227 terms

Inflammation & Inflammatory Response, Immune system, UCD

Chap 3 Porth, Immune system, UCD
1. an automatic response to cell injury that: nuetralizes harmful agents & removes dead tissues
2. characterized by elaboration of inflammatory mediators & movement of fluid & leukocyes from vascular system into extravascular tissues
3. An irritation of a tissue caused by infection or injury.
refers to inflammation
Classic physical responses of inflammation
redness, swelling, heat, pain or discomfort & loss of funciton
Manifestations of acute inflammatory response
Immediate vascular changes (vasodilation & increased capillary permeability, influx of inflammatory cells such as neutrophils, & sometimes widespread effects of inflammatory mediators which produce fever & other systemic signs & symptoms
Manifestations of chronic inflammatory response
Due to infiltration with macrophages, lymphocytes, & fibroblasts, leading to persistent inflammation, fibroblast proliferation & scar formation.
Acute inflammation
adaptive response triggered by noxious stimuli & conditions such as infection & tissue injury, short duration, few minutes to several days
chronic inflammation
long duration ,days to years, associated with proliferation of bloodvessel tissue necrosis & fibrosis (scarring)
endolithial cells:
line epithelial lining of bloods vessels, produce antiplatelet & antithrombotic agents, vasodilators & vasoconstictors
small membrane bound disks, inflammatory mediators
leukocytes/white blood cells
major cellular component of inflammatory response
neutrophils, eosinophils, & basophils - specific cytoplasmic granules & multilobed nucleus
moncyrtes, macrophages & lymphocytes - lack cytoplasmic granules Have single nucleus
1) principal leukocytes in acute inflammation
early responders
2) phagocytic, predominate in early inflammatory responses
3) polymorphonuclear
4) Increase in acute infections
5) Ingest bacteria, dead cells & cellular debris
6) short lived & become a componenet of the purulent exudate
Granular WBC - Weak phagocytes, vascular mediator
1) Protection from infections caused by parasites - Bind on IgE (helminths)
2) Involved in allergic reactions
3) slower reaction (2-3 hrs P/Neutrophils) 2-3% circulation
4) interact w/basophils, long life span, chronic inflammation
1) granulocyte that has 2 lobes
2) nonphagocytic
3) releases histamine, prostaglandins, serotonin & leukotrienes; vasoactive mediators
4) associated with allergic responses
5) precurser of mast cell
6) mediated by IgE
Mast cells
1) derived from same stem cells as basophils, but only activated when lodged in tissue sites;
2) release histamine, cytokines, chemotactic facotrs, leukotrienes, prostaglandins when activated
Agranulocytic: a relatively large phagocytic white blood cell that circulates in the bloodstream and has a single ovoid nucleus. once these cells migrate into the tissues from the blood, they become macrophages:
produced in bone marrow
Develop from monocytes, a type of white blood cell.
1) Either fixed or wandering, Irregular shape with short branching projections.
2) Capable of engulfing bacteria and cellular debris.
3) contibute to initiation of healing process
4) typically arrive at the inflammatory site 24 hours or later after neutrophils
A class of white blood cells that consist of small and large lymphocytes. The small lymphocytes bear variable cell-surface receptors for antigen and are responsible for adaptive immune responses. B cells, T cells, NK cells (large granular), of innate immunity
Plasma cells
Devleop from Activated B lymphocytrs & produce antibodies against persistent antigens in inflammatory site
Adhesive molecules- (L-selectin on lymphocytes, P selectin and E selectin on endothelial cells)
Adhesive proteins
E-selectin, L-selectin, P-selectin
30 structurally simiar poteins that promote cell-to-cell & cell-to-extracellular matrix inteactions built into the plasma membrane that interconnects the extracellular matrix and the cytoskeleton.
adhesion molecules
Proteins located on the cell surface involved with the binding with other cells or with the extracellular matrix (ECM).
Acute inflammation triggers
Infections, immune reactions, mechanical , chemical agents, trauma, chemical, tissue necrosis from any cause
LAD I and II, Leukocyte Adhesion deficiency
Inability of cell to control adhesion of selectins w/immune system
Contibute to pathogenesis of RA (excessive expression of cell adhesion)
functio laesa
loss of function
acute phase response elicits:
cardinal signs of inflammation: rubor, tumor, calor, dolor, functio laesa as well as fever, anorexia, hypertension, increased heart rate, corticoid steroid and ACTH release occur during this phase.
vascular stage of acute inflammation
increased blood flow: vasodilation
structural change of acute inflammation
increased vascular permeability: plasma proteins leave circulation
cellular stage of acute inflammation
emigration of leukocytes from microcirculation & accumulation at injury site
First line of defense: Immune system
Innate/natural immunity - responds early & rapidly; very effective
2nd line of defense: Immune system
Inflammation (immunity) - functions immediately as an effective barrier to microbes
3rd line of defense
adaptive/acquired immunity -resonds less rapidly, but more effectively. Use of lymphocytes, antibodies
physical & mechanical barriers:
The skin, linings of GI, Genitourinary & respiratory tracts:
Act by:
Sloughing off of cells
coughing & sneezing
mucus & cells
Biomechanical barriers
Synthesized & secreted saliva, tears, ear wax, sweat & mucus
anitmicrobial peptides
normal bacterial flora
Inflammatroy response: 2nd line of defense triggers
Caused by a variety of materials:
Infection, mechanical damage, ischemia, nutrient deprivation, temperature,extremes, radiation, etc.
Local manifestations
Inflammatory mediators
Compounds which stimulate inflammation
1) first mediator of inflammation,
2) released from mast cells & damaged tissue.
3) Causes vasodilation & increased capillary permeability
Inflammatory agents
histamine, prostaglandins, leukotrienes
Plasma protein systems
Complement system
Coagulation System
Kinin system
Inactive enzyme
MAC (membrane attack complex) complement actions
Cell lysis, including bacterial & altered blood cells
C3a, C5a, complement actions
activates basophils & mast cells, vascular permeability, release of inflammatoroy mediators that produce smooth muscle contraction, changes in endothelial cells to enhance migration of phagocytes
C3a complement actions
anaphylatoxin bronchospasm, mast cell degranulation
opsonization- coating of particles (microbes) for more efficient recognition by phagocytes
35b67 complement actions
Chemotaxis (complement actions)
C5a complement actions
Neutrophil activation
Coagulation clotting systems
Forms a fibrinous meshwork at an injured or inflamed site:
1) prevent spread of infection
2) keeps microorganisms & foreign bodies at site of greatest inflammatory cell activity
3) forms a clot tht stops bleeding
4) provides a framework for repair & healing
main substance in an insoluble protein
Kinin system
1) functions to activate & assist inflammatory cells
2) primary kinin is bradykinin
3) causes:
a. dilation of blood vessels
b. pain
c. smooth muscle contraction
d. vascular permeability
e. leukocyte chemotaxis
Classic Manifestations of Inflammation:
Local: pain, swelling, warmth, redness, LOF
Systemic: fever, leukocytosis, malaise
Vascular stage:
Prostaglandins & leukotrienes affect blood vessels
arterioles & venules dilate
increase blood flow to injured area
redness & warmth result
capillaries become more permeable
allows exudate to escape into tissues
swelling & pain result
What mechanism causes the redness associated with the inflammatory process?
Prostaglandins & leukotrienes cause vasodilation, which brings more blood to the injured/affected area as well as redness/erythema & warmth.
watery fluids, low in protein, early inflammation
red blood cells present due to damage to capillary beds & blood vessels, indicates bleeding
fibrinogen, thick & sticky meshwork, clotted exudate, indicates more advanced inflammation
on mucous membrane, necrotic cells on fibropurulent exudate
pus, WBC's, proteins & tissue debris, indicates a bacterial infection
pus forming
localized area of inflammation containing purulent exudate
site where epithelial surface (skin or GI) becomes necrotic & eroded
Cellular stage:
WBC enters injured tissue:
destroys infective organisms
remves damaged cells
releases more inflammatory mediators to control further inflammation & healing
Duties of leukkocytes:
1) enter injured area
2) express adhesive proteins
3) attach to blood vessel lining
4) squeeze between the cells
5) follow inflammatory mediators to injured area
6) release many inflammatory mediators @ injured area
Leuckocytes release these inflammatory mediators @ injured area:
Histamine & seratonin
platelet activating factor
cytokines: colony stimulating factors; interleukins (IL), interferons, tumor necrosis factor (TNF)
Nitric Oxide (NO)
Which leukocytes participate in the acute inflammatory response?
a. eosinophils
b. monocytes
c. neutrophils
d. all of the aobve
e. a & c
e. a & c
Granulocytes & monocytes play a role in the acute phase of the immune reponse. Eosinophils & neutrophils are granuloctes, so all of the leukocytes listed participate.
Other inflammatory mediators:
coagulation & fibrinolysis proteins
complement system
C-reactive protein
Leukocytes release interleukins & tumor necrosis factor during the acute phase response which
affects thermoregulatory center - fever
affects CNS - lethargy
causes skeletal muscle breakdown
During the acute phase response, the liver makes fibrinogen & C-reactive protein which:
facilitate clotting
bind to pathogens
moderate inflammatory responses
Fever during the systemic manifestations of inflammation, is:
caused by exogenous & endogenous pyrogens
act directly on the hypothalmus
An increased number of circulating leukocytes
Systemic manifestations of Inflammation:
Increased plasma protein synthesis (C-reactive, fibrinogen, haptoglobin, amyloid, ceruloplasmin)
Acute phase reactants synthesised during inflammation
C-reactive protein, fibrinogen, haptoglobin, amyloid, ceruloplasmin, etc.
Body temperature is controlled through negative feedback loops. T/F
True, when body senses a change out of the norm, it activates mechanisms that oppose that change (vasodilation & sweating with increased temperatures; vasoconstriction & shivering with decreased temperatures. This is known as negative feedback.
Vasodilation & sweating occur
with increased body temperatures/fevers
Vasoconstriction & shivering occur
with decreased body temperatures
White blood cell response to inflammation
Inflammatory mediators cause WBC production
WBC count rises
Immature neutrophils released into blood
During chronic inflammtion, macrophages:
Accumulate in the damaged area & keep releasing inflammatory mediators
With non specific chronic inflammation:
fibroblasts proliferate
scar tissue forms
During Granulomatous inflammation:
Macrophages mass together around foreign bodies
Connective tissue surronds & isolates the mass
Chronic inflammation of 2 wks or longer
is often related to an unsuccessful acute inflammatory response
Characteristics of chronic inflammation include:
dense infiltration of lymphocytes & macrophages
granuloma formation
epithelioid cell formation
giant cell formation
Ulcerative colitis:
involves the colon & rectum & only the mucosal layer is affected.
The hallmark sign & symptom of Ulcerative Colitis is:
Bloody diarrhea & lower abdominal cramps
There is an increased risk of cancer after
8-10 years of ulcerative colitis disease
Assessment of ulcerative colitis disease:
Number of stools/day
sed rate
albumin level
Plasma protein that maintains the proper amount of water in blood
Crohn Disease signs & symptoms
Intermittent bouts of fever, diarrhea, & RLQ pain
may have RLQ mass, tenderness
Can affect any portion of GI tract
To DX Crohn disease
Uper GI series with small bowel follow thru plus either colonoscopy or barium enema
Treatment for crohn disease
stop smoking, drugs similar to UC
Crohn disease can be found:
any portion of GI tract
30% small bowel
50% small & large bowel
15-20% large bowel
Treatments of IBD (Inflammatory Bowel Disease)
Acute pancreatitis leads to
Deep abdominal pain
digestion of elastic tissue
inactivation of surfactant in the lung which can cause pulmonary edema & the development of acute respiratory distress syndrome
Glucose intolerance
Symtpoms of acute pancreatitis
GI bleeding & ulcers
Treatment for acute pancreatitis includes:
fluids & electrolytes
collid treatments for shock
demerol for pain
nasogastric suctionto rest digestive system
vasoconstrictor drugs if shock
Acute Pancreatitis is defined as:
acute autodigestion of the pancreas
40-60% are associated with ETOH abuse, gallstones & other billary diseases
Also associated with trauma to abdomen, hyperlipidemia & certain types of drugs
Activation of enzymes in acute pancreatitis:
Serum amylase is one of first to increase
serum trypsin
serum phoshoipase A
serum elastase
Tissue Repair is stimulated by
growth factors stimulate local cells to divide
Tissue organization is
controlled by the extra cellular matirx
Tissue regeneration
Injured tissue is replaced by the same kind of cells
fibrous tissue repair:
injured tissue is replaced by connective tissue
Granulation tissue leads to
scar tissue
immune resonse
The collective, coordinated response of the cells & molecules
elicit adaptive immune repsonses - memory of the substance is developed so repeat exposure to same microbe produces quicker & more vigorous response
Humoral immunity
mediated by antibodies which are produced by B lymphocytes
Cell mediated immunity
defends against intracellular microbes, such as viruses, provided by T lymphocytes.
Cellular elements of the blood: RBC's WBC's, platelets
derived from hematopoietic stem cells in bone marrow
Myeloid progenitor is precurser to:
monocytes/macrophages, granulocytes & dendritic cells of innate immune system which are produced in bone marrow.
Phagocytic cells
monoctyes/macrophages, granulocytes, dendritic cells
dendritic cells
cell with long fingerlike processes
Lymhoid progenitor in the bone marrow is precurser to:
lymphocytes (B&T) & natural killer cells.
naive lymphocyte
mature B or T lymhocyte that has not previously encountered antigen or is not progeny of antigen-stimulated mature lymphocyte
B lymphocytes
cells capable of producing antibodies, mediate humoralimmunity
T lymphocytes
Cell-mediated immunity; antigen receptors recognize peptide fragments of proteing antigens
Helper T cells
Help B lymphocytes produce antibodies & help phagocytic cells destroy ingested pathogens
cytotoxic T cells
kill or lyse intracellular microbes
CD proteins
Cluster of differentation, numerical, defines particular cell type or staged of cell differentiation & are recognized by cluster/group of antibodies
CD4 Helper cells
measures progressionof HIV infection
Natural Killer Cells NK
recognize & kill tumor cells, abnormal body cells & cells infected with intracellular pathogens (viruses & intracellular bacteria)
Central Lymphoid organs
bone marrow & thymus provide environment for immune cell production & maturation
Peripheral Lymphoid Organs
lymph nodes, spleen, tonsils, appendix, Peyer patches of intestine, mucosa associated lymphoid tissues in respiratory, GI tract, & reproduction systems
Lymph channels, blood vessels & capillaries
Immune cells circulate through these various tissues & organs to seek out and destroy foreign material.
Thymus, fully functional @ birth
generates mature immunocometent T lymphocytes which express appropriate receptors
Thymic selection
abiltiy of T cells to recognize foreign antigens & distinguish self from non self; process of maturation
B cell maturation
occurs in bone marrow; here cells multiply, mature & acquire immunoglobulin (Ig) signalining molecules & cell markers that distinguish self from nonself
fluid which drains from the epithelia, connective tissues, & most parenchymal organs
T lymphocytes, B lymhocytes
_____are more abundant in paracortex of lymph node; ____ are more abundant in follicles & germinal centers located in outer cortex of lymh node.
specialized areas of lymph node
outer cortex
inner medulla
secondary lymphoid organ
filters antigens from blood
comprised of red and white pulp
red pulp
well supplied with arteries & area where senescent & injured RBC's are removed
white pulp
contains concentrated areas of B & T lymphocytes permeated by macrophages & dendritic cells
mucosa-associated lymphoid tissues (MALT)
Nonencapusulated clusters of lymphoid tissue located around membranes lining respiratroy, digestive & urogenital tracts
short acting soluble protein molecules which provide cell-to-cell communication; mediate actions of immune systems cells
Interleukins (ILs)
made by leukocytes & act on leukocytes
Interferons (IFNs)
interfere with virus multiplication
ability of cytokine to act on a different cell type
cytokines that stimulate migration & activation of immune & inflammatory cells
CC chemokines
2 cysteines located adjacent to each other; attract mononuclear leukocytes to sites of chronic inflammation
CXC chemokines
2 cysteines separated by amino acie; attract neutrophils to sites of acute inflammation
Chemokines receptors
CCR1, R = receptor, 1 = number of gene
Colony stimulating factors (CSF)
cytokines that stimulate bone marrow pluripotent stem & progenitor or precursor cells to produce large number of erthrocytes, platelets, lymphocytes, neutrophils, moncytes, eosinophils, basopils & dendritic cells
toll-like receptors
transmembran receptor involved in activation pathway for pathogen snesors of innate immunity (Drosophila)
coating materials which bind particles (microbes) for efficient recognition by phagocytes
acute-phase proteins
Complement system
1) Can destroy pathogens directly, increased phagocytosis, destruction & clearance of pathogen from the body
2) Activates or collaborates with every other component of the inflammatory response, enhances inflammatory response
3) Pathways: classical, lectin, alternative
3 phases of complement system reaction
1. initiation or activation
2. amplification of inflammation
3. membrane attack response
Key complement protein is
protein C3, which is cleaved into larger C3b smaller C3a fragments.
alternative pathway of the complement system
is activated on microbial cell surfaces in the absence of antibodies and is a component of innate immunity
classical pathway of the complement system
activated by certain types of antibodies bound to antigen & is part of humoral immunity
Lectin pathway of the complement system
activitaed by a plasma lectin that binds to mannose on microbes & activates the classical system pathway in the absence of antibody
C3a fragment
stimulates inflammation by acting as chemoattractant for neutophils
C3b fragment
attaches to microbe & acts as an opsonin for phagocytosis, & enzyme to cleave C5 into 2 components
C5a fragment
produces vasodilation & increaes vasular permeability as part of complement system
C5b fragement
leads to late-step membrane attack responses as part of complement system
Initial activation phase of complement system (innate immunity)
Microbe recognized by 1 of 3 paths which intiates
C3 all stages
Early-step inflammatory responses of complement system (innate immunity):
Enzymatic cleavage of C3 produces C3b, & C3a
C3a stimulates inflammation & chemotaxis
C3b opsinizes bacteria & cleaves C5 to C5a & C5b
C5a is vasodilator & will increase vascular permeablilty
substances used to enhance the adaptive immune response to any antigen. To exert its effect an adjuvant must be mixed with the antigen before injection or vaccination.
Vaccinations are produced by
antigens without microbes, so need adjuvants in order to elicet the same adaptive immune as microbes would.
antigens or immunogens
substances foreign to the host that can stimulate and immune reponse
secreted proteins, AKA: Antibodies. Soluble proteins secreted by activated B cells and plasma cells in response to an antigen
antigenic determinant/epitopes
• Portions of exposed surface of antigen that actually make it an antigen (trigger immune response)
• Sites where antibodies bind, site on an antigen that reacts with specific antibody or T-cell receptor
smaller molecules that are not antigenic by themselves, but become antigenic when combined with larger carrier molecules (usually proteins)
adaptive immune response characteristics:
1. Involves complex series of interactions btwn component immune system & antigens of foreign pathogen
2, able to distinguish btwn self & nonself, recognize & specifically react to lg numbers of different microbes & pathogens
3. Rememers the specific agents/has a memory
humoral immunity characteristics:
1. consists of protection provided by B lymphocyte-derived plasma cell
2. these produce antibodies that travel in the blood and interact with circulating & cell surface antigents
Cell mediated immunity charcteristics
1. Protection provided by cytotoxic T lymphocytes
2. Protects against virus-infected or cancer cells
Passive immunity represents
temporary type of immuity that is transferred from aonter source (i.e., in utero mother to infant)
Active immunity
the response by the person's immune system that is acquired through immunization or actually having a disease.
Inflammatory cytokines
Inerferons: released by virus infected cells & immune cells
TNF & interleukins: stimulate CRP release from liver - acts as opsinin
Once inflammation begins, it does not arrest because inflammation is:
stero-specific: must go through all steps
Has no memory - will not produce single cellfor antigen
Complement "a" fragments:
1. increase vascular permeability
2. actvate neutrophils
3. Vasodilate
Complement "b" fragments:
responsible for opsinisins:
Coat a foreign material w/substance so that it is easier for macrophages to recognize it & take it out
Chemotaxic factors:
attract white blood cells into areas of inflammation
soluble mediators of innate immunity:
Opsoninins-tag microbes for recognition: Antibodies IgG & IgM can also act act as opsinins
Inflammatory cytokines: interferons, inerleukins
Late step of complement system (innate immunity)
Neutorphils attracted to microbe
C5b organizes membrane attack complex with C6-C9
Microbe is lysed (killed)
General properties of adaptie immunity:
recognizes & repsonds to a large number of SPECIFIC antigens
Remembers initial exposure - enables quick response to subsequent exposures
antigens of adaptive immunity
Foreign substances that stimulate an immune response
Recognized by immune cell receptos or antibodies
Generally large molecules with multiple antigenic epitopes
Cells of adaptive immunity:
Antigen presenting Cells: APCs (present antigents to T cells)
Macrophages - mature from monocytes, fixed/mobile
Dendritic cells - found in mucus membranes & skin
Lymphocyte characteristics:
1. generated from stem cells in bone marrow
2. B cells mature in marrow - move to lymphoid tissue
3. T cells mature in thymus - move to lymphoid tissue
4. Each has specific surface receptor
5. Each targets a specific antigen
6. 10 (12) different types of lymphocytes
7. Activated when correct antigen binds to surface receptors
8. Antigen must be presented on correct type of MHC
Major histocompatibility complex molecules
Cell surface molecules that present antigens
Class I MHC (Major histocompatibility complex molecules) are found:
nucleated cells
recognized by cytotoxic T (CD8) cells
Class II MHC (Major histocompatibility complex molecules are found
on APC's (antigen presenting cells) & B cells
recognized by T helper (CD4) cells
IgG (immunoglobulin G)
Attack bacteria
cross placenta - providing passive immunity to the fetus
Can contribute to hemolytic disease of newborn (anti-Rh antibodies)
IgE (immunoglobulin E)
inflammation & allergic response
Attaches to antigens on mast cells - histamine release
Xolair is monoclonal antibody against IgE - use to fight asthma
IgD (immunoglobulin D)
Surface of B cells, can play a role in the activation of the B cell involved
IgM (immunoglobulin M)
first antibody made when antigen detected:
circulates as a 5 antibody starburst
effective in forming immune complexes
may also attack bacteria that are insensitive to IgG
IgA (Immunoglobulin A)
found primarily in glandular secretions:
mucus, tears, saliva
attack pathogens before they gain access to internal tissues
immediate transient response of inflammation
occurs with minor injury
develops rapidly after injury
usually reversible & of short duration (15-30 min)
immediate sustained response of inflammation
Occurs with more serious injury
usually due to direct damage of endothelium by stimuli, i.e., burns, products of bacterial infections
affects all levels of microcirculation (arteriols, capillaries & venules)
delayed hemodynamic response of inflammation
increased permeability begins after a delay of 2-12 hours
lasts for several hours or days
involves venules as well as capillaries
injuries due to radiation (sunburn)
Sequences of events in cellular response to inflammation includes leukocyte
1. margination & adhesion
2. transmigration
3. chemotaxis
4. activation & phagocytosis
leukocyte accumulation during cellular stage
leukocytes extend pseudopodia
endothelial cells separate
leukocytes move through vessel wall
tethering is
the slow flow of leukocytes moving along the enothelial cell surface
cyclooxygenase pathway
synthesis of prostaglandins
lipoxygense pathway
synthesis of leukotrienes
induce vasodilation & bronchoconstriction
inhibits inflammatory cell function
causes pain
Induces smooth muscle contraction
constrits pulmonary airways
increases microvascular permeability
produces vasoconstriction
promotes platelet function
Leukotriene (LT)C4, LTD4 and LTE4 (slow reacting substance of anaphylaxis - SRS-A)
Cause slow, sustained constriction of bronchioles
inflammatory mediators in bronchial asthma & anaphylaxis
Omega 3 polyunsaturated fatty acids
Considered anti-thrombotic & anti-inflammatory
fish oil
flax seed, canola oil
green leafy vegetables
walnuts & soybeans
Omega 6 polyunsaturated fatty acids
contain high proportions of arachidoinc acid
prothrombotic & pro-inflammatory
Nitric Oxide (NO)
appears to reduce cellular phase of inflammation
relaxation of vascular smooth muscle
antognism of platelet adhesion, aggregation & degranulation
antimicrobial actions - host mediator against infection
severe bacterial infection
Systemic inflammatroy response syndrome
cause generalized vasodilation
increased vascular permeability
intrvascular fluid loss
myocardial depression
circulatory shock
thermoregulatory center
located in hypothalamus regulates body temperature
thermostatic set point
level at which body temperture is regulated so that core temperature is maintained within normal range
pilomotor muscles
raise skin hair
produce goose bumps
reduce surface area available for heat loss
arteriovenous (AV) shunts
located under skin surface that allow blood to move directly from the arterial to the venous system
open - heat released
closed - heat retained
radiation of heat
transfer of heat through the air or a vacuum
direct transfer of heat frm one molecule to another
heat transfer throght the circulation of air currents
insensible perspiration
water that diffuses through the skin independent of sweating
fever - elevated body temperature
neurogenic fever
fever withorigin in the central nervous system
usually result of damage to hypothalamus caused by CNS trauma
intracerebral bleeding
increase in intracranial pressure
intermittant fever
temperature that returns to normal at least once every 24 hours
remittant fever
temperature does not return to normal & varies a few degrees ineither direction
associated w/URI, Legionella & mycoplasma infections
sustained or continuous fever
temperature remains above normal with minimal varitions (<.55 C or 1 F)
recurrent or relapsing fever
temperature in which there is one or more episodes of fever, each as long as several days w/one or more days of normal temperature btwn episodes
TB, fungal infections, Lyme disese, malaria
prodome or first stage of fever
nonspecific complaints: mild headache & fatigue
general malaise
fleeting aches & pains
chill/second stage of fever
uncomfortable sensation of being chilled & onset of generalized shaking even w/temperature is rising
Shivering causes body temp to reach new set point
flush or third stage of fever
cutaneous vasodilatation occurs & skin beomes warm & reddened
defervescence or fourth stage of fever
initiation of sweating
manifestations of fever
increase metabolic rate
increased need for O2
use of body proteins as energy source
w/prolonged fever, increased breakdown of endogenous fat stores
FUO fever of unknown origin
temperature elevation of 38.3 C/101F or higher that is present for 3 wks or longer
Fever treatment
Antipyretic drugs: aspirin, acetaminophen, ibuprofen - protect vital organs
sponge baths
Hydrate & simple carbohydrates