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INTENSIVE CARE NEPHROLOGY

Q.475. What is the role of proinlflammatory cytokines in the pathophysiology of sepsis?

 

INTENSIVE CARE NEPHROLOGY

intensive care nephrology beyond basic intensive care unit nephrology nephrology and intensive care associates
Single kidney

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Q.475. What is the role of proinlflammatory cytokines in the pathophysiology of sepsis?

A. Proinlflammatory cytokines: 👉 [TNFa– IL1B-IL6-IL8]  released in response to infectious stimuli: TNFaIL1B  wide range effects incl.:  {activation of macrophage , lymphocytes, reticulocytes, incr. expression of adhesion molec-ules & incr. production of inflammatory cytokines.}

Q.476.What is the role of antiinlflammatory cytokines in the pathophys-iology of sepsis?

A. Antiinflammatory cytokines 👉[TNF B- IL10-IL13] they  Reduce the pro-inflamm. cytokines (TNFa – IL1B), furthermore, in animal models, these cytokines ð a KEY component of Sepsis, As: infusion of TNFa– IL1B  Shock state, and A.B. to these cytokines   attenuate the shock-like state.      

Q.477.What is the role of Neutrophil in the pathophysiology of sepsis?

A. Neutrophils: in critically ill ptn. Abn. Neutrophil function  Reduced migration & superoxide production & bacterial killing = ALL impair host def-ence mechanisms.

Q.478.What is the role of other mediators?

A. Other mediators:

1)   PGE2: Responsible of V.D. of septic shock.

2)   Thromboxane A2: V.C. & Platelet & leukocyte aggregation.  œœ

3)   PAF: produced by many cells in resp. to inflmm. stimuli & stimulate leukocyte adhesion to endothelium.

4)   NF.KB : (a transcription f. located in cytoplasm of mast cells) Recently: stimulation of cells by cytokines, bacteria or viral by-products   Translocation of NF. KB  fr. cytoplasm to nucleus, where it regulates transcription of target genes, wch. activate & modulate cytokines, chemokines & receptors of [Sepsis-SIRS-ARDS -MODS.].

Q.479. How can the coagulation system affected by sepsis?

 A. Sepsis

*      Protein C & downregulate its convertion to active protein C  Thrombosis.

*      Dramatic  of anti-thrombin III.(which inhibit thrombin III & f.X.)   microthrombosis  MODS.

Q.480. What are Toll-like receptors? What is its significance?

A. Toll-like receptors: [T.L.Rs.] (toll=mark):[Proteins tht recognize sp. patt-ern of a pathogen]. Ten human T.L.Rs, when stimulated  Cascade of Signal-ing events  production of cytokines & effector molecules, incl. (TNFaIL1-IL6.) wch’re the Iry transduction of the inflamm. resp. to the invading organism.

Q.481.What is the role of the kidney in T.L.R.s. expression?   

A. T.L.Rs. are necessary for HOST DEFENCE , The kidney express most of the T.L.Rs., but T.L.R. 2 & 4 most studied, because they have a potential role in mediating G+ve (Tol 2) & G -ve (Tol. 4) signaling.             

- A possible role of Local T.L.Rs. in mediating R.F. is evaluated, moreover, Local T.L.Rs.  directly mediate AKI seen in sepsis.

Q.482. Describe the clinical features of sepsis?

A. C.F. > [fever-hypothermia- tachycardia-tachpnea-leukocytosis-leukopenia]. Many cytokines > Sn & Sm. e.g. TNFa & IL1   Fever, .. Failure to dev. fever M.R., hyperglycemia, hypoglycemia, hypocalcaemia, hyponatremia, hypokalemia, hypomagnesemia & hypophosphatemia all are seen.

- Sev. sepsis  Hypotension due to   N.O. release & dcr. circulatory volume.

- Intravascular vol. depletion occ. due to:

1)   Incr. insensible losses.   

2)   Incr. microvascular permeability.

3)   Dcr. systemic vascular resistance. (SVR).

- Once resuscitation occur  Hyperdynamic CVS é   C.O. &   SVR.

Q.483.What  is the effect of sepsis on the heart  & respiratory system?

 A. Sepsis   Myocardial depression LVED volume & LVES volume, the accused f. TNFa– IL1, ……. also, N.O.  -ve intrope.

- Hypoxia & tachypnea, ARDS= 40 %.   Adrenal insufficiency= 40 %.

- DIC, Lab  thrombocytopenia,   PT,   a.PTT,  D-dimer.

Q.484.What is the effect of sepsis on the CNS & peripheral nerves?

 A. Septic encephalopathy= the most common in ICU, due to  

1)   Impaired mitochondrial function.

2)   Impaired O2 extraction by the brain.

3)   Disruption of astrocyte end-feat.                     

4)    All inflmm. mediators Neural inj., confusion, lethargy, obtundation & coma.

5)   Critical illness polyneuropathy due to  axonal degeneration, ch.ch. by hyporeflexia, weakness, distal more than proximal.

Q.485. Explain, how could the kidney be affected in sepsis?

  A.  Incidence: 9-60%.    M.R.: 50%

- Clinically: ATN  up to [Bilateral Cortical Necrosis]. 

               

- Hypotension  Renal hypoperfusion  AKI.  As does nephrotoxic ag.s.

 Role of Cytokines:   

1.    TNFa   Release fr. (mesangial) cells:  

i.             Leukocytes accumulation in the glomeruli.

ii.            Apoptotic glomerular endothelial cell death.

iii.          Endothelin production.

2.    IL1:     

                                         i.    V.C.

                                        ii.    Neutrophil aggregation.

                                       iii.    More cytokine release.

3.    Thromboxan E2  [RBF,  GFR, Afferent V.C.].  œœ

4.    Leukotriens released é endotoximia RBF & GFR.

5.    PAF (platelet aggreg. factor) Both aff. & eff. arteriolar resistance &  GFR.

6.    Endothelin 1  incr. é response to septic mediators incl. TNFa  Renal V.C., inhibition of Na+ & water reabsorption by collecting tubules.

Q.486.What are the potential contributors of MODS in sepsis?

A. Potential contributors of MODS:

  Hypoperfusion.     

  Microvascular thrombosis.

ƒ  Mitochondrial dysfunction.

  Ischemia /Reperfusion injury.

  Circulating inflammatory load.

  Diffuse endothelial cell injury.

  Increased tissue N.O.

ˆ  Bacterial toxin translocation.

Q.487.What are the main tools in management of sepsis?

  A. Three main items:

 I. Eradication of infection.    II. Hemodynamic support.     III. Activated vitamin C.

Q.488.What are the recommendations in infection eradication?

  A. A.B. coverage  should be   Double é :    

1)   Pseudomonas aerogenosa.

2)   Febrile Neutropenia.

3)   Intra-abdominal infection.

Q.489. How can you perform hemodynamic support in sepsis?

 A. At least 10 L./crystalloid/1st 24h., as profound hypotension occ. due to: [Volume depletion- Peripheral V.D.- Incr. permeability]. So, aggressive vol. resusc-itation, boluses of fluid given until reperfusion occur, e.g. urine output.

- Colloid Vs crystalloids   No evidence of preference. 

Q.490.What is the goal-directed therapy in hemodynamic support?

A. Goal-directed therapy a use of the foll. end-points to improve M.R.: 

  C.V.P.

  Hematocrit.

ƒ  Mean arter. B.P.

  C.V. O2  saturation.

- Tools:👉

1)   Dopamine & Nor.  1st choice in sepsis:Dopamine: limited use, as sepsis incr. its chrono. effect   tachycardia & arrhythmia. - Nor.: as effective as dopa. in   B.P, but less cardiac effect, it doesn’t   C.O. as dopa.

2)   Epinphrine: used in refractory hypotension, but  s. lactate.

3)   Vasopressin: of posterior pituitary V.C. & antidiuresis. It’s incr. (20-200) times in shock, it cn spare Nor.,   B.P. & cardiac index.

-Alth. [Nor.] Profound glom. affer. V.C., [Vasopressin]   G. effer.V.C GFR, but Vasopressin coronary V.C.   AMI. & hs No +ve inotropic effect.

4)   Doputamine: cn be used to  O2, but cn potentiate hpt., due to B2 V.D., it is recommended for low cardiac index (< 2.5 L/min/m2) after vol. resuscitation, but if B.P. 80 , it shd be used with Nor., to mediate peripheral V.C.

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Q.475. What is the role of proinlflammatory cytokines in the pathophysiology of sepsis?
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