Pathophys #2: Mechanisms Of Self Defense: Inflammation & Immunity

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First line of defense (nonspecific)

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skin, mucosal barrier
-normal immune fuction

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second line of defense
(nonspecific)

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inflammation,
general to any kind of threat

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Third line of defense
(specific)

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Immune response

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Characteristics of immune
System (5)

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1-Self Tolerance/non-self intolerance: HLA's 6 MHC halplotype, ex: supertypes defend against HIV
2- Self Regulation-w/o input from other body systems
3-specificity-specific cell type or antigen ex: chicken pox
4-Diversity-Develop immunity to new things w/in your lifespan
5-Memory-Long term immunity

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Haplotype

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Your personal version of those varients on that particular MHC gene. Explains why people respond to diseases differently. Ex: Super types and HIV

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Antigen

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A forgein substance that illicts an immune response. Require immunocompeant cells (lymphocytes) Ex: capable of stimulating an immune response, bacteria, pollen, food...

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Immunogen

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An antigen that induces the formation of immune cells. Stimulates growth of specific types of immune cells.

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Antigenic Determinant (epitope)

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The portion of the anitgen molecule that is recognized by the antibody. There can be more than one

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Innate Immunity (Natural Immunity)

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Inborn Immunity. Able to distinguish self from non self, but not able to distinguish b/t agents.

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Adaptive Immunity (Aquired)

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Develop later in life; Aquired after you were born. Passive or Active.
Passive: From mother or IVIG,
Active: vaccine, exposure to dx.
Humoral (b-cell) vs. Cellular (t-cell)

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Humoral (B cell)

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part of Adaptive immunity:
Principal defense of microbes and their toxins. Cells that DO NOT go to the thymus. These cells come from the liver as stem cells then develop into a lymphocyte, then go to a different place in the bone marrow= B cells

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Cellular (T cell)

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Part of Adaptive Immunity: T cells are good at fighting pathogens (viruses). Stem cells => Lymphocytes => THYMUS= mature into T cells. See thymus*

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Thymus

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Where T cells mature. Very developed in an infant. Preparing person for life with T cells. In adult, apoptosis takes place in the thymus and is not very well developed.

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Antigen presenting Cell (APC)

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APC (ex: a macrophage or dendritic cells). T cell can't suck up antigen by itself, so it needs this APC to present the antigen to it.

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Dendritic cell

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Most potent of APC's; key part of innate immunity

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Plasma Cell

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Humoral Immunity:
A B cell that has transformed into a plasma cell that now can secrete antibodies. B cells don't secrete antibodies until they are plasma cells.

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Memory Cells

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B cells that are floating around in the blood stream waiting for the "next time" they are needed.

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Immunoglobulin
IgG

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gammaglobulin. Can be made into a medication. Most abundant, only one that crosses the placenta: transfers from mom to baby. Present in all body fluids

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Immunoglobulin
IgA

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Found in saliva, tears, colostrum

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Immunoglobulin
IgM

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early responder, no crossing placenta

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Fuctions of Immunoglobulins
(Antibodies)

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agglutination (clumping), opsonization (coating), neurtalization, activation of inflammatory processes

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Primary Response of the Immune system

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Stiumulates the naive B cells to become activated. They release antibody IgM (first antibody formed in response to an antigen). Doesn't last long.

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Secondary Response of the Immune System

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Person is exposed to dx again (from first time), and IgG long lasting response. Ex: Booster shot. Need two shots to get long lasting response

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Cellular Immunity (T cells)

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T lymphocytes that mature in the thymus:
-work with other T cell & B cells
-control intracellular viral infx
-reject forgein tissue grafts
-cause delayed hypersent rxns
Several Types of T's.

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Types of T cells (6)

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1) memory
2) Lymphokine-producing
3)Cytotoxic (Tc) "master regulator"
4) Helper Th (CD4)
5)Suppressor Ts
6)Natural Killer (NK)

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"Cluster of Differentiation"
markers (CD)

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Marker on the cell membrane:
Helper T cells: CD4 (HIV)
Cytotoxic: CD8 (master regulator)

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Cytokines

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Cellular Immunity:
Chemicals that are put out by T cells. Two types: Lymphokines or monokines

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Acute Inflammation-superficial

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Superficial hallmarks: redness, heat swelling, pain, loss of fct.

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Acute inflammation-microscopic

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Microscopic hallmarks: vasodilation, increased vascular permeability, WBC adherence and migration to tissues
2 PHASES

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Acute inflammation Microscopic
1st Phase: Vascular

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Vascular Phase: Vasoconstriction (short) quickly followed by vasodilation and increased vascular permability=proteins leak out into tissues= exudate

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Acute Inflammation Microscopic:
2nd phase: Cellular

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Cellular Phase: WBC roll and adhere to endothelial cells and eventually transmigrate out b/c of increased capilary permability. "Digest" there way out of the vessel. Good! b/c need to find their way to the area of injury

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Types of WBC's (6)

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1) Basophils
2) Band cell
3) Neutrophil
4) Lymphocytes (T & B)
5) Eosinophil
6)Monocyte (mature into macrophages)
MENLBB

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Mast cells

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Component of inflammation:
Degranulate and release histamine and other inflammatory mediators

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Endothelial Cells

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Component of inflammation: Contract, express adhesion molecules, release iNO (pulmonary vaso)

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Granulocytes

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Component of inflammation:
Include Neutrophils, basophils, eosinophils: phagoctyes

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Role of Monocytes in inflammation

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Component of inflammation:
(immature in bloodstream) and macrophages (mature, in tissues): Phagoctyes

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Role of Platelets in inflammation

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Component of inflammation: Aggretate to stop bleeding, release chemical mediator of inflammation such as serotonin

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Role of Lymphoctyes in inflammation

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Component of inflammation:
secrete lymphokines

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Interleukins

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Example of a cytokine.
Produced by WBC in response to an antigen. Causes an acceleration of the immune response

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Interferons

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Example of a cytokine.
Produced by a host cell infected witha virus. Stimulates healthy neighbor cells to produce stuff that inhibits the virus to get to it.

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Cytokines

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soluable proteins secreted by cells of both the innate and adapative immune systems. They mediate many fuctions of cells

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Chemokines

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Cytokines that stiumlate the migration and activation of immune and inflammatory cells

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Colony-stiumlating factors

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stimulate the growth and differentiation of bone marrow progenitors of immune cells

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Chemotaxis

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leukoctyes migrate in response to a chemical signal. Can move toward the bacteria and phagocytize it.

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Complement System
(Cascade)

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Is started by an antigen (microbial invasion). Very important part in the inflammatory process. Many different proteins involved. Two pathways involved: Classical or Alternative.

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C-reative protein

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CRP
predictor of cardiovascular dx.
Level of inflammation in the body

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Ertythorcyte Sedimentation rate (ESR)

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Or Sed rate. Increased CRP results in increased ESR. Imprecise dx activity for inflammation.

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Lipooxygenase pathway

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When arachidonic acid is metabolized=> This is one of the two possible pathways. If you stop this pathway, use drugs like anitlukotrienes (singulair)

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Cyclooxygenase pathway

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When arachidonic acid is metabolized=> This is one of the two possible pathways. If you stop this pathway, use drugs like aspirin, NSAIDS to stop prostaglandins & thromboxane.

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Corticosteroid medications

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These medications prevent arachidonic acid from being formed and broken down. Works high up on the chain.

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Chronic inflammation

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Acute inflammation that sticks around. Formation of fibroblasts and granulomas form (bulky tissue).

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Immunodeficiency Diseases" Two types

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Too little immunity
Primary-Congenital
Secondary-Born healthy

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Primary Congenital Immunodeficiency Disease

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Gene for specific components of the immune response missing or malformed (T, B cells...etc.) Ex: DiGeorge Syndrome, SCIDS...born with it.

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Seconary Immunodeficiency Disease

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Born healthy! Aquired later. Can be caused by: Biologic determinants (ex: pregnancy), nephrotic syndrome, surgery, trauma, dx's, nutrition, cancer, infx...etc.

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Hypersensitivities

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Inappropirate response to environmental antigens
(allergy), self-antigens (autoimmune), or other person's antigens (alloimmune-transplant). Altered immune homeostasis & genetic susceptibility. Can be immediate or delayed. 4 types.

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Hypersensitivities: 4 types

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1) IgE mediated (allergy rxn)
2) antibody mediated
3) immune complex
4)cell-mediated

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Type 1 IgE Mediated (Allergy)

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Allergic rxn:
many clinical effects range from mild to severe (death). MUST be mediated by IgE to be an allergy.

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Type II antibody mediated hypersensitivity

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tissue-specific rxns. Antibodies bind to tissue-specific antigen: IgG of IgM binds to cell surface antigens and injures or kills cells. Ex: transfusion rxn, Myasthenia gravis.

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Type III Immune complex mediated injury

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3 phases:
1) immune complex formation
2) immune complex deposition in tissues (ex: lungs)
3) activation of the complement cascade
Ex of dx: vasculitis in SLE, Raynaud's

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Type IV hyper sensitivity (cell mediated)

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NO antibodies involved; sensitized T lymphocytes. T cells are activated by the re-introduction of an antigen. Takes 24-72 hours to develop.
Ex: TB test response, poison ivy.

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Autoimmune diseases

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May result from type II, III, IV
Digest own tissue-not able to recognize self from non-self
More common in females

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HIV

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retrovirus: carries genetic info in RNA rather than DNA. Attacks CD4 cells (helper cells)

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Therapies for HIV

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1)Entry inhibitors
2)Reverse-transcriptase inhibitors
3)Integrase inhibitors
4)Protease inhibitors

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Stages of HIV invading a T cell: life cycle of the virus

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1)HIV binds to CD4 helper T cell (attachment)
2) gets into cell membrane of T cell (internalization and uncoating of the virus)
3)RNA floating around of free
4) HIV gets its RNA into cell's DNA to replicate.
Transcription
5)New HIV Virus is born and T cell is now dead.

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Category C AIDS illness

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Stage in AIDS that person is at risk for opportunistic infections (Karposi's sarcoma, PCP...)