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
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