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Q.575. Describe the evolution of MIA syndrome?



 hemodialysis complications hemodialysis meaning hemodialysis machine hemodialysis procedure hemodialysis and peritoneal dialysis

Q.575. Describe the evolution of MIA syndrome?  

A. Malnutrition, Inflammation & Atherosclerosis syndrome describes wasting as part of an inflmmation state ass. é CVS dis. It's not responsive to 🠝 dietary intake. MIA explains the 🠝 CVS risk é failing kidney. The evolution of athero. is an inflmm. process, é 🠝 evidence that CRP enhances this process. CKD ptn have 🠝 levels of CRP & other proinflmm. cytokines incl. IL-6. The low s. albumin seen in MIA reflects 👉 ongoing inflammation & effect of 👉 cytokines on GIT, “rather” poor nutritional intake. 👍

Q.576. What are the common coagulation disorders that occur 2ndry to renal disease?

A. Uremic bleeding 🠟 hemostatic mechanisms (esp. Iry hemostasis, incl. vWF & Plt. adhesion) Ø clinical bleeding: bruises, G.I., venipuncture… due to:

I. “Low Hct.”: Hct. inversely related to B.T. (🠝 B.T. é R. anemia). As Hct rises 🠝Plt. adhesion to subendothelium. As RBCs travel through B.V. é fast stream at the center of lumen, plt. diffuse radially 

more adhesion to sites of injury, so, dcr. in Hct fast Plt. passage in the center of lumenless chance for adhesion. Conversely, Hct rise &  bld. viscosity (e.g. by diuretics)incr. thrombotic risk. Uremic electrolyte procoagulant activity due to phosphatodylserine exposure. So, maintain Hct at 30 in RF ptn.  👈

II. Plt. dysfunction”: Before DX, Plt. count is N., or mildly dcr., but function is impaired due to uremic toxins (urea, Cr., phenolic a. & methylguanidine). Dcr. affinity to vWF & 🠟 expression of Gp1b receptor Ineffective adhesion to subendothelium.

-      🠝 N.O., PGI2, Ca & cAMP 🠞V.D. 🠟 Plt. aggregation.

III. Thrombocytopenia”🠞bleeding, due to:

                                                     i.    Heparin-induced.

                                                    ii.    Contact to “artificial surface” in HDX.🠞Thrombosis.

Q.577. How to investigate for uremic bleeding?    

A. Uremic bleeding therapy:

1)   CBC: essential to ensure adequate H.B., Hct. & plt. count.

2)   Coagulation tests: P.T/aPTT: N. in uremics, abn. in DIC. Fibronigen & D Dime-rs: Ac. Phase reactant, incr. é inflmm. & accumulate in CKD (Renal clearance).

3)   B.T.: N.=2-7 min. Largely replaced by PFA 100.  

4)   PFA 100 system: in vitro system wch try to reproduce high shear circulation involving vWF binding & plt. adhesion, activation & aggregation. It’s sensitive to abn. in vWF & plt. adhesion. Closures times is shorten in DX & DDAVP.

Q.578. How to manage uremic bleeding? 

A. Choice depends on clinical circumstances:

(1) DDAVP:(Arginine Vsaopressin): acts on endothelial vasopressin V2 recep. & cAMP- signaling 🠊 exocytosis of vWFfr. Weibel-balade bodies where it’s stored. DDAVP infusion 🠊larger vW f. VIII multimer + 🠟B.T. It’s the 1st choice for ur. bleeding as it hs rapid onset + ½ life =10 h. & B.T. returns baseline in 48 h.

-Single infusion of 0.3 ug/kg us. sufficient for R. biopsy & No overload or change in electrolytes, despite 🠝 in osmolality, but it’s C.I. in cardiac💢insufficiency.

(2) Cryoppt.: rich in vWf, f VIII & fibrinogen: reverse abn. in hemostasis in min-utes, used if DDAVP failed or in emergency surgery, if intravasc. vol. tolerated

(3) Platelet Tx.:  4-5 h. hemostatic effect. Pre-storage leucodepletion: 🠟incidence of alloimmunization with subsequent Plt. refractoriness.

(4) Red cell Tx.: Allow margination of Plt. & improve markers of Plt. activation.

(5) Tranexamic acid (Cyklokapron) 5 mg/24 h.: 🠟 fibrinolysis by forming a rever-sible complex é plasminogen & 🠟its conversion to plasmin. Single dose used + DDAVP, which 🠝 release of tPA.

(6) Recombinant activated f. VII.: 90 ug/kg., for emergency: binds directly to activated Plt.: thrombin burst: short ½ life. So, given/2h.

(7) Epo:Erythopoiesis, 🠝 Hct. & facilitating plt. margination & signaling thr. tyrosinephosphorelation 🠝 metabolically active reticulated plt. & improve HB scavenging effect for N.O. Effect is delayed several days (not suitable for Ac. Cases).

(8) Conjugated estrogen: i.v.0.6 mg/kg/30 min/5d., onset: 6 h.]7-21 d. It 🠝 vWF & f. Viii,🠟protein S levels: improve bleeding, used é elective surgery & suitable for .

(9) DX.: especially.D.: improves platelet dysfunction & help in 🠟uremic bleeding.

Q.579. What precautions should be taken if a uremic patient should be biopsied?

A. 20% of C.O.: kidney (highly vascular):bleeding risk:2-8 % overt, it reach-es 90 % é C.T. (hidden bleeding & peri-R. hematoma). Degree depends é R.I., é highest level é uremics. So, DDAVP 0.3 ug/kg, 30 min before biopsy:🠝 Risk of bleeding. Pre-biopsy evaluation incl.: 

PT & aPTT.

Hct. & Plt. count.

Stop asprin & NSAID intake.

Personal & family bleeding history.

- Stop Asprin, 2 w. before biopsy (greater effect on Plt. in uremics thn N.).

- Stop warfarin, 5 d. before biopsy, or replace é Heparin & stop it é day of biopsy. Transjuguler  biopsy is safer in risky ptn.

-2/3rd of bleeding events occ. é 1st 8 h., so 24 h. observation are advised.

Q.580. What thrombotic disorder can be seen in a uremic patient?

A. Despite effect of uremia on Plt., CKD ptn. hv a hypercoagulable state with :

1)   Enhanced thrombin generation due to tissue f. pathway activation.

2)   Reduced antithrombin level

3)   Resistance to activated protein C.

4)   Plt., monocyte & endothelial cell actvation or injury.

-Incr. hepatic synthesis of f. II, V, VII, VIII, X & XIII : Augment thrombin form-ation & fibrinolytic activity reduced. Thrombotic comp. occ. in: [Site of vascular access- DVT- coronary, cerebral, retinal].



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Q.575. Describe the evolution of MIA syndrome?
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