Pathophysiology > Immunity > Flashcards

Immunity Flashcards

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1
Q

Inflammation

A
  1. recruitment of other WBCs = chemotaxis
  2. stabalizes tissue for repair
  3. swelling localizes damage
  • vasodilation & increased capillary permeability
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2
Q

Innate Immune system vs Adaptive Immune system

A

INNATE: you are born with these

  1. Physical Barriers - skin, mucous membranes
  2. Chemical Barriers - saliva, tears, stomach acid, sweat, earwax = lysosomes
  3. Inflammation - nonspecific laukocytes
    * external system within the body = GI tract, Respiratory tract

ADAPTIVE: aquired

  • changes within us due to exposure
  • build and change across our lifetime
  • hygenine hypothesis - we are too clean and not getting the exposure we need for healthy immune systems
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3
Q

stress and disease

A

Physiostress (infection, disease, external factors of stress) release CORTISOL during times of stress from adrenal cortex and stress makes us IMMUNOCOMPROMISED

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4
Q

Immunity

A
  • BARRIERS: Integumentary System (skin and mucous membrane)
  • first line of dense against infection and injury
  • constant/continuous defense
  • nonspecific
  • Inflammatory response - hematology mediated
  • very hard to turn off once stimulated
  • second line of defense in response to injury or infection
  • Immediate response
  • nonspecific
  • mast cells, granulocytes (neutrophils, do’s, bass’s) Mono’s/Macro’s, platelets, endothelial cells = non-specific white blood cells
  • mast cells and bass cells are Pro-inflammatory = release histamine and heparin as an immediate inflame response
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5
Q

Adaptive Immunity

A
  • Lymphocytic System
  • 3rd line of dense
  • specific, acquired, memory. humoral
  • in response to antigen exposure
  • VERY Specific
  • delay between exposure to antigen and maximum response
  • T & B lymphocytes, macrophages, and plasma cells
  • anitbodies
  • cell-mediated immunity = t cells
  • anitbody-mediated immunity = b cells
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6
Q

Innate- immunity

A

multilevel system of interactive defense

  • 1st line of defense = innate resistance, barriers
  • physical and biochemical (skin and mucous membranes)
  • 2nd line of defense = inflammation (innate)
  • rapid, non-specific
  • 3rd line of defense = adaptive (acquired) immunity = memory
  • specific, memory
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7
Q

innate immunity - 1st line of defense

A

BARRIERS

  • physical and mechanical
  • skin
  • linings of GI, GU and Resp. Tracts
    • sloughing of cells removes bacteria from layers, coughing, sneezing, vomiting, mucous and cilia
  • Biochemical Barriers
  • synthesized and secreted - “washing” saliva, tears, ear wax, sweat, mucus
  • antimicrobial peptides (skin, urethra)
  • normal bacterial flora
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8
Q

Innate- Innate Immunity - 2nd line of defense

A

Inflammatory Response - response to injury or vascularized tissue
- Classic symptoms of local effect
S swelling - increased blood flow
H heat - vasodialtion
A a loss of function - damages, inflammation, trigger to not use
R redness - bloodflow
P pain - tissue releases chemicals to tell body “don’t use me”

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9
Q

Innate- Why is inflammation physiologic?

A

it is a normal, good-functioning response in the body

  1. stabalizes tissue
  2. recruits WBCs
  3. stops spread of infection
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10
Q

Innate- Why is inflammation pathologic?

A 
hard to turn off inflammation
chronic inflammation
1. fluid dynamics change - edema, BP
2. Stress on system - effects heart rate, BP, heart muscle
3. immunosuppressed - low WBC count
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11
Q

Innate- Diapedesis

A

leukocyte extraction, cells leave blood stream for tissues

  • monos (in blood))/macros (in tissues) pacman, phagoctes
  • neutrophils
  • eosinophils
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12
Q

Innate- chemotaxis

A

moving leukocytes to injured site

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13
Q

Innate- phagocytes

A

= monocytes & macrophages, neutrophils

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14
Q

Innate- hematology of immuno

A
  • WBCs = leukocytes
    1. Granulocytes: cytoplasmic pockets
  • B basophils
  • E eosinophils
  • N neutrophils
    2. Agranulocytes
    Lymphocytes, monocytes (immature in bloodstream)
  • T & B cells = specific fighters
  • NK cells “take out bad guys”
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15
Q

Innate - Neutrophils

A
  • first responder
  • most abundant of WBCs
  • primary phagocyte
  • ingest, destroy anything foreign or damages
  • chemotaxis = called to injured site
  • diapedesis = go in blood to injured site
  • phagocyte - 1st in early inflammation (6-12 hours)
  • mediators - attract and activate complement proteins and mast cells (cytokines)
  • pus = “war zone” = dead tissues, cells, dead reg. tissue
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16
Q

Innate mast cells

A
  • release histamine and heparin
  • start the inflammation process
    1. vasodilation
    2. increased capillary permeability: gives us signs of SHARP

Degranulation: cytomplasmic granules activate and release

  1. histamine release = vascular effects
    - increased blood into microcirculation
    - histamine also increase vascular permeability
    - histamine increases adherence of leukocytes to the endothelium
    * these all equal inflammation
  2. Chemotaxis of more neuters
  3. chemotaxis of more dos

Chemotactic factors:

  • neutrophil chemotactic factor = kill bacteria in early stages
  • eosinophil chematic factor = regulate inflammatory response
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17
Q

Innate - mast cell - synthesis

A 
causes 3 major effects:
1. paltelet activation factors: clotting
Activation of arachnoid acid to:
2. vascular effects via leukotienes
3. vascular effects and pain via prostaglandins
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18
Q

Innate- mast cell arachidonic acid pathway

A

mast cell synthesis produces 4 products

  1. leukotrines: leukocytes = increase inflammation
    - similar effects to histamine in late stages. inreaseses inflammation and brings more WBCs
  2. prostaglandins: endothelium = inhibits platelet agreg and induces vasodialtion
    - similar effects to leukotrines and PAIN
    - increase inflame and cap perm and pain
  3. platelet-activation factor (thromboxanes) = platelets
    - increase platelet agree and vasoconstriction
    - increase clotting and inflame
  4. Prostacyclin = regulates other 3 effects = decreases clotting, inflame, and pain = apririn, ibuprofen
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19
Q

Innate- Monocytes and Macrophages

A
  • appear 24 hours ager injury - replace neutrophils
  • attracted by macrophage chemotactic factor from neutrophils
  • phagocytic cell
  • APC activates adaptive immune system “antigen-presenting cell”
  • ingests pathogen, takes parts of the protein it ingests and shows off to other cells to show them what to kill
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20
Q

Innate- Eosinophils

A
  • primary defense against parasitic worms
  • regulate vascular mediators from mast cells histamine
  • NOT phagocytic
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21
Q

Innate- phagocytosis

A
  • process by which a cell ingests and disposes of foreign material
  • cells migrate out of the blood - though basement membrane
  • pavementing = line up along basement membrane
  • diapedesis = leukocyte extraction into blood stream
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22
Q

Innate - Natural Killers (NK) cells

A
  • special kind of T cell
  • nonspecific lymphocyte
  • primary fxn is to kill - viruses, abnormal host cells (cancer or tumor cells and non-specific abnormal cells that don’t look right)
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23
Q

Innate - cellular products - proteins

A

Cytokines: cell communication signals

  • interleukins - pyrogens (cause fever)
  • interferons - viral infections (let neighbor cells know about it)
  • tumor necrosis factor

Chemokines: chematic cytokines
* induce leukocyte chemotaxis - causes chemotaxis at injured sites

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24
Q

Innate- plasma protein systems

A
  • proteins made in the LIVER and circulate the blood
  • inactive enzymes (proenzymes)
  • sequential activation = cascade communication confirmation. are you sure? are you really sure? really really?

3 plasma proteins essential to effective inflame/immune response:

  1. complement system: immune responses series of protein cascades
  2. coagulation system: clotting
  3. Kinin system: increase pain and inflammation
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25
Innate- complement system
* activates innate and adaptive responses * triggers and modulates a variety of immune activities and acts as a linker between the two branches of the immune response * maintains cell homeostasis by eliminating celuarl debris and immune complexes 1. opsonization = taggin a cell for destruction 2. chemotactic = attracts WBCs 3. produces membrane attack complex - pokes holes in bacterial membrane
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Innate - cytokines
cell communication for immunity
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Innate immunity Inflammation
- local manifestations: increase vasodilation & permeability - vascular changes with leakage - vasodilation and increase permeability - SHARP *exudative fluid - serous (watery, early), fibrous (thick, blotted, more advanced. amber color, thick, sticky, more proteins), Purulent (bacterial infection, pussy and smelly), hemorrhagic (bloody) Inflammation causes systemic effects: * fever = infection - endogenous (within, interleukins), exogenous (pathogen produced - act on hypothalamus - reset and turn on pyro * leaukocytosis , increase number WBCs * increases plasma proteins (LIVER) - acute phase reactants - 10-40 hours. increase clotting factors * CHONIC INFLAMM = lasting longer than 2 weeks. often unsuccessful acute inflammatory response - stimulus isn't removed - chronic injury, smoking-related
28
adaptive immunity
* 3rd line of defense = T & B cells * Aquired, specific - cell-mediated T cells - humoral/antibody-mediated B cells 3 important things to remember about adaptive: 1. memory of antigens 2. specificity 3. antibodies
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adaptive - Immunity Terminiology active vs. passive natural vs. artificial
ACTIVE = acquired - producing memory, activates T & B cells PASSIVE = straight antibodies, no memory ``` NATURAL= we get exposed naturally in our environment ARTIFICAL = injection into body ``` * Natural Active = common illness and infection, memory * Artificial Active = injection and produce B and T cells = vaccination * Natural Passive = mother breastfeeding passing on antibodies through breatmilk; in womb antibodies travel through placenta * Artifical Passive = inject antibodies; AFTER the fact - rabies shot, ebola antigens, anti-venom
30
adaptive - Anitgens and Antibodies
* Antigens = Foreign or non self particles/proteins(ag) - viruses, bacteria, cancer ,fungi, parasites - noninfectious = pollens, foods, bee venom - dugs, vaccines, transfusions, transplants * B cells produce antibodies * antigens react with antibodies or receptors on B and T cells * Antibodies = proteins produced by immune system - immunogens/immunoglobins/ig *EPITOPE = region of the antigen that is recognized by antibody
31
adaptive - Tolerance
* tolerance = us not killing "self cells" because we recognize them - if you loose tolerance then you get autoimmune issues TWO ARMS: 1. ab mediated/humoral - B cells - antibodies = bacteria, viruses, toxins 2. cell-mediated - T Cells - react directly with ag on cell surfaces - NK - stimulate other leukocytes (cell to cell or cytokines) T - cytotoxic cells - verses infected cells and cancer
32
adaptive - T cells vs. B Cells
* T cells = made in bone marrow, mature in thymus - thymus teaches the cells self vs. non-self. Starts in puberty then shrinks to fatty tissue by adulthood * B cells = made and mature in bone marrow T CELLS: 1. memory cells 2. cytotoxic T cells (poke holes in cell) 3. helper T cells (stimulate both T and B cells) 4. Suppressor T cells (ramp down response) Antigen activates B CELLS: 1. memory cells 2. plasma cells --> antibodies
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adaptive - Clonal diversity
produces millions of T and B cells each with different receptors - immunocompetent cells become active if meet up with specific antigen - hang out in lymphatic tissue waiting for antigens to come or helper T cell to activate them = recognition and activation of lymphocytes - first phase in fetus - recognition of millions of antigens
34
adaptive - APC cell
antigen-presenting cell, lymphocyte - accessory cells (also dendritic) - APC activates helper T cells --> tell antibodies to release
35
adaptive - MHC
Major Histocompatibiity complex = flagging to determine self from non-self * 2 classes: * *MHC1 = endogenous pathogens = viruses & cancer - on all nucleated cells - ag binds with MCH1 to activate cytotoxic T cells (CD8) * *MHC2 = extracellular pathogens = bacteria & toxins - on phagocytic cells: macrophages, APC, B lymphocytes - Ag bings with MHC2 to activate helper T cells (CD4) * **MHC1 = CD8 * **MCH2 = CD4
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MHC1
all nucleated cells fxn: present processed antigen to - 1. cytotoxic CD8 and T cells = cancer prevention. 2 .NK cells = constant screening (no binding with MHC needed)
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MHC2
APCs - dendritic, B cells, macrophage | Fxn- presents processed antigen fragment to -> CD4 T cells
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CD cells
cluster of differentiation - additional membrane bound proteins - FXN: aids in the function of the immune cells - defines the functionally distinct subset of cells * CD4 helper T cells - binding receptor-from APCs * CD8 cytotoxic T cells - binding receptor: from all nucleated cells
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adaptive - Antibodies
IgG - most abundant, transported across placenta, four classes IgA - secretions IgM - largest, fetal life IgD - low concentration IgE - allergic responses, parasite infections * Direct Functional Effects: neutralization, agglutination, precipitation * Indirect Functional Aspects: opsonization, complement
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Secretory (mucosal) immune system
- lymphoid tissue that protects the external surface of the body - Ab present in tears, sweat, saliva, mucus and breast milk
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cell-mediated immune response
- viruses, tumors, pathogens resistant to neutrophils and macrophages - mature T cells: cytotoxic (Tc, attack and destroy directly by using cells); Regulatory Helper T (Th, cell mediated, humoral mediated, suppressors); memory cells
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adaptive immunity
tighly regulated | **MORE INFO**
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Primary and secondary Immune Responses
PRIMARY - initial exposure - latent period (B cell differentiation) - after 5-7 days (igm antibodies detected) - an IgG response follows ``` SECONDARY - more rapid - large amounts of Ab are produced - rapid response 2 hours to memory cells - IgM - similar 1 hour response IGg - greater number ```
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active vs. passive immunity
ACTIVE - antibodies or T cells produced after either a natural exposure to an antigen or after immunization PASSIVE - performed Ab or T lymphocytes are transferred from a donor to a recipient * passive immunity of the fetus = IgG (crosses placenta)
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Immune Dysfunction
1. hypersensitivities 2. infection 3. immune deficiencies
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humoral immunity
antibody mediated, b cell activation to make antibodies
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IgG
- most abundant - lasts a long time in the blood - transports across the placenta - Type ii hypersensitivity - the amount of it shows the level of immunity you have to something
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IgM
- largest antibody - 1st responder - shows if you have a current infection - synthesized during fetal life - type ii hypersensitivity
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IgA
- secretions | - tear, saliva, mucous, breast milk
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IgE
- allergic responses: stimulates mast cells and inflammation - parasite infections - Type i hypersensitibity - anaphylactic
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direct and indirect functional effects of antibodies
direct: neutralization, agglutination, precipitation indirect: opsonization - tagging for killing by phagocyte & Complement - assists both innate and adaptive responses
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Primary Immune Response
initial exposure -- latent period (B cells start to differentiate) -- after 5-7 days IgM antibodies are detected -- an IgG response follows
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secondary immune response
- explosive, more rapid - large amounts of antibodies are produced - IgM appears within an hour - IgG in much great numbers - can clear within 2 days
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active vs. passive immunity
ACTIVE: antibodies or T cells produced after either a natural exposure to an antigen or after immunization PASSIVE: preformed antibodies or t lymphocytes are transferred from a donor to a recipient exp: IgG for hepatitis A exposure or tetanus toxoid
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AIDS
- helper T count falls below 200 | - anywhere above = HIV
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inappropriate immune responses
1. exaggerated - allergies 2. misdirected - autoimmunity (against self) 3. against beneficial foreign tissues - alloimmunity (transplant rejection) 4. insufficient - immune deficiency
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Type I Hypersensitivities
1. ANAPHYLACTIC HYPERSENSITIVITY 2. Type 1 3. IgE antibody 4. Immediate (minutes) 5. Mast Cells 6. allergic asthma, hay fever, urticaria (hives), conjunctivitis, rhinorrea (runny nose), gastroenteritis (vomiting, diarreah) EXP: bee sting 1st profuce IgE antibodies -- 2nd IgE binds to antigens -- activates mast cells -- creates inflammation
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Type II Hypersensitivities
1. Cytotoxic Hypersensitivity = Automimmunity against healthy tissue Specific 2. Type II 3. IgG, IgM 4. hours - days 5. Phagocyte 6. graves disease (creates antibodies against thyroid), rheumatoid arthritis, lupus (attacks muscles, cells) EXP: systemic lupus erythematosus - antibodies against nucleic acids, erythrocytes, coagulation proteins, etc.
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Type III Hypersensitivity
1. Complex Mediated/ Antigen-Antibody - antigens get "stuck" in healthy tissue 2. Type III 3. ANY antibody 4. days - months 5. rare to no leukocyte involvement 6. wrong blood transfusion, serum sickness, * C3B + neutrophils * alloimmunity - rejection of foreign transplanted tissue, blood
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Type IV Hypersensitivity
1. delayed reaction 2. Type IV 3. Years 4. NO antibodies 5. T Cells 6. poison ivey, latex sensitivity, celiac disease, * mediated via T cells and takes time to develop 3 types: DElayed type = antigen is injected into dermis (PPD test TB exposure); Contact Hypersensitivity = absorbed into epidermis (latex sensitivity); gluten-sensitive enteropathy = absorbed by the GI (celiacs)
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Bacterial Infection
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Pathophysiology
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