Patho II Exam 1

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FattyRunRun
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62009
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Patho II Exam 1
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2011-01-25 18:06:54
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Patho Packet 1
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  1. Three tiers of
    defense
    • Mechanical Barriers:
    • · Skin,
    • Mucous Membrane (protection of organs against MO, create environ. where things
    • don’t cross readily
    • · Chemical Barriers: Saliva,
    • Tears (dilute toxins and remove from body)

    • Inflammation
    • · Without inflammation: Cannot heal any
    • wound sustained/or clean up and rid the MO

    Immunity

    o B Cell, T Cells responses is specific immunity

    o Defense is specific to the MO (invader)

    o And have defense for future also
  2. Cardinal
    Signs of Inflammation
    • · Redness,
    • Heat, Pain, Swelling at site of injury

    • o Redness:
    • Due to vessel dilation and increased blood flow

    • o Heat:
    • Due to vessel dilation and increased blood flow

    • o Swelling:
    • Increase Pressure (Fluids, Proteins,
    • Cells, leave the blood and goes to the site of injury)

    • o Pain:
    • increase blood flow/swelling cause pain
    • because substances that are released irritate the nerve endings
  3. What are the
    local changes that will occur because of inflammation?
    • · Increase
    • blood flow at the site: (hyperemia) redness at site

    • o Mediators
    • (cell or plasma derived) go to the site of injury and recruit other
    • cells/proteins to have inflammatory response.

    • · Increase
    • capillary membrane permeability

    • o Make
    • WBC/proteins/etc that do not want to cross membrane want to cross the
    • membrane.

    • · Diapedesis
    • of WBC from the blood to the site of injury

    • o Movement
    • of WBC due to built in mechanism

    • · Walling
    • off Effect of Inflammation

    • o Create
    • mesh work and ID where the site of injury is and put a gate around that area

    • o Only
    • want certain things to take place in that gated area so we can clean up the
    • debris, MO, and prepare it optimally to initiate wound healing and repair
    • mechanism
  4. Plasma derived mediators
    • o Complement
    • system:

    • § IMP
    • for the removal of MO from SOI/clean up

    • o Kinin
    • system:

    • § Principle
    • player is bradykinin

    • ú Participates
    • with vasodilatation at the SOI

    • ú Serves
    • to facilitate the sensations of pain

    • · Bradykinin
    • will irritate the nerve endings to cause pain.

    • o Coagulation
    • system:

    • § Clotting:
    • trying to create the mesh work around the SOI

    • § Not
    • trying to increase the blood flow to the entire body but only that SOI

    • § Trying
    • to create a clot to highlight the vasodilatation at that SOI by restrict blood
    • from moving in and out that area so we maximum the movement of substance out of
    • the blood to the SOI

    • o Fibrinolysis
    • System:

    • § Opposite
    • to coagulation system

    • § Anti-
    • coagulation: increase the blood flow, and increase the deliver of the mediators
    • for the pro-inflammatory response to the SOI
  5. Cell derived
    mediators:
    • · Mediators
    • comes from cells

    • o Prepackaged
    • (ready for release)

    • o Needs
    • to be synthesized and then released
  6. Acute
    Inflammation

    Immediate Effect
    Knife cut:

    • o First,
    • increase in blood flow

    • § Increase
    • in H from mast cells, Bradykinin released which promotes vasodilatation at SOI
    • (not whole body)

    • § And
    • vasoconstriction at the periphery of the injury

    • § Local
    • heat at SOI

    o Histamines:

    • § Endothelial
    • cells constricts and thus produces gaps/holes in vessels walls

    • § The
    • junctions aren’t as tight as they used to be so substances in blood can move
    • through these holes to the SOI

    • § Increase
    • in permeability: fluids proteins, etc leave blood and goes to site of injury

    • § Process
    • is reversible

    • ú Acute,
    • because once fx is done, the substances leave back to the blood
  7. Diapedesis
    (aka extravasation)
    • Movement
    • of WBC from blood to tissue

    • · As
    • a result of the H being released, the jx are relaxed and have promotion of the
    • expression of receptors

    • · Receptors
    • called p-selectin pops up on the surface
    • of the endothelium and interact with the proteins that are always expressed on
    • the surface of a Neutrophil.

    • · Neutrophils want to stay in the blood,
    • but we need these neutrophils to go to SOI, so the neutrophil will capture the
    • receptor and cause the movement out of the blood through the relaxed jx and
    • into the SOI.

    • · Macrophages:
    • phagocytes (clean up the debris and IDing bacteria. that are tagged for
    • destruction)
  8. Time Course
    Chart
    • · 1st
    • line of defense

    • o Local
    • macrophages

    • § Very
    • large amounts of neutrophils present in the first 4 to 6 hours after
    • injury

    • § After
    • 4-6 hours: your body is now starting the clean up the injury

    • § Takes
    • care of the situation acutely

    • · 2nd
    • line

    • o recruit
    • more macrophages

    • § local
    • macrophages that causes more neutrophils to go to SOI

    • · 3nd
    • line of defense

    • o Monocytes:
    • immature macrophages

    • § Take
    • a while to get to the SOI

    • § Once
    • at the site, they will mature and become macrophages and perform the fx

    • § More
    • prolonged progression of immature/mature macrophages over (18 to 24 hours peak)

    • § Diminishes
    • out after 48 hours


    • · After
    • 24 hours: increase in T lymphocytes

    • o Immune
    • response

    • o Takes
    • even longer
  9. Leukocyte
    Adhesion Deficiency
    • · No
    • P-selectin receptors on surface the
    • endothelial cells

    • o Neutrophils
    • can’t target the area, so no WBC can get to the SOI to take care of injury or
    • MO

    • · Disease
    • in children that have recurrent bacterial infection because you don’t get rid
    • of the MO from the primary invasions because can’t get the WBC there to take
    • care of the MO.
  10. Lines of Defense
    • · 1st:
    • localized macrophages (mins) by chance they are present during the injury.
    • chemical mediators and plasma derived mediators that promote localized
    • macrophages to be 1st line of defense

    • · 2nd:
    • localized macrophages triggers/attracts further mediators to attract more
    • macrophages to the SOI

    • · Chemotaxis:
    • movement of cells to that attractive environment by chemical presence

    • · 3rd:
    • prolonged monocytes: immature/mature macrophages goes to SOI after 18 hours

    • · more
    • macrophages to prepare site for wound healing and repair
  11. Complement system:
    • : target MO for removal and
    • destruction
  12. o Clotting/
    coagulating system and Fibrinolytic system
    • § Decrease
    • or increase blood supply depending need
  13. o Acute-phage
    proteins
    • § IO1
    • beta promotes fever
  14. Systemic Changes during
    inflammation
    • · When
    • sustain injury or MO invasion, can produce systemic changes

    • · Changes
    • that occurs to assist us in controlling the MO invasion or to prepare body to
    • rid the invader

    · Fever


    • · General
    • Malaise (sleepy) – shutting our system down a little bit, allow body to rest so
    • give chance for responses to occur locally or globally around body

    • · Decrease
    • own activity to allow body to response accordingly

    • · Appetite
    • suppression, pain, pulse rate are the effects of bradykinin
  15. Diagnostic Test
    • · Neutrophil
    • count in peripheral blood (painful and long)

    • · Increate
    • erythrocyte (RBC) sedimentation rate (ESR):

    • o Blood
    • sample and spun/center fuse it down into a medium

    • o Goes
    • to a certain level and stays there

    • o You
    • will see an increase in fibrin and cause RBC to clump together and it will spin
    • at a different level. Increase ESR means inflammatory event

    • · Increase
    • acute phase proteins in the blood

    • o Proteins
    • that aren’t usually in the blood, but because of the inflammatory event, you
    • see the presence of these proteins

    • § Ex.
    • C- reactive proteins most common, made in liver and it usually tags bacteria
    • cells/ injured cells for destruction
  16. Benefits of
    Inflammation
    • · Heal
    • wound

    · Fever

    • o Increase
    • body temperature to create an unfavorable environment for MO to grow.

    • o Stimulates
    • an immune response (specificity assigned to the invaders)

    • · Clots
    • (walling-off effects)

    • o Occurs
    • to seal off the injury/MO and don’t let it spread to rest of body

    • · Clean
    • up area up to return to normal fx, extra fluids dilutes toxins and chemicals
    • also
  17. Review on Fever
    • · Release
    • of pyrogens in circulations

    • · Travels
    • to hypothalamus

    • · Resets
    • and increase in the set point

    • · Results:
    • body conserves heat

    • · Increased
    • in body temperature

    • · Body
    • response: warm, sweaty, lethargy

    • · To
    • combat the MO to grow further

    • · Once
    • the MO gone, can return back to normal

    • · Fever
    • gone
  18. Chronic
    Inflammatory Disease
    · Not just a prolonged local acute inflammation

    • o Ex.
    • Mouse is not a small rat

    • · Still
    • inflammation

    • · Area
    • of body in which mechanism is activated and it just stays on

    • · Constantly
    • have exposure to the certain organs to mediators that promote inflammation

    • o Crohn’s
    • disease

    • § Inflammation
    • of body organs that compromise it’s fx

    • · Inflammatory
    • response that is prolonged

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