Q.385. Why does the B.P. increase é Epo therpy?

 

Erythropoietin therapy

Revise please the abbreviation list on:

https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372

Q.385. Why does the B.P. increase é Epo therpy?

A. Two  ✌ main reasons:

I. Incr. RBCs mass 🠊🠝P.R.

II. Incr. “vascular reactivity”, due to:  👌

              (1)  🠋 N.O. production  🠊 Loss of its V.D. effect.

(2)   Release of Endothelin & V.C. protanoids  🠊 incr. Cytosolic Ca+.

(3)   Trophic effect of Epo on endothelial cell growth.

Q.386.What is the role of oral Iron in ttt. of anemia in H. DX. patient?

A. Pooooor, 😌😌😌 why? :

1. Poor compliance, due to G.I. upset, two cp./d at least, poor education.

2. Poor efficacy, need to be taken é empty stomach, poor absorption.

3. Poor absorption: Po4 binders interfere é iron absorption.

 (Ca acetate 27%- Ca Hco3. 19% - Sevelamer Hcl 10%)

** Oral iron can only be used in:  1. P.D.       2. Pre-DX.  … as much less iron losses.

Q.387.Then if it is used, how to enhance its efficacy?

A. Tools:  👉

1)   Dose: 200 mg elemental iron = 3 t. of 325 mg “ferrous So4”.  A new agent, “heme iron polypeptide” ➤ more effective & tolerable.

2)   Intake: between meals, at least one h. apart fr. Po4 binders (interfere é absorption).

3)   Avoid S.R. (slow release) forms, as it absorbed proximally (Duodenum).

Q.388.What is the suggested strategy for i.v. iron therapy?  †

A. Two ✌ possible strategies:

I. Periodic replacement: if iron def. detected🠞 Short replacement course of 1000 mg Iron, cn be divided é 2-3 w.

II. To anticipate iron def. by small weekly doses: 12.5-100 mg i.v. to improve Epo resp.  .

-      Iron profile assessment 🠞 should be quarterly=/3m.

-     3 forms are available:

1.    Iron sucrose: polynuclear iron CHO.

2.    Iron dextrose🠞 vasoactive mediators fr. Mast cells 🠞 31 deaths é U.S.    💀💀

3.    Iron gluconate: Ferric gluconate.

Q.389. How to monitor iron therapy?

A. Evidence-based iron monitoring:                                                                                                i. Initial therapy & not recording iron def.Ø monthly monitoring, until:                                  ii. Stable dose Epo/Iron🠞 3 monthly (quarterly).                                                              Two important tests:       i. TSAT.       ii. S. Ferritin.    … Moreover,   iii. PHR: Percent % hypochromic RBCs.    iv. CHr: Reticulocyte HB content.   

- For Specifity & Sensitivity reasons, use:👆 S. ferritin for  👉 iron “Overload” evaluation.    &

TSAT for  👉iron “Deficiency” evaluation.

Q.390.What are the recommended targets for the aforementioned parameters?

A. Target ferritin: NKF. (K/DOKI) 2006 guide lines🠞

                   {🠝100 ng/ml (P.D & Pre-DX.). & 🠝 200 ng/ml (H.DX.)}.

                       * T.S.A.T. 🠞🠝20 % (20-50%)  & * CHr 🠞 29  Pg.

- CHr🠞 Excellent, stable & accurate ,while (PHR) % hypochromic RBCs, used for iron status in H.DX., not accurate, affected by bld storage. (🠋MCV).

- CHr🠋(29-31) pg.🠞 need for iron thpy,.. Reticulocytes🠞 circulate in circul-ation only for 24 h. So, they reflect ACUTE changes in Iron Status.

Q.391. Is there is another tool to declare iron overload rather than ferritin?

A. SQUID🠊[Superconducting Quantum Interference Device]🠞 Excess iron is present in the liver of 70 % of H.DX. ptn. Significance is undetermined.

Q.392. Can we treat anemic patient with iron during acute infection?

A. Risk of infection incr. é ferritin é500-1000 (some claim: it’s just a reflection infection.), So, the best thing is to AVOID I.V. iron during episodes of acute infection.

Q.393. Explain?

A. In CKD: i.v. iron

🠞🠝 oxidative stress, enzymuria, proteinuria & generation of “superoxide radicles”.  … As:

1)   I.V. iron does release some iron directly into circulation.

2)   The released amount, overwhelm the ability of transferrin to buffer them 🠞 “free labile” iron into circulation.

3)   This free labile iron🠉 oxidative stress & pathological events e.g. ath-erosclerotic vessel dis..

- A potent role of iron in accelerated CVS disease (as iron deficiency🠞 protective 🠞 against atherosclerotic vascular disease) is documented.

Q.394. When to consider the response of Epo is delayed or diminished?

A. Failure to reach target Hct over 4-6 m. é adequate iron stores é dose of 450 i.v./ 300 s.c. u/kg/w. (rHEpo), or failure to maintain Hct é this dose.

Q.395. So, when to start work up for Epo resistance?

A. Start work up for Epo resistance é:

1)   Inadequate H.B. level for Epo.-dose.

2)   More Epo-dose needed to maintain Hct.

3)   Dcr. in H.B. é constant dose of Epo.

4)   A dose of 🠉500 i.u./kg/w. rHuEpo, failed to incr. H.B. to🠉11 g.