to run a fever due to their blunted response so may intervene
quicker
acute inflammation
healing occurs in 2 to 3 weeks, usually leaving no residual damage
neutrophils are predominant cell type at this site of inflammation
chronic inflammation
may last for years
injurious agent persists or repeats injury to site (keeps coming back or never clears)
predominant cell types involved are lymphocytes and macrophages
has lasting effects
primary prevention (health promotion) - inflammation
prevention of injury
adequate nutrition
early recognition of inflammation
immediate treatment
proper storage and preparation of food
secondary prevention - inflammation
no specific screenings
diagnostics for early identification
CBC
CRP, ESR = non specific inflammatory markers
MRI, CT, PET scans
tertiary intervention - inflammation
observation
vital signs
fever management
fever management
moderate: up to 103, uncomfortable but should not harm healthy person
severe: greater than 104 causes delirium, altered mental status, seizures, brain damage
risk factors for inflammation
age (young and old)
immunocompromised
uninsured/underinsured (don't go in till its BAD)
nursing and inter-professional management
drug therapy - inflammation
aspirin: blocks prostaglandin synthesis
acetaminophen: blocks prostaglandin synthesis, has effect on hypothalamus, does not
thin blood
NSAIDs: inhibits prostaglandin synthesis, SE: GI irritation and bleeding
Corticosteroids: antipyretic, prevents chemical mediators from being excretes,
immunosuppressive, used in short spurts for acute situations
