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55 terms

Pathophysiology Test 1 Chapter 3

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state the purposes of inflammation
inflammation is an automatic response to cell injury that
neutralizes harmful agents
removes dead tissue
damaged cells release inflammatory mediators
these compounds stimulate inflammation
what are the cells of inflammation
endothelial cells that line blood vessels, circulating platelets and leukocytes, connective tissue cells (mast cells, fibroblasts, tissue macrophages), and components of the extracellular matrix. The principal leukocytes in acute inflammation are neutrophils, whereas macrophages, lymphocytes and plasma cells, eosinophils, and mast cells predominate in chronic inflammation.
endothelial cells role in inflammation
provide a selective permeability barier to exogenous (microbial) and endogenous inflammatory stimuli; regulate leukocyte extravasation by expression of adhesion molecules and receptors; contribute to the regulation and modulation of immune responses through synthesis and release of inflammatory mediators; and regulate immune cell proliferation through secretion of hematopoietic colony-stimulating factors (CSFs).
platelets role in inflammation
release a number of potent inflammatory mediators, thereby increasing vascular permeability and altering the chemotactic, adhesive, and proteolytic properties of the endothelial cells
leukocytes (white blood cells)
major cellular components of the inflammatory response
include the granulocytes (neutrophils, eosinophils, basophils, mast cells) and the agranulocytes (monocytes/macrophages and lymphocytes)
neutrophils
first cells to appear at the site of acute inflammation usually arrivine withing 90 minutes of injury
eosinophils
have a longer life span that neutrophils therefore play a role in chronic inflammation
interact with basophils and are prominent in allergic reactions such as hay fever and bronchial asthma
basophils and mast cells
basophils are most prominent in allergic reactions mediated by immunoglobulin E (IgE)
basophils are precursors of mast cells
mast cells derive from the same hematopoietic stem cells as basophils but do not develop until they leave the circulation and lodge in the tissue sites
monocyte/macrophages
monocyte/macrophages produce potent vasoactive mediator including prostaglandins and leukotrines, platelet-activating factor (PAF), inflammatory cytokines, and growth factors that promote regeneration of tissues.
capable of phagocytosis and are active in bacterial killing
-help clean up
lymphocytes and plasma cells
participate in immune-mediated inflammation caused by infectious agents as well as non-immune-mediated inflammation associated with cell injury and death
state the five cardinal signs of acute inflammation, and describe the physiologic mechanisms involved in the production of these signs
rubor (redness)
tumor (swelling)
calor (heat)
dolor (pain)
functio laesa (loss of function)
acute inflammation has two stages
the vascular stage and the cellular stage
vascular stage
characterized by increased blood flow (vasodilation) and structural changes (increased vascular permeability) that allow plasma proteins to leave the circulation
-prostaglandins and leukotrines affect blood vessels
-arterioles and venules diolate: increasing blood flow to injured area, congestion in vascular beds, redness and warmth result
-capillaries become more permeable: allowing exudate to escape into the tissues, swelling and pain result
cellular stage
involves the emigration of leukocytes (mainly neutrophils) from the microcirculation and their accumulation at the site of injury or infection
-white blood cells enter the injured tissue :
destroying infective organisms
removing damaged cells
releasing more inflammatory mediators to control further inflammation and healing
what mechanisms causes the redness (erythema) associated with the inflammatory process
prostaglandins and leukotrines cause vasodilation, which brings more blood to the injured/affected area. The symptoms caused by this vasodilation are redness/erythema and warmth
acute inflammation
the early (almost immediate) reaction of local tissues and their blood vessels to injury
it typically occuurs before the adaptive immune response becomes established and is aimed primarily at removing the injurious agent and limiting the extent of tissue damage
chronic inflammation
in contrast to acute inflammation, which is usually self limited and of short duration, chronic inflammation is self perpetuating and may last for weeks, months, or even years
instead of the vascular changes, edema, and predominantly neutrophilic infiltration seen in acute inflammation, chronic inflammation is characterized by infiltration with mononuclear cells (macrophages, lymphocytes, and plasma cells) and attempted connective tissue repair involving new vessel formation (angiogenesis) and fibrosis
-macrophages accumulate in the damaged area and keep releasing inflammatory response
-nonspecific chronic inflammation: fibroblasts proliferate, scar tissue forms
-granulomatous inflammation: macrophages mass together around foreign bodies, connective tissue surrounds and isolates the mass
angiogenesis
new vessel formation growth of new capillary blood vessels
inflammatory mediators
may be derived from the plasma or may be produced locally by cells at the site of inflammation
list four types of inflammatory mediators
plasma is the source of four major mediators of inflammation, including kinins, products of the coagulation/fibrinolysis system, proteins of the complement system, and c reactive protein
function of kinins
one kinin, bradykinin, causes increased capillary permeability and pain
function of coagulation
the clotting system contributes to the vascular phase of inflammation mainly through fibrin products formed during the final steps of the clotting process
function of the complement system
consists of a cascade of plasma proteins that plays an important role in both immunity and inflammation
complement proteins contribute to the inflammatory response by 1. causing vasodilation and increasing vascular permeability 2. promoting leukocyte activation, adhesion, and chemotaxis and 3. augmenting phagocytosis
the acute inflammatory response involves the production of
exudates
name the five types of inflammatory exudates
serous, hemorrhagic, fibrinous, membranous, purulent
serous
protein rich fluid
watery fluids low in protein content that result from plasma entering the inflammatory site
hemorrhagic
occur when there is sever injury that causes damage to blood vessels or when there is significant leakage of red cells from the capillaries
hemorrhagic inflammation is serious business. Some of the most pathogenic agents cause hemorrhagic inflammation. Think Ebola. The holes in the blood vessels are big enough to let even the erythrocytes out. Prognosis may be guarded
fibrinous
contain large amounts of fibrinogen and form a thick and sticky meshwork, much like the fibers of a blood clot
membranous or pseudomembranous
develop on mucous membrane surfaces, and are composed of necrotic cells enmeshed in a fibropurulent exudate
purulent
pus- plasma with both active and dead neutrophils, fibrinogen, and necrtoic parenchymal cells
composed of degraded white blood cells , proteins, and tissue debris
ex. abscess
leukocytes function
leukocytes enter the injured area
leukocytes express adhesive proteins
attach to the blood vessel lining
squeeze between the cells
follow the inflammatory mediators to the injured area
leukocytes release many inflammatory mediators at the injured area such as:
histamine and serotonin
platelet- activating factor
cytokines
-colony stimulating factors
-interleukins
-interferons
-tumor necrosis facor
nitric oxide
cytokines
hormone-like, low molecular weight proteins produced by many cell types (principally activated macrophages and lymphocytes, but also endothelium, epithelium, and connective tissue types) that modulate the function of other responses, although well known for their role in immune responses, these proteins also play important roles in both acute and chronic inflammation
define the systemic manifestations of inflammation
the most prominent systemic manifestations (what it does to the body) of inflammation include the acute phase response, alterations in white blood cell count (leukocytosis or leukopenia), and fever.
shift to the left
WBC count is normal value of 4,000
increases to 10,000, 15k, 20k in acute inflammatory conditions
normal life span of neutrophil is 10 hours, constantly replaced to be adequate
excessive demand for phagocytes, immature forms of neutrophils (bands) are released from bone marrow
"shift to the left" indicates increase in bands in severe infection
which leukocytes participate in the acute inflammatory
eosinophils
monocytes
neutrophils
all of the above
all of the above- granulocytes and monocytes play a role in the acute phase of the immune response. Eosinophil and neutrophils are granulocytes, so all of the leukocytes listed participate
Eosinophils tend to be associated with higher in allergic response but are not exclusive
what happens in the acute phase response
leukocytes release interleukins and tumor necrosis factor which:
-affect thermoregulatory center = fever
-affect central nervous system = fever
-skeletal muscle breakdown
Liver makes fibrinogen and C-reactive protein
-facilitate clotting
-bind to pathogens
-moderate inflammatory responses
white blood cell response
inflammatory mediators cause WBC production
WBC count rises
immature neutrophils (bands) released into blood
fever
it is caused by a cytokine-induced upward displacement of the set point of the hypothalamic thermoregulatory center
define core temperature
the temperature in the deep tissues of the body
describe the mechanisms of heat production
metabolism is the bodys main source of heat production.
fine involuntary actions such as shivering and chattering of the teeth can produce a threefold to fivefold increase in body temp.
physical exertion also increases body temperature
how is heat lost throughout the body
conduction, radiation, convection,and evaporation
conduction and heat loss
conduction involves the direct transfer of heat from one molecule to the other
blood carries or conducts heat from the inner core of the body to the skin surface
normally, only a small amount of body heat is lost through conduction to a cooler surface
convection and heat loss
convection refers to heat transfer through the circulation of air currents
normally, a layer of warm air tends to remain near the bodys surface; convection causes continual removal of the warm layer and replacement with air from the surrounding environment
the wind chill factor that often is included in the weather report combines the effect of convention caused by wind with the still air temperature
radiation and heat loss
radiation involves the transfer of heat through the air or a vacuum
heat loss through radiation varies with the temperature of the environment
environmental temp must be less than that of the body for heat loss to occur about 60% of the bodys heat loss occurs through radiation
evaporation and heat loss
evaporation involves the use of body heat to convert water on the skin to water vapor
evaporative heat losses involve both insensible perspiration and sweating
causes of fever
fever can be caused by a number of microorganisms and substances that are collectively called pyrogens.
fever is a nonspecific response that is mediated by endogenous pyrogens released from host cells in response to infectious or noninfectious disorders.
how is fever resolved
fever is resolved when the condition causing the increase in the set point of the thermostatic center in the hypothalamus is resolved
describe the four stages of fever
prodrome- a chill, during which the temperature rises; a flush; as temp increases, minor complaints such as mild headache, fatigue
second stage- chilled, shivering, shaking, uncomfortable skin is pale
flush- cutaneous vasodilation occurs and the skin becomes warm and reddened to cool body
sweating- could be absent
fever manifestations
anorexia, myalgia (pain in muscles), arthalgia (pain in joints), fatigue, often headache
define neurogenic fever
absolute reset of temp in hypothalamus
traumatic brain injury
a long term elevation of body temperature due to a disruption of the normal body temperature set point as a result of damage to the hypothalamus
explain what is meant by intermittent, remittent, sustained, and relapsing fevers
intermittent fever- one in which temp returns to normal at least once every 24 hours usually associated with conditions such as gram-negative/gram-positive sepsis, abscesses, and acute baterial endocarditis
remittent- the temp does not return to normal and varies a few degrees on either direction it is associated with viral upper respiratory tract and mycoplasma infections
sustained- temp remains above normal with minimal variations seen in persons with drug fever
relapsing- one in which there is one or more episodes of fever, each as long as several days, with one or more days of normal temperature between episodes may be caused by a variety of infectious diseases including tuberculosis, fungal infections, lyme disease, malaria
body temperature is controlled through negative feedback loops
true or false
true- when the body senses a change out of the norm it activates mechanisms that oppose that change (vasodilation and sweating with increased temperatures; vasoconstriction and shivering with decreased temperatures) this is known as negative feedback. positive feedback on the other hand senses a change but activates a mechanism that exaggerates the change.
discuss the clinical guidelines specific for children 0 to 36 months of age in regards to the treatment of fever
younger children have decreased immunological function and are more commonly infected with virulent organisms. the guidelines define fever in this age group as a rectal temperature of at least 38 C (100.4 F)
fever in elderly
slight elevations may indicate serious infection or disease
tend to have a lower baseline temperature bc of the percieved lack of a significant fever
unexplained changes in functional capacity, decreased mental status, weakness, and weight loss may be only signs of infection
probably due to blunted fever response in the thermoregulatory center