Renal/Uro Flashcards
Define AKI in terms of Creatinine/UO/GFR
* Stage 1 (Risk)
* Stage 2 (Injury)
* Stage 3 (Failure)
* (Loss of Function)
* (End-stage)
- > 1.5x baseline Cr (7 days) or rise >26 (2days), UO 0.5ml/kg/hr in 6 hrs, >25% decline
- 2x baseline Cr, UO 0.5 in 12 hrs, >50% decline
- 3x baseline Cr, UO Anuria in 12 hrs/0.3 in 24 hrs, >75% decline
- Loss of function for >4 weeks; req dialysis
- > 3mo, req dialysis
Investigations - AKI
Bedside (obs, urinalysis, ECG)
Bloods (U&E + eGFR, LFTs, FBS, CRP) + cultures
Imaging (renal u/s / CT KUB / XR KUB / Doppler)
Special tests (renal biopsy / immune or virology screen)
Urinalysis to distinguish pre-renal from intra-renal
- Casts
- Urine Na
- Urine FeNA (fraction of excreted Na+ compared to amount reabsorbed)
- Serum Urea:Creatinine ratio
- Urine osmolarity
Pre-renal:
hyaline casts, Low Na+ & Low FeNA, high Urea:Creatinine, high urine osmolarity
Kidneys preserve Na+ - hence don;t secrete Na+ in urine - to maintain blood volume/treat hypovolaemia
Intra-renal:
brown granular casts, High Na+, Normal Urea:Creatinine, Low osmolality (dilute)
High Urea:Creatinine ratio in Pre-renal because Cr isn’t being re-absorbed due to reduced GFR.
Mx of AKI - fluid balance and electrolyte monitoring, stop nephrotoxics, treat underlying cause.
List nephrotoxic drugs (DAMN my PCL)
Which of these are not technically nephrotoxic but need to be stopped in AKI due to increased risk of toxicity?
- Diureitcs
- Aminogycosides, ACE-I, ARBs
- Meformin, Morphine
- Nitrates and NSAIDs
- Phenytoin
- Contrast media
- Lithium –> diabetes insipidus
Increased risk of toxicity - digoxin, metformin, lithium
NSAIDs and ACE-Inhbs effect on renal blood flow:
Reduction in GFR - worsening or causing AKI.
NSAIDs cause vasconstriction of afferent arteriole.
ACE-Inhbs cause vasoldilation of efferent arteriole.
The combination together reduces blood flow into the glomerulus and increases blood flow out of it - aka reducing the GFR
Define CKD and the 3 ways it can be classified?
Abnormal kidney function present for >3 months with significant health implications:
* GFR 1, 2, 3a/b, 4, 5: >90, 60, (45, 30) 15, <15
* ACR (Albuminuria) 1-3: <30, 30-300, >300
* Underlying disease
Top 3 Causes in UK for CKD
- Diabetes
- HTN
- Glomerularnephritis
General mx for CKD:
* Treat underlying cause; optimise modifiable RF
* Slow disease progression
* Treat complications
* Nephrology referral for RRT
Conservative measures include lifestyle modifications, stopping nephrotoxics - what diet is recommended?
Low K+ and PO42-
Fluid restriction
Complications of CKD
- Uraemia
- Electrolyte imbalance - hyperkalaemia
- Anaemia of chronic disease (normocytic)
- Acid-base imbalance: Acidosis
- Reduced synthesis of 1,25-dihydroxycholecalciferol –> Hypocalcaemia, renal osteodystrophy, secondary hyperparathyroidism
- Fluid overload, oedema
- Gout
Nephrotic vs nephritic syndrome
* Nephrotic = proteinuria (>3g/day), hypoalbuminaemia (<30g/l), oedema (reduced oncotic pressure) +/- hypercholesterolaemia
* Nephritic= haematuria, HTN, oliguria +/- proteinuria/oedema
EPO injections are not effective if…
Iron deficient.
One of their side effects is IDA (brittle hair, glossitis, oncholysis etc)
Extra-renal features of autosomal dominant polycystic kidney disease
Screening investigation
- Liver cyst (most common)
- Berry aneursym –> SAH
- CVS - mitral valve prolapse
- Other GI cysts
Screening: ultrasound abdomen
Paediatric Glomerulonephritides: nephrtic px. Disease and typical causative organism.
* 1-2 wks post URTI/skin inf with raised anti-streptolysin O, immune complex deposition, and starry sky appearnace on bx.
* AKI, haemolytic anaemia and low Plt, following bloody diarrhoea. Shistocystes on blood film.
* Throat infection followed by purpuric rash on buttocks and extensor surfaces, abdominal pain, haematuria & polyarthritis.
* Inherited connective tissue disorder causing eye problems (retinitis pigmentosa and lenticonus), ear problems (sensorineural deafness) and nephritic syndrome. Basket weave on bx.
- Post-strep GN (after strep pyogenes URTI or skin infection)
- Haemolytic uraemic syndrome (after shiga-producing E-Coli)
- Henoch-Shonlein Purpura (various causative organisms)
- Alport’s syndrome;need a basket for transport
Generally managed conservatively. HUS may require IV Fluids and HSP NSAIDs for arthralgia. Alport’s with BP management (ACE-Inhb).
Paediatric Glomerulonephritides - nephrotic px
* Kid with loss of albumin & transferrin in urine, podocyte effusion on electron microscopy, requiring Prednisolone.
* Can present in teens but most common nephrotic presentation in adults. Scarring on bx. Normally 2ndary to other renal disease, req steroids +/- I/s.
- Minimal change disease (no changes seen on light microscopy)
- Focal segmental glomerulosclerosis
Adult glomerulonephritides - nephritic sx:
* Young male with reucrrent eps of recurrent macroscopic haematuria; note 1-2 days post URTI. Immune complex deposition; association with HSP and other autoimmune dx.
* * HLA-DR2 associatied disease with bimodal presentation (20s & 60s) affecting connective tissue of lungs & kidneys
* P-ANCA associated small vessel vasculitis presenting with haematuria & haemopytisis
* C-ANCA associated “ following an URTI/LRTI
* P-ANCA associated “ presenting with severe asthma
- IgA Nephropathy (diffuse proliferative) - monitor proteinuria (No treatment –> ACE-I –> CS)
- Anti-GBM disease (Good-pasture’s)
- Microscopic polyangitis
- Granulomatosis with polyangitis (wegners)
- Eosinophilic granulomatosis with polyangitis (Churg Strauss)
Adult glomerulonephritides - nephrotic sx
* Common cause of ESRD. Rule of 1/3 (recover, relapse, chronic). Spike & dome appearance (thickened GBM) on bx.
* Rare disease with poor prognosis.Tramline of double BM on bx. Type 1 - low C4, type 2 - low C3.
- Membranous nephropathy
- Membranoproliferative GN (mesangiocapillary)
Renal transplant - underlying cause & mx.
1. Hyperacute (mins -hrs)
2. Acute/ T-cell mediated (<6 mo)
3. CHronic (>6mo)
- Existing antibodies to ABO/HLA causing necrosis. Reqs Graft removal.
- Mismatched HLA. Asx/ raised CR/proteinuria. Reversible with steroids/IS.
- Antibody & T-cell mediated, causing fiborosis. Note recurrence of renal disease e.g. MCGN, IgA, FSGS.
Prostate cancer - after doing a PR exam & PSA test:
* First line investigation
* Next investigation to establish diagnosis (two methods)
* Scan for bony mets?
-
Multiparametric MRI
(results reported as Likert scale 1-5 from very low suspicion to definite cancer) - Prostate biopsy e.g. Likert scale 3+ and clinical suspicion etither transrectal (TRUS; ultrasound probe) or transperineal (needle)
- Isotope bone scan / radionucleide/bone scintigraphy (injection into bone - cancer cells take up more isotope so stand out)
Prostate cancer
Scoring System
1. Based on histology from prostate biopsy, where 6 is low and 8> is high risk:
2. General for cancer
1. Gleason: greater the score, the more poorly differentiated the tumour is (1-5): made up of 2 numbers (total 10) (1 = most prevalent pattern, 2 = second most prevalent pattern)
2. TNM (Tumour X-4, Nodes X,0,1, Metastasis 0,1)
Prostate cancer
Mx guided by MDT.
* Conservative
* Medical
* Surgical
- Watchful waiting (early stage)
- Radio x, - external beam/brachytherapy (metal seeds into prostate)
- Hormone x e.g. androgen-receptor blockers, GnRH agonists
- Surgery - radical prostatectomy
Key complications of radical prostatectomy
Erectile dysfunction
Urinary incontinence
Medical mx for prostate ca - type/MOI of each drug:
* Goserelin
* Bicalutamide
* Cyproterene acetate
* Albiterone
- GnRH analogue - paradoxically suppress the testosterone production (suppression of HPG axis by overstimulation)
- anti-androgen
- anti-androgen
- androgen synthesis inhibitor
Varicocele -* swelling of the veins (pampiniform plexus) within the spermatic cord that drain the testicles*
* Typical presentation:
* Examination finding:
* Ix
* Surgery only required if (3)
- Dragging sensation, worse when standing up
- Disappears when lying down; feels like “bag of worms”
- Ultrasound with Doppler
- Testicular atrophy, pain or infertility
Epididymal cyst - fluid filled cyst attached to to the head of the epididymis, normally asx/incidental finding.
* Examination findings (4)
- Soft
- Round
- Attached to epididymis, seperate from testicle itself
- May be able to transilluminate if large enough
Hydrocele
* Location
* Examination findings
* Rule out (2)
- In tunica vaginalis (pouch surrounding testes)
- Smooth, fluctuant lump, testicular palpable within hydrocele, irreducible
- Hernias (reducible, bowel sounds present) & cancer
Testicular cancer
* Types
* Prognosis? % cure rate?
* Presentation/examination findings?
* Tumour markers (3)?
* Scoring system?
* Mx - medical, surgical, other
* Note - long term side effects after treatment
- Semimoma or non-semimoma (terotoma)
- Good, 90%
- Painless lump on the testicle (hard, irregular, attached, non-fluctuant, no transilluminescence)
- AFP raised in terotomas, beta-hCG, LDH
- Royal Marsden Staging 1-4 (isolated –> retroperitoneal –> lymph nodes –> metastasis)
- Chemotherapy, Radiotherapy, Sperm banking to save sperm for future use post treatemtn
Testicular torsion
* Presenting sx
* Common trigger?
* Examination findings (5)
- Sudden severe unilateral testicular pain + abdominal pain & vomiting Typically 12-18.
- Sports - vigorous exercise.
- Firm, swollen, elevated/retracted testicle. Absent cremasteric reflex. Testicle may be rotated / or in horizontal lie
can just present with abdominal pain
Birth abnormality of reduced fixation of scrotum to the tunica vaginalis –> risk factor for testicular torsion
Bell-Clapper
Immediate mx testicular torsion
- urosurgical emergency
- NBM, analgesia
- Surgery within 6 hrs of presentation- orchoplexy or orchidectomy
Causes of reduced cremasteric reflex
- Spinal injury L1/L2
- Damage to ilioinguinal nerve
- Can be normal variant
- Testicular torsion
Epididymo-orchitis presents with unilateral testicular pain & swelling. Commonly caused by UTI (E Coli) or STI (e.g. Chlamydia).
* What sign is positive?
* Ix UTI / STI
* Mx UTI / STI
*
- Positive Phren’s test - pain is alleviated when testicle is lifted
- UTI (MSU–> MC&S), STI (urethral swab)
- If UTI - Quinolones (for gram-ve) Ofloxacin/Levofloxacin
- STI - IM Ceftriaxone + Doxycycline.
Referral guidelines haematuria at >45 and for >60 - what is the difference?
2WW for visible haematuria (unexplained)>45 and microscopic haematuria for >60, + dysuria/ raised WCC
Management for patient with renal stones, associated sepsis and hydronephrosis
If hydronephrosis - ureter is almost completely occluded.
Urgent decompression –> nephrostomy tube or indwellling stent.
Kidney stones
Appropriate management for scenarios:
- initial management before CTKUB for pain relief
Definitive mx
- <5mm
- 5-10mm
- 10-20mm
- >20 or complex
Prevention of stone formation (3 medications,general diet change)
Which procedure is contra-indicated in pregnant females?
If the stones were ureteric what would also be considered alongside intervention?
- IM Diclofenac or IV Pct
- Watchful waiting
- Lithotripsy (ESWL; external beam; req analgesia)
- Uretoscopy (via ureter to renal pelvis; stone retrieval+/- stent formation)
- Percutaneous niphrolithotomy (+ intracorpeal lithotripsy/fragmentation; procedure through back)
Management to reduce stone formation:
- Thiazide diuretics for calcium stones: block Na+/Cl- transporter in the DCT, in turn increases calcium reasorption into the blood.
- Chloestyramine - for oxalate stones.
- Allopurinol (xanthine oxidase inhibs) or oral bicarbonate - decreases uric acid stones
- general: low Na+
- ESWL is contra-indicated in pregnant women
- Alpha blockers
Bladder cancer - transitional cell carcinoma (95%)
* Risk factors
* Grading & two main types
* Inv (3)
* Mx (medical - chemo/immunotheapy, surgical - 3)
* Clarify the difference between the ileal diversion techniques
* other types of bladder cancer - less than 5% of cases
- smoking, aromatic amines (rubber/dyes)
- TNM (non-muscle invasive, muscle invasive)
- CT KUB, cytoscopy and biopsy
- Intravesical chemo with BCG, TURBT, radical cystectomy, ileal conduit
- One is external bag: urostomy with ileal conduit; one is internal: continent urinary diversion*
- squamous cell and adeno
Renal cancer
* Types - 2 most common, 2 others
* Triad for RCC
* Grading
* Ix
* Mx
- Most common = renal cell carcinoma (clear cell, papillary, chromophobe). Less common = Transitional cell/Wilm’s (nephroblastoma).
- Loin pain, loin mass, haematuria. Cannon ball mets.
- CT KUB
- Radiotherapy, nephrectomy (partial/radical), TK-inhibitors
Acute tubular necrosis (ATN)
most common cause of AKI seen clinically; polyuric –> oliguric –> recovery,
- 2 main causes
- features
- ischemia and nephrotoxins
- over time iischemia (e.g. from hypovolaemia after infection) causes renal cell hypoxia and necrosis
- AKI & muddy brown casts in urine
BPH
benign enlargement of the prostate gland due to dihydrotestosterone, putting pressure on the prostatic urehtral
* % of men with enlarged prostate at 50, and with symptoms
* presentation
* O/E - DRE
* investigations
* management - medical 1st and 2nd line (can be combination therapy)
* surgical options - 4
- 50%, 30%
- LUTS - storage (retention, overflow incontinence, nocturia); voiding (hesitancy, poor stream, terminal dribbling, straining)
- O/E: smooth enlarged prostate with retained central sulcus
- bloods - PSA (if suspicious of ca, or obstructive), U&E, urine dip –> MC&S, U/S or Transrectal ultrasound (if ca?)
- Alpha agonists - smooth muscle relaxation of the prostatic urethra - Tamsulosin, Doxazosin
- 5-alpha reductase inhibitors - prevent conversion of testosterone to its more potent form - Finasteride, Dutasteride
- Transurethral resection of the prostate (TURP), TEVAP (electrovaporisation), HoLEP (holium laser) open prostatectomy
BPH
International Prostate Symptom Severity Score:
0-7
8-19
20-35
Mildly symptomatic
Moderate
Severe
Anion gaps (sum of positive ions - sum of negative ions) - for distinguishing causes of **metabolic acidosis **
Normal range = 4-12 (varies?)
- High anion gap implies…?
- Name of a normal anion gap - causes
-calculation
- Normal = hyperchloraemic metabolic acidosis =** loss of H+ ions** (renal tubular acidosis, Addisons, GI bicarbonate loss - prolonged diarrhoea)
- High anion gap = hypochloremic
accumulation of H+ (lactate, ketones, urate, salicylates) - eg. lactic acidosis, DKA, aspirin overdose - (sum of positive ions) - (sum of negative ions)
- Aka (NA+ + K+) - (Cl-+HCo3-)
HIGH = EXCESS H+ IN BLOOD
Prescence of hyaline casts
secreted by DCT
- exercise
- loop diureitcs
- normal
- fever
Renal tubular acidosis
all associated with a norman anion gap (hyperchloraemic metabolic acidosis; loss of organic acids)
Renal tubular acidosis of the distal tubules type 1 and 4
Type 1 RTA (DCT)
- Inability to excrete H+ ions and failure of H+/K+ exchange leads to:
- Conditions causing this pathology (rheum, anaemia, endocrine)
- presentation
Type 4 RTA (Collecting duct)
- Reduced aldosterone –> reduced potassium and H+ ion excretion
- results (3)
- causes of low aldosterone
- mx targets underlying cause
Other types
- Type 2
- Type 3
Type 1 RTA
- **Hypokalaemia; **metabolic acidosis (blood), alkaline urine
- SLE, Sjorgren’s, Marfan’s, Sickle cell, hyperthryoidism, genetic, PBC
- Recurrent UTI, Arrythmias, muscle weakness, FTT in kids, bone disease
- treat with oral bicarbonate
Type 2 RTA
* Hyperkalaemia, metabolic acidosis, low urinary pH
* adrenal insufficiency, diabetic nephropathy, medications (ACE-inhibitors, spironalactone “potassium sparing diuretic”)
* treat hyperkalaemia
* oral bicarb
* fludrocortisone in aldosterone deficiency
**Type 2 **
- PCT; hypokalaemia
- inherited causes e.g. Fanconi
Type 3
- mixed 1 and 2
Urinary tract infection
Management:
- women
- pregnant women (symptomatic or asymptomatic bacteriuria)
- men
- catheterised (symptomatic or asymptomatic)
Women
- Trimethoprim/Nitrofurantoin 3 days
- MSU if >65 yrs or visible/non-visible haematuria
Pregnant women (symptomatic and asymptomatic)
- Nitrofurantoin 1st line/ Amoxicillin/Cefalexin 2ndline 7 days
- Note avoid Nitro in 3rd rimester (risk of neonatal haemolysis) and trimethorprim in first trimester (teratogenic)
- Send MSU in all cases
Men
-Trimethoprim/Nitro for 7b days
- like non-pregnant women but longer course
- Send MSU in all cases
Catheterised
- Do not treat asymptomatic
- if asymptomatic treat 7 day (rather than 3 day)
- consider removing or changing cagtheter if in place for longer than 7 days
-
Acute pyleonephritis
Consider hospital admission if fever, rigors, chill, vomiting, confusion - systetmic signs of infection
- local antibiotic guideline
- BNF recommendations:
- Length of course
- Broad spec cephalosporin or quinolone (non-pregnant women)
- 10-14 days
Renal tubular acidosis
- unable to excrete H+ into urine, causing acid to build up into the blood
- also unable to excrete ammonia so this causes - hyperchloremic metabolic acidosis amd jhypokalaemia
*
Acute interstitial nephritis (AIN)
* Triad
* Common trigger, other causes (3)
* Urinalysis findings
* can also present with … in young females (TINU)
* mx
- Fever, eosinophilia and rash, in context of reduced renal function + Arthralgia
- drugs - most common cause - Penicillin, Rifampicin, NSAIDs, Allopurinol, Furosemide
- Systemic disease - eg sarcoid
- Infection - eg staph
- Urinalysis = sterile pyuria and white cell casts - white cells in urine with absence of bacteria
- uveitis - red painful eye
- stop offending drug +/- steroids
