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Q.566. What is the effect of underlying disease on the immune system in CKD patients?

 

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Q.566. What is the effect of underlying disease on the immune system in CKD patients?

A. D.M. is the most common cause of ESRD in UK & Europe. W.H.O. lists DM as a cause of secondary immunodeficincy disease. Hyperglycemia both innate & adaptive immune system é defect in chemotaxis, phagocytosis & cidal activity of lymphocytes & neutronphils. Other dis.: [Amyloidosis, M.M., autoimmune dis.] abnormalT-cell & A.B. function.

Q.567. How could the treatment of underlying disease affect the immune function in CKD?

1)   Im/m.: CNI, steroids, cytotoxic thpy & biologics im/m. effect of uremic syndrome. Different im/m. T-cell (CNI) & B-cell (MMF & rituximab) function. So, these effects should be discussed é ptn, é continuous monitoring (WBCs) & proper A.B. in time.

2)   Pph.:  removal of Ig. & complement  risk of infection (theoretical/ no evidence.).

Q.568 What are the recommended vaccinations in CKD & ESRD?

A. Most guidelines advocate the foll. vaccinations in CKD & ESRD:

1)   Hepatitis B;

2)   Pneumococcus,

3)   Influenza,

4)   Tetanus,

5)   Meningiococcus (serogroup B). Ptn. é CKD & ESRD are less likely to respond to these vaccination.

Q.569 What are the general recommendation in influenza/HBV vaccinations (Vcc.)?

(A) Influenza Vcc: 🠞 signif. morbidity/mortality, espicially im/m. ptn. including CKD. In U.K. all CKD ptn. incl. in Vcc. programs 🠞signif. decrease in hospitalization & death in ESRD ptn..

(B) HBV. Vcc.: recmmended for ptn appr. ESRD to avoid transmission among ptn.s & between ptn. & staff. Resp. to Vcc. 🠟as s. Cr.& age rise. It’s successful in mild/ moderate CKD & only 37% in HDX. ptn.s who us. require larger dose than é Normal kid. func.. Immune defects🠞🠟 Vcc. resp.: impaired T-helper cell function, occur due to abn. cytokine signaling & 🠟 expression of HLA Class II molecules by Ag-presenting cells in CKD & ESRD.

- Typical HBV. Vcc schedule:  40 ug., repeated in:    1, 2 & 6 m.    

- Seroconversion: occ. when HB.s A.B. is >10 IU 3 m. after last vaccination.

Q.570. How can immune dysfunction affect cancer evolution in uremics?

A. Immune surveillance is an important mechanism for early detection & deletion of potentially cancerous cells. Immune dysf🠝risk of cancer in a 3 way:  👌 

1)   Direct effect of uremic toxins on immune cell function.

      2)   Underlying renal condition.                         

      3)   ttt of underlying renal condition.

 - This only theoretical, Not evidence-based, only mild🠝in Kid. & UT on DX. ptn.

Q.571 What is the suggested relation between cancer incidence and both Iry renal disease and ongoing therapy?   👉

💣 👽 { Calciphylaxis with Arterial Calcification.} 👀

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A. I. Cancer & “Iry”R. dis.:

1)   Von Hipple-Lindau disease.: auto. dom. familial cancer [multiple benign & malignant tumors: Kid., adrenals, CNS & pancreas].

2)   Analgesic NephropathyTransitional cell carcinoma.

3)   Balkan Np. Transitional cell carcinoma.

     II. Cancer & ttt. of R. dis.:

1)   Cph: 🠝 incid. of neoplasia (cancer U.B.), which may appear decades later.

2)   Im/m. é CKD & ESRD: 🠝 risk of cancer.

3)   R.Tx.: certain cancers: more common: non-melanoma “skin” cancer, Post Tx. lmphoprolifertive diso. Risk of neoplasia is linked to reg. used, é mTORs e.g. rapamycin:  Antiproliferative effect & 🠟 risk of neoplasia.

Q.572. What are the treatment options in patients with Calcific Uremic Arteriopathy?  👉

💣  👽  { Calciphylaxis with Arterial Calcification.}  👀

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A. I. Cancer & “Iry”R. disease:

A. Treatment options for Calcific Uremic Arteriopathy (CUA) (Calciphylaxis):

(1) Reduction of pro-calcifying factors:

*      Intensified: daily HDX., switch fr. P.D. to HDX., Low Ca Dzt.

*      Avoid vit. D & Ca supplements, Ca-free Po4 binders, bisphosphonate (cautiously é adynamic bone dis.).

*      Pec.(Parathyroidectomy): in severe hyperpara, or use of Cinacalcet - Etelcalcitide.

(2) Improving the status of calcification inhibitors:

Halt vit. K. antagonists (Warfarin).

Aggressive ttt. of infections or other pro-inflmm. stimuli to incr. fetuin-A level (-ve Ac. phase reactant).

Experimental:

o   Vit. K2 high dose.

o   Fetuin-A (by FFP, or Pph.)

(3) Prevention or reversal of Ca-phosphate precipitation:

   Administration of sodium thiosulfate.

(4) Supportive measures:

·         Avoid local tissue trauma by atraumatic wound care é gentle debridement of necrotic tissues & avoid s.c. injections.

·        Improve O2 supply by Hyperbaric therapy.

·        Anticoagulation. (Heparin, LMWH).

·        Adequate pain management.

·        Adequate infection control

                                                        


Q.573. What are the causes of intradialytic hemolysis?

A. Intradialytic hemolysis:

     I.        Incorrect osmolarity of dialysate.

   II.        Microangiopathy: Drug-induced: e.g Quinine Sulfate.

 III.        Glucose-6-Po4 def.: Exacerbated by oxidants (e.g Quinine Sulfate.).

  IV.        Reductive dge: Formaldehyde (also may activate cold agglutinins).

    V.        Cell membrane fragility:

*      Insufficient DX.

*      Zinc def.

  VI.        Thermal dge:

  Overheated Dzt. (> 47 °C ).

  Underheated Dzt: (<35°C): anti-N Cold agglutinins activation (formaldehyde).

VII.        Oxidative dge: Methemoglobulinemia:

1.   Chloramines,

2.   Copper.

3.   Nitrate/Nitrites.

4.    Drugs (e.g. Quinie So4).

VIII.        Interference with RBCs metabolism:

1) Copper: affects cellular thiols.

2) Aluminum: affects iron uptake.

3) Formaldehyde: inhibits glycolysis.

4) Hypophosphatemia:2,3-diphosphoglycerate def.

  IX.        Traumatic fragmentation:

(1) Dialyzer roller pump.

(2) Single-needle DX.

(3) Excessive suction arterial access site.

(4) High blood flow thr. a small needle.  

(5) Kinked DX cath./tubing.

(6) RT atrial subclavian cath.

Q.574. What are the causes of HDX-associated seizures?

A. “HDX-associated seizures:

     I.        Uremic encaphaloopathy.

   II.        Hyperensive encaphaloopathy.

 III.        DX. disequilibrium syndrome.

  IV.        Focal neurologic disease:

1)   Atheroemolism.

2)   Intracranial hge.

3)   Thrombotic microangiopathy.

    V.        Cerebral anoxia due to sustained hypotension:

1)   Hge.

2)   Sepsis.

3)   Cardiac arrhythmia.

4)   Hypersensitivity reaction.

  VI.        Metabolic:

(1)       Hypoglycemia.

(2)       Hypocalcemia.

(3)       Hypomagnesemia.

(4)       Hypernatremia: Hyperosmolarity.

(5)       Severe acid-base disturbances.

VII.        Drugs:

(1) Dialytic removal of anticonvulsats.

(2) Erythropoiesis-stimulating drugs.

(3) Epileptogenic drugs: [Theophylline, Penicillin, Meperidine (its toxic metabolite: normepredine)].

VIII.        Other toxins:

  1. Alcohol withdrawal
  2. Aluminum intoxication.

Q.575. Describe the evolution of MIA syndrome?   👵👵

A. Malnutrition, Inflammation & Atherosclerosis synd. describes wasting as part of an inflmm. 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 inflmmation process, é evidence that CRP enhances this process. CKD ptn have  levels of CRP & other pro-inflmm. cytokines incl. IL-6. The low s. albumin seen in MIA reflects ongoing inflammation & effect of cytokines on GIT, “rather” poor nutritional intake. 

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