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102 Cards in this Set

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Lack of resistance to a disease. Vulnerability or lack of immunity(protein). Effected by:general health, Nutricion, Age(neonates,no time to build the immunite response), Stress
Ability to ward off disease
Nonspecific resistance:
Generally present defenses against any pathogen (not directed toward anyparticular pathogen)
FIRST line of defense
Specific resistance:
Immunity, resistance to a specific
THIRD line of defense Imunity/has a concept of Memory. Memory to a specific phatogen/custom made,custom taylor.
born with it. Born with certain resistance.
Species:Pathogens may only infect a limited range of species.
eg. Mumps:Infects humans not dogs or cats.Anthrax: Cattle and humans but no birds.
Reasons for species resistance (Manu unknown)
Physiology:eg. Anthrax:
Temperature is the Key!
Humans:37 oC Birds 41-45oC
Pasteur exposed chickens to Anthrax then lowered their body temperature. The chickens died of antrax.
Anatomy / plant diseases
(immune disease)
(certain chemical receptors plant phathogens require do not exist in/on the human body.) Rose rust-potato fungi,bred mold. Immune compromise.
(Immune disease)
Fish tapeworm Diphyllobotrium latum. Ingested in raw fish. Any species that doesn't eat fish is unlikely to get this disease.
Race or Strain
e.g. caucasians are more susceptible to diphtheria,influenza, and gonorrhea. Blacks and Americans Indians are more susceptible to TB.
Hormone levels effect the immune system.
females produce less seratonin(tobehappy)
woman are different then males.
autoimmune disease/females live longer,better immune system
Mechanical/Physical Barriers
1)intact skin:
Epidermis consist of tightly packed cells with Keratin, a protective protein. Acts as a barrier to most microbes.
Mechanical/physical barriers
2)Mucous membranes:
Line body cavities that open to the exterior.e.g.Digestive,repiratory,urinary,and reproductive tracts. The ephithelial layer of mucus menbranes secretes mucus which acts as a trap and physical barrier.Much less protective than skin.
anything in the open environment tents to colonize with normal flora.
Mechanica/physical barriers
3)hairs of the ears and nose
4)ciliary/mucociliary escalator:
3)wax in nosse,hair in nose filter and trap microbes.
4)microbes trapped in mucus are transported away from the lungs.
Mechanical/physical barriers
5)Lacrimal apparatus
6)Salivary Glands
5)Manufactures and drains away tears continual washing of the eyes.
6)Wash microbes from teeth and mucus membranes of the mouth
Mechanical/physical barriers
8)Vaginal secretions
7)flow of urine moves microorganism out of the urinary tract.
8)help remove microorganism from of the vagina.
9)Coughing, sneezing, vomiting, diarrhea.
Chemical Defenses
Sebaceous Glands:
Secrete SEBUM: contain fatty acids:gives the skin a low pH(3-5)
Sweat Glands
Produce perspiration contains:NaCL and Lysosyme
Gastric Juice
Contains HCL low pH(1.2-3.)acidic
Iron-binding proteins in the blood. Limits avaliable iron needed for microbial growth.
Second line of defense is goint to consis of what two aspects?
Phagocytosis and inflamation.there is going to be chemicals in the second line of defense. Blood
Mechanical physical and chemical barriers
Blood:the fluid portion
Formed Elements
the different in plasma and serum is the cloothing factors
Erythrocytes (RBCs come from bone marrow)(BM they are born in the yock site)
Leukocytes (WBCs)
leukocytes (WBCs)
Have granulates in the cutoplasm and a lobed nucleus.
2)Basophils -produce histamine
Agranulocytes 2 types
1)monocutes/macrophages-phagocytosis when they mature into macrophages
2)lymphocytes-tcell bcells produce antibodies destroy target cells by cytolysis and apoptosis.
Differetial Blood Count
determines the relative percent of each WBC type. Many infections cause an increase or decrease in WBC numbers.
Leukocytosis:increase in total WBC count-indicative of an infection-cancer
decrease in WBC count.
Neutropenia:decreasein neutrophil count
Eosinophilia:Increased Eosinophil count eg. allergies and parasitic infections. Lymphocytosis:Increased Lymphocyte count.
Functions of WBCs
Basophils/Mast Cells
Neutrophils:Phagocytic (youngones are called bands)
Basophils/mast cells: produce histamine
Eosinophils:toxic to parasites, some phagocytosis.
Monocytes:phagocytic as mature macrophages
Lymphocytes:Involve in specific immunity.
Mononuclear Phagocytic/Reticuloendothelial System (RES)
Consist of phagocytosis which enter certain tissues and remain there:Fixed macrophages/histocytes:ingest bacteria and debris as they flow past. Found in the Liver:Kupffer cells
Nervous System:
alveolar macrophages
Microglial cells
langerhan's cells
Also located in Spleen, Lymph nodes, bone marrow and peritoneal cavity.
GI track are called dendretic cells
other macropaghes are called wandering macrophages.
Inflamatory Response
Response to tissue damage by a combination of nonspecific defenses. Characterized by:Redness(rubor),pain(dolor),Heat(calor),Swelling(tumor/Edema)
You are almost there keep it up!!!
Yes! You are almost there keep it up!!!
Functions of Inflamation
2)Confining or walling
3)Repair or replace
1)destroy the injurious agent, and remove it
2)Condining or walling off the injurious agent and it's by products.
3)to repair or replace damaged tissues.
in response to injury acute-phase proteins (complement,cytokine, fibrinogen and kinins)are activated and their concentration increases.
Injured tissues release:Histamine,kinins,Prostaglandins,leukotrienes.
These substances dilate(increase the diameter)of blood vessels.
Redness and Heat Increased permeability:Margination and emigration/diapedesis of WBCs Increased WBCs at siteof injury PMNs reach site first (short lived) Monocytes reach site within 24hr. (longer lived)
Increased flow of fluids from blood to tissue spaces.
The final stage of inflammation, begings during the active phase of inflammation.
FEVER-still inflammation
(systemic increase in body temperature) Endogenous Pyrogens (Interlukin 1)IL-1 and alpha tumor necrosis factor. secreted by WBCs(monocytes and macrophages)
Act on the hypothalamus(body's thermostat)Hypothalamus releases prostaglandins.
Increase in body temperature
Inhibits the growth of some organims
Speeds up body's chemical reactions. Decreases avaliable iron. When IL-1 is eliminated, body temperature falls(crisis)
a group of over 30 proteins found in the blood. Complements antigen antibody reactions. Binds to IMMUNE COMPLEXES.
What are the several functions of complement system?
Cell lysis:Membrane attack complex
WBC chemotaxis:attracts phagocytes
Opsonization or immune adherence: enhanced phagocytosis
Inflammation. complement of cytolysis.
Interferons (IFNs)
Alpha IFN & Beta IFN
cause cells to produce ANTIVIRAL PROTEINS that inhibit viral replication
Interferons (IFNs)
Gamma IFN
Increases the activity of neutrophils and macrophages in phagocytizing bacteria
Immune system:2parts
Humoral Immune System
involves specific antibodies in the blood and lymph.(the body's humors)Produced by B cells.
Immune system:2parts
Cellular Immune System
involves T cells. that do not produce antibodies but secrete cytokines specialized lymphocytes respond to INTRACELLULAR Ags
T & T stands for...
T cell mature in the...
after maturation they migrate to lymphoid tissue.
Define terms
Acquired Immunity
Resistance to infection due to activity of ANTIBODIES
a)active Immunity-you are producing antibodies
b)Passive immunity-you are getting antibodies from another source.
Define terms
Naturally Acquired Immunity
1)Stimulus:contacts with a live microbe by natural processes. eg infection;illness(U may become infected)
2)Response:Symptoms of disease or subclinical RXN-Active production of specific antibodies to the pathogen.
3)Duration:long term(months-years),sometimes life long. Lots of exceptions:eg. Influenza Life Long.
Define Terms
Artificially Acquired Active Immunity
Antigen is intertionally introduced into the body.
a)Killed pathogens(or their proteins alone)
b)Attenuated/weakened live phatogens
c)Inactivated toxins (toxoids)Tecnoshoot - toxin
2)RESPONSE:Production of specific antibodies without developing sysptoms of diseases(or prodromal sysmptoms only)
3)DURATION:Variable (months-years-life time)
Define Terms
Passive immunity
Immunity acquired through transfer antibodies.
Define Terms
Naturally Acquired Passive Immunity
1)Mother to fetus through the placenta (placenta transfer)or in colostrum/milk during nursing.
2)Response:No immune response. Acquisition of antibody only.
3)Duration:short term (a few weeks-months)
Define Terms
Artificially Acquired Passive Immunity.
1)Antibodies formed in one individual transferred/injected into another individual. Immune serum/gamma globulin
2)Response:No Immune response, acquisition of antibody only.
3)Duration:Very Short (2-3 weeks)eg venomous snake bites, Tetanus,Hep.A,Diphtheria,Botulism.
Specific immune response involves production of specific antibodies (Ab) against SPECIFIC antigens(Ag)
The Nature of antigens/Immunogens
Definition:An IMMUNOGEN
is any substance that when introduced into the body STIMULATES the production of specific antibodies. An ANTIGEN is any substance that COMBINES with those specific antibodies. The term antigen is often used to mean both an antigen and an immunogen.
The Nature of antigens/Immunogens
Foreign/Non-self matter eg Microorganisms,toxins, foreign tissues. Chemically:Complex molecules:eg Protein or polysaccharide
has reactivity(combines with specific antibodies)without immunogenicity(stimulating production of specific antibodies)unless bound to a carrier.
Antibodies are not formed against a whole organism but specific regions or chemical groups.
Nature of Antibodies/Immunoglobulins.
a protein produced by B lymphocytes in response to an immunogen/antigen and is capable of combing with that antigen.
Nature of Antibodies/Immunoglobulins.
Gamma Globulins
from separation of blood proteins by electophoresis (antibodies)
Nature of Antibodies/Immunoglobulins.
Antibody Structure
two heavy chains and two light chains. Heavy and light chains both have a "C" or constant portion and a "v" or variable portion
V portion
Vp:is different for each kind of Ab and gives the Ab its specificity.Ag binding occurs at the V portion
C portion
Constant for each class of Ab.
(antigen binding fragment)The two "arms" FcL(Crystallizable fragment)The "trunk" of the antibody. Contains the COMPLEMENT BINDING SITE.
Clases of Antibody
Monomer 80% of serum antibodies (most aboundant Ab in rerum) Can cross the placenta: protects fetus & newborn.
Fixes complement. Enhance phagocytosis, neutralize toxins & viruses.
Clases of Antibody
Pentamer. Fixes complement in blood, lymph, on B cells. Agglutanates microbes; First Ab produced in response to infection.
Clases of Antibody
Main Ab in mucus secretions, and breats milk. Mucosal protection. This protects the portal of entry
Clases of Antibody
Intibodies in blood and lymph. Receptor on B cells.
Clases of Antibody
Monomer on mast cells and basophils, in blood. Allergic reactions; Lysis of parasitic worms.
1st response :Contact with the Ag for the fisrt time.
1) Plasma cells --->Antibodies
2)Memory cells are formed
2do. Response/Anamenestic response
Memory cells activated -> Plasma cells -> Abs formed quickly and in large numbers.
Involves interaction of macrophages and specific T lumphocytes (T-Cells) are in the lymph nodes.
Phatogens entering the gastrointestinal or respiratory tracts pass through. Peyer's patches which contain T cells differentiate into EFFECTOR T-cells when stimulated by an Ag some effertor T-cells become memory cells.
T Cells types
Helper T Cells (CD4, TH)
TH1: Activated Cells related to cell-mediated immunity
TH2 Activate B Cells to produce IgM, and IgE
T cells types
T cells (CD8.Tc)
Destroy target cells with perforin
Delay Hypersensitivity T Cells (Tc) Associated with allergic reaction, transplant rejection. and tuberculin skin test.
T cells types
Turns off immune response when Ag is no longer present.
T cells types
ACTIVATED MACROPHAGES Macrophages stimulated by ingesting Ag or by cytokines.
NATURAL KILLER CELL Lymphocytes that destroy virus-infected cells and tumors.
T-dependent Antigens
T-independent Antigens -Antibody-Dependent Cell -Mediated Cytotoxicity
The immune system does not mornally attack self tissues or compounds. Theory: Clonal deletion:During embryonic development lymphocytes with antigen receptors for molecules present in the body are destroyed.
(MHC) Human Leukocyte Antigen Complex HLA. Glaycoproteins in plasma membrane that enable the immune system to distinguish self from nonself.
Class I MHC:On all nucleated cells.
Class II MHC:On macrophages and B Cells.
Anaphylactic Rxn/Anaphylaxis
Involves IgE antibodies which bind to Basophils/Mast cells.
1st exposure
IgE (to the allergen)In formed and binds to Mass cells by Fc Portion. (no symptoms at this point)
2nd exposure
(Histamine, Leukotriene and prostaglindins released)
1)dilates blood vessels
2)Increased permeability of capillary vessels
3)contraction of smooth muscles
4)Increased mucus secretion
5)Increased secretion of HCI in stomach
Type I / Immediate Hypersensitivity (10-20min)
2 Major Types
1. systemic Anaphylaxis
Severe, sometimes fatal. Develops rapidily after antigen/allergen is introduced to a sensitized individual. eg.Bee Sting:Schock and Ashphyxia
Flushing of skin
shortness of breath, schock
Constriction of smooth muscles in the lungs)
AsphxiaL Death due to respiratory failure
Treatment: Adrenaline/Epinephrine.
Type I / Immediate Hypersensitivity (10-20min)
Locatized Anaphylaxis/Atopic Disease
more common, eg Hayfever, Asthma,Hives, Ags: Plant pollen,Fugal spores Dust, animal danger, dust mites. Foods
Involves IgE
Allergic Rxn of Upper Respiratory system
Signs/Symp:Itchy, tearing eyes, congested nasal passages, runny nose and sneezing.
Treatment: Antihistamine
Allergic Rxn of the lower respiratory system. signs/symp: wheezing and shortness of breath.
Treatment: adrenaline/Epinephrine (Leukotrienes not Histamine)
Prevention of Anaphylactic Reactions.
Skin test to identify allergens
Prevention of Anaphylactic Reactions
Carefully ingecting small, repeated doses of the allergen into the skin. Patient produces IgG antibosy rather then IgE. IgG acts as "blocking" Ab.
Prevent binding of allergen to IgE on Mast cells ->No release of histamines ->No symptoms.
Type II (Cytotoxic) Reactions
Involves IgG or IgM antibodies and complement.Complement activation causes cell lysis or damege by macrophages. Transfusion Rxns & Rh Incompatibility)
ABO Blood Groups
four major types based on CABOHYDRATE antigens on surface of RBC's
A,B,AB and O
Rh Incompatibility (D Ag)
Erythroblastosis Fetalis/Hemolytic Disease of the newborn (HDN)
Results from Rh Negative mother exposed to Rh positive cells by prior birth or transfusion. (sensitized)
->Produce anti-Rh antibodies (igG) which can cross the placenta.
-> reacts with fetal RBCs-> Lysis of RBCs. Results in release of toxins (bilirubin) and anemia.
Treatment:Exchange transfusion:Removal of fetal Rh+ cells and transfusion with Rh-blood.
Prevention:Rho Gam: Passive immunization of Rh-mother with anti-Rh antibodies.
Drug-induced Thrombocytopenic Purpura.
Type III Immune Complex Hypersensitivity
Excess Immune Complexes
are deposited in tissues -> localized inflammation and tissue damage. Non-self Ag:Serum Sickness Self AgL Autoimmune Disease Rheumatoid Arthritis. SYSTEMIC Lupus Erythematosus
Type IV (Delayed) Hypersensitivity
Contact Dermatitis (T cell mediated)
T-cell mediated response. Allergen binds to some of your own cells. e.g. Poison Oak, Poison Ivy.
T-cells infiltrate tissue -> Cytokines-> activate inflammatory cells -> destroy target cells.
Production of Autoantibodies (Antibodies agains ones own tissues or chemical substances) or self reactive T-cells.
Paul Ehrlich
(Horror Autotoxicus)
The father of Autoimmunity
Magic Bullock!
the need not to react to self. Dliverately attemted to immunize animals against their own tissues.
Type I
Type II
Type III
Type IV
Type I-Due to antibodies agains pathoges
Type II-Antibodies react with cell-surface antigens
Type III-(Immune Complex)-IgM, IgG, complement immune complexes deposit in tissues
Type IV-Mediated by T cells
Theumatic Fever and Acute Glomerulonephritis
Follows infection with GROUP A STREPTOCOCCI Cross reactive antibody can bind to heart, cartilage, muscle, and kidney tissue.
(Rf~15,000 deaths/yr US)
Type I
Graves disease Type 2
Attachment tto AutoAbs to receptors for Thyroid-stimulating hormone (THS) on follucle cells of the thryroid gland. Stimulation of follicle cells overproduction of thyroxin.
Hyper Thyroidism: Gotier, increased metabolic rate, nervousness, tremor, difficulty concentrating, heat intolerance, dirarrhea, and palpitations.
Type 2
Myasthenia Gravis:
AutoAbs bind to acetylcholine receptors at tneuromuscular junctions, causes dregadation of receptors, muscle weakeness and fatigue. loss of muscle function, paralysis, respiratory failure and death.
Type 2
Systemic Lupus Erythematosis (SLE or Lupus)
Auto Abs produced against a variety of tissues and DNA.
Most involvedL Kidneys, Bone marroe, skin, Nervous system, Jounts, Muscles, Heart and G.I tract.
Type 3
Systoms:Fever, skin rashes, arthritis, effusions (fluid build up) and inflammation in pleural. pericardial.peritoneal caities and CNS.
Can cause a life-threatening, progressive, immune complex-mediated glomerulonephritis.
90% of cases are in females of childbearing age.
Rare in males (Klinefelter's syndrome XXY)
Rheumatod Arthritis
Associated with advanced age (80% of population) Characterized by cronic inglammation of the jounts. AutoAbs (Rheumatoids factor) form immune complexes with IgG, binds to synovial membrane of joints, activated complement, scar tissue and joint destruction.
Type 3
Multiple Sclerosis (MS)
Damage to maelin Sheath type 4 (demyelination)of CNS (Brain and Spinal Cord) T-cells attact myelin, decreased ability to conduct nerve impulses, muscular weakness, tremor, difficulties in speech and vision. paralysis.
Hashimoto's/Autoimmune Thyroditis
T-cells destroy the follicle cells that produce thyrosin. Hypothyroidism: Malaise, lethargy pain, fever, and increased risk of pyogenic infection.
Type 4
Diabetes Mellitus:
Type I
(Juvenile-onset/Insulin dependent)
T-cells attack islet cells of the pancreas, inflamatory reaction, cell lyses, decreased insulin secretion.
Acquire Immune Deficiency Symdrome
HIV: Humans immunodefiency virus (retroviridae) Envelope with transmembrane spikes
gp 120 (glucoprotein) spikes enable HIV to attach to host cells with the CD4 (helper T-cell) receptor: T cells, macrophages, dendritic cells, and monocytes
Upon entering a cell viral RNA is transcribed into DNA by the enzyme
Reverse transcriptase Viral DNA becomes integreated into the host cell chromosome. Integrated DNA may be active or latent.
Clinical categories of HIV infection
Category A
Category B
Category C
A- Asymptomatic or lymphadenopathy (swollen lymph nodes)CD4 count 500/mm3 or above.
B- Various symptoms & persistent infections (oral candidiasis) CD4 count between 200-499/mm3
C- Clinical AIDS various opportunistic infections. Less than 14% of T-cells present are CD4 cells
CD4 count below 200/mm3 people have AIDS
Transmission of AIDS:
Direct contact with body Fluids. Blood:10-1000 IP (infectious particles)/ml
Semen:10-50 IP/mL
Saliva:Generally <1 IP/mm
Treatment for AIDS:
Nucleoside Analogs(AZT, ddl, and ddC)
inhibit reverse transcriptase as it synthesizes DNA. Resemble thymidine but lack the corect attachment point for the next nucleotide.
Protease inhibitors (ritonavir, and indinavir)
Block and enzyme needed to assemble the virus.
Problems:No idea animal model, virus targets the immune system itself, Mutation rate of HIV, needs both antibody and killet T-cell response Effective vaccne will also have to stimulate a mucosal immune response. (IgA) cross reactive antibodies.