W06: UTI, GLOMERULAR DISESE, Benign Prostate Disease, The Kidneys in Systemic Disease Flashcards
Discuss the clinical presentation and principles of management of patients with renal pain and ureteric colic.
a
Describe the presentation, investigations of urinary tract infections.
INVESTIGATIONS:
MSU: urinalysis @ ward
MSU: microbiology, baacteruria 10^5
if UTI frequent: USS or IVU or isotope studies
Levels of infection within the urinary tract
Kidney
- Acute Pyelonephritis
- Chronic Pyelonephritis
Bladder
* Cystitis
Urethra
*Urethritis
Prostate
*Prostatitis
Epididymis/Testis
*Epididymo-orchitis
RF to UTI
Immunosuppression
Steroids
Malnutrition
Diabetes
Sexual intercourse and poor voiding habits
Congenital abnormalities e.g. duplex kidney
Stasis of urine e.g. due to poor bladder emptying
Foreign bodies eg catheters, stones
Oestrogen deficiency in postmenopausal women
Fistula between bladder & bowel
Common aetiological agents of UTI
gram -ve
- e. coli
- proteus mirabilis
- klebsiella
gram+ve
- cog -ve staph.
- enterococci
Presentation of UTI
children: diarrhoea, systemic, n/v, nil eating, crying
adults: flank pain, dysuria, turbid offensive urine, urgency,
Presentation of pyelonephritis
systemic, loin tenderness at renal angle, dehydration, turbid urine
Presentation of pyelonephritis
systemic, loin tenderness at renal angle, dehydration, turbid urine
Describe the treatment of urinary tract infections.
- Fluids
- Antibiotics
Amoxicillin (3-5 day course or 3g x 2), cephalosporin, Trimethoprim - Severe infections
Intravenous antibiotics
Normally functionning UTract Vs Abnormal
normal = seldom renal dmg, produce normal IVU
* radiographic study of the renal parenchyma, pelvicalyceal system, ureters and the urinary bladder. This exam has been largely replaced by CT urography.
abnormal = anatomical/neuro, DM, stones,
Reflux Nephropathy
chronic in nature, childhood recurrent infection association
reflux + infection
*USS and biochem to assess progression
= findings of patchy interstitial scarring, tubular atrophy, and loss of nephron mass. It is often detected during a routine evaluation in early adulthood or during pregnancy
Quantification of Bacteriuria
≥ 10^5
Chronic Pyelonephritis
Radiological diagnosis
Scarring & clubbing
Hypertension / CRF
Explain the approach to diagnosis and management of patients with haematuria and proteinuria.
d/t inflammation of the kidneys (nephritic state)
Explain the diagnosis, pathological, and clinical manifestations of glomerulonephritis.
Glomerulonephritis is primarily diagnosed via biopsy
= Haematuria (non-visible or visible) Proteinuria (low grade or nephrotic) Hypertension Renal impairment
PROLIFERATIVE GLOMERULONEPHRITIS: presence of immune cells
= more nephritic in nature
NON-PROFILIEFRATIVE GLOMERULONEPHRITIS: normal/scarring but normal number of cells
= more nephrotic in nature
• diffuse or focal, global or segmental
State the management principles of glomerulonephritis.
> Lifestyle
BP Control
> Steroids
Imm Supp: Rituximab
Cyclophosphamide
Nephritic vs Nephrotic
NEPHROTIC: massive proteinuria (≥3.5 g/day) resulting in significant hypoalbuminaemia (serum albumin ≤30 g/L).
- associated with oedema (due to reduced oncotic pressure), hyperlipidaemia and hypercoagulability.
- Oedema (e.g. peri-orbital, lower limb, ascites)
- Xanthelasma and/or xanthoma
- Leukonychia
- Shortness of breath (with associated chest signs of pleural effusion – e.g. stony dullness in lung bases)
NEPHRITIC (more immune/inflamm in nature):
haematuria, mild to moderate proteinuria (typically less than 3.5g/L/day), hypertension, oliguria and red cell casts in the urine.
- dysmorphic rbcs sidement
- HT
- renal impairment
IgA NEPHROPATHY
common cause, M>F,
IgA deposition in the mesangium and mesangial proliferation.
- haematuria + proteinuria
- crescent deposition
Post Infectious Glomerulonephritis
Follows 10-21 days after infection typically of throat or skin; genetic predisposition
Most commonly with Lancefield group A Streptococci.
> diuretics for oedema
antihypertensives
Crescentic glomerulonephritis
d/t
1) ANCA
2) anti-glomerular basement membrane (GBM)
nephritis +/- resp. haemorrhage (goodpasture’s syndrome)
3) IgA vasculitis; SLE; post-infectious
= immune nature
GBM disease tx
anti-GBM
> aggressive immunesuppression: steroid, plasma exchange, and cyclophosphamide
NON-PROLIFERATIVE GLOMERULONEPHRITIS
Focal and segmental glomerulonephritis
Membranous Nephropathy
> Treat oedema: salt and fluid restriction and loop diuretics.
Hypertension: use Renin-Angiotensin-Aldosterone-blockade.
Reduce risk of thrombosis: Heparin or Warfarin.
Reduce risk of infection e.g. pneumococcal vaccine.
Treat dyslipidemia e.g. statins.
Significance of MINIMAL CHANGE DISEASE
commonest in children; sudden onset of oedema/days
> steroids for remission but relapse common
PREDNISOLONE then TAPER.
+ ?thromboprophylaxis
> relpse tx: (imm-suppr.) Cyclophosphamide Cyclosporin Tacrolimus Mycophenolate mofetil Rituximab
end-staage kidney disease risk is low
Focal and segmental glomerulosclerosis
(nephrotic)
Pathology reveals focal and segmental sclerosis with distinctive patterns e.g.
tip lesion, collapsing, cellular, perihilar, and not otherwise specified.
• steroid resistant; high risk end stage progression
> Trial of steroids, positive response , even partial remission, carries better prognosis.
Alternative options: cyclosporin, cyclophosphamide, and Rituximab.
