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
Risk factor for bladder cancer
Increased age
Male
Smoking
Occupational exposure:
Aromatic amine —> textiles, dye, rubber, paints
- Transitional cell carcinoma
Schistosomiasis / areas with high prevalence (Egypt) - squamous cell carcinoma
Sx of Px with bladder cancer
Painless haematuria (macro / microscopic)
Dysuria
_Constitutional Sx:)
Weight loss
Fatigue
Investigation and Dx of bladder cancer
Flexible cystoscopy + biopsy - gold standard
If if high risk +/ suspected muscle invasion - CT abdo / pelvis
Tx for bladder cancer
Medical
Chemo / radiotherapy
Surgical:
TURBT - transurethral resection of bladder tumour
Radical cystectomy - last resort
What type of cancer is prostate cancer
Adenocarcinoma of the posterior peripheral prostate
Malignant neoplasm of glandular epithelium
Risk factors for prostate cancer
Genetic - BRCA 1 / BRCA 2 (for breast cancer too) // HOXB13
Increased age
FHx
Afrocaribbean ethnicity
Sx of prostate cancer
LUTS (like BPH) but with systemic cancer Sx (weight loss, fatigue)
± Bone pain (lumbar) - typically metastasise in bone (sclerotic lesions), liver, lung, brain.
Investigation and Dx of prostate cancer
Digital rectal exam - Asymmetrical, hard, nodular prostate
Increased PSA
Multiparametric MRI - 1st line
Transrectal USS + biopsy = gold standard
Gleason grading score
Score used in prostate cancer
Gleason grading score (out of 5; done twice) - based off biopsy
Low grade: ≤6
Intermediate: 7
High grade: 8-10
Tx for prostate cancer
Local
Prostatectomy
Metastatic
Hormone therapy (because this is the most hormone sensitive cancer)
Bilateral Orchidectomy - best
GnRH agonist (Goserelin)
Radio/Chemotherapy
Why can hormone therapy be used in prostate cancer
Androgen-dependent, meaning they rely on androgen hormones (e.g., testosterone) to grow.
Decrease testosterone —> decrease cancer growth
What type of drug is goserelin and why is it used in prostate cancer
GnRH agonist
Weird - agonist for GnRH increases LH + FSH … BUT… results in exogenous suppression of HPG axis (hypothalamic pituitary gonadal)
- so reduced hormones reduces prostate cancer growth
What is the most common cancer in young men
Testicular cancer
Types of testicular cancer
Germ cell (90%)
Seminoma (most common)
Teratoma
Non-germ cell (<10%)
Leydig
Sertoli
Sarcoma
Risk factor for testicular cancer
Undescended testes - Cryptorchidism
Infertility
FHx
Sx of testicular cancer
Painless lump in testicle
That
Does not transilluminate
May show signs of metastases: cough/sob (lung) / bone pain (bone)
Investigation and Dx of testicular cancer
Urgent doppler USS testes - 1st line + diagnostic
Tumour markers:
ß-hCG - raised in seminoma
AFP - raised in teratoma
LDH - raised non-specifically in tumours
Chest X-ray for metastasis
Tx for testicular cancer
Radical orchidectomy (1st line)
Adjuvant: chemo/radiotherapy
Give 2 causes of obstructive uropathy
BPH
Stones
Pathophysiology of obstructive uropathy
Obstruction —> urine retention + increased KUB pressure —> causes refluxing/backlogged urine in renal pelvis —> leading to HYDRONEPHROSIS (dilation renal pelvis; more prone to infection)
Types of UTIs
Upper UTIs: pyelonephritis
Lower UTIs: cystitis, Prostatitis, urethritis, epididymo-orchiditis
Location of UTIs
Upper UTIs: kidneys
Lower UTIs: bladder and below
Which organisms can cause a UTI
KEEPS
Klebsiella pneumonia
E.coli - most common
Enterobacter
Proteus mirabilis
Staphylococcus saprophyticus
Which organism accounts or 80% of UTIs
UPEC
UroPathogenic E.Coli
Who is more affected in UTIs
Women
Shorter urethra so closer to anus + easier for bacteria to colonise
Investigation and Dx for all UTIs
1st line: Urine dipstick
+ve leukocytes
+ve nitrites (bacteria breakdown nitrates—>nitrites)
- can consider uti with just +ve nitrites; not just +ve leukocytes though
± Haematuria
^shows uti likely
Gold standard: midstream MC & S (microscopy, culture, sensitivity)
^confirms uti + ID’s pathogen
Define pyelonephritis
Infection of renal parenchyma + upper ureter.
Ascending transurethral spread
Organisms causing pyelonephritis
UPEC - most commonly
Any of the KEEPS:
Klebsiella
E. coli
Enterobacter
Proteus mirabilis
Staphylococcus saprophyticus
Risk factors for pyelonephritis
Urine stasis - renal stones
Young women <35
Catheters
Pregnancy
Immunocompromised
Sx of pyelonephritis
Learn triad differentiating it from cystitis
Fever, Loin pain, N&Vomiting
± Pyuria (pus in urine)
Investigation and Dx for pyelonephritis
Same for all UTIs
1st line: urine dipstick
+ve leukocytes
+ve nitrites (bacteria breakdown nitrates—>nitrites)
- can consider uti with just +ve nitrites; not just +ve leukocytes though
± Haematuria
^shows uti likely
Gold standard: midstream MC & S (microscopy, culture, sensitivity)
^confirms uti + ID’s pathogen
Do Ix for renal stones in case
Tx for pyelonephritis
Paracetamol; analgesia
+
ABx: Ciprofloxacin or Co-amoxiclav
Cephalexin; if pregnant
Define cystitis
Infection of the lower urinary tract; affecting bladder
Risk factor
Women
Post-menopause
Catheter
Bladder lining damage
Sx of cystitis
Increased frequency, urgency
Dysuria
Nocturia
Suprapubic tenderness
Confusion / delirium esp. in adults
Investigation and Dx of cystitis
Same for all UTIs
1st line: urine dipstick
+ve leukocytes
+ve nitrites (bacteria breakdown nitrates—>nitrites)
- can consider uti with just +ve nitrites; not just +ve leukocytes though
± Haematuria
^shows uti likely
Gold standard: midstream MC & S (microscopy, culture, sensitivity)
^confirms uti + ID’s pathogen
Tx for cystitis
ABx
Trimethoprim / Nitrofurantoin
Amoxicillin if pregnant
Define urethritis
Inflammation of the urethra ± infection
Most commonly a sexually acquired condition
Types of urethritis
Infective has 2 types:
Gonococcal (less common) - Neisseria Gonorrhoea
Non-Gonococcal (more common) - Chlamydia Trachomitis
non-infective:
Trauma
What type of bacteria is chlamydia trachomatis
Obligate intracellular gram -ve aerobic bacillus
What type of bacteria is Neisseria gonorrhoea
Gram -ve diplococcus
Which micro organisms can cause infective urethritis
Neisseria gonorrhoea
Chlamydia trachomatis
Risk factors for urethritis
Unprotected sex
Multiple sex partners
Sx of urethritis
Dysuria ± urethral discharge (blood/pus)
Urethral pain
Investigation and Dx of urethritis
NAAT - nucleic acid amplification test —> detects STIs (Neisseria / chlamydia)
Urine dipstick (+ve if infectious UTI) + MC + S (will detect pathogen ID if UTI) : gram -ve diplococcus = gonorrhoea
Tx for urethritis
Neisseria G:
IM Ceftriaxone + Azithromycin
Chlamydia T:
Azithromycin ( / doxycycline)
Complication of urethritis
Reactive arthritis
Cant see (conjunctivitis)
Cant pee (urethritis)
Cant climb a tree (arthritis)
Define epididymo-orchitis
Inflammation of epididymis, extending to testes
At the back of each testicle is the epididymis. Sperm are released from the testicle, into the head of the epididymis, connected at the top of the testicle. The sperm travel through the head, then body, then tail of the epididymis. Sperm mature and are stored in the epididymis. The epididymis drains into the vas deferens.
Usually due to urethritis (STI) - more in <35y/o
OR
cystitis (KEEPS) extension - more in >35y/o
Cause of epididymo-orchitis
Usually due to urethritis (STI) - more in <35y/o
OR
Cystitis (KEEPS - Enteric bacteria) extension - more in >35y/o
OR
Mumps (viral)
How does epididymo-orchitis affect
Males
- infection of the epididymis + testes
Sx of Px with epididymo-orchitis
Unilateral, tender, red swollen testicle
Pain relieved by elevating testis (+ve Prehn’s sign)
Cremasteric reflex intact
LUTS
Differential Dx of epididymo-orchitis
Testicular torsion
- Acute presentation like epididymo-orchitis with testicular pain but higher change of testes death so Tx like torsion until proven otherwise
(+ additional Sx: N+V, cryptorchidism / bell clapper)
Investigation and Dx of epididymo-orchitis
NAAT - for NG / CT
Urine dipstick
Urine MC+S
Tx for epididymo-orchitis
If STI:
Neisseria G—>** IM Ceftriaxone + Azithromycin**
Chlamydia T—> Azithromycin / doxycycline
If UTI
Ciprofloxacin - quinolone = powerful broad-spectrum antibiotics for gram -ve esp
Co-amoxiclav
The difference between nephrotic and nephrotic syndrome
NephrOtic
Proteinurea
Hypoalbuminemia
Oedema
± hypertension
Nephritic
Haematuria
Oliguria
Oedema
Cause of nephrotic syndrome
1º -
Minimal change disease (MC in children)
Focal segmented glomerulosclerosis (MC in African / Hispanic descent)
Membranous nephropathy (adults; causcasian)
2º -
Diabetic nephropathy
Amyloidsis
Signs and Sx of Px with nephrotic syndrome
Proteinuria - Frothy urine
Hypoalbuminaemia
Oedema
Hyperlipidaemia
Investigation and Dx of of nephrotic syndrome
Take kidney biopsy
Minimal ∆ disease
Light microscopy - NO CHANGE
E- microscope - podocyte effecement + fusion
Focal segmental glomerulosclerosis
Light microscopy - segmental sclerosis; less than 50% glomeruli affected though
Membranous nephropathy
Light microscopy - thickened glomerulus basement membrane
E- microscope - subpodocyte immune complex deposition, spike and dome appearance
Treatment for nephrotic syndrome
Minimal ∆ disease - corticosteroids (12 weeks)
Focal segmental glomerulosclerosis + membranous nephropathy respond less well to steroids
Define nephrotic syndrome
When glomeruli are damaged becoming more permeable ~ T cells in the blood, releasing cytokines: glomerular-permeability factor (GPF), that specifically damages the foot processes of the podocytes, making them flatten out (effacement)
Allows proteins to be filtered through into the urine (proteinuria)
*Main protein lost ~ Albumin; leads to less in blood (hypoalbuinaemia) ~
This then leads to peripheral and peri-orbital oedema Because there’s reduced oncotic pressure.
Px becomes hypercoaguable too ~ due to loss of anti-thrombin III protein ~ so increased thrombosis formation.
Loss of immunoglobulins increases risk of infection*
How much proteinuria is indicative of nephrotic syndrome
≥ 3.5g per day
Define nephritic syndrome
Inflammation that damages glomerular basement membrane
This leads to haematuria and RBC casts in urine ~ can then lead to renal failure; presenting with
…
Oliguria
Arterial hypertension
Peripheral and peri-orbital oedema.
Causes of nephritic syndrome
Type III hypersensitivity reaction
IgA nephropathy (Berger’s disease) - most common cause
Post Strep. Glomerulonephritis
SLE
Haemolytic uraemic syndrome
Type II hypersensitivity
Goodpasture’s syndrome
Explain how post strep. Glomerulonephritis presents in a Px with nephritic syndrome
Visible haematuria (blackish / coke-cola like)
HTN
Oliguria
Usually seen 2 weeks after Px had pharyngitis from group A/B haemolytic streptococcus ~ strep. Pyogenes
investigation & Dx:
Light microscope - hyper cellular glomeruli
E- microscope - subendothelial humps
Immunofluorescence - starry sky ~deposition of IgG, IgA & C3 in G. Basement membrane
Tx:
Self-resolves in children
In adults could lead to
Explain how IgA nephropathy presents in a Px with nephritic syndrome
Visible haematuria (blackish / coke-cola like)
HTN
Oliguria
Px presents 1-2n days after tonsillitis viral infection / gastroenteritis viral infection
~ more commonly seen in Asian populations
~associated with HIV
Dx:
Immunofluoresence - IgA complex deposition
Light microscopy shows mesangial hypercellularity
Tx:
Non-curative
BP control - ACEi (1st line control)
How to Dx lupus nephritis
2º to SLE (ANA deposits in endothelium)
Cause of nephritic syndrome
+ve ANA
+ve Anti-dsDNA
Tx for lupus nephritis
Corticosteroids + immunosuppressants
Define goodpasture’s
Anti-Glomerular basement membrane (GBM) antibody disease
Autoimmune disease whereby circulating antibodies target the lungs and kidneys, causing pulmonary haemorrhage and glomerulonephritis.
Tx for goodpastures
Corticosteroids - prednisolone
+ plasma exchange
Complication of nephritic syndrome
RPGN
Rapidly progressing glomerulonephritis
Dx for rapid progressing glomerulonephritis
Progress to end stage renal failure v.fast
Inflammatory crescents in bowman’s space
True or false: wegener’s granulomatosis C-ANCA +ve
Yes true
Autoimmune vasculitis is P-ANCA positive
Define Polycystic kidney disease
Cyst formation throughout the renal parenchyma
- bilateral enlargement + damage
Aetiology / cause of PKD
Familial inherited:
Autosomal recessive - much less common
Presents in neonates and is usually picked up on antenatal ultrasound scans. It is the result of a mutation in the polycystic kidney and hepatic disease 1 (PKHD1) gene on chromosome 6.
Autosomal dominant - most common
Presents more in males; Px at 20-30y/o
Mutation in PKHD1 (85%) / PKHD 2 (15%)
Pathophysiology of pkd
PKHD 1 / 2 genes encode for polycystin (Ca2+ channels) in the cilia of nephron…
When filtrate passes cilia move and open Polycystin; influx of Ca2+ inhibits excessive growth… so….
When theres a mutation, you get decreased ca2+ influx and cilia grow excessively
What chromosome is pkhd 1 found
16
What chromosome is pkhd 2 found
4
Signs and Sx of polycystic kidney disease
Bilateral flank / back or abdominal pain ± hypertension & haematuria
(I.e. chronic loin pain)
Extra-renal cysts: esp in circle of Willis (berry aneurysm; if ruptured becomes subarachnoid haemorrhage) / prostatic cysts
Investigation and Dx of polycystic kidney disease
Kidney uss
Enlarged bilateral kidneys with multiple cysts
Genetic testing
Tx for pkd
Non curative
Tolvaptan - vasopressin receptor antagonist
Antihypertensives for hypertension.
Analgesia for renal colic related to stones or cysts.
Antibiotics for infection. Drainage of infected cysts may be required.
Give examples of non-malignant scrotal diseases
Scrotal mass —> cancer till proved otherwise
Epidyidymal cyst
Hydrocele
Varicocele
Testicular torsion
Define and Dx epididymal cysts
Extra testicular cysts (above + behind testis) that will transilluminate
Dx: USS scrotum
Define and Dx hydrocele
Fluid collection in tunica vaginalis
- cyst that testicle sites within that will transilluminate
Dx: USS scrotum
Define and Dx a varicocele
Bag of warms (on LHS mostly)
Distended Pampiniform plexus because of increased left renal vein pressure causing reflux - typically painless.
Dx: clinical
Define testicular torsion
Spermatic cord twists on itself; occlusion of testicular artery causes ischaemia —> gangrene of testis if not tx
Surgical emergency
Risk factors for testicular torsion
Bell clapper deformity - horizontal lie of testes
Signs and Sx of testicular torsion
Severe unitesticular pain (hurts to walk)
Abdominal pain; N&V
-VE PREHNS SIGNS - lifting testis doesn’t alleviate the pain
No cremasteric reflex
^Both seen in epididymo-orchitis - DDx^
Dx for testicular torsion
surgical exploration - if high risk of torsion.
USS to check testicular blood flow
Could later do a urinalysis - to see if sign of epididymo-orchitis
Tx of testicular torsion
Urgent surgery within 6hrs (for >90% success)
- all cases require bilateral orchiplexy (fixing of testes to scrotal sac to overcome bell clapper deformity; if not viable, do orchidectomy)
