gabungan ppt inflamasi

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    SYSTEMIC RESPONSE TO

    INJURY AND METABOLIC

    SUPPORT

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    SYSTEMIC RESPONSE TO INJURYAND METABOLIC SUPPORT

    1. Overview: Injury-Associated Sytemic Inflammatory Response

    2. The Detection of Cellular Injury

    3. Central Nervous System Regulation of Inflammation in Response toInjury

    4. The Cellular Stress Responses5. Mediators of Inflammation

    6. Cellular Response to Injury

    7. Transcriptional and Translational Regulation of the Injury Response

    8. Cell-Mediated Inflammatory Response

    9. Endothelium-Mediated Injury

    10.Surgical Metabolism

    11.Nutrition in the Surgical Patient

    12.Enternal Nutrition

    13.Parenteral Nutrition

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    EVELINA MEILANY

    Overview: Injury-Associated SytemicInflammatory Response

    The Detection of Cellular Injury

    Central Nervous System Regulation ofInflammation in Response to Injury

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    The Cellular Stress Responses

    Mediators of Inflammation

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    Cellular Response to Injury

    Transcriptional and Translational Regulationof the Injury Response

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    SANG AYU KADEK WIDIARI

    Cell-Mediated Inflammatory Response

    Endothelium-Mediated Injury

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    CELL-MEDIATED

    INFLAMMATORY RESPONE

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    PLATELETS

    Platelets are small (2m), circulating fragments of a

    larger cell precursor, the megakaryocyte, that is located

    chiefly within the bone marrow.

    While their role in hemostasis is well described, that

    platelets play a role in both local and systemic

    inflammatory responses, particularly following ischemia

    reperfusion.

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    L!P"#$%&' * %+$&LL !!-%

    %he specific functions of these cells recognition and

    killing of intracellular pathogens (cellular immunity/ %h0

    cells), regulation of antibody production (humoral

    immunity/ %h2 cells), and maintenance of mucosal

    immunity and barrier integrity (%h01 cells). %hese

    actiities hae been characteri3ed as proinflammatory

    (%h0) and anti inflammatory (%h2), respectiely, as

    determined by their distinct cytokine signatures

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    'pecific immunity mediated by helper % lymphoctes subtype 0 (%"0)

    and subtype 2 (%"2) after in4ury.

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    DENDRITIC CELLS

    dendritic cells (*$s) are also actiated in response to

    damage signals, to stimulate both the innate and the

    adaptie immune responses.

    *$s are speciali3ed antigen+presenting cells (P$s)

    that hae three ma4or functions.

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    '#P"L'

    &osinophils are immunocytes whose primary functions

    are antihelminthic.

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    !'% $&LL'

    !ast cells are important in the primary response to

    in4ury because they are located in tissues.

    !ast cells are thought to be important cosignaling

    effector cells of the immune system ia the release of L+

    5, L+6, L+7, L+8, L+09, L+05, and L+06, as well as

    macrophage migration:inhibiting factor.

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    MONOCYTE/MACROPHAGES

    !onocytes are mononuclear phagocytes that circulate in

    the bloodstream and can differentiate into macrophages,

    osteoclasts, and *$s on migrating into tissues.

    !acrophages are the main effector cells of the immune

    response to infection and in4ury, primarily through

    mechanisms that include phagocytosis of microbial

    pathogens, release of inflammatory mediators, and

    clearance of apoptotic cells.

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    &-%;#P"L'

    eutrophils are among the first responders to sites of

    infection and in4ury and, as such, are potent mediators of

    acute inflammation.

    eutrophils do facilitate the recruitment of monocytes

    into inflamed tissues

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    ENDOTHELIUM-MEDIATED INJURYVASCULAR ENDOTHELIUM

    Under physiologic conditions, vascularendothelium has overall anticoagulant propertiesmediated via the production and cell surfaceexpression of heparin sulfate, dermatan sulfate,

    tissue factor pathway inhibitor, protein S,thrombomodulin, plasminogen, and tissueplasminogen activator.

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    NEUTROPHIL-ENDOTHELIUMINTERACTION

    The regulated inflammatory response to infectionfacilitates neutrophil and other immunocytemigration to compromised regions through theactions of increased vascular permeability,

    chemoattractants, and increased endothelialadhesion factors referred to as selectins that areelaborated on cell surfaces

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    CHEMOKINES

    $hemokines are a family of small proteins (< to 05 k*a)

    that were first identified through their chemotactic and

    actiating effects on inflammatory cells.

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    ENDOTHELIUM-MEDIATED INJURY

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    NITRIC OXIDE

    itric o=ide (#) was initially known as endothelium+

    deried rela=ing factor due to its effect on ascular

    smooth muscle.

    # synthesis is increased in response to

    proinflammatory mediators such as %>+? and L+0@, as

    well as microbial products, due to the upregulation of

    i#' e=pression

    ncreased # is also detectable in septic shock, where it

    is associated with low peripheral ascular resistance and

    hypotension.

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    'implified seAuence of selectin+mediated neutrophilendothelium

    interaction after an inflammatory stimulus.

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    PROSTACYCLIN

    Prostacyclin is a potent asodilator that also inhibits

    platelet aggregation.

    Prostacyclin acts through its receptor (a B+protein:

    coupled receptor of the rhodopsin family) to stimulate

    the en3yme adenylate cyclase, allowing the synthesis of

    c!P from adenosine triphosphate (%P). %his leads to

    a c!P+mediated decrease in intracellular calcium and

    subseAuent smooth muscle rela=ation.

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    ENDOTHELINS

    Endothelins (ETs) are potent mediators ofvasoconstriction and are composed of threemembers: ET-1, ET-2, and ET-3.

    ET release is upregulated in response tohypotension, LPS, injury, thrombin, TGF-, IL-1,angiotensin II, vasopressin, catecholamines, andanoxia

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    &ndothelial interaction with smooth muscle cells and with

    intraluminal platelets.

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    PLATELET-ACTIVATING FACTOR

    %he receptor for P> (P>;)

    P>; ligation results not only in the upregulation of

    numerous proinflammatory genes including $#C+2,

    i#', and L+8, but also in the generation of lipid

    intermediates such as arachidonic acid and

    lysophospholipids through the actiation of PL2.

    "uman sepsis is associated with a reduction in the leels

    of P>+acetylhydrolase, which inactiates P> by

    remoing an acetyl group.

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    NATRIURETIC PEPTIDES

    %he natriuretic peptides, atrial natriuretic factor (>)

    and brain natriuretic peptide (DP), are a family of

    peptides that are released primarily by atrial tissue but

    are also synthesi3ed by the gut, kidney, brain, adrenal

    glands, and endothelium.

    %hey are both increased in the setting of cardiac

    disorders/ howeer, recent eidence indicates some

    distinctions in the setting of inflammation.

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    ELLA PUTRI SAPTARI

    Surgical Metabolism

    Nutrition in the Surgical Patient

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    SURGICAL

    METABOLISM

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    METABOLISM DURING FASTING

    Fuel metabolism during unstressed fasting statehas historically served as the standard to wichmetabolic alterations after acute injury andcritical illness are compared

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    In the healthy adult , principal sources of fuel

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    y ,p pduring short term fasting (

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    METABOLISM AFTER INJURY

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    LIPID METABOLISM AFTER INJURY

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    KETOGENESIS

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    CARBOHYDRATE

    METABOLISM

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    PROTEIN & ASAM AMINO

    ACID METABOLISM

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    ESTIMATION OF ENERGYREQUIREMENTS

    NUTRITION IN THE

    SURGICAL PATIENT

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    VITAMINS AND MINERALS

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    OVERFEEDING

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    SYIFA MASHFUFAH AGMA

    Enternal Nutrition

    Parenteral Nutrition

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    CELLULAR RESPONSE TO INJURY

    Cytokines act on their target cells by binding tospecific membrane receptors

    Cytokine receptors that belong to theimmunoglobulin receptor superfamilies. Several

    of these receptors have characteristic signalingpathways

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    JAK - STAT SIGNALING

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    JAKs and STATs are central players in theregulation of key immune cell function.

    Suppressor of cytokine signaling (SOCS)molecules are a family of proteins that function

    as a negative feedback loop for type I and IIcytokine receptors by terminating JAK-STATsignaling

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    All SOCS proteins are able to regulate receptorsignaling through the recruitment of proteasomaldegradation components to their target proteins

    A deficiency of SOCS activity may render a cell

    hypersensitive to certain stimuli, such asinflammatory cytokines

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    GPCRs function by detecting a wide spectrum ofextracellular signals, including photons, ions,small organic molecules, and entire proteins.After ligand binding, GPCRs undergo

    conformational changes, causing the recruitmentof heterotrimeric G proteins to the cytoplasmicsurface.

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    The G subunits also include the Gq pathway,which stimulates phospholipase C- to producethe intracellular messengers inositoltrisphosphate and diacylglycerol. Inositol

    triphosphate triggers the release of calcium fromintracellular stores, whereas diacylglycerolrecruits protein kinase C to the plasmamembrane for activation

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    TNFR1 also induces apoptosis by activatingcaspase 2 through the recruitment of receptor-interacting protein (RIP)

    TRANSCRIPTIONAL AND

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    TRANSLATIONAL REGULATION OFTHE INJURY RESPONSE

    Many genes are regulated at the point of DNAtranscription and thus influence whethermessenger RNA (mRNA) and its subsequentproduct are expressed.

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    DNA TRANSCRIPTION

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    The DNA access of protein machineries involvedin transcription processes is tightly regulated byhistones.

    The role of histone modifications in the

    regulation of gene expression is referred to asepigenetic control.

    Histone methyltransferases in proinflammatorygene programs

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    mRNA transcript including 3 mechanisms: (a)splicing (b) Capping and (c) the addition of apolyadenylated tail