Loading ...

Followers

KIDNEY PROTECTION

Q.260. What is Fanconi syndrome(F.S.)?

 

KIDNEY PROTECTION

tubulointerstitial diseases ppt tubulointerstitial diseases of the kidney ppt tubulointerstitial renal diseases glomerular and tubulointerstitial diseases pathology of tubulointerstitial disease tubulointerstitial disease symptoms causes of tubulointerstitial nephritis how to diagnose tubulointerstitial nephritis tubulointerstitial disease causes

Q.260. What is Fanconi syndrome(F.S.)?

A. A generalized disorder of R. tub. transport [Po4.uria, a.a.uria, glucosuria+ Loss of K+, uric a., HCO3]. Transport abnormal are mainly proximal but can also occur é distal tub.. Partial F.S. can occur, but if multiple transport defects occur this means multiple processes e.g.: Krebs cycle, Na, K+-ATPase, are defective. Ultrastructural abn. involve mitochondria & endoplasmic reticulum. C.P.: {Rickets, osteomalacia, metabolic acidosis, stunted growth (children) & hypo-kalemia]. In “Pediatric”: Cystinosis is ass. é F.S.. In adults, hypoPo4 is Sm.-tc. and acquired F.S., may be ass. é M.M., Wilson’s dis. & tub. toxins. F.S. may be an 👉early feature of M.M.  

Q.261. What is difference between renal tubular disorder & tubulointerstitial diseases?

A. Interstitial dis. are ch.ch.by: [inflammation or fibrosisbetweentubules that transport abnormalities, wch’r 2ndry to the inflmm. or fibrotic process].   While...

- R. tub. defects: ch.ch. by [transport abn.+”preserved R. architecture]. Filtered substances [Gluc., a.a., Po4, Ca, Mg.,Na, K+, uric a.] us. reabsorbed in proximal tub., then their excretion is regulated in distal tub.. A reduction in transport of any of them inadequate reabsorption & appearance in urine. Defects may be genetic or acquired.

Q.262. What causes Nephrogenic diabetes insipidus (D.I.)?

A. Inability of the collecting ducts “to respond to Vasopressin🠞 D.I., due to:

(1) Toxic: [Amphotericin B., Li-thpy, HyperCa+, sev. hypok+, distal nephron injury].

(2) Genetic loss of function of proteins incl.: V2 vasopressin receptor & water channel, aquaporin-2.

(3) Obstructive injury.

 

Q.263. What is “Heymann” Nephritis?

A. Injection of crude preparation of (tub. brush border extract) called (Fx1A) into allogeneic rats 🠞 [A.B. mediated response, mimic M.N. in humans + tubulointerstitial injury]. The responsible Ag. MEGALIN.

Q.264. What are the causes of Ac. tubulointerstitial nephritis (TIN)?

A. Aetiology of Ac.TIN :

1)   A.B.: [Cephalosporins- Ciprofluxacin- Sulfonamide].

2)   NSAIDAllopurinol- Aza- Acyclovir.

3)   Infection: {CMV-EBV-HIV- Mumps- Leptospira- Legionella.}

4)   Idiopathic:(Im/m):Anti-tub. B.M dis.

5)    TINU: Tubulointerstitial Nephritis & Uviitis syndrome.  

- All NSAID esp. [Fenoprofen & Refocoxib (vioox)]:🠞 Risk of TIN disease.

Q.265. What is the hallmark of Ac. tubulointerstitial nephritis?

A. The hallmark of TIN.: { Eosinophilic & Lymphocytic inflamm. cell infiltration é interstitium, Sparing 👉 B.V. & Glomeruli}.     

Q.266. What is the clinical Triad of Ac. tubulointerstitial nephritis?

A. Classic clinical Triad of Ac. TIN.:   👌

*      Fever.

*      Rash.

*      Arthralgia.

 

Q.267. When can Sarcoidosis be expected?


tubulointerstitial diseases ppt tubulointerstitial diseases of the kidney ppt tubulointerstitial renal diseases glomerular and tubulointerstitial diseases pathology of tubulointerstitial disease tubulointerstitial disease symptoms causes of tubulointerstitial nephritis how to diagnose tubulointerstitial nephritis tubulointerstitial disease causes