GU Flashcards
What is the function of the proximal convoluted tubule?
Reabsorption of: - some water and Na+ - some other ions - all glucose and amino acids
What is the function of the distal convoluted tubule?
Regulating acid-base balance - By secreting H+ and absorbing HCO3- - Also regulates Na+ level
What is the structure of the collecting duct in the kidney?
Principal cells: - Regulate Na+ reabsorption and K+ excretion - Respond to aldosterone and ADH Intercalated cells: - Exchange H+ for HCO3-
What is the structure of urothelium?
- Complex stratified epithelium - Can stretch in 3 dimensions - Layer of umbrella cells - make it urine proof
What is the innervation of bladder contraction?
Autonomic parasympathetic (cholinergic) - S3-S5 nuclei - Drive detrusor contraction
What is the innervation of bladder relaxation?
Autonomic sympathetic (noradrenergic) - T10-L2 nuclei - Urethral contraction (smooth muscle component but remember the main part of the sphincter is skeletal muscle) - Inhibits detrusor contraction
What is the innervation of A-δ fibres (bladder stretch) and C fibres (bladder pain)?
Sensory Autonomic - S2-S4 nuclei
Treatment for pyelonephritis
Analgesia: Paracetamol - Antibiotics: Ciprofloxacin or co-amoxiclav (if pregnant, give cefalexin) - Refer to hospital if there are signs of sepsis
Treatment for chlamydia
First line: doxycycline - if CI or not tolerated: azithromycin - if CI: erythromycin…or ofloxacin but this is CI in pregnancy - Sexual intercourse should be avoided until treatment is complete - Partner must Also be treated
Treatment for gonnorrhoea
- IM ceftriaxone 1g - Refer to GUM clinic
Treatment for early syphilis
- Single deep intramuscular dose of benzathine benzylpenicillin - Refer to GUM clinic - Notify all partners in the last 3 months
What are kidney stones made from?
Calcium - Calcium oxalase (80%) - Calcium phosphate (20%) Other types: - Struvite (RF = UTI) (1-5%) - Uric acid (10-20%) - Cystine (1%) - Drug induced (1%)
Aetiology of calcium oxalate stones
Low urine volume - Hypercalciuria - Hyperuricosuria - Hyperoxaluria - Hypocitraturia
Aetiology of calcium phosphate stones
Low urine volume - Hyperclciuria - Hypocitraturia - High urine pH - Hyperparathyroidism - Renal tubular acidosis
Aetiology of cystine stones
Cystinuria, a genetic disorder that causes cystine to leak through the kidneys into the urine
Drugs that impair urine composition
Acetazolamide - Allopurinol - Aluminium magnesium hydroxide - Ascorbic acid - Calcium - Furosemide - Laxatives - Vit D - Topiramate
Drugs that crystallise in urine
Allopurinol/oxypurinol - Amoxicillin/ampicillin - ceftriaxone - Ephedrine - Indinavir - magnesium trisilicate - Quinolones - Sulphonamides - Triamterene - Zonisamine
Epidemiology of kidney stones
- M:F about 2:1 - Uncommon in children - Age 30-50 but decreasing
Pathophysiology of kidney stones
- Excess solute in collecting duct - Supersaturated urine, favours crystallisation - Stones cause regular outflow obstruction - Hydronephrosis -> dilation + obstruction of renal pelvis
Presentation of kidney stones
- Unilateral loin to groin pain that is colicky (fluctuating) - Patient can’t lie still (DDx = peritonitis) - Haematuria and dysuria - UTI symptoms/recurrent UTIs
Three common obstruction sites for kidney stones
Pelvoureteric junction - Pelvic brim (where ureter crosses over iliac vessels) - Vesicoureteral junction
Diagnosis of kidney stones
First line: KUBXr - 80% specific for renal stones, cheap + easy Gold standard: Non-contrast CT KUB - 99% specific for stones Bloods: FBC (raised Calcium and Phosphate) U+E (haematuria) Ultrasound if pregnant
Treatment for kidney stones
- Symptomatic -> hydrate, non-opiate analgesia or NSAIDs - Antibiotics if UTI present - Alpha blocker to help stones pass (up to 10mm) - Surgical elective treatment if stones are too big to pass (5mm<)
Methods of surgery for kidney stones
- Extracorporeal shock wave lithotripsy (ESWL) - non-invasive, smaller stones - Percutaneous nephrolithotomy (PCNL) - larger stones, 20mm+ - Uteroscopy (URS) - energy sources including lasers break up stones - Open surgery (last resort when all else fails)
What is acute kidney injury?
Abrupt decline in kidney function (hours-days) characterised by high serum creatinine + urea and low urine output
NICE criteria for acute kidney disease (any one)
- Rise in serum creatinine of > 25μmol/L within 48 hours - 50% or greater rise in serum creatinine over 7 days - A fall in urine output to less than 0.5ml/kg/hour for more than 6 consecutive hours
Risk factors for acute kidney injury
65+ - Comorbidities - Cognitive impairment (less water intake) - Hypovolaemia of any cause - Oliguria - Nephrotoxic drug use including contrast agents
Why shouldn’t you use contrast agent when kidney disease is suspected?
Contrast would need to be excreted by the kidney
Pathophysiology of acute kidney injury
Accumulation of usually excreted substances: - K+ (arrhythmias) - Urea (pruritis + uremic frost, confusion if severe) - Fluid (pul + peripheral oedema) - H+ (acidosis)
Pre-renal AKI
Due to hypoperfusion of the kidneys, leading to decreased GFR - Hypovolaemia - Reduced cardiac output (cardiac failure, liver failure, sepsis, drugs) - Drugs that reduce blood pressure (ACE-i, ARBs, NSAIDs, loop diuretics)
Renal AKI
A consequence of structural damage to the kidney, eg: tubules, glomeruli, interstitium, bvs. May result from persistent pre-renal and post-renal causes, damaging renal cells - Toxins and drugs (eg: antibiotics, contrast agent, chemo) - Vascular causes (eg: vasculitis, thrombosis, etc) - Glomerular, tubular (MC) or interstitial causes
Post-renal AKI
Least common (10%) - due to acute obstruction of the flow of urine -> increased intratubular pressure and decreased GFR - Renal stones - Blocked catheter - Enlarged prostate - GU tract tumours - Neurogenic bladder
Diagnosis of AKI
- Establish cause (pre, intra, post) w KDIGO classification - Check K+, H+, urea, creatining w U+E - FBC + CRP check for infection - Renal biopsy will confirm intrarenal cause, ultrasound for post renal
Best way to establish cause of AKI
Urea:Creatinine > 100:1 = Prerenal < 40:1 = Renal 40-100:1 = Postrenal
Treatment for AKI
Treat complications - Fluid rehydration with IV fluids for pre-Renal AKI - Stop Nephrotoxic medications - Relieve obstruction in post-Renal AKI - last resort = Renal replacement therapy
When would haemodialysis be given for AKI
Acidosis (pH<7.1) Fluid overload (oedema) Uremia K+ >6.5 /ECG change
Normal eGFR
120mL/min/1.73m2
When is metformin contraindicated?
When eGFR < 30
CKD G scores (eGFR)
G1. ≥ 90ml/min/1.73m2 G2. 60-90ml/min/1.73m2 G3a. 45-59ml/min/1.73m2 G3b. 30-44ml/min/1.73m2 G4. 25-29ml/min/1.73m2 G5. <15ml/min/1.73m2
Best clinical readings to quantify CKD
eGFR - Albumin:creatinine (more sensitive measurement of proteinurea than PCR)
Aetiology of CKD
T2DM - Hypertension - Glomerulonephritis - PKD - Nephrotoxic drugs
Risk factors for CKD (other than diseases)
Older Age - Family history - Smoking
Pathophysiology of CKD
- Many nephrons damaged, increased burden on the remaining nephrons - Compensatory RAAS but this increases transglomerular pressure -> shearing and loss of BM selective permeability -> proteinuria/haematuria - Angiotensin 2 upregulates TGF-beta and plasminogen activator-inhibitor-1 -> mesangial scarring
Presentation of CKD
- Asymptomatic early on (lots of nephrons = reserve supply) - Symptoms due to substance accumulation + renal damage (diabetic nephropathy) - Pruritis, loss of appetite, nausea, oedema, muscle cramps, pallor
Complications of CKD
Anaemia (Low EPO) - Osteodystrophy (Low Vit D activation) - Neuropathy and encephalopathy - CVD and Hypertension - Haematuria and proteinuria
Diagnosis of CKD
- FBC for anaemia - U+E for eGFR - Early morning urine dipstick for haematuria and albumin:creatinine (>70mg/mmol = significant proteinuria) - Ultrasound shows bilateral renal atrophy
Treatment for CKD
No cure so treat complications: - Anaemia: Fe + EPO - Osteodystrophy: Vit D supplements - CVD: ACE-i and statins - Oedema: diuretics - Stop NSAIDs - Stage 5 (end stage renal failure) -> RRT (dialysis) - Ultimately if ESRF, cure is renal transplant
CKD A scores (albumin:creatinine)
A1. < 3mg/mmol A2. 3-30mg/mmol A3. >30mg/mmol
A patient has a score of A1 combined with G1 or G2. Can they be diagnosed with CKD?
No. They need at least an eGFR of <60 or proteinuria
What is chlamydia caused by?
Chlamydia trachomatis, a gram negative intracellular bacillus
Epidemiology and risk factors for chlamydia
- Most common STI in the UK - Under 25 and sexually active - New sexual partner or more than one sexual partner in the last year - Lack of consistent condom use - Unprotected sex
Presentation of chlamydia and gonorrhoea
Vaginitis and cervicitis - Proctitis - Epididymo-orchitis - Pelvic inflammatory disease - Pharyngitis - Reactive arthritis
Symptoms of lymphogranuloma venereum (a type of chlamydia)
Tenesmus - Anorectal discharge (often bloody) and discomfort - Diarrhoea or altered bowel habits
Diagnosis of chlamydia
Nucleic acid amplification testing - Women - vulvovaginal or endocervical swab - Men - first-void urine
What do GUM clinics screen for?
Chlamydia - Gonorrhoea - Syphilis (blood test) - HIV (blood test)
What is gonorrhoea caused by?
Gram-negative diplococcus Neisseria gonorrhoeae - Spread By penetretive Sexual intercourse Most commonly
Risk factors for gonorrhoea
Frequent or unprotected Sexual intercourse - Multiple Sexual partners - MSM - Chlamydial infection
Symptoms in gonorrhoea
50% of women and 90% of men are symptomatic
Symptoms of rectal and pharyngeal gonorrhoea infection
Rectal infection is usually Asymptomatic but may cause anal discharge and pain or discomfort - Pharyngeal is Asymptomatic in Most cases but is occasionally associated with a sore throat
How do nucleic acid amplification tests work?
Check if a gonococcal infection is present or not - By looking at gonococcal RNA or DNA
Diagnosis of gonorrhoea
Nucleic acid amplifiction testing - Microscopy shows Gram negative diplococci - Swab infected areas
Pathophysiology of syphilis
Spirochete bacteria called Treponema pallidumial - Gets in through skin or mucous membranes, replicates and then disseminates through the body
Risk factors for syphilis
MSM - IVDU - Sex workers - Multiple or unprotected Sexual partners
Primary syphilis
- Painless ulcer called a ‘chancre’ at the original site of infection (usually genitals) - Femoral lymphadenopaty - Presents 9-90 days after exposure - Usually resolves spontaneously over 3-10 weeks
Secondary syphilis
- Systemic features, skin lesions, alopecia, mucous patches and early neurosyphilis - Presents 4-12 weeks after initial chancre - Untreated symptoms slowly resolve over 3-12 weeks but may recur
Latent syphilis
- Asymptomatic - Less than 2 years duration from initial infection - Late latent - more than 2 years
Tertiary syphilis
- Gummatous, cardiovascular and neuro syphilis - Presents 15-40 years after initial infection
Diagnosis of syphilis
Antibody testing for T.pallidum - Samples from site of infection Can be tested to confirm the presence of T.pallidum with dark field Microscopy and PCR
Five most common UTI pathogens
Klebsiella E.coli Enterobacter Proteus S.saphrophyticus MC is uropathogenic e.coli
Why are females more affected by UTIs?
Shorter urethra - Closer to anus - Easier for bacteria to colonise
Diagnosis of all types of UTI
First line:✨Urine dipstick✨ +ve leukocytes +ve nitrites (bc bacteria break down nitrates into nitrites) +/- haematuria Gold standard: Midstream MC + S - Confirms UTI - Identifies pathogen
What is pyelonephritis?
Infection of the renal parenchyma and upper ureter, ascending transurethral spread
Most common causative pathogens of pyelonephritis (most to least common)
Uropathogenic E.Coli - Kleblsiella - Proteus - Pseudomonas - Enterobacter
Presentation of pyelonephritis
Triad: loin pain, fever, n+v
Patients who have significant symptoms or do not respond to treatment w pyelonephritis
Renal abscess - Kidney Stones
What is cystitis?
UPEC infection of the bladder - Most common in young sexually active women
Aetiology of cystitis
urine stasis - bladder lining damage - Catheters
Presentation of cystitis
Suprapubic tenderness and discomfort, worse with a full bladder - High frequency and urgency - Visible Haematuria
Infective vs non-infective urethritis
Infective: Gonococcal (LC) and non-gonococcal (MC, chlamydia) Non-infective: Trauma
Risk factors for urethritis
MSM and unprotected sex
Presentation of lower urinary tract infections
- Dysuria - Frequency +/- urethral discharge, urethral pain (Urethritis)
Diagnosis of urethritis, epididymo-orchitis and prostatitis
Normal diagnosis for UTIs - As well As NAAT (nucleuc acid amplification testing) to detect STI
What is epididymo-orchitis?
- Inflammation of the epididymis, extending to the testes Usually due to: - Urethritis (<35 years) - Cystitis extension (>35 years) - Can also be caused in the elderly from a catheter
Presentation of epididymo-orchitis
Unilateral scrotal pain and swelling - Prehn’s sign positive - Cremaster reflex intact - DDx = rule out testicular torsion
Treatment of urethritis and epididymo-orchitis
Dependent on cause
Acute vs chronic prostatitis
- Acute bacterial prostatitis - more rapid onset of symptoms - Chronic prostatitis - symptoms lasting for at least 3 months, can be subdivided. Types of chronic prostatitis: - Chronic pelvic pain syndrome - no infection - Chronic bacterial prostatitis - infection
Most common cause of prostatitis
E.Coli
Presentation of prostatitis
Perineal, penile or Rectal pain - Acute urinary retention, obstructive voiding symptoms - Low back pain, pain on ejaculation - Tender, swollen warm prostate on examination
Functions of the prostate
- Produces testosterone and dihydrotestosterone (5x more potent) - Produces PSA - liquefies semen
Risk factors for benign prostatic hyperplasia
- Age (50+) - Men (obviously) - Afrocarribean = high testosterone
Pathophysiology of benign prostatic hyperplasia
Inner transitional zone of prostate (muscular, gland) proliferates - Causes narrowing of the urethra
Presentation of benign prostatic hyperplasia
LUTS
What happens in benign prostatic hyperplasia if the urethra is totally occluded?
Anuria - Retention - Hydronephrosis - UTI - Stones
Diagnosis of benign prostatic hyperplasia
Digital rectal examination (DRE) - Smooth, enlarged Prostate-specific antigen (PSA) - To rule out prostate cancer (but unreliable as it can be raised in both, but more in cancer)
Treatment for benign prostatic hyperplasia
- First line: Alpha blocker (tamsulosin) - Second line: 5 alpha reductase inhibitor (finasteride) - decreases testosterone production and therefore prostate size - Last resort, surgery - TURP - transurethral resection of the prostate (SE = retrograde ejaculation)
Risk factors for renal cell carcinoma
- > 40 - Smoking - Obesity - Male - Hypertension - Haemodialysis (15% chance) - Von-Hippel Lindau syndrome (also tuberous sclerosis, Burt Hogge Dube and hereditary papillary RCC)
What is Von-Hippel Lindau syndrome?
- Autosomal dominant loss of tumour suppressor gene - ROC (50%) bilaterally - Renal + pancreas cysts - Cerebellum cancers
Presentation of renal cell carcinoma
- Often asymptomatic and found incidentally, 25% metastasised cases at presentation - Triad: loin pain, haematuria, abdo mass - May have left sided varicocele - Anaemia (low EPO)
Diagnosis of renal cell carcinoma
First line: Ultrasound - Gold standard: CT chest/abdo/pelvis
Renal cell carcinoma metastases
- Spreads to the tissues around the kidney, within Gerota’s fascia - Often spreads to the renal vein, then IVC - “Cannonball metastases” in the lungs are a classic feature of renal cell carcinoma
Staging of renal cell carcinoma
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Treatment for renal cell carcinoma
- Sometimes watch and wait - Radiofrequency ablation or cryotherapy (only if tumour is <4cm) - Gold standard: Partial nephrectomy - Radical (full) nephrectomy (most common)
What is a Wilms tumour?
- Renal mesenchymal stem cell tumour - Seen in children (<3 years) - Much rarer - Aka: nephroblastoma
What type of cancer is renal cell carcinoma?
PCR epithelial carcinoma
What type of cancer is bladder cancer?
transitional cell carcinoma of bladder (mc, and mc subtype is transitional urothelium) - if Patient has schistosomiasis, they are more likely to have squamous cell carcinoma
Risk factors for bladder cancer
- Smoking - Age 55+ - Males - Occupational exposure to aromatic amines, eg: painter, hairdresser (dyes), mechanic working with tyres (rubber) - Chemo/radiotherapy (cyclophosphamide)
Presentation of bladder cancer
Painless Visible Haematuria - LUTS - Recurrent UTIs
Diagnosis of bladder cancer
Gold standard: flexible cystoscopy + upper tract imaging
NICE 2 week wait referral criteria for bladder cancer
Age 45 or above with: - Unexplained visible haematuria - or visible haematuria that persists after UTI treatment Age 60 or above with: - Unexplained non-visible haematuria - and either: dysuria or raised white cell count
NICE two week wait referral criteria for renal cancer
45 or over with: - Unexplained visible haematuria without UTI - or visible haematuria that persists after treated UTI
Treatment for bladder cancer
T1: Transurethral resection of bladder tumour T2-3: Cystoprostatectomy in men, anterior extentoration in women T4: Palliative or chemo/radiotherapy Intravesical therapy: mitomycin and BCG to reduce recurrence
What type of cancer is prostate cancer?
Adenocarcinoma of outer peripheral prostate
Risk factors for prostate cancer
Genetic: BRCA1, BRCA2, HOXB13 - increased Age - Afrocaribbean ethnicity
Presentation of prostate cancer
LUTS - Systemic cancer symptoms (weight, loss, fatigue, night pain) - Bone pain
Prostate cancer metastases
Typically to Bone (thick sclerotic lesions) - Typically lumbar back pain - Also liver, lung, brain
Diagnosis of prostate cancer
DRE + PSA in community - Gold standard: Transrectal Ultrasound - Biopsy gives Gleason score - higher = worse
Treatment of metastatic prostate cancer
Hormone therapy - Bilateral orchidectomy (best) - GNRH receptor agonist eg: goserelin - Radio/chemo therapy
What type of cancer is testicular cancer?
Germ cell (90%+) or non germ-cell (<10%) tumour Germ = seminoma (mc) or teratoma Non germ = sertoli, leydig, sarcoma
Risk factors for testicular cancer
- Most common cancer in young men 20-45 (more common in caucasians) - Cryptorchidism (undescended testes) - HIV - Previous testicular cancer - Infertility - Family history
Presentation of testicular cancer
- Painless, hard, irregular lump in testicle - Does not transilluminate - May show lung metastasis signs, eg: cough -> consider chest x-ray - Gynaecomastia (breast enlargement) if it is a Leydig cell tumour (rare)
Diagnosis of testicular cancer
- Examination including lymph nodes, testes and scars from previous orchidopexy- Urgent (Doppler) ultrasound of testes (90% diagnostic) - Bloods for tumour markers - CXR if resp symptoms - Staging: CT chest/abdo/pelvis
Tumour markers for testicular cancer
beta hCG - raised in seminomas - AFP - raised in teratomas - LDH raised non-specifically
Royal Marsden staging system for testicular cancer
- Isolated to testicle 2. Spread to retroperitoneal lymph nodes 3. Spread to lymph nodes above diaphragm 4. Metastasised to other organs (mc: lymphatics, lungs, liver, brain)
Treatment of testicular cancer
- Urgent inguinal orchidectomy (+ offer sperm banking) - Adjuvant chemotherapy Or radiotherapy
Most common causes of obstructive uropathy
Benign prostatic hyperplasia - Kidney Stones
Pathophysiology of obstructive uropathy
obstruction - retention and increased Kidney ureter bladder (KUB) pressure - Refluxing/backlogged urine in Renal pelvis - Hydronephrosis - dilated Renal pelvis, more infection prone
Treatment of obstructive uropathy
- Relieve kidney pressure -> catheterise urethra, urethral stent - Treat cause/infection
Autosomal recessive PKD
- Much less common - Mutated PKHD1 gene on chromosome 6 - Infancy or prebirth - High mortality - Congenital abnormalities - eg: Potter’s sequence: flattened nose + clubbed feet
Autosomal dominant PKD
- Most common - Mutated PKD1 (85%) or PKD2 (15%) - More males - Presentation at 20-30 years
Pathophysiology of polycystic kidney disease
Normally - PKD 1+2 codes for polycystin (Ca2+ channels) - Usually, cilia move and polycystin open - Ca2+ influx inhibits excessive growth PKD - PKD gene mutated - Lack of Ca2+ influx - Excessive growth of cilia - Results in polycysts
What is PKD?
Cyst formation through Renal parenchyma - Bilateral enlargement and damage
Presentation of PKD
- Bilateral flank/back or abdo pain - Hypertension - Haematuria (when cysts rupture), resolves within a few days - Renal stones more common - End stage renal failure at around 50 years
Extrarenal cysts
- Particularly in Circle of Willis - Berry aneurysm if rupture -> subarachnoid haemorrhage
Diagnosis of PKD
Kidney Ultrasound shows enlarged Bilateral kidneys with multple cysts - Also Genetic testing
Treatment of PKD
non-curative - Manage symptoms
Aetiology of nephritic syndrome
- IgA nephropathy/Berger’s disease - mc - Post strep glomerulonephritis - SLE - Goodpasture’s syndrome - Haemolytic uraemic syndrome - All examples of Type 3 hypersensitivity, except for Goodpasture’s which is Type 2
Risk factors for IgA nephropathy
Asian populations - associated with HIV - Teenagers or young adults
Presentation of IgA nephropathy
- Visible haematuria (ribena/coke) - 1-2 days after tonsilitis - Viral infection (or gastroenteritis viral infection)
Diagnosis of IgA nephropathy
Immunofluorescence Microscopy shows IgA Complex deposition - Biopsy
Treatment of IgA nephropathy
- Non-curative - 30% progress to ESRF - First line: BP control (ACE-i)
Presentation of post-strep glomerulonephritis
- Visible haematuria - 2 weeks after pharyngitis from Group A, beta-haemolytic strep (S.pyogenes)
Diagnosis of post strep glomerulonephritis
Light microscope - hypercellular glomeruli - Electron microscope - subendothelial immune Complex deposition - Immunoflorescence - starry sky appearance biopsy???
Complications of post strep glomerulonephritis
Self limiting usually - Sometimes may progress to rapidly progressing Glomerulonephritis
Pathophysiology of SLE nephropathy
Lupus nephritis secondary to SLE - ANA deposition in endothelium
Diagnosis of SLE nephropathy
ANA positive - Anti-ds DNA positive how??? bloods???
Treatment of SLE nephropathy
Steroids - Hydroxychloroquine - plus immunosuppressants, eg: cyclophosphamide
Pathophysiology of Goodpasture’s syndrome
- Presence of autoantibodies (anti-GBM) to alpha-3 chain of Type 4 collagen in glomerular and alveolar membrane - Pulmonary and alveolar haemorrhage, lung fibrosis and glomerulonephritis
Treatment for Goodpasture’s syndrome
- Corticosteroids - Plasma exchange (to get rid of anti-GBM antibodies) - Cyclophosphamide (for immune suppression)
What is RPGN?
Subtype of glomerulonephritis that progresses to ESRF very fast (weeks to months)
Diagnosis of RPGN
Biopsy shows Inflammatory cresents in Bowman’s space
Causes of RPGN
- Wegener’s granulomatosis (c-ANCA +ve) - MPA (pANCA +ve) - Goodpasture’s
Aetiology of nephrotic syndrome
Primary: - Minimal change disease (mc in children) - Focal segmental glomerulosclerosis (mc in adults) - Membranous nephropathy (caucasian adults) Secondary: - Mc to diabetes
Presentation of nephrotic syndrome
- Proteinuria (frothy apple juice🧃) (>3.5g/24hours) - Hypoalbuminaemia (<30g/L) - Oedema (eg: puffy face) - Hyperlipidemia + weight gain
Diagnosis of minimal change disease
On biopsy: - Light biopsy = no change - Electron biopsy = podocyte effacement + fusion
Diagnosis of focal segmental glomerulosclerosis
On biopsy: - Light microscopy -> segmental sclerosis - < 50% glomeruli affected
Diagnosis of membranous nephropathy
On biopsy: - Light microscopy - thickened GBM - Electron microscopy - subpodocyte immune complex deposition, spike + dome appearance
Treatment of nephrotic syndrome
- Steroids for 12 weeks with variable response - Minimal change = responds well to them - Focal segmental glomerulosclerosis + membranous nephropathy = less well :(
What does a scrotal mass indicate?
Cancer until proven otherwise
What is an epididymal cyst?
- Extratesticular cyst above and behind testis - Transilluminates - Diagnosed by scrotal ultrasound - Dissolves in 10 days
What is hydrocele?
Cyst that testicle sits within - Transilluminates - Diagnosed with scrotal Ultrasound
Pathophysiology of hydrocele
Fluid collection in tunica vaginalis
Pathophysiology of varicocele
Distended pampiniform plexus - due to increased left Renal vein pressure causing reflux
Complication of varicocele
Infertility
Presentation of varicocele
Bag of worms (on left hand side mostly) - Typically Painless, painful when more severe - Diagnosed clinically
Pathophysiology of testicular torsion
Spermatic cord twists on itself - Occlusion of testicular artery
Risk factor for testicular torsion
Bell clapper deformity (“horizontal lie” of testes)
Presentation of testicular torsion
- Severe unitesticular pain - hurts when walking - Abdo pain - Nausea and vomiting - Cremastering reflex lost - Prehn’s negative
Diagnosis of testicular torsion
First, surgical exploration - then, Ultrasound to Check testicular blood flow
Treatment of testicular torsion
- Urgent surgery within 6 hours (90-100% successful) - All cases require bilateral orchiplexy (fixing of scrotal sac to overcome biclapper deformity) - If testes non-viable = orchidectomy
Classification of incontinence
Stress incontinence (sphincter weakness) - Urge incontinence (detrusor or bladder overactivity) - Mixed incontinence - Overflow incontinence - Spastic paralysis (neurological UMN lesion)
What is retention?
Inability to pass urine even when bladder is full (500+mL)
Causes of retention
obstruction - Stones - BPH - neurological flaccid paralysis (hypotonia of detrusor, As LMN)
Treatment of retention
Catheterise
Storage lower urinary tract symptoms (LUTS)
Occur when bladder should be storing urine -> need to pee Frequency Urgency Nocturia Incontinence More common in females
Voiding lower urinary tract symptoms (LUTS)
Occur when bladder outlets obstructed -> hard to pee Poor Stream Hesitancy Incomplete emptying Dribbling after finishing urination More common in males
What diseases can present as both nephrotic and nephritic?
Diffuse proliferative Glomerulonephritis - Membranoproliferative Glomerulonephritis
General presentation of nephritic syndrome
- Visible/non-visible haematuria (+little proteinuria) - Oliguria (little urine, salt + water retention) - Hypertension - Oedema
Difference in pathophysiology of nephrotic vs nephritic syndromee
Nephrotic - Podocyte injury - Scarring Nephritic - GBM breaks - Inflammation - Bowman crescents
Treatment of post-strep glomerulonephritis
Antibiotics to clear the strep - Supportive care
Pathophysiology of Henoch Schoenlein purpura
Small vessel vasculitis - Affects Kidney and joints due to IgA deposition - IgA nephropathy only in kidneys - HSP everywhere Do Biopsy
Presentation of Henoch Schoenlein purpura
Purpuric rash on legs - Nephritic symptoms - Joint pain due to IgA deposition
Diagnosis of Henoch Schoenlein purpura
Diagnosed clinically - Confirmed with Renal Biopsy
Treatment of Henoch Schoenlein purpura
Corticosteroids - ACE-i/ARB
Presentation of Goodpasture’s syndrome
Dyspnoea - Coughing problems - Oliguria - Haematuria
Diagnosis of Goodpasture’s syndrome
lung and Kidney Biopsy - damage and Ig deposition - Serology - Anti-GBM positive
What is Prehn’s sign?
- Used to determine the cause of testicular pain - Performed by lifting the scrotum and assessing the consequent changes in pain - Prehn’s sign positive = pain relief upon elevation
What is the cremasteric reflex?
Stroke inner thigh, ipsilateral testicle should elevate
Presentation of epididymitis
- Acute unilateral pain - Sometimes following previous infection - Prehn’s sign positive
Treatment of epididymitis
Stat IM ceftriaxone (if organism unknown) - plus doxycyline
Suprapontine incontinence
Mid brain functioning but not controlled By cortex (will present with neuro problems like dementia or cerebral palsy) - reflex bladder and bowel - involuntary urination and defaecation - Coordinated sphincter complete emptying
Spastic SCI incontinence
Conus functioning but not controlled By brain (sphincter isn’t being told to relax By pons) - reflex bladder and bowel - involuntary urination and defaecation - Dyssynergic sphincter Incomplete emptying
Flaccid SCI incontinence
Conus destroyed or non-functional - Areflexic bladder and bowel - fill until they Overflow - non-functional sphincter
Management of stress incontinence
Women:- Pelvic floor re-education/physiotherapy - Duloxetine (caution) - Surgery (last line) Men: - Artifical urinary sphincter
Stress incontinence causes
Women: - Post-pregnancy trauma Men: - Neurogenic - Iatrogenic (prostatectomy)
Management of overactive bladder
Behavioural therapy or physiotherapy - Anticholinergic therapy - Mirabegron (B3 agonist) - Botox - Neuromodulation - bladder augmentation
Spinal reflexes for bladder
- Reflex bladder contraction - sacral micturition centre - Guarding reflex - onuf’s nucleus (rhabdosphincter - skeletal muscle so somatic) - Receptive relaxation - sympathetic
What is an unsafe bladder?
One that puts the kidneys at risk - caused by prolonged high pressure
Transitional cell carcinoma of the upper tract
- Less common - Same risk factors as bladder cancer - Haematuria, loin pain, “clot colic” - Managed by nephroureterectomy
Supportive treatment of nephrotic syndrome
- Control fluids - diuretics, ACE-i/ARB, spironolactone - Statins - Anticoagulation (espesh when albumin <20g/L) - Abx in children
What is erectile dysfunction?
- Persistent inability to attain amd maintain an erection sufficient to permit satisfactory sexual performance - Commonly found in men over 40 - Up to 10% of men are affected
Pathophysiology of erectile dysfunction
Neurogenic - failure to initiate - Arteriogenic - failure to fill (mc) - Venogenic - failure to store
Innervation of the penis
sympathetic - T11 - L2 - parasympathetic - S2-S4
Aetiology of erectile dysfunction
Atherosclerosis - Diabetes - Age - Hypogonadism - Trauma to Pelvic plexus - Iatrogenic - surgery that damages Pelvic plexus, drugs - Psychosomatic
Treatment of erectile dysfunction
Treat underlying cause - Psychosexual counselling if necessary - Intracavernosal injection - Vaccuum assisted device - Implant
Treatment of localised prostate cancer
Radical prostatectomy - Radiotherapy - external beam, bachytherapy - Watchful waiting
What is a consequence of autosomal dominant PCKD?
IBS
Reactive arthritis (Reiter’s triad)
- Can’t see - conjunctivitis - Can’t pee - urithritis - Can’t climb a tree - arthritis
Complications of AKI
Hyperkalaemia (Most important) - Rhabdomyolysis
Complication of pyelonephritis
Hydronephritis from dilated renal pelvis
What is pyuria?
The presence of leukocytes in the urine
Complicated vs uncomplicated UTIs
Uncomplicated - non pregnant women Complicated - everyone else
Teatment of asymptomatic bacteruria
Do not treat if they’re over 65 (???)
What to do while waiting UTI test results
First line (trimethroprim) if patient is symptomatic
Investigations for upper UTI
Midstream urine - blood cultures
Prevention of uric acid stones
Deacidification of urine to pH 7-7-5
Prevention of cystine stones
Excessive overhydration - urine alkalinisation - Cysteine binders
Treatment for cystitis
- Trimethroprim (avoid in pregnancy) or nitrofurantoin (avoid in 3rd trimester) - If pregnant, take amoxicillin instead
Treatment for epididymo-orchitis
Depends on if it’s caused by an STI (NG/CT) or UTI - treat either appropriately
Treatment for urethritis
N.Gonorrhoea - IM ceftriaxone or azithromycin - C.Trachomatis - azithromycin (or doxycycline)
Symptoms in chlamydia
70% of women and 50% of men are asymptomatic
