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.
Membranous Nephropathy
Commonest cause of nephrotic syndrome in adults; idiopathic
*serum markers
2º: Malignancies, SLE, Rheumatoid arthritis., Drugs: NSAIDs, gold, penicillamine.
> usual steroid/ imm supp
List the common benign diseases of the prostate and state the principles of their clinical presentation, investigation
Investigations: MSU, flow rate study, post-void residual USS, bloods (PSA),
- renal tract USS
- cystoscopy for HAEMTURIA
- ⇧PSA or abn DRE = prostate biopsy
Recognise and understand the complications associated with benign prostatic obstruction, and the indications for surgical treatment
a
Benign Prostatic Hyperplasia
fibromuscular and glandular hyperplasia; primarily affects transition zone; disordered dihydrotestosterone
⇧age
- moderat to severe LUTS
- progression to BOObstr.
LUTS
symptoms indicative of nature of syndrome
OBSTRUCTIVE = VOIDING: hesistancy, poor stream, terminal dribbling, incomplete emptying
IRRITATIVE = STORAGE: freq, nocturia, urgency, incontinnce
BPO Tx
uncomplicated BPO (benign prost. obstr.)
* wait
* Alpha blockers = relax
* 5 alpha reductase inhibitors / 5ARI (Finasteride or Dutasteride) = testosterone to dihydrotestos.; ⇩prostate size
= Combination most effective in preventing progression; ⇩prostatic bleeding
- Surgical intervention
• TURP (prostate size <100cc) - prost. resection GOLD STANDARD; sfx: bleeds, infection, retro ejac., regrowth = recurrent haematuria or BOO (blad. outf. obstr.)
Open retropubic or transvesical prostatectomy (prostate size >100cc)
Endoscopic ablative procedures
complicated
> Sx
BOO Tx
(blad. outf. obstr.)
> mostly sx = TURP
> alternatively: LT catheter but has issues such as catheter trauma, blockages, frank haematuria or recurrent UTI
ACUTE URINARY RETENTION
painful inability to void with a palpable and percussible bladder; 500ml-1L+
> catheter
if no renal failure, alpha blocker and remove catheter
CHRONIC URINARY RETENTION
painless, palpable and percussible bladder AFTER voiding; 400 to >2L residual and voiding possible
*detrusor underactivity, or longstanding BOO (BPO, stricture) = LUTS
> symptomatic = catheter, CISC, TURP
CISC
Clean intermittent self-catheterisation (CISC) is the intermittent insertion of a catheter into the bladder by the patient in order to assist drainage of the urine when normal voiding is not possible.
UPPER TRACT OBSTRUCTION & LOWER TRACT OBSTRUCTION presentation and complications
UPPER:
PAIN, frank haematuria
*palpable mass, microscopic haematuria
compl.: INFECTION, SEPSIS, RENAL FAILURE
acute: renal funct. ?normal
chronic: high pressure v low pressure, partial or complete obstruction
LOWER:
incontinence, retention, infection and sepsis, frank haematuria, stone formation, RFailure
high-p = painless, incontinent, ⇧cr., bilateral hydronephrosis
low-p = painless, dry, normal cr, normal kidneys
UPPER OBSTRUCTION MGMT
RESUSCITATION: iv access, abg, cultures, fluid monitoring; analgesia
+abx?
+ HDU care? renal replacement rx?
*IMAGING
- EMERGENCY TX OF OBSTRUCTION:
- percutaneous nephrostomy insertion under LA
- retrograde stent insertion via cystoscopy
> stone = ureteroscopy and laser lithotripsy +/- basketing or ESWL
> ureteric tumour = radical nephro-ureterectomy
> PUJ obstr. = laparoscopic pyeloplasty
What is radical nephro-ureterectomy
Laparoscopic radical nephroureterectomy is a minimally invasive surgical procedure to remove the renal pelvis, kidney and entire ureter, along with the bladder cuff, in an attempt to provide the greatest likelihood of survival for patients with transitional cell cancer.
LOWER OBSTRUCTION MGMT
> catheter
> foley cathater
- EMERGENCY TX OF OBSTRUCTION:
- urethral catheter
- suprapubic catheter
underlying > BPE = TURP > stricture = optical urethrotomy > meatal stenosis = meatal dilatation > phimosis = circumcision
Complications of obstruction
DECOMPRESSION HAEMATURIA: vascular shearing d/t compliance of tissue, self-limiting
POST-OBSTRUCTIVE DIURESIS: 200ml/hr++, osmotic diuresis = Na thus H2O depletion
> saline input
The following are absolute indications for surgical intervention in patients with benign prostatic obstruction except:
a. refractory acute urinary retention
b. refractory chronic urinary retention
c. renal failure
d. recurrent UTI
e. bladder stones
refractory chronic retention bc can catheterise
The following are causes of acute urinary retention in men except:
a. spinal cord compression
b. urinary tract infection
c. constipation
d. pain from laparotomy wound
e. cystoscopy under local anaesthetic
cystoscopy under local anaesthetic
Long-term urethral catheters (e.g. silicone-based ones) should not be left in-situ for longer than:
a. 1 week b. 4 weeks c. 8 weeks d. 12 weeks e. 16 weeks
maximum duration of short term urethral catheters is 4 weeks
vs
long term catheters duration = min. of 4, up to 12w
What is the ‘gold standard’ investigation for renal colic?
a. Renal ultrasound scan
b. MRI of renal tract
c. IVU
d. CT-KUB
e. Plain KUB X-ray
CT-KUB
The following are common types of renal tract stones except:
a. Calcium phosphate
b. Calcium oxalate
c. Calcium bicarbonate
d. Uric acid (urate)
e. Magnesium ammonium phosphate (struvite)
Calcium bicarb (teeth, bones)
*with Calcium oxalate being commonest, alongside calcium phosphate being common too
Investigations of urinary tract obstructions
1) * CT-KUB *
non-contrast, low dose, no nephrotox., renal failure
+visualise stones and obstructions in emergency setting
- not as useful if ureter/collecting system undilated
- RENAL USS: upper tract hydronephrosis, hydroureter but cannot visualise cause of obstruction d/t obstruction of bowel gas
- IVU (old)
- CT Urogram - different phases; higher radiation, nephrotoxic, CI in RFailure, greater sensitivity for obstructing masses (carcinomas, pelvic mass)
- MAG3 isotope study = split renal function (ideally 50/50) = used for chronic unilateral upper obstruction esp chronic PUJ obstruction
DIABETIC NEPHROPATHY
hyperfiltration, altered glomerular composition, renal hypertrophy, and glomerular HT
= albuminuria + deposition of ECM
=> glomerulosclerosis, interstitial fibrosis
- increasing proteinuria associated w/ declining GFR
- commonest cause of ESRD
LUPUS NEPHRITIS: common signs, and mgmt
F>M; systemic fever fatigue mouth ulcers rash joints, butterfly rash
common for Pt. to develop lupus nephritis; glomerulonephritis w/ immune deposits
+ proteinuria (nephrotic syndrome)
+ haematuria, RBC casts
+ creatinine+++
> corticost.
or imm suppr.
MYELOMA: signs and dx
multiple myeloma = plasma cell profileration = XS Immunoglobulins
⇧ESR, anaemia, Wt loss, fractures, infections, backpain
LYTIC LESION; URINE DIP = HEAVY PROTEINURIA
- bone aspirate
- serum paraprotein
- urinary BENCE-JONES PROTEIN
- skeletal survey
Cast nephropathy, hypercalcaemia, hyperuricaemia, amyloidosis
Signs of systemic disease with renal involvement
1) SPLINTER HAEMORRHAGES, PURPURA, RAYNAUD’S
2) SCLERITIS, UVEITIS, RETINAL VASCULITIS, HYPERTENSIVE RETINOPATHY
3) VASCULITIC RASH, SCLERODERMA
+hypertension, creps, joint swelling tenderness, stroke encephalopathy
Investigations in systemic renal suspicions
URINE DIP
Bloods - ANCA (anti-MPO/anti-PR3 antibodies), ANA, dsDNA antibodies, Complement levels C3, C4, Blood cultures
Radiology – CXR, USS abdomen, CT thorax
Echocardiography
Kidney Biopsy
