Inflammation Flashcards
what is inflammation
a local response of vascular tissue to cell injury/death
3 aims of inflammation
- prevent spread (localize injurious agent)
- removes agent, damaged cells, debris
- assist with healing
whenever inflammation occurs there is always
tissue damage
the suffix for inflammation is
-itis
clinical/cardinal signs of inflammation
- erythema
- swelling
- warmth
- pain
- loss of fx
what are the 2 responses of acute inflammation
- vascular
- cellular
what are the 3 main stages of the vascular response of acute inflammation
- vasoconstriction
- vasodilation
- increased permeability
during acute inflammation, vasoconstriction is what kind of response
a neuro response
during acute inflammation, what is the purpose of vasoconstriction
- minimize blood loss and reduce flow in order for a clot to form
during acute inflammation, why is the vasoconstriction phase so short
because resources and nutrients for healing must reach the site
during acute inflammation, injury activates what
plasma and inflammation cell mediators
what are 2 examples of inflammation cell mediators
histamines and prostaglandin
during acute inflammation, inflammation cell mediators trigger what
vasodilation and increased permeability of blood vessels
during acute inflammation, what does vasodilation cause
increased blood flow to the area (hyperemia)
during acute inflammation, why does exudate form in the tissue
due to increased permeability of the blood vessels
during acute inflammation, what is the fluid shift
when fluid (exudate) moves out of the blood vessels and into the tissue
during acute inflammation, what does the fluid shift cause
swelling, and therefore pain and loss of function
during acute inflammation, histamine causes what 2 processes
- vasodilation
- permeability
during acute inflammation, prostaglandin causes what 3 processes
- vasodilation
- permeability
- pain
during vasodilation what do erythrocytes do
they stack in the rouleau formation
what are 2 manifestations of hyperemia
- erythema
- warmth
what is diapedesis
when cells move out of the blood vessels with fluid from the blood (exudate)
what are the 3 stages of the cellular response of acute inflammation
- chemotaxis
- margination
- diapedesis
what is chemotaxis (inflammation)
mediators attract neutrophils and other leukocytes to the site of injury
explain what happens during margination (inflammation)
selectins (adhesion molecules) help neutrophils to attach to the endothelium
explain what happens during the diapedesis (transmigration) phase of inflammation
cells enter the interstitial space which allows for phagocytosis of microbes and debris
what 3 processes occur during chronic inflammation
- angiogenesis
- fibrosis
- necrosis
what are the 5 types of exudate
- serous
- purulent (suppurative)
- hemorrhagic
- membranous
- fibrinous
what are the main components of serous exudate? what does it indicate?
mostly fluid (serum), few proteins and cells. indicates mild injury
what are the main components of purulent (suppurative) exudate? what does it look like? what does it indicate?
pus = necrotic debris, WBC, proteins
cloudy, thick, foul smell
more severe injury, likely bacterial infection
what does hemorrhagic exudate contain? what does it indicate?
RBC’s due to severed vessels
indicates severe injury
what does membranous exudate contain? what does it look like?
necrotic cells in fibropurulent exudate
appears membranous due to fibers
what does fibrinous exudate contain? what does it look like?
fibrogen
appears like sticky, mesh
what 3 things do all exudates contain in varying amounts
- fluid
- cells
- protein
what are some symptoms of systemic manifestations
malaise, headache, fatigue, fever
is fever a deliberate process
no
what is the temperature set point of the body
hypothalamus
what are 3 things fever does
- increases rate of cellular repair
- decreases growth/reproduction of pathogens
- enhances phagocytosis and immune response
what are pyrogens
fever causing chemicals
exogenous pyrogens are released by
bacteria
endogenous pyrogens are released by
defense cells
explain the process of triggering a fever
- bacteria release exogenous pyrogens
- exo. pyrogens trigger endogenous pyrogens
- endo. pyrogens cause synthesis of PGE2
- PGE2 binds to the hypothalamic receptor
- this binding triggers the temperature set point to adjust via cAMP
what is PGE2
prostaglandin type E2
what are serum markers
markers that are present in the serum and are specific for certain diseases
what is CRP and what does it indicate
C- reactive protein - a serum marker
inflammation
what does CRP help with
aids complement with defense
is CRP a specific or non specific marker of inflammation
non specific
should we treat inflammation?
only if it is causing pain
inflammation is beneficial for healing
what is the process for treating inflammation
- apply cold
- elevate
- apply pressure
- later apply heat
what does applying cold to inflammation do
decreases vasodilation which decreases swelling
why does elevation help treat inflammation
blood must work against gravity
therefore decreases hyperemia and blood flow - decreases swelling
what does applying pressure to inflammation do?
opposes the formation of exudate (in interstitial fluid)
decreases blood flow
what does applying heat to inflammation do
increases phagocytosis and the immune response
what do NSAIDS act on
decrease prostaglandin synthesis which decreases pain
why are steroidal anti-inflammatory drug useful
they are very efficient
steroidal anti-inflammatory drugs cause what
very pressing side effects
what do steoidal anti-inflammatory drugs act on
- decrease permeability (decrease exudate formation)
- decrease mediator release (inflm relies of mediators)
- inhibit leukocyte and mast cell activity at the site
