Inflammation + Fever (CHP 9 + 14) Flashcards
Outline the process of inflammation. Differentiate between the vascular and cellular phases of inflammation. Describe the local and systemic effects of inflammation on the body. Discuss the phases of tissue resolution and repair.
__________ leakage of a fluid or drug from a blood vessel or tube into the surrounding tissue
extravasation
___________: A response involving cell orientation or cell movement that is either toward (positive) or away from (negative) a chemical stimulus.
chemotaxis
_________: The process by which certain cells engulf/ingest and consume foreign material, other cells and cell debris.
phagocytosis
_________ Producing or containing pus
Purulent
_______ Fluids, cells, or other substances that have been slowly exuded or have escaped from blood vessels and have been deposited in tissues or on tissue surfaces.
Exudate
__________ cells: continue to divide and replicate throughout life, replacing cells that are constantly destroyed
labile
_________ cells: normally stop dividing when growth ceases
stable
__________ cells: cannot undergo mitosis
permanent
_______: gape or burst open
dehisce
-itis
inflammation
what are the body’s 3 lines of defense?
skin
mucous membrane
inflammatory response
what is the skin’s main job? and it is the _______ defense
protect, largest
what are mucous membranes?
moist, inner lining of some organs and body cavities (cover the GI tract, any openings)
examples of mucous membranes
mouth, lungs, stomach
it is good to have an ____________ response
inflammatory
what are the main goals of an inflammatory response? (3)
eliminate the cause of the injury, remove damaged tissue, generate new tissue
what are cardinal signs?
local reaction to injury
what are the 5 cardinal signs?
Rubor/redness
Tumor/swelling
Calor/heat
Dolor/pain
Function laesa/loss of function
how are systemic signs caused? (Inflammation)
when chemical mediators (cytokines) from the local site enter the bloodstream and spread to the body
what is the main example of a systemic sign of inflammation?
fever
duration of acute inflammation
minutes to hours
________ host protective response of _____ tissues and their _____ to injury is critical for restoration of tissue _________
early
local
BV’s
homeostasis
what is acute inflammation caused by?
infections
immune reactions
blunt and penetrating trauma
physical or chemical agents
tissue necrosis
why is tissue necrosis caused by acute inflammation?
poor blood flow/O2 to tissues = death (diabetes)
what are the 2 components of acute inflammation?
vascular
cellular
what is the vascular component of acute inflammation (police cars)
leads to increased blood flow
what is the cellular component of acute inflammation (firetrucks)
migration of leukocytes
what is the duration of chronic inflammation
days to years
chronic inflammation is _____-__________, which means the
self-perpetuating
chronic inflammation has a greater chance of ________ due to proliferation of ____________
scarring
fibroblasts
what are fibroblasts
a type of cell that contributes to the formation of connective tissue, a fibrous cellular material that supports and connects other tissues or organs in the body
what is chronic inflammation caused by?
1. ________ or progressive ______ inflammatory process
2. _____-_____ smoldering responses that fail to evoke an _______ response (__________ , surgical sutures)
3._________mechanisms (autoimmune disorder)
- recurrent, acute
- low-grade, acute, asbestos
- immunologic
getting sick and not fully recovering before getting sick again, and a repeat of this cycle is an example of
recurrent acute inflammatory process
__________ cells are barriers/lining vessels and are semi-permeable
endothelial
bouncers
endothelial cells
what cells are the primary achievers of homeostasis?
platelets
what do platelets do
clot blood
if a lab draw reveals a high value of eosinophils it means that infection is due to _______/______
allergy/parasitic
what are basophils’ main job?
dilate BV’s (police escorts for firetrucks)
where do mast cells form?
at the site, once they are lodged
“overseer” cells
mast cells
what cells are the primary phagocytes?
neutrophils
“1st responders”
neutrophils
neutrophils: arrive ________, engulf and _______
early, remove
where are neutrophils generated from?
bone marrow
neutrophils have a ____ shelf life and are ________ in creation until the inflammation is gone
10
constantly
what cells clean debris (“janitor”)
macrophages
what cells are the “bridges” between removal and healing?
macrophages
if the labs show that neutrophils are high but all other lab values are normal, what does this mean?
inflammation is early on
with really big infections, the body has to send _______ which are ______ neutrophils to try and keep up
bands
immature
________ mature at the site to macrophages
monocytes
the vascular stage of inflammation is characterized by changes in the small ______ at the site of injury (tissue ________ / ______ sign)
BV’s
tissue
cardinal
the vascular stage of inflammation begins with MOMENTARY ________ followed RAPIDLY by __________ which allows for _______ capillary _________
vasoconstriction
vasodilation
increased
permeability
why do capillaries vasodilate?
so the “bouncers” et more blood in with nutrients/gas/etc
the vascular stage of inflammation involves ________ and _______ resulting in _________ capillary blood flow which is seen as ______ and ________ (cardinal symptoms)
arterioles
venules
increased
redness and heat
because vascular permeability is increased, there is an outpouring of protein-rich fluid (______) into the _____________ space which leads to _________, impaired _______, and ______
exudate
extracellular
swelling
function
pain
what are the chemical mediators for the vascular dilation phase of acute inflammation? (3)
histamine
prostaglandins
complement proteins (C3a, C5A)
what are the chemical mediators for the increased vascular permeability phase of acute inflammation? (3)
histamine
kinines
prostaglandins
what are the chemical mediators for the emigration of inflammatory cells phase of acute inflammation? (3)
C5a
leukotrienes
cationic proteins of neutrophils
what does the cellular phase of inflammation involve?
delivery of leukocytes (WBCs) to the site of injury
why are leukocytes helpful at sites of inflammation?
host defense via phagocytosis
what are the 3 stages of the cellular stage of inflammation?
margination
transmigration
chemotaxis
___________ is the movement of ________ to _____ to the periphery of BV’s wall
margination
phagocytes
adhere
_________ is when the phagocytes move out of the cells
transmigration
what is the first step of phagocytosis?
recognition of bacteria/debris and adherence (binding) of phagocytes to debris
what is the second step of phagocytosis?
engulfment/ingestion of the bacteria/debris
what is the third step of phagocytosis?
creation of a phagosome (bacteria/debris is completely eliminated from the source)
what is the fourth step of phagocytosis?
fusion with a lysosome that kills what is inside
what is the fifth step of phagocytosis?
creation of a phagolysosome which is walled up and exited out of the body
what are the walls made of in the fifth step of phagocytosis?
fibrin wall/barrier formation
summary of inflammation:
1. ___________ increases blood flow to injured tissue
2. increased vascular ______________ (edema at the site and _____ shifts)
3. ____ migration to site for healing purposes
4. ________ aggregation (clot formation to stop _____)
5. stimulation of _____ endings at the site (pain)
- vasodilation
- permeability, fluid
- WBC
- platelet, bleeding
- nerve
acute inflammation has two kinds of “_____“-derived mediators, what are they?
plasma
cell
acute inflammation: CELL-derived mediators have two types:
performed mediators
newly synthesized
acute inflammation: PLASMA-derived mediators have three types:
acute-phase proteins
factor XII activation
complement proteins
performed mediators (a kind of ____-derived mediator) have 3 types
cell
mast cells
platelets
neutrophils/macrophages
newly synthesized (a kind of ____-derived mediator) have 3 types
leukocytes
leukocytes/macrophages
macrophages/lymphocytes/endothelial cells
local manifestations of acute inflammation
cardinal symptoms (5)
exudate
drainage that is normal/expected
watery, from plasma (due to increased permeability)
serous exudate
bloody, severe vascular injury
hemorrhagic exudate
thick/smelly/sticky/meshwork, due to a large amount of fibrinogen (part of the fibrin wall - scar formation)
fibrinous exudate
develop on mucous membranes, necrotic cells
membranous exudate
pus, dead WBCs, proteins, and tissue debris from the injury site
purulent exudate
popped blister
serous exudate
systemic manifestations of inflammation (7)
fever
leukocytosis
lymphadenitis
anorexia
somnolence
malaise
shock
during a fever, the body gets a new set point from the _______, low -grade fevers are good because they naturally kill the infection
hypothalamus
4 subtypes of leukocytosis
neutrophilia
eosinophilia
neutropenia & lymphocytosis
increase in neutrophils = ______
means ______ Infection
neutropenia
bacterial
sign of parasitic & allergic responses
eosinophilia
________ = decrease in neutrophils
_________ = increase in lymphocytes
signals a _______ infection
neutropenia
lymphocytosis
viral
the reaction of lymph nodes that drain the affected area, painfully palpable nodes = inflammatory
lymphadenitis
SIRS meaning
systemic inflammatory response syndrome
shock:
1. generalized __________ ( BP drops)
2. __________ vascular permeability
3. intravascular fluid _____
4. myocardial ________
5. _____________ shock
- vasodilation
- increased
- loss
- depression
- circulatory
this protein is normally not present (0-3 mg/dL), but ________ acute inflammation or tissue ___________
CRP (C-reactive protein)
increases
destruction
CRP and ESR are elevated with ________ and help determine ________, but not _______
SIRS
severity
location
_________ sedimentation rate (ESR) is less ________ and __________ with inflammation
erythrocyte
specific
elevates
FEVER:
1. release of fever producing _______ from _______ cells
2. reset thermostatic point in __________
3. body responses: (4) –> fever
4. body reaches new _____ ______
5. temperature reducing response: (3)
- cytokines and inflammatory
- hypothalamus
- vasoconstriction, shivering, piloerection, increased metabolism
- set point
- vasodilation, sweating, increased ventilation
tissue _________: repair of the injured tissue with cells of the same type
regeneration
the 2 “R’s” of tissue repair
regeneration and replacement
tissue _________ (_______ injury): replacement of cells with CT (involves granulation tissue and formation of ______ tissue)
replacement
severe
scar
__________ tissues: contain the functioning cells of an organ or body part
parenchymal
_______ tissues: consist of the supporting CT, BVs, nerve fibers, ECM
stromal
bridge = ______ tissues
support beams = ______ tissues
parenchymal
stromal
what is the primary objective of wound healing?
fil the gap created by tissue destruction and to restore the structural continuity of the injured part
repair by ________ formation: fills the gap created by tissue ______, but does not repair the structure with functioning ________ cells - different cell types (weaker)
scar
death
parenchymal
heals outside in
primary intention
primary is _____ than secondary wound healing
faster
primary wound healing leads to minimal ______ because the _____ cells and tissues are used
scarring
same
example of _______ healing: sutured incision
primary
example of _______ healing: larger wound healing and burns
secondary
heals from the inside out
secondary
greater loss of tissue
secondary
barriers to wound healing: (3)
insufficient inflammatory response
poor nutrition (vitamins, minerals, protein)
poor blood flow and lack of O2 (diabetes)
3 phases of wound healing
inflammatory
proliferative
contraction and remodeling
primary healing may end up being secondary if there is _________ or contamination
infection
__________ phase: begins at time of injury with formation of blood ____
inflammatory
clot
__________ phase: migration of _____ into wound site
inflammatory
WBCs
__________ phase: __________ are first responders, they ingest and remove bacteria and cellular _____, then ___________ arrive
inflammatory
neutrophils
debris
macrophages
_________ phase: the focus is on building new tissue to fill wound space
proliferative
_________ phase: 1. growth of new BVs 2. formation of new surface layer at the wound ________, previously destroyed by the wound, via _____________
proliferative
edges
epithelization
_________ phase: key cell __________ for healing and growth
proliferative
fibroblast
___________ phase: begins approximately 3 weeks after injury and continues for ___ months
contraction and remodeling
6
___________ phase: development of fibrous scar
contraction and remodeling
__________ phase: decrease in vascularity and continued remodeling of scar tissue
contraction and remodeling
scar is capable of _______ tensile strength, which makes it ___ visible
increasing
less
scar tissue is ALWAYS ________ than normal tissue ex) C-section no more vaginal births
weaker
factors that affect wound healing (6)
