Urology Flashcards
AKI
- aetiology: define, types, risk factors, stages
Acute decline in kidney function leading to dysregulation of fluid balance and electrolytes and retention of nitrogenous waste products
RF:
- Age >65 years
- History of:
- CKD
- HF
- Liver disease
- Diabetes
- Multiple myeloma
- contrast administration
- NSAIDs/ACEi’s or ARBs/Diuretics
Three types of AKI:
1) Prerenal: decreased renal perfusion- low urinary sodium. Raised urea:creatinine ratio over 20BUN:1Cr. No issue with kidneys so urea and creatinine still being filtered but at slower rate so urea rises quite a bit but creatinine doesnt. since eGFR is lower the RAAS system is activated and since tubular cels are functioning can stimulate sodium and water takeup as well as potassium excretion. Urine osmolality over 500, not much sodium or water in the urine as it follows urea and is taken back up. Low fraction f sodium excreted
Causes:
- Hypovolaemia (haemorrhage, diarrhoea, vomiting)
- Hypotension (shock, sepsis, anaphylaxis)
- Heart Failure, liver failure (portal hypertention), pancreatitis
- Renal artery Stenosis
- Drugs : NSAIDs, ACEi, tacrolimus, hypercalcemia
If suspect renal artery stenosis: Magnetic resonance angiography. Will have asymmetrical kidneys. If bilateral, cannot give ACEi
2) Intrinsic: direct kidney damage- high urinary sodium. Can be due to Acute tubular necrosis, drug induced(allergic reaction), vascular disease or Glomerulonephritis. Tubular injury so cannot excrete creatining and reabsorb urea. The tubular cells die and create muddy brown casts which are seen in the urine, these clumps of cells build up and increase the pressure in the kidney tubule which further impedes kidney filtration. less than 15BUN:1Cr. RAAS system activated due to low eGFR but no working tubular cells to bind to so it doesnt work. In the urine: high sodium, high water, high urea, high fraction of sodium excreted, less than 350 osmolality. High creatinine in the blood
(1) Acute tubular necrosis most common cause: damage to tubular cells due to (low blood flow+ toxins)
- ischamia (shock+sepsis, HF, Renal artery stenosis, GI fluid loss)
- nephrotoxins (exogenous or endogenous)
-Endogenous: Myoglobin from rhabdomyolysis (high CK), haemoglobin from haemolysis, Uric acid from tumour lysis syndrome, Monoclonal light chains from multiple myeloma
- Exogenous: Aminoglycosides (gentamycin), Cisplatin, vancomycin, antivirals, NSAID, contrast agents, anti-freeze
On microscopy of ATN see muddy brown granular casts in the urine. If rhabdo see high CK.
High urine sodium but low urine osmolality
(2)-Acute interstitial nephritis ( allergic reaction to a drug, or inflammation induced intirinsic AKI) due to Penicillin/ABx, PPIs and NSAIDs. Sarcoidosis, amyloidosis, autoimmunr (SLE and sjorens) and infections can also cause inflammation
- fever, arthralgia, rash, eosinophillia (type IV hypersensitivity)
- Urinalysis: white cell casts as immune reaction
- Urine Dip: Leukocytes +++, micro amounts of blood and protein
- Bloods: Raised IgE, eosinophilia
- No bacteria unless pylonephritis (flank pain, LUTI, fever)
(3) Vascular Disease causing intrinsic AKI: thombi develop in the glomerulus
(1) Haemolytic uraemic syndrome : haemolytic anaemia (jaundice and schistocytes), thrombocytopenia (petechiae and purapura), Blood diarrhoeal illness (shiga toxin e.coli). Supportive management
(2) Thrombotic thrombocytopenia purpura: Abnormally large and sticky multimers of von Willebrand’s factor cause platelets to clump within vessels. Same symptoms as HUS also fever and neurological signs (headache, confusion, seizures). Give prednisolone start PLasmapheresis
-bilirubin, platelets, reticulocytes, haptoglobin in urine
(4) Glomerulonephritis : can present as nephrotic or nephritis syndrome (antibody-antigen complexes deposited on glomeurlus)
- bloody urine, RBC case, protein in urine
3) Postrenal AKI: Any condition that results in bilateral obstruction of urinary flow from renal pelvis to urethra. Block causes pressure to build up in the tubular capsule so low eGFR. Kidney tubular cells work so urea still being rabsorbed and creatinine excreted but at a slower rate. RAAS still functions too. Urine= low sodium, low fration of excreted sodium, low urea, low water. over 20BUN:1 creatinine (in early stages post renal looks like prerenal). In later stges the pressure increases so much it balloons the tubular capsule with fluid which presses on and damages tubular cells, killing them. RAAS can no longer function. Urine: high sodium, high urea, high water, lower than 350 osmolality/ less than 15BUN:1Cr. Late stages mimic intrinsic AKI.
Causes:
- Kidney stones
- External compression of ureter e.g. due to tumour
- BPH, prostate cancer, urethral injury, catheter
- Anticholinergic drugs for incontinence (detrusor contracts too much)
- Neurogenic bladder
- MS
- Spinal cord lesions
- Peripheral neuropathy
AKI STAGING
KIDIGO criteria
- Stage 1
- Creatinine rise of 1.5x compared to baseline
OR
- Serum Creatinine <0.3 mg/dL/hour (over 26.5μmol/l)
OR
- Urine output <0.5 ml/kg/hour for 6-12 hours
- Stage 2
- Creatinine rise of 2-2.9x compared to baseline
OR - Urine output <0.5 ml/kg/hour for 12 hours
- Creatinine rise of 2-2.9x compared to baseline
- Stage 3-
- Creatinine rise of 3x compared to baseline
OR - Serum Creatinine <4.0 mg/dL/hour >354 μmol/L,
OR - Urine output <0.3 ml/kg/hour for 24 hours
OR - Anuria for 12 hours (lack of urine production)
- Creatinine rise of 3x compared to baseline
AKI
- clinical features
- investigations
- management
- prognosis + complication
Decreased urine output → Oliguria (reduced urine output) or anuria (complete absence of urine output)
Kidneys can no longer excrete protons in urine: metabolic acidosis as protons retained: arrythmias and hypertention
Prerenal/Volume depletion:
- Hypotension
- Tachycardia
- Reduced skin turgor
- Orthostatic hypotension
- Thirsty
Fluid Overload (Na+ and H2O retention):
- Peripheral or pulmonary oedema
- Hypertension
- HF
- SOB
Signs of uraemia (builds up in kidneys as cant be filtered out and absorbed back in). Leads to platelet dysfunction
- Bleeding, lack of coagulation
- Anorexia
- Nausea
- Seizures
- Encephalopathy
- Asterixis
- Pericarditis (pericardial cavity inflamed, can progress to cardiac tamponade)
Postrenal- renal obstruction signs :
- Distended bladder (suprapubic distension)
- Incomplete voiding → Lower urinary tract symptoms
- Pain over bladder or flanks
Arrythmias
- Hyperkalaemia: muscle weakness and paraesthesia, bradycardia, v fib, heart block
INVESTIGATIONS
Bloods and Urine investigations
- Increase in serum creatinine (small inc in pre renal and early post renal, large increase in intrinsic)
- Increase in serum urea
- Change in urine osmolality (prerenal - high, intirinsic low
- Decrease in urine output
- Potassium increased: severe if K over 6.5 or see ECG changes (tented t waves, loss of p, broad QRS)
- Protein positive on urine dipstick= must be intrinsic. Acute interstitial nephritis = +++ leukocytes, eosinophils
,,,glomerulonephritis= Positive blood,,,, infection if WBC cast and bacteria,,,, muddy cell cast if acute tubular necrosis
Renal Ultrasound if cause unknown
In post renal will be able to see the obstruction, may see bilateral hydronephrosis because of the backup of fluid. Then need a bladder scan.
Chest X-Ray + ECG
ABG: metabolic acidosis due to uraemia
MANAGEMENT
1) stop DAMN nephrotoxic medication + treat underlying cause
- diuretics
- aminoglycides (gentomycin) and ACEi
- Metformin if eGFR under 45 (can accumulate, become toxic and cause lactic acidosis
- NSAID (only continue aspirin at cardio-protective doses
2) Manage volume status:
pre renal AKI: if hypovolaemia then IV fluids- crystalloid unless potassium over 5.5 then saline,,,
if hypervolaemic (IV loop diuretic furosemide or dialysis or fluid restrict)
if pulmoanry oedema: sit upright, GTN, high flow oxygen
3) Hyperkalaemia
- 5.5-5.9= calcium polystyrene sulfonate
- 6.0-6.4 (no ecg chnage) IV gluconate 10% 30mL to stabilise cardiac membrane/ IV glucose +++ Insulin (Actrapid) to drive K+ into cells along with dextrose to prevent hypoglycaemia
- 6.5 and over or over 6 with ECG changes: Calcium resonium can remove potassum, insulin+ gluose+ salbutomol
If metabolic acidosis: sodium bicarb
4)Patient may require catheterisation if post-renal AKI
5)Post renal: if BPH: alpha blockers (-zosin), or 5 alpha reductase inhibitors (finasteride and dutasteride)
IF not responding to medical treatment : dialysis
Acidosis
Electrolytes (refractory hyperkalaemia)
Intoxication ( drugs accumulating)
Oedema (refractory pulmonary oedema)
Uraemia (pericarditis/encephalopathy/epilepsy)
complications
- Hyperphosphataemia
- Hyperkalaemia
- Uraemia
Benign Prostatic Hyperplasia
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Benign glandular and stromal hyperplasia of the transitional zone of the prostate
DHT is a prostatic growth factor,
As men age they have andorgen/oestrogen imbalance
RF: over 50 years, FHx
Prevalence increases with age
- 42% of men 51-60 affected
- 82% of men 71-80% affected
Pathological BPH vs clinical BPH: only clinical has symptoms
Cannot give amitriptyline in BPH
CLINICAL FEATURES
Features of uncomplicated lower urinary tract symptoms (LUTS).
1) Voiding (obstructive) symptoms: SW HIPS
- straining to urinate
- weak stream
- hesitancy (difficulty initiating urination)
- intermittency
- post-void dribbling
- sensation of incomplete emptying
2) Storage (irritative) symptoms: FUN
- Frequency
- Urgency
- Nocturia
Complicated urinary tract infection = fever and dysuria. Uncomplicated BPH dont have fever
INVESTIGATIONS
Transrectal ultrasound-guided needle biopsy : gold standard for diagnosis
Urinalysis:
- uncomplicated BPH: no findings
- Pyuria: UTI
- Haematuria: cancer
Bloods: if PSA (prostate specific antigen) is high suggests presence of underlying prostate cancer or prostatitis. Helps guide treatment in LUTS
International Prostate Symptom score: mild 0-7, mod 8-19, severe 20-35 to look at severity of symptoms
Post-residual volume: look for urinary retention (over 300ml)
DRE:Smooth enlarged prostate, palpable midline groove
MANAGEMENT
Conservative : behavioural and lifestyle - education about the condition, reducing fluids at night, limiting caffeinated and alcoholic beverages, avoiding or modifying the timing of diuretics or medications that increase urinary retention, and use of techniques to help control bladder symptoms
Symptoms bothering but no indication for surgery:
- behavioural and lifestyle
- alpha blocker (-osin e.g terazosin, doxazosin, tamsulosin): relax the smooth muscle or bladded to decrease resistance
- 5 alpha reductase inhibitor (-asteride e.g. finasteride or dultasteride): Reduced conversion of testosterone to DHT, which leads to reduced prostate growth
- phosphodiesterase-5 (PDE-5) inhibitor : only if comorbid and ED- tadalafil
Surgery: if complications due to BPH: bladder stones, gross haematuria, UTI, refractory urinary retention, dont respond to medication, cant take side effects
prostate 30g or less: Transurethral incision of the prostate (less invasive, lesser rates of retrograde ejac and blood transfusion than TURP)
prostate 30-80g: Transurethral resection of the prostate (TURP): can cause retrograde ejaculation, urethral strictures, perforation of prostate, TURP syndrome (high sodium, fluid overload, glycine toxicity
PROGNOSIS
Mild symptoms usually well controlled with medications
Most patients get significant relief from surgery
What is prostatitis
- presentation
- management
- Pain in perineum/penis/rectum/back
- Obstructive voiding symptoms
- Fever and rigors
- DRE → tender, boggy prostate (warm, tender, soft, mushy)
Management
- Quinolone (e.g. ciprofloxacin) for 14 days
- Screening for STI
What are the side effects of the medications used for BPH
Alpha blockers
- Dizziness
- Postural hypotension
- May also cause retrograde ejaculation
5 Alpha reductase inhibitors:
- Diminished libido
- Erectile Dysfunction
- Gynaecomastia
- Decreases levels of PSA
Bladder Cancer
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Usually Transitional cell carcinomas (Urothelial carcinoma)
RF:
- Smoking biggest RF in west
- Male
- Over 65
- Aniline dye: Painters and Hairdressers
- Pelvic radiation
- Chronic UTIs
- Positive family history for bladder cancer
RF for squamous cell bladder cancer:
- Areas where schistosomiasis is endemic (Middle East)
- Long term catheterisation (>10 years)
CLINICAL FEATURES
- Gross painless haematuria (macroscopic haematuria is common)
- Dysuria → associated with aggressive bladder cancer (pain/burning during urination)
- Urinary frequency and urgency
INVESTIGATIONS
1st line: urinalysis for haematuria
Staging:
- Renal and bladder ultrasound (microhaematuria)- may see hydronephrosis due to tumour causing obstruction
- CT/MRI abdomen and pelvis (gross haematuria)
- Chest X ray: look for mets
Diagnostic gold standard: Cystoscopy and biopsy → visualises bladder tumours and enable pathological diagnosis
60 year old with unexplained non-visible haematuria and either dysuria or a raised WCC on a blood test: Should be referred using the suspected cancer pathway within 2 weeks
MANAGEMENT
Non muscle invasive/low risk: Transurethral resection of bladder tumour (TURBT)
Muscle invasive/high risk: Radical cystectomy → Removal of bladder, prostate and seminal vesicles
Mets: Palliative systemic chemotherapy
PROGNOSIS
non invasive = high survival rate, mets= 12% survival
Chronic Kidney Disease
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Abnormality of kidney structure or function (GFR <60 mL/minute/1.73m^2) that is present for ≥3 months
RF:
- Diabetes
- Hypertension
- Obesity
- Advanced age
- Substance use
- AKI
- Black or Hispanic ethnicity
Causes:
- Diabetic nephropathy
- Hypertensive nephropathy
- Glomerulonephritis
- Polycystic kidney disease: genetic cause- autosomal dominant, must screen relatives with abdominal US
CLINICAL FEATURES
symptoms caused because of:
Uraemia → Lack of excretion of toxic substances
Anaemia → Lack of EPO produced by kidney
Hyperphosphataemia → Lack of excretion of toxic substances
symptoms:
- Often asymptomatic → may be finding of routine blood test or urine test
- Fatigue (due to anaemia)
- Oedema (Peripheral/Pulmonary) due to Na/H2O retention
- Nausea
- Pruritus due to uraemia
- Hypertension
- Hypocalcaemia ( 1 alpha hydroxylase deficiency) : muscle twitch, arrythmias, tetany, paraesthesia
INVESTIGATIONS
Hypocalcaemia suggests chronic not acute
Renal profile: high creatinine, high potassium, <60 mL/minute/1.73 m^2, eGFR not a good measurement if high or very low muscle mass as will have varying creatinine, if bodybuilder or older or malnourished or muscle wasting issue then do serum cystatin C and cystatin C- based on eGFR estimation
Urinalysis: Hameaturia and proteinuria, high urinary albumin (30-300)
Renal Ultrasound: small kidneys
Bloods: high serum creatinine, low calcium(chronic), high phosphate, high PTH, low vitamin D. Must give alfacalcidol (vit d supplement) and reduce dietary intake of phosphates or prescribe a phosphate binder (sevelamer)
CKD Staging:
G1 egFR over 90, G2 eGFR 60-89: only CKD if abnormal kidney function e.g. abnormal U&Es (creatinine high) or proteinuria.
albuminuria A1 less than 3mg/mmol 30mg/g is Low risk,,, A2 30-300 mg/g or 3-30mg/mmol is moderate risk,,,, A3 is over 300mg/g or over 30mg/mmol
G3a: eGFR 45-59, A1 is moderate risk, A2 high risk, A3 very high risk
G3b: eGFR 30-44, A1 is high risk, A2 very high risk, A3 very high risk
G4: 15-29 : a1,2,3 very high risk
G5: less than 15 (kidney failure): a1,2,3 very high risk
TREATMENT
Stage G1-2
- ACE inhibitor (pril) or ARB (angiotensin block- sartan)
- Lisinopril if ACR >30
- Losartan
- Statin
- Consider if stage 2: Dapagliflozin (SGLT2 inhibitor)
Stage G3 to 4
- ACEi
- Dapagliflozin
- Statin simvastatin ± ezetimibe
Stage G5
Other:
- Vitamin D supplements → Alfacalcidol (doesn’t require activation in kidneys)
- Fluid and salt restrictions to maintain fluid balance
- if anaemia: erythropoeitin stimulating agent epoetin alfa
- if iron deficiency anaemia: Correct it with ferrous sulphate first then give EPO stimulating agent (ESA)
- if secondary hyperparathyroidism: G3-5 diet first then + calcium carbonate, sevelamer or alendronic acid (phosphate binding),
- if metabolic acidosis: sodium bicarb oral
COMPLICATIONS:
- metabolic acidosis (inability to excrete acid)
- hyperkalaemia
- anaemia
- renal osteodystrophy (elevation in PTH due to hypocalcaemia)
- cardiovascular disease
- pulmonary oedema
PROGNOSIS
- Mostly progressive and leads to end-stage renal disease and the need for renal replacement therapy
- Can’t be cured, but can be controlled and managed
Dehydration
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
State of reduced total body water volume
Causes:
- Insufficient water intake- particularly in the elderly and the critically ill
- Diuretics
- DI
- Diarrhoea
- Vomiting
- Burns
- Sweating
CLINICAL FEATURES
- Thirst
- Headache
- Weakness
- Dizziness
- Fatigue
- Dry cool skin, dry mucus membranes, delayed CRT, reduced skin turgor
In infants: irritability, lethargy, sunken fontanelle
INVESTIGATIONS
Bloods: Hypernatraemia
Urine : high osmolality (higher than serum osmolality - serum and urine osmolality being similar suggests renal failure or diuetic,,, serum urine low suggests DI)
MANAGEMENT
Oral rehydration therapy
IV fluid resuscitation: careful of hypernatraemia too quickly as can cause cerebral oedema
COMPLICATIONS
- Hypovolaemic shock → Pre-renal AKI
- Thrombosis
- Increased risk of UTIs
Free water deifict(L)= total body water x ((actual serum Na minus ideal Na) divided by ideal Na))
Epididymitis + Orchitis
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Epididymitis: Inflammation of the epididymis (cord that connects the testis with ductus deferens), usually as a result of an infection.
Causes:
- UTI: common in older men and children usually E.coli
- STI: young males under 35 years old: number 1: Chlamydia trachtomitis,, number 2 Neisseria gonorrhoeae
Orchitis: Inflammation of the testis
Causes:
- Unprotected sexual intercourse
- Bladder outflow obstruction
- UTIs
- Immunosuppression
- Vasculitis
- Mumps: notifyable disease should of got MMR as causes orchitis and pancreatitis.
- fever
- malaise
- muscular pain
- parotitis (earache or pain on eating)
CLINICAL FEATURES
Epididymitis
- Unilateral scrotal pain and swelling, develops over several days and radiates to the ipsilateral flank
- Tenderness along posterior testis
- Positive Prehn sign (pain relief on elevation of the testes) negative in testicular torsion, positive in epididymitis
- Hot, erythematous, swollen hemiscrotum
- Low grade fever
History of:
- Symptoms of lower UTI (dysuria, frequency, urgency)
- Symptoms of STI (penile discharge)
Orchitis:
- Sudden onset of nausea & vomiting
- Sudden fever
- Swollen and tender testicle(s) although primarily unilateral
INVESTIGATIONS
Urinalysis: pyuria (white blood cells (leukocytes) or pus in your urine) or bacteriuria
Urine microscopy: WBC
Gram stain + culture of urethral secretions
If sexually active young person: NAAT of urethral secretions for STIs
Older Adult low risk of sexual history: Urine culture (MSU for MC&S)
Duplex ultrasound of the scrotum → rule out testicular torsion
MANAGEMENT
Symptoms:
- NSAIDs
- Application of cold pack
- Bed rest
- Scrotal elevation
If amiodarone- stop it
If idiopathic or viral just supportive for symptoms
Infection treatment:
Emperic treatment of : ceftriaxone 500mg intramuscularly single dose, plus oral doxycycline 100mg twice daily for 10-14 days until know cause
ABx based on most likely cause
- Doxycycline if <35, it covers chlamydia
- Ceftriaxone if gonorrhoea suspected
- Ciprofloxacin or levofloxacin if >35 (not in epileptics) or gay sex as may be enteric
PROGNOSIS:
epididymitis usually gets better after ABx
COMPLICATIONS
Epididymitis:
- Epididymo-orchitis → Spread of infection from epididymis to the testicle
- if mumps: Orchitis
Orchitis:
- Atrophy
- hypofertility
Clinical presentation of testicular torsion
- age <20 yrs
- severe pain
- more acute onset
- -ve prehn sign (lift the scrotum up and pain is relieved= epidydymitis, if no pain relief then torsion)
Nephrotic Syndrome
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
Collection of signs and symptoms indicating damage to the glomerular filtration barrier
- Massive proteinuria
- Hypoalbuminaemia
- Oedema
Causes:
1) Minimal change disease: idiopathic usually children with peri-orbital oedema, associated with URTI and non-hodgkins lymphoma,, Cytokine mediated damage of podocytes (role is to prevent protein entering filtrate),, light microscopy will be normal,,, electron microscopy will show fusion of podocytes,, give prednisolone, 2nd Cyclophosphamide
2) Membranous glomerulonephritis: adults,, deposition of immune complexes on basement membrane,, associated with malignancy, SLE, Hep B and C, Autoimmune disease,,, light microscopy BM thickening,, electron microscopy spike and dome appearance,, associated with Anti-phospholipase A2 receptor antibodies,, Low T4,, doesnt really respond to steroids
3) Focal segmental glomerulosclerosis: Afro-caribbean,, Sclerosis of glomeruli leads to damage and loss of podocytes,, renal biopsy on light microscopy shows Segmental areas of mesangial collapse and sclerosis,,, electron microscopy : Effacement of foot processes of podocytes ,, associated with obesity, diabetes, HIV, heroid, sickle cell, give corticosteroids
4) Diabeteic nephropathy (secondary): usually have retinopathy and neuropathy, urine microalbuminuria, light microscopy: mesangial expansion, GBM thickening, Kimmelstiel-Wislon nodules (in early stages on kidney USS see enlarged kidneys- also see enlarged kidneys in amyloidosis, PKD, HIV associated nephorpathy,,, managed with diabetic control and BP ACE/ARB
5) Amyloid nephropathy (secondary): Elderly patients,, associated with multiple myeloma and chronic inflam diseases : TB RA,,, affects Kidney → Deposition of amyloid in kidney (breathlessness, weakness and hepatosplenomegaly),,, congo red staining: Apple-green birefringence
CLINICAL FEATURES
xanthalasma and xanthomas (high lipid and cholesterol)
leukonchymia and tiredness (low albumin)
oedema (low protein so fluid leaks to interstitium)
breathlessness (pumonary oedema)
frothy urine (protein)
- Massive Proteinuria >3.5g/24 hours → may cause foamy urine
- Oedema → starts with periorbital oedema, then may lead to peripheral oedema (or pulmonary oedema)
- Hypoalbuminaemia (<25 g/L)
- Hypotension and low eGFR
- Hyperlipidaemia → Low blood protein increases lipid synthesis
- Hypercoagulable state- Due to loss of antithrombin III (also protein C and protein S) and rise in fibrinogen levels. This increases risk of thrombosis
- Increased infection risk: loss of immunoglobulins
INVESTIGATIONS
Urine dipstick : +++ proteins (or more)
24 hour urine protein: >3.5g/24 hours
Urine sediment microscopy : fatty casts
Bloods: low serum albumin, high cholesterol, low calcium, check for serum and urine immunoglobulins, Hep B and C screen
Ultrasound and renal biopsy -> light and electron microscopy and immunoflurescence
MANAGEMENT
Oedema:
- Dietary sodium restriction
- Fluid restriction
- Diuretic therapy (furosemide)
Proteinuria:
RAAS inhibitors
- ACEi’s (ramipril)
- ARBs (Losartan)
Prophylactic anticoagulation
- LMWH
- Warfarin
Infection Risk:
Vaccination
COMPLICATIONS
- Infection due to urinary loss of immunoglobulins
- VTE due to urinary loss of antithrombin
- Hyperlipidaemia due to increased hepatic production of lipids to restore the serum oncotic pressure
What is nephritic syndrome (NOT NEEDED)
CLINICAL FEATURES
- Haematuria
- Proteinuria
- Oedema
-
Membranoproliferative Glomerulonephritis (MPGN)
Type 1: Immune complex deposits resulting from chronic infection e.g. hep B or C
electron microscopy: Tram track appearance
Type 2: Complement deposits e.g. in SLE
low circulating levels of C3
electron microscopy?Dense deposits
Symptoms:
Mixed picture of nephrotic and nephritic syndrome
Management
Steroids
-
Rapidly Proliferative Glomerulonephritis (RPGN)
Proliferation of cells in Bowmans space → crescent shape (so it’s aka crescenteric glomerulonephritis)
Three types
Type 1 :Goodpasture Syndrome
- Mainly nephritic
- Anti-GBM antibodies → autoantibodies against type IV collagen
Symptoms:
- Pulmonary features (haemoptysis and SOB)
- Nephritic syndrome
Type 2 (Immune-complex mediated) 4 diseases
1) Poststreptococcal Glomerulonephritis-
- Nephritic
- Smoky urine
- Proteinuria
- 1-2 weeks post throat infection or gastroenteritis
Anti-strepsolysin O titre: to confirm recent infection
Immunofluorescence: Starry sky appearance
Low C3
2) IgA Nephropathy- features
- 1-2 days post GI/resp infection
- Bloods positive for IgA
- Young male
- Recurrent episodes of macroscopic haematuria
3) Henoch-Schonlein Purpura (IgA Vasculitis)
- Palpable purpuric rash
- Abdo pain
- Polyarthritis (joint pain)
- Usually seen in children
- Bloods positive for IgA
4) SLE- immune complex deposits trigger type III hypersensitivity reaction
Type 3 (Pauci-Immune): cANCA and pANCA
1) cANCA- Granulomatosis with polyangiitis (aka Wegner’s granulomatosis)
Feature
- Saddle nose shape
- Epistaxis
- Sinusitis
Consider if ENT, resp and kidney issues at the same time
2) pANCA-Microscopic polyangiitis and Eosinophilic granulomatosis with polyangitis (Churg Strauss)
- MP
Features:
- Purpuric rash
- Pain/numbness/tingling in hands and feet
- EGP Churg
- Granulomatous inflammation
- Asthma-like symptoms
- Eosinophilia
Prostate Cancer
- aetiology: define, types, risk factors, stages
- clinical features
- investigations
- management
- prognosis + complication
A malignant tumour of glandular origin (adenocarcinoma), situated in the prostate
2nd most common cancer, 5th men killer
RF:
- Age >50 years
- Family history
- Black African ethnicity
- BRCA 1 & 2
CLINICAL FEATURES
Typically asymptomatic just rf
May present with complicated LUTS
- Urinary retention
- Haematuria
- Incontinence
- Flank pain
Abnormal DRE
- Asymmetrical
- Hard
- Nodular enlargement of prostate
- Loss of midline sulcus
Advanced prostate cancer:
- Fatigue
- Weight loss
- Bone pain
- Neurological deficits
- Lymphoedema
INVESTIGATIONS:
1st bedside :PSA Antigen >4 ng/mL
Not cancer-specific → elevated in benign conditions
- BPH
- UTI
- Prostitis
1st bedside: DRE
Scan
1st prebiopsy Multiparametric MRI
Gold standard:Transrectal ultrasound-guided needle biopsy:
- May detect adenocarcinoma
- Gleason staging
Bone scan: check for mets will be raised ALP
Pelvic CT/MRI scan
MRI spine: look for mets that cause spinal compression: incontinence and weakness
Grading: Gleason score- lower is better
MANAGEMENT
Localised: Active monitoring and watchful waiting
Localised advanced: T3/4 on gleason
- Radical prostatectomy: can cause ED
- Beam Radiotherapy: inc risk of bladder, colon and rectal cancer
- Brachytherapy
Metatastic prostate cancer:
Hormonal therapy:
- GnRh agonist : Goserelin: initally can cause tumour flare bone pain, bladder obstruction so also pretreat with flutamie and give cyproterone with treatment. General side effects: ED, low libido, inferitility, gynaecomastia
Androgen antagonists
- Darolutamide
- Enzalutamide
-GnRH antagonists-
- Degarelix
- Gosrelin
DLR (docetaxal+ -lutamide+ -relin/relix
Testicular Cancer
aetiology: define, types, risk factors, stages
clinical features
investigations
management
prognosis + complication
Common in young adult men → 20-34 years old
Usually Seminomas : can be non-Seminomas aka tetratomas or non-germ cell tumours
RF:
- Cryptorchidism (undescended testes)
- Infertility
- Age <45
CLINICAL FEATURES
- Painless unilateral hard nodular testicular mass
- Negative transillumination test (light does not shine through)
- Gynaecomastia: due to seminoma secreting hCG (increased oestrogen:androgen ratio)
- May be associated hydrocele- Transilluminates, Not separate to testis, Fluctuant
- Lymphadenopathy
- Metastatic Disease
- cough
- SOB
- chest pain
- Bone pain (backache)
Usually travel to para-aortic lymph nodes
INVESTIGATIONS
1st Ultrasound with colour doppler of testis → shows testicular mass
Tumour markers:
- Alpha fetoprotein
- Beta-hCG
- LDH
In seminoma
- Normal AFP
- Raised beta-hCG sometimes
- Raised LDH sometimes
In non-seminoma germ cell?
- Raised AFP
- Raised Beta-hCG
- Normal LDH
Look for mets:
- CXR
- CTAP
Dont biopsy just remove the testicle
MANAGEMENT
Pre surgry: Sperm cryopreservation → Tumours are associated with decreased fertility
Surgery: Radical inguinal orchidectomy
Also given:
Radiotherapy and chemotherapy
Urinary Incontinence
aetiology: define, types, risk factors, stages
clinical features
investigations
management
prognosis + complication
Common condition characterised by uncontrollable leakage of urine
Usual in elderly females
RF: BMI over 25, more births
Causes:
- Neurological: MS, spinal injury
- Genitourinary: pelvic floor trauma, sphincter deficiency, bladder outlet obstruction, pelvic floor weakness
- Reversible Causes: diuretic, UTI
CLINICAL FEATURES: 4 types
1) Urge Incontinence: Overactivity of bladders detrusor muscle, leads to strong, sudden sense of urgency, followed by involuntary leakage
RF’s
- Advancing age
- High BMI
- Smoking
- Caffeine
2) Stress incontinence: Leaking small amounts when coughing, laughing or sneezing (activities that increase intra-abdominal pressure)
RF’s
- Vaginal childbirth
- Hysterectomy
3) Mixed incontinence: Combo of stress and urge incontinence
4) Overflow incontinence: Due to bladder outlet obstruction, overdistended bladder due to urinary retention causing leakage (e.g. due to prostate enlargement). Can be caused from drugs causing urinary retention:
- TCA (amitriptyline) due to cholinergic effect
- Opioids
will have palpable bladder, suprapubic tenderness, delerium if elderly
INVESTIGATIONS
Bedside:
Bladder Diaries: To assess frequency and volume of micturition (3 days)
Exclude pelvic organ prolapse: Vaginal exam- can assess the ability to initiate voluntary contraction of pelvic floor muscles
Tests:
Cough stress test, Empty supine stress test
Urine Dipstick and Culture: exclude UTI
Postvoid urinary residual volume : ≥100 mL
- chronic HIGH pressure if renal function is impaired or if there is hydronephrosis → typically due to bladder outflow obstruction
- chronic LOW pressure if normal renal function and no hydronephrosis
Susupected bladder outflow obstruction:
Urodynamic studies
- Increased detrusor pressure
- Reduced urine flow rate
Diagnostic for urinary retention: Bladder USS
MANAGEMENT
lifestyle
- Weight loss
- Diet changes (decrease alcohol and caffeine)
- Smoking cessation
Stress incontinence:
1st Pelvic floor muscle training
Surgery: Retropubic mid-urethral tape procedure
Meds: pseudoephedrine,, Duloxetine (Combined noradrenaline and serotonin reuptake inhibitor)
Urge Incontinence:
1st Bladder retraining → Lasts for minimum of 6 weeks: aim to increase the intervals between voiding
Meds: Antimuscarinics (Oxybutynin)
COMPLICATIONS
- Depression
- Psychological stress
- Dermatitis/skin infections (from prolonged contact with urine)
- UTIs
- AKI
