Q.287. What is the most common type of bacterial infection in patient life?
VI. U.T.I.
Revise please the abbreviation list on:
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Q.287. What is the most
common type of bacterial infection in patient life?
A. UT.I.☜ is the most common bacteria infecting a patient in his life span.
Q.288. What are the criteria of diagnosis of UT.I.?"
A. Criteria of Dgx.:
🠞Urine examination [10] leukocytes/cmm3.
🠞Culture Validity (bacterial
colony count)105 colony forming unit, at least.
🠞Nature of organism: The most common:👉Enterococcus fecali s(G-ve).
Q.289. Which patient is more susceptible
for UT.I.?
A.“Susceptibility” for UT.I. (hematogeous or ascending):
(1) Obstruction of urine flow (even é short period).
(2) Intratubular
chemical injury.
(3) Vascular factors: intra renal V.C, R.V.
V.C.
(4) Hgc. hypotension.
(5) Analgesics.
(6) K+ depletion.
(7) Renal
massage.
(8) P.K.D.
Q.290. What is the suggested mechanism for ascending infection?
A. Two possible mechanisms:
v V.U.R.:
Congenital abnormalities é ureter insertion.
v Intrarenal ☜ reflux:
Papillae é opening
ducts
allow spread of organisms to R. parynchyma, inflmm., scarring & Ch. P.N.
Q.291. Is there any role for ACEI/ARBs in ttt. UT.I.?
A. ACEI/ARBs have Antisclerotic effect thr. : Down-regulation
of TGF-B (trans-forming
growth f. B. ) Prevention of R. Scarring. As, ch. P.N. & ch. inflmmation TGF-B & Platlet G.F. R. Scarring.
Q.292. How can D.M. increase the susceptibility to UTI.?
A. D.M.:
1)
Dc. Np.⮚Impair bladder emptying.
2)
D.M.⮚Papillary necrosis.
3)
D.M.⮚🠟🠟host defense mechanisms.
4)
D.M. ⮚Necrotizing invasive bacteriaEmphysematous infection..
Q.293.What are the direct possible factors precipitating Emphysematous cystitis or pyelonephritis?
A. “Emphysematous” cystitis or P.N. us. expected due to :
v Gas forming organisms invasion.
v High glucose level.
v Impaired
tissue perfusion.
Q.294.What is the relation between UT.I.
& patient age & sex?
A. Between infancy & 55 y. old (prostate), UTI is us.
predominantly a ♀ dis., in pediatric ch. P.N. is the most
common cause of H.T.
Q.295.What is the impact of V.U.R &
reflux nephropathy on kidney function?
A. V.U.R & reflux Np.: ⮚
(1) H.T.
(2) Retardation
of Renal growth.
(3) Obstruction &
other congenital anomalies.
(4) Progressive
G.losclerosis 2ry FSGS Proteinuria = 1.2-5.8 g/24h.
Q.296.What are the general impacts of UT.I.?
A. UT.I.
⮚ H.T.
⮚Incr. M.R.
⮚ Loss of renal function.
⮚Fetal & pregnancy outcome affection.
Q.297. When can you expect Renal tuberculosis?
A. Any unexplained (sterile) pyuria/hematuria think of T.B.
v Renal T.B. is the most common site of extrapulmonery T.B.
v Genitourinary T.B. us. results fr.: [Silent Bacillemia] ass. é pulm. T.B.
v Common
Sms:
[Dysuria- Hematuria – Flank pain] é PPD +ve (95%).
Q.298. What are the radiological findings? How to make a tissue diagnosis?
A. C.T. finding: 🠞 {Gross stricture - Cavities - & Calcification}.
Pathology: {
Granulomatous inflammation + Caseation Necrosis + Papillary
Necrosis +
Cavity formation } = R. T.B.
Q.299. How to treat? What is the proof of cure?
A. 5 different situations in “T.B.” therapy: ✋
I.
“Uncomplicated” U.T. T.B. é “drug-sensitive”
organism:
1st (2 m. [Rifampicin + INH + Pyrazinamide] +
4 m. [Rifampicin + I.N.H.]. in ♀ +
more (3-6) m. in ♂ (prostate T.B. nidus) .. total 12 m.
II.
If Pyrazinamide
is not tolerated[Rifambicin/INH] extended 9 m. for ♀ & added (3-6) m. for ♂ .
III.
“Caseating”
Kidney:
[Rifampin/I.N.H.] 12-18
m.سنه ونص
IV. AIDS: 9-12 m.
of ttt. considered. Relapse is common, so, incr. dur. of ttt.
V.
Drug resistant: until C. & S. is available, at least two bactericidal drugs (Rifambicin/INH/ Pyrazinamide) + one of (Ethambutol /Ofloxacin/ Strept-omycin). Once C. & S.
available continue for 12 m., but if only one
bactericidal drug available add (Ethambutol)
for 24 m. at least.
VI. If
ptn cannot
tolerate two bactericidal drugs
(SE), use only One + (Ethambutol) for 24 m.
-
The Proof of cure documented by👉culture & 👉 follow up urogram or U/S., to exclude Obstructive
uropathy caused by the “healing
process”, wch may necessitate surgical salvage.
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