GU Flashcards
Define nephrolithiasis
Aka renal stones / renal coliculi / urolithiasis
Stones form when solutes leave the urine and crystallise
Where are stones usually formed in the body
Kidney
Ureter
Urethra
Bladder
What are renal stone precipitates most commonly formed from
Calcium oxalate
• Accounts for 90%
Its black/dark brown in colour —> radiopaque on X-ray (shows as a white spot) - as its absorbing more light
Types of stones formed
Calcium oxalate - most common
Calcium phosphate
Struvite (Risk factor for it - UTI)
Uric acid (urate) stones (Radiolucent on X-ray - transparent)
Cysteine
Risk factors for renal stones
Chronic dehydration
Hx of renal stones
Hypercalcaemia / hypercalciuria —> HyperPTH
Kidney disease —> Polycystic kidney disease
Foods —> chocolate, rhubarb, spinach, nuts
Are stones more common in men or women
Males
Sx for renal stones
Symptoms
• Severe flank pain - Loin to groin that is colicky - intermittent pain
• N & V
• Urinary urgency / frequency
• Haematuria - Micro / Macroscopic
• Fever - If suggests uric acid stone / pyelonephritis
Signs
• Flank/Renal angle tenderness
• Hypotensive & tachycardia
• Pyrexia - septic stone
Typical age for renal stone development
20-40 yrs old
Pathophysiology for renal stones
When excess solute or reduced solvent—> Supersaturated urine —> favours crystallisation—> stone leads to regular outflow obstruction—> Hydronephrosis
Dilation and obstruction in renal pelvis (increases damage + risk of infection)
Complication of renal stones
Hydronephrosis - AKI / renal failure
Urosepsis (Infection)
Recurrence of stone - very common
Investigation and Dx for renal stones
KUB X-ray - 1st line
Non-Contrast CT KUB - Gold standard and diagnostic!!!
DO NOT USE Contrast CT for suspected renal stones as it needs to be excreted —> harmful if theres an obstruction
Urinalysis - microscopic Haematuria ± pyuria if pyelonephritis is present
Bloods + U&Es
Tx for renal stones
< 5mm should pass
Symptomatic relief - IV fluids (hydrate) + Analgesia (Diclofenac - NSAID) - IV for severe pain
± Alpha 1 blocker (Tamsulosin) - helps with pain, not always used though
± Antibiotic for sepsis (Gentamycin - for pyelonephritis)
Surgery:
ESWL - extracarporeal shock wave lithotripsy
Breaks stones down with sound waves of stones 5-10mm / < 20mm
PCNL - Percutaneous nephrolithotomy
Keyhole removal of stones >20mm
If hydronephrosis - emergancy, so do Percutaneous nephrostomy
Commenest site of renal stone obstruction
PUJ - Pelvo-Uretric Junction (Distal i.e. ureter entering bladder point)
Pelvic brim - ureter crossover iliac vessel
VUJ - Vesico-uretric Junction (*proximal i.e. top of Exeter joining kidney)
What worsens renal stone pain
Diuretics + fluid
Define AKI
Acute drop in kidney function, characterised by:
Increased Creatinine & Urea
Decreased urine output
What is the diagnostic AKI criteria
RIFLE criteria used to detect AKI:
Increase in serum creatinine by ≥ 26 micromol/L within 48hrs
Increase in serum creatinine by ≥ 50% within past 7 days
(≥ 1.5x baseline serum creatinine in 7 days)
Decrease in Urine output by < 0.5mL / kg / hour for more than 6 hours
KDIGO criteria used for severity of AKI:
Stage 1 -
Rise in creatinine by ≥26.5 µmol/L … OR …
Rise in creatinine to 1.5-1.9x baseline … OR …
Fall in urine output to < 0.5 mL/kg/hour for ≥ 6 hours
Stage 2 -
Rise in creatinine to 2.0 to 2.9x baseline … OR …
Fall in urine output to <0.5 mL/kg/hour for ≥12 hours
Stage 3 -
Rise in creatinine to ≥ 3.0 times baseline, or
Rise in creatinine to ≥353.6 µmol/L or
Fall in urine output to <0.3 mL/kg/hour for ≥24 hours, or
The initiation of kidney replacement therapy, or,
In patients <18 years, fall in eGFR to <35 mL/min/1.73 m2
Pathophysiology of AKI
Damage from AKI —> inability to remove toxins & regulate pH —> accumulation of the following:
K+ —> Hyperkalaemia - Arrhythmias
Urea —> Hyperuremia - Pruritus / Uremic frost
Fluid —> Oedema - Pulmonary ± peripheral oedema
H+ —> Acidosis
Causes of AKI
Whenever someone asks you the cause of renal impairment always answer “the causes are pre-renal, renal or post-renal”.
Pre-renal
Hypovolaemia - Dehydration / haemorrhage
Reduced cardiac output - Heart or liver failure / sepsis
Drugs - NSAIDS / ACEi / IV contrast
Renal
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis
Toxins (sepsis / ABx)
Post-renal
Obstructive uropathy - Renal stones / BPH
Drugs - Anticholinergics / CCBs
How can ACEi cause AKI
ACEi causes afferent arterioles constriction
Therefore reduced perfusion to kidney —> AKI
Pre-renal cause
Top 3 causes of AKI
Cardiogenic shock
Sepsis
Major surgery
Most common renal cause of AKI
Tubular - acute tubular necrosis
Px triad of: Fever, rash, eosinophilia
Risk factors for AKI
Increased age
Co-morbidities: HTN, chronic H.F, T2DM
Nephrotoxic drugs: NSAIDS, ACEi, ARBs, Gentmicin, IV contrast
Sepsis
Signs of AKI
Oedema:
Bibasal crackles,
Increased JVP,
Peripheral oedema
Palpable bladder
Hyperuremia
Uremic frost
Pruritis
Hyperkalaemia
Arrhthmias
Increased H+
Metabolic Acidosis
^ Px can present depending on the substances accumulated - Remember Pathophysiology
Signs of hypovolaemia
Dry mucous membranes
Decreased skin turgor
Reduced blood pressure
Sx of AKI
Reduced urine output ± urine colour change
Confusion / drowsiness
Dypnoea ± swollen ankle —> Oedema
Suprapubic pain —> Urinary retention
Haematuria —> Glomerulonephritis
Which criteria is used for AKI
RIFLE criteria +
KDIGO system
Ecg changes for Hyperkalaemia
Tall tented T wave
Wide QRS
Absent P waves
Investigation and Dx of AKI
- Investigations are aimed at making the diagnosis, assessing the severity of the AKI and finding an underlying cause.*
U&Es: K+, H+, Urea, Creatinine
FBCs + CRP: Sign of infection
VBG: Metabolic acidosis
Renal biopsy - to confirm intrarenal cause / USS - to confirm pot-renal cause
Tx for AKI
Treat complications:
Hyperkalaemia —> stabilise cardiac membrane - Calcium gluconate
Fluid overload - Furosemide
Metabolic acidosis - Sodium bicarbonate
Treat underlying cause
Discontinue nephrotoxic drugs
Rehydrate Px - IV fluids
Renal replacement therapy - last resort:
Haemo-dialysis: A FUK
Acidosis
Fluid overload
Uraemic - present as Encephalopathy / pericarditis
HyperKalaemia
Define chronic kidney disease
Progressive deterioration in renal function
eGFR <60 for ≥ 3months
Normally at 120
Risk factor for CKD
Diabetes mellitus
HTN
^Most common
Increased age
Glomerulonephritis
Nephrotoxic drugs (NSAIDS, lithium)
What is a G score
Stage of renal failure… Based on the eGFR mL/min/1.73m2
G1. 90+
G2. 60-89
G3. A) 45-59 B) 30-44
G4. 15-29
G5. < 15 (known as “end-stage renal failure”)
Sx of CKD
Early on Px = asymptomatic as theres still lots of nephrons
Sx start due to substance accumulation + renal damage (e.g diabetic nephropathy)
Sx:
Lethargy
Pruritis —> uraemic
Nausea
Frothy urine
swollen ankle —> fluid overload
Hypertension
Whats an A score?
Renal function based on the albumin:creatinine ratio:
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol
- The patient does not have CKD if they have a score of A1 combined with G1 or G2*
Pathophysiology of CKD
Progressive reduction in kidney function leading to mesangial scarring (support tissue in glomerulus)
The most common cause of CKD is diabetes, excess glucose in the blood starts sticking to proteins in the blood — non-enzymatic glycation.
Affects the efferent arteriole and causes it to get stiff and more narrow increases pressure —> hyperfiltration.
the supportive mesangial cells secrete more and more structural matrix expanding the size of the glomerulus.
Diminishes the nephron’s ability to filter the blood —> chronic kidney disease.
- In hypertension, the walls of arteries supplying kidney thicken in order to withstand the pressure —> narrow lumen. A narrow lumen means less blood and oxygen gets delivered to the kidney, resulting in ischemic injury to the nephron’s glomerulus.
Macrophages and foam cells called slip into the damage glomerulus and start secreting growth factors like Transforming Growth Factor ß1 (TGF-ß1).
These growth factors cause the mesangial cells to regress back to their more immature stem cell state known as mesangioblasts and secrete extracellular structural matrix. This excessive extracellular matrix —> glomerulosclerosis, hardening and scarr, and diminishes the nephron’s ability to filter the blood*
Complications of CKD
Anaemia —> reduced EPO, reduced RBC
Osteodystrophy —> reduced Vit D activation
Neuropathy + encephalopathy —> hyperuraemia
Cardiovascular disease e.g pericarditis / arrhythmias
Investigation and Dx of CKD
Estimated glomerular filtration rate (eGFR) U&E blood test. Two tests are required 3 months apart to confirm a diagnosis of chronic kidney disease. - use its staging —> G score
Proteinuria can be checked using a urine albumin:creatinine ratio (ACR). A result of ≥ 3mg/mmol is significant. - use A -score
Haematuria can be checked using a urine dipstick. A significant result is 1+ of blood. Haematuria should prompt investigation for malignancy (i.e. bladder cancer).
Renal ultrasound can be used to investigate patients with accelerated CKD, haematuria, family history of polycystic kidney disease or evidence of obstruction.
Tx of CKD
No cure so Tx complication:
Anaemia - Fe + EPO
Osteadystrophy - Vit D (calcitriol) / bisphosphonates
CVD - ACEi (1st line - exacerbational - cause of AKI but used for HTN)
Oedema - diuretics
For stage 5 (ESRF) - dialysis (renal replacement therapy) / renal transplant (curative)
When is metformin CI in CKD
EGFR < 30
Define BPH
hyperplasia of the stromal and epithelial cells of the prostate. It usually presents with lower urinary tract symptoms.
What scoring system is used in BPH
IPSS
International prostate symptoms score
Difference between BPH and prostate cancer proliferation
BPH usually non malignant proliferation of inner transitional zone of prostate
Prostate cancer usually proliferation of outer peripheral zone
Risk factor for BPH
Increased age
Male
Afrocarribean
Fx
Diabetes
Obesity
Castration - protective
Pathophysiology of BPH
Hyperplasia of both glandular epithelial cells and stromal (connective tissue) cells.
With age, there is an increase in activity of 5-alpha reductase —>
Increases dihydrotestosterone (DHT) and oestrogen. DHT acts on androgen receptors within the prostate causing hyperplasia
BPH predominantly affects the peri-urethral region of the prostate called the transition zone, resulting in compression of the prostatic urethra.
Prostate cancer usually occurs in the peripheral zone. Anatomically, the median and lateral lobes are usually enlarged.
Signs / symptoms of BPH
LUTS —> more so voiding Sx
Storage - frequency, urgency, nocturia, incontinence
Voiding - weak stream, hesitancy, terminal dribbling, dysuria
Lower Abdominal pain - acute urinary retention
Signs
Smooth, enlarged, and non-tender prostate
Lower abdominal tenderness and palpable bladder
Investigation and Dx of BPH
Digital rectal exam
Smooth, enlarged prostate
Prostate-specific Antigen (PSA)
May be raise - more so in cancer though - unreliable
IPSS
Tx for BPH
Lifestyle modification
decrease caffeine
Drugs
alpha-1 blocker (tamsulosin) - 1st line
Relaxed SMC around bladder neck
5-alpha reductase (finasteride) - 2nd line
Reduces testosterone conversion —> reduces prostate size
Surgery
Last resort
TURP - transurethral resection of prostate
Complication for transurethral resection of prostate
Retrograde ejaculation
What type of neoplasm is renal cell carcinoma
Adenocarcinoma affecting proximal convoluted tubule epithelium
Remember adenocarcinoma = malignant glandular epithelial neoplasm
What is the most common renal cancer
Renal cell carcinoma
Types of renal cell carcinomas
Clear cell carcinoma
Papillary carcinoma
Chromophobe
Pathophysiology of Renal cell carcinoma
Majority = sporadic
Some are hereditary
Deletion in the VHL tumour suppressor gene (Von Hippel Lindau) —> causes increased IGF-1 —> increased cell growth…
Risk factors for renal cell carcinoma
Age
Male
Von hipped lindau disease
Haemodialysis
Sx of renal failure
Remember classic triad for RCC
Haematuria
Flank pain
Palpable mass
_Left sided varicocele_
Left testicular vein drains into the left renal vein; a left RCC can invade the renal vein causing backpressure and varicocele formation
Right testicular vein drains directly into the IVC, therefore a right RCC does not cause a varicocele
Other Sx related to cancer (constitutional Sx)
Weight loss
Fatigue
Paraneoplastic features of renal cell carcinoma
EPO —> polycythaemia
Renin —> hypertension
PTHrP / bony metastases —> hypercalcaemia
Investigation and Dx of renal cell carcinoma
1st line - USS
Gold standard - CT Chest / Abdo / Pelvis (more sensitive)
Could do urinalysis (haematuria) / FBC (anaemia of chronic disease or polycythaemia)
Staging - Robson staging 1 - 4
Tx for renal cell carcinoma
Nephrectomy (partial / radical)
Could also do;
Radiofrequency ablation
Define Wilms tumour
Renal mesenchymal stem cell tumour seen in children (< 3y/o)
AKA nephroblastoma
What type of cancer is bladder cancer
2 types…
Urothelial / Non-rothelial
Urothelial:
Transitional cell carcinoma of bladder —> most common (90%)
Non-urothelial:
Squamous cell carcinoma (7%)—> higher in Px with schistosomiasis
Adenocarcinoma —> very rare
