Renal/Urology Flashcards
AKI
- Diagnosis
- Causes
- Presentation
- Investigation
- Management
Diagnosis
Stage 1- 1.5-1.9x increase in Cr OR <0.5ml/kg/hr u/o for 6h
Stage 2 - 2-2.9x increase in Cr OR <0.5ml/kg/hr u/o for 12h
Stage 3 - >3x increase in Cr OR <0.3ml/kg/hr u/o for >24h OR initiation of RRT
Refer to nephrology if: renal transplant, unknown cause of AKI, inadequate response to tx, complications, stage 3 AKI, CKD stage 4 or 5, if needing RRT (see below), vasculitis, glomerulonpehiitis, myeloma
Causes
- Pre-renal - volume depletion/low BP, drugs (ACEi, aminoglycosides, NSAIDs, diuretics)
- Renal - nephritic syndromes, toxins (e.g. rhabdo (myoglobin), contrast), ATN
- Post-renal - obstruction e.g. BPH, stones
Presentation
- Oliguria
- Uraemia -> confusion, itching, pericaditis
- Acidosis
- Hyperkalaemia -> arrhythmias
Investigation
- U&Es + other routine bloods
- USS KUB
- Urinalysis - ATN/Renal cause - kidneys lose ability to hold onto Na (to preserve circulating volume) + concetrate the urine -> urine Na >40 and urine osmol <350). Pre-renal the kidneys try to help - urine Na <20 and urine osmol >500)
- (ATN is most common cause of AKI can be due to ischaemic (hypovolaemic) or toxins (e.g. meds).
- Determining between acute vs chronic kidney disease - chronic tend to have small kidneys bl on USS (except polycystic kidney disease, early diabetic nephropathy + amyloidosis) also in CKD you get hypocalcaemia/secondary hyperparathyroidism
Management
- Treat Cause
- Meds review
- Treat complications e.g. hyperkalaemia
- Consider referral for RRT: refractory hyperkalaemia, metabolic acidosis, complications of uraemia, fluid overload
CKD
- Diagnosis
- Causes
- Presentation
- Investigation
- Management
Diagnosis
- Stage 1 - eGFR >90 w/ other signs of kidney disease
- Stage 2 - eGFR 60-90 w/ other signs of kidney disease
- Stage 3a - eGFR 45-59
- Stage 3b - eGFR 30-44
- Stage 4 - eGFR 15-29
- Stage 5 - eGFR <15 or need for RRT
eGFR is adjusted for race, age, sex, Cr level
N.B. if eGFR >60 + no other signs of kidney disease then this is NOT CKD
Causes
Most common:
- Diabetic nephropathy
- HTN
Other:
- Chronic glomerulonephritis
- Chronic pyelonephritis
- Adult polycystic kidney disease
- BPH
- Myeloma
Presentation
Asymptomatic. Can -> uraemia (fatigue, weakness, anoreixa, vomtiing, metallic taste in mouth (urea), pruritis, restless legs, bone pain)
Blood gas = metabolic acidosis w/ resp compensation
Complications –> increased CVS risk, anaemia (low EPO), renal bone disease (low Ca2+ + phosphate -> PTH raised -> increased bone resorption -> osteitis fibrosa cystica), fluid overload
Investigation
- Urinalysis + ACR
- Certain patients should have regular screening: DM, HTN, >60yo, recurrent UTI, urinary obstruction, systemic illness, fam hx stage 5 CKD or PCKD
Management
- Manage cause (if HTN ACEi first line, if eGFR <45 furosemide can also help)
N.B. rise in Cr of 30% or drop in eGFR by 25% is acceptable but keep an eye on U&E
- Monitor Cr + eGFR
- Dose modifications/meds r/v
- Nephrology referral for: anaemia, bone disease (1st line: reduce dietary phosphate, 2nd: phosphate binders (stops if complexing w/ Ca + causing hypocalcaemia)
- RRT for stage 5 CKD
- General dietary advice: low protein, phosphate, sodium + potassium
Autosomal Dominant Polycystic Kidney Disease
- Inheritance
- Presentation
- Investigation
- Management
Inheritance
- Autosomal dominant
- Can be type 1 (85% of cases, presents w/ renal failure earlier) or type 2
Presentation
- HTN, recurrent UTIs, flank pain, haematuria, palpable kidneys, renal impairment, stones
- Extra-renal: liver cysts (can -> hepatomegaly), berry aneurysms (can -> subarachnoid), mitral valve prolapse, aortic root dilatation + aortic dissection, Other cysts: pancrease, spleen
Investigation
- Screening of relatives w/ abdo USS + diagnose if:
- <30 w/ 2 cysts (uni or bilateral)
- 30-59 w/ 2 cysts in both kidneys
- >60 w/ 4 cysts in both kidneys
Management
- Supportive in most
- Some may have tolvaptan (vasopressin antagonist) if CKD 2 or 3 AND evidence of rapidly progressing disease
-
Haematuria
- Causes
- Investigation/Referral Criteria
Causes
*Microscopic *
-Transient: UTI, menstruation, vigorous exercise (resolves in 3d), sexual intercourse
Persistent: cancer (bladder, renal, prostate), stones, BPH, prostatitis, urethritis, renal: IgA nephropathy, thin basement membrane disease
Spurious: rhabdo (myoglobin), foods (beetroot), drgus (rifampicin, doxorubicin)
Macroscopic
- painless macroscopic think bladder Ca
- UTI/pyelonephritis
- Stones
- Pelvic trauma
- Renal: IgA nephropathy, thin basement membrane diseases
- Iatrogenic: TRUS/TURP, traumatic catheterisation, renal biopsies, ESWL
Investigation
- In all: check ACR, U&Es, BP (if proteinuria needs renal ref), HTN could be ?nephritic syndrome)
2WW if:
- >45 AND unexplained visible haematuria (without UTI) OR visible haematuria persisting/recuring despite successful tx of UTI
- > 60 AND unexplained nonvisible haematuria AND either dysuria or raised WCC on bloods
Non-urgent ref if
- >60 w/ reucrrent or persistent unexplained UTI
Who doesn’t need referring? Age <40yo w/ normal renal function, no proteinuria + normotensive
Bladder Cancer
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
Can be TCC (most common), SCC (chronic inflam eg. schisosomiasis), adenocarcinoma, sarcoma
Risk factors:
- Smoking (both TCC + SCC)
- Aniline dye exposure (eg. printing or textiles) (2-naphthylamine or benzidine dye)
- Rubber manufacuring
- Cyclophosphamide
Presentation
- Painless haematuria (micro or macroscopic)
- Recurrent UTIs or LUTs
- Sterile pyuria (rarely)
- Weight loss, lethargy, pelvic pain (if locally advanced)
Investigation
- 2ww referral for >45 + macroscopic haemturia + no UTI or >60 + microscopic haematuria w/ dysuria or raised WCC
- Cystoscopy, biopsy CT staging
Management
- Surgical eg. TURBT (if in situ/T1), radical cystectomy (w/ ileal conduit formation or bladder reconstruction (from small bowel) +/- chemotherapy
- If bladder recon w/ small bowel needs B2, folate checking annually (?def due to less absorption)
Sterile Pyuria
Causes
Investigation/Management
Causes
- Most common is actually infection: recently or partially treated UTI, UTI w/ slow-growing organism, STI
- Other: appendicitis, post-menopausal atrophic vaginitis/trigonitis, prostatitis, genitourinary TB, schistosomiasis (rare in UK), sarcoidosis
- Malig: Bladder Ca (normally w/ haematuira), Renal disease
Investigation
- MSU for miscroscopy + culture, test for chhlamydia/gonorrhoea, U&Es, ACR, BP, upper tract USS
- If persistent refer to urology for further assessment
Haemolytic Uraemic Syndrome
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
Generally seen in young children –>
- AKI
- Microangioathic haemolytic anaemia
- Thrombocytopenia
Can be:
Primary (rare) - due to complement dysregulation
Secdonary (typical HUS):
- Shiga toxin producing E.Coli = most common cause (90%)
- Pneumococcal infection
- HIV
- Rare: SLE, drugs, Ca
Presentation
- Most due to E.coli shiga toxin –> bloody diarrhoea, abdo pain, fever, n+v
- Then features of HUS - anaemia, AKI, thrombocytopenia
Investigation
- FBC (anaemia w/ -ve direct coomb’s), thrombocytopenia, evidence haemolysis on film eg. schistocytes, helmet cells
- U&Es: AKI
- Stool culture: STEC infection, PCR for shigella toxin
Management
- Supportive: fluid, transfusion, dialysis +/- plasma exchange (normally only if not associated w/ diarrhoeal illness)
Renal Cell Carcinoma
Risk factors
Presentation
Investigation
Management
Risk Factors
- Smoking, von-Hippel-Lindau, tuberous sclerosis
- only slight increase in ADPKD
Presentation
- Classic triad: Haematuria, Loin pain, Abdo Mass
- pyrexia unknown origin
- Endocrine: EPO (-> polycythaemia), PTHrp (->hypercalcaemia), Renin (-> HTN), ACTH (cushing syndrome)
- Left varicocele
- Stauffer syndrome (paraneoplastic) –> cholestasis + hepatosplenomagly
Investigation
- Urinalysis, Bloods
- USS
- CT staging
- Biopsy
Management
- Confined disease - partial/total nephrectomy
- Chemo generally ineffective. Can use immunotherapy or biologic agents
- (if patient otherwise well + primary is resectable then can do resection of solitary mets)
Nephrotic vs Nephritic syndrome
- Classic Triads
- Investigations
- Causes + their management
Triads
*Nephrotic *- oedema, proteinuria, hypoalbuminaemia
- Other features: dyslipidaemia, hypercoaguability (loss of antithrombin), reduced immunity (loss of immunoglobulins)
- Presentation - peripheral oedema (aduts), facial oedema (children), frothy urine, fatigue, recurrent infections
Nephritic - HTN, AKI, haematuria
- Other: mild proteinaemia, mild oedema
- Presentation: haematuria, mild oedema, signs of uraemia (fatigue, pruritis, nausea)
- Red cell casts in urine
Investigations
- Nephrotic range of proteinuria >3.5g/day
Causes
Nephrotic
- Minimal change disease (most common in children)
most idiopathic but can be associated w/ mono, NSAIDs, hodgkins lymphoma
Present: nephrotic. renal biopsy: fusion of podocytes + effacement of foot processes
Mx: 1st: PO steroids (80% = steroid responsive),2nd= cyclophosphamide
most relapse at least once but tends to stop before adulthood - good prog
- Membranous nephropathy (most common in adults)
- Focal segmental glomerulosclerosis
Nephritic
- IgA Nephropathy (aka Berger’s disease)
most common glomerulonephritis
Present: macroscopic haematuria following URTI, young, male (renal failure is rare)
Associated conditions: Henoch-Schonlein, alcoholic cirrhosis, coeliac
Mx: if isolated haematuria then no tx just monitor. If slight reduced GFR or persistent proteinuriaa ACEi. If failure to respond to ACE: immunosupression w/ steroids
- Post-streptococcal glomerulonephritis
Present: 7-14d post group A B-haemolytic strep (normally S. Pyogenes), headache, malaise, visible haeamtura, proteinuria, HTN, oliguria, raised anti-streptolysin O (confirms recent strep), low completement
Differentiate from IgA: bigger gap between infection + onset, low complement + proteinuria in post-strep
good prog, supportive mx, resolves spon - Rapid progressive glomerulonephritis (anti-GBM or ANCA vasculitis)
What are the following?
- Alport’s Syndrome
- Goodpasture’s Syndrome
Alports Syndrome
Inheritance: X-linked dominant, problem w. collagen -> abnormal glomerular BM
Present: microscopic haematuria, progressive renal failure, B/L sensorineural deafness and eye problems: lens protrusion, retinitis pigmentosa
Diagnosis: genetic testing, renal biopsy (shows splitting of BM -> basket weave appearance)
Goodpasture’s Syndrome
Autoimmune condition affecting lungs + kidneys
Present: 10-30yo, haemoptysis, fatigue, fever, nosebleed, nephrotic syndrome
Diagnosed w/ renal biopsy, serum Ab, urinalysis
Renal Transplant
Immunosupressants
Complications
Immunosupressants
Example regime:
- Initial: ciclosporin/tacrolimus + monoclonal Ab
- Maintenance: ciclosporin/tacrolimus w/ MMF or sirolimus
- ADD steroids if >1 steroid reponsive acute rejection
Side effects:
- Ciclosporin - higher rate of rejection than tacro
- Tacrolimus - imparied glucose tolerance/DM
- Mycophenonlate mofetil - GI SEs + marrow supression
- Sirolimus: hyperlipidaemia
All patients on long-term immunosupression need monitoring for complications:
- CVS disease
- Renal failure (tacrolimus/ciclosporin are nephrotoxic also monitor for graft regection + recurrent of original disease)
- Malignancy - SCC + BCC (non melanoma skin ca)
Complications
- Post op: ATN of graft, UTI, vacular thrombosis, urine leakage, UTI
- Hyperacute Rejection (mins-hours)
Due to pre-existing Ab against ABO or HLA antigens. Type II hypersensitivity. Graft MUST be removed/no other tx
- Acute Graft Failure (<6/12)
due to mistmatched HLA, normally asymp -> rising Cr, pyuria + proteinuria. May be reversible w/ steroids + immunosupression - Chronic Graft Failure (>6/12)
*Recurrence of original disease or fibrosis of transplanted kidney *
Rhabdomyloysis
Causes
Presentation
Investigation
Management
Causes
- long-lie, crush injuries, prolonged epileptic seizure, coma, statins (esp if co-prescribed w/ clarithromycin)
Presentation
- AKI w/ disproportionately raised Creatinine + raised CK
- Dark urine (myoglobinuria), hypocalcaemia (as myoglobin binds calcium), raised phosphate (released from myocytes), raised K+, metabolic acidosis
Ix
- Raised Creatine Kinase
- AKI (w/ raised Creatinine)
Management
- IVI to maintain good u/o
- +/- urinary alkalinisation
UTI
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
Causative organism: E.Coli, Klebsiella, proteus
In structural abnormality: Pseudomonas
Gram -ve organisms are nitrite +ve (e.g. E.coli) but gram +ve are nitrite -ve (eg. staph saprophyticus)
Presentation
- Dysuria, frequency, urgency, haematuria, confusion, rigors, suprapubic pain
- pyeloneph: rigors, nausea/vomiting, loin pain
Investigation
- Urine dip all <65yo
- Culture: >65yo, catheter, pregnant women, haematuria (visible or not)
Management
Uncomplicated (women)
- 3 days nitrofurantoin or trimethoprim
Complicated
- Men: 7 days nitro or trimethoprim
- Catheter: 7 days nitro or trimethoprim + consider changing catheter if been in more than 7 days (N.B. do not treat asymptomatic bacteriuria in catheterised)
- Pregnancy: 7 days - nitro in early preg, cefalexin or amoxicillin later (avoid trimethoprim throughout- esp 1st trimester)
- Asymptomatic bacteriuria in preg: 7 days abx as above (due to risk of pyeloneph) + do further culture as test of cure.
Pyelonephritis
- 10-14days broad spectrum abx (co-amox, cephalosporin or quinolone)
What are the following and their management?
Erectile Dysfunction
Priapism
Signs of Urethral Injury
Erectile Dysfunction (impotence)
- Causes: pscyhological or organic (CVS, DM, low testosterone, neuro disorders, pelvic surgery), mens (anticholinergics, antidepressants, antihypertensives etc)
- Management depends on cause:
- Psychological - therapy (then similar to organic)
- Organic: lifestyle/meds modification 1. PO phosphodiesterase inhibitors (unless taking nitrates) (eg. sildenafil) 2. Intraurethral or intracavernosal alprostadil 3. vacuum pump device 4. refer to urology (?penile prosthesis)
- If hypogonadism: testosterone supplementation
Priapism
- Persistent erection, >4h, not associated w/ sexual stimulation, painful (if not painful or any hx of trauma this suggests non-ischaemic cause)
- Can be: ischaemic (blocked outflow) or non-ischaemic (too much inflow)
- Causes: idiopathic, sickle cell, meds eg. sildenafil, antidepressants, cocaine; trauma
- Ix: cavernosal blood gas analysis (differentiates ischaemic/non); doppler USS, FBC/tox screen (?cause)
- Mx:
- Ischaemic = emergency - aspiration of blood + injection of saline flush to clear pooled blood +/- phenylephrine or surgery
- Non-ischaemic - observe initially, non emergency
Signs of Urethral injury
- perineal bruising, bood at external urethral meatus, high riding prostate on PR
- do NOT attempt catheterisation. Refer urgently to urology.
What are the following/their management?
- Balanitis
- Phimosis
- Paraphimosis
Balanitis
can have multiple causes, including pre-malignant lesions. Swab all to confirm organism. +/- biopsy if ?pre-malignant lesion (bowens disease, bowenoid papulosis or erythroplasia of Queyrat)
- Candida: rash w/ soreness/itch - tx w/ clotrimazole cream or PO fluconazole + screen partners
- Anaerobic infection: foul smelling discharge, inguinal lymphadenopathy - PO metronidazole
-
Aerobic infection -> non-specific balanitis - mx depends on sensitivities
-* Lichen sclerosus* - white patches on glans, itch, sore, splitting. Can -> phimosis + urethral stenosis + risk of malignant transformation to penile Ca. Needs biopsy to diagnose. Mx w/ strong topical steroids
-* Zoon’s *(plasma cell) balanitis: older uncircumcised men due to irritation from urine -> well-circumscribed organe-red glazed areas on glands w/ multiple pinpoint red spots - biopsy to exclude malig - mx w/ circumcision + topical steroids - Psoriasis - looks similar to elsewhere - emollients, steroids, calcitriol
- Circinate balantitis - occurs in reactive arthritis - white areas on glans that coalesce to form geographic area w/ white margin - screen for STI + tx accordingly
- Irritant/Allergic - eczematous rash - emollients/soap sub +/- hydrocortisone
Phimosis = inability to retract
Cause: physiologic (resolves w/ time); pathologic (scarring, infection, inflammation)
Pres: difficult retraction, pooling or urine, smegma, balanitis, urinary retention, painful erection
Management: topical steroids + manual retraction. If ineffective or causing problems (e.g. recurrent UTI, paraphimosis, recurrent balanitis) or pathological cause then may need circumcision
Paraphimosis = inability to replace = emergency (risk of necrosis)
Causes: not replaced post-catheter, phimosis
*Pres: erythema, pain, swelling, *
*Mx: manual reduction +/- surgery (longitudinal incision made)
