Q.260. What is Fanconi syndrome(F.S.)?
KIDNEY PROTECTION
Revise please the abbreviation list on:
https://draft.blogger.com/u/0/blog/post/edit/8610857019469578230/4564412989605988372
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 fibrosis “between“ tubules
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) NSAID – Allopurinol- 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?
A. Sarcoidosis can be expected é : 👌
1.
Hypercalcemia.
2.
Unexplained R. F.
3.
Nephrocalcinosis.
4.
Tubular dysfunction.
5. I.G.
Q.268. How to ttt.?
A. Sarcoidosis ttt.:
(1) Prednisone 1 mg/kg.
(2) Chloroquine:🠋1 & 25 D.H.
cholcalciferole.
(3) Ketoconazol esteroidogenesis Vit. D.
(4) Infleximab: Chimeric anti-TNFa.
Q269. Enumerate
the most commonly drug-induced granulomatous AIN?
A. Drug-induced “granulomatous“AIN :(Drugs
most commonly involved
are in bold):
I.
Antimicrobials:
(1) Ampicillin.
(2) Methicillin.
(3) Penicillin G. (benzylpenicillin).
(4) Ciprofluxacin.
(5) Cotrimoxazole.
(6) Polymixin
B.
(7) Nitrofurantoin.
(8) Rifampicin.
(9) Sulfonamides.
II.
NSAID:
(1) Fenoprofen.
(2) Ibuprofen.
(3) Piroxicam.
(4) Indpmethacin.
(5) Diflunisal.
III.
Analgesics:
(1) Glafenin.
(2) Floctafenin.
(3) Clometacin(Clometazin).
IV.
Anticonvulsants:
(1) Phenytoin.
(2) Carbamazepine.
V.
Diuretics:
(1) Furosemide.
(2) Triametrene.
(3) Tienilic acid.
VI.
Aniulcers: Cimetidine.
VII.
Others:
(1) Allopurinol.
(2) Phenindione.
(3) Captopril.
(4) Chlorpropamide.
(5) Betanidine.
(6) Fenofibrate.
(7) Lamotrigine.
(8) Cyamemazine.
Q.270. Describe the criteria of analgesic nephropathy?
A. Analgesic
nephropathy criteria:
(1) Dcr. renal size.
(2) Bumpy contour.
(3) Papillary calcification.
Q.271. Enumerate the causes of Granulamatous interstitial
nephritis?
(SEE)
A. Granulamatous I.N.:
(1) T.B.osis.
(2) Sarcoidosis.
(3) Beryliosis.
(4) Wegener’s granulomatosis.
(5) Allergic
interstitial nephritis. (NSAID &5 A.S.A.) (see above).
Q.272. Describe the medical diseases associated with calcium stone formation 👆 ? 😎
A. Calcium stone formation can be present
in the foll. medical
conditions:
(1) Iry hyperpara.: PTH 🠉 bone resorption, [1,25(OH)2D3] R. synthesis & gut Ca+ absorption⮞ Hypercalcemia.
(2) RTA ⮞
💢
Acidemia:⮞ bone buffer (Ca+) release & dcr. ur. citrate
excretion.
💢
Po4 wasting:⮞ HypoPo4, 1,25(OH)2D3 R. synthesis & hypercalcemia.
(3) Granulomata:(T.B.
& Sarcoidosis) 🠉1,25(OH)2 D3 extra.R synthesis & 🠉 Gut Ca+ absorption.
(4) Milk-alkali synd. or incr. intake of Calcium-containing antacids.
(5) Gout & Hyperuricemia ⮞ Uric a. crystals ppt.
in acid urine⮞Ca oxalate
crystals nucleate & aggregate on the surface of uric a.
crystals.
(6) Iry/enteric
hyperoxaluria 2ndry to enteric bowel dis. Steatorrhea & bile salts ⮞ 🠉 intestinal
permeability to oxalate, 🠉Gut oxalate absorption or due to Iry dis.
Q.273. How can Sarcoidosis & Sjögren's syndrome affect the kidney?
A. “Tubulointerstitial” disease is common
in these diseases. Sarcoidosis also ⮞ Hypercalcemia & Ca+ stone formation (Nephrocalcinosis).
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