Q.575. Describe the evolution of MIA syndrome?

 

HEMODIALYSIS

 

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 2^ndry 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 lumen⮞less 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 1^st 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.

-2/3^rd of bleeding events occ. é 1^st 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].