Renal Flashcards
AKI
defined as an acute drop in kidney function (under 48 hours). It is diagnosed by measuring the serum creatinine.
AKI criteria
- Rise in creatinine of ≥ 26.4 micromol/L in 48 hours (>1.5-1.9 x reference) or <0.5ml/kg/hr for >6 hours
- Rise in creatinine of ≥ 50% (>2-2.9 x reference) in 7 days or Urine output of < 0.5ml/kg/hour for > 12 hours
- Increase >3 x reference SCr or increase to >354 and <0.3ml/Kg/hr for >24 hours
risk factors for AKI
- CKD
- Heart failure
- Diabetes
- Liver disease
- Previous AKI
- Peripheral vascular disease
- Older age (above 65 years)
- Cognitive impairment
- Nephrotoxic medications such as NSAIDS and ACE inhibitors
- Use of a contrast medium such as during CT scans
Pre-renal (inadequate supply of blood to kidneys reducing filtration of blood)
- Hypovolaemia: Haemorrhage, volume depletion (e.g. D&V, burns and dehydration)
- Hypotension: cardiogenic shock and distributive shock (sepsis or anaphylaxis)
- Renal Hypoperfusion: Heart failure, NSAIDs/ACEi/ARBs/hepatorenal syndrome
Renal causes of AKI
- Glomerulonephritis
- Interstitial nephritis: Drugs (NSAIDs, antibiotics, PPI), Infection (TB) and systemic (sarcoidosis)
- Tubular injury: Ischaemia, drugs (gentamicin), contrast and rhabdomyolysis
- Acute tubular necrosis
- Vasculitis/renovascular
Post renal causes (obstruction to outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function)
- Kidney stones
- Ureter or urethral strictures
- Enlarged prostate or prostate cancer
- Masses such as cancer in the abdomen or pelvis
sign/symptoms of AKI
- Constitutional symptoms e.g. Anorexia, weight loss, fatigue, lethargy
- Nausea & Vomiting
- Itch
- Fluid overload: Oedema, SOB
Signs
- Fluid overload incl hypertension, Oedema, Pul oedema, effusions (pleural & pulmonary)
- Uraemia incl itch, pericarditis
- Oliguria
AKI Iv
Urinalysis: protein, blood, nitrites, glucose, WCC
U&E
FBC and coagulation screen
immunology: ANA, ANCA, GBM
protein electrophoresis and BJP
USS
biopsy
Management of AKI
- assess for hydration: BP, HR, UO, JVP, CRT, Oedema
- IV Fluid hydration (fluid challenge for hypovolaemia) - crystalloid (0.9% NaCl) or colloid: not 5% dextrose
- bolus of fluid, if >1000mls and no improvement, seek help
- heart failure: fluid overload be careful - Stop nephrotoxic medications e.g. NSAIDS and ACEi
- Relive obstruction in post renal AKI
- Dialysis: anuria or uraemia
AKI complications
Hyperkalaemia
fluid overload, heart failure and pulmonary oedema
metabolic acidosis, uraemia (encephalopathy or pericarditis)
CKD
abnormal kidney function and/or structure
CKD risk factor
AKI CVD disease diabetes hypertension Glomerulonephritis Polycystic kidney disease age related decline Medication: NSAIDs, ACEi/ARBs and lithium Smoking Untreated urinary outflow tract obstruction proteinuria
CKD Iv
U&Es and eGFR (2 tests + 3 months apart)
Proteinuria (ACR) and Haematuria (dipstick)
renal USS
ACR stages
A1: <3
A2: 3-30
A3: >30
CKD stages
G1: >90 G2: 60-89 G3a: 45-59 G3b: 30-44 G4: 15-29 G5: <15`
Accelerated CKD
sustained decrease in GFR of 25% or more and a change in GFR category within 12 months
Or
a sustained decrease in GFR of 15 ml/min/1.73m2 per year
Renal consequences of CKD
- Local – pain/ haemorrhage/ infection
- Urinary – haematuria/ proteinuria
- Impaired salt and water handling
- Hypertension
- Electrolyte abnormalities
- Acid-base disturbance → ESRD (End stage renal disease)
slowing CKD management
- ACEi - Reduce proteinuria
- Treat glomerulonephritis
- Exercise, maintain a healthy weight and stop smoking
- Special dietary advice about phosphate, sodium, potassium and water intake
- Offer atorvastatin 20mg
Anaemia of CKD
Target 100-120Hb, exclude B12 and folate, check ferritin (>100) and TSats > 20%
- Oral iron - IV iron - EPO
Bone disease of CKD
- Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised. - Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.
CKD: Bone disease management
- Active forms of vitamin D (alfacalcidol and calcitriol) – don’t need activation by kidneys
- Phosphate binders
- Salt reduction, K+ and fluid restriction
- Bisphosphonates
Dialysis 3 main purposes
excess fluid, solutes and waste products.
Dialysis based on
- Diffusion e.g. urea, K+, Na+ and infusion of HCO3-
- Convection: water across semipermeable membrane
- Adsorption: atoms, ions or molecules from a substance
adhere to a surface of the adsorbent
e.g. plasma proteins
Dialysis indications
A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia symptoms such as seizures or reduced consciousness
eGFR < 7ml/min
Haemodiafiltration (HDF)
haemodialysis is primarily diffusive, haemodiafiltration is increasingly convective, in nature. greater the convective force, the greater will be the generated volume of the pressure-driven ‘ultrafiltrate’. • Large volumes of ultrafiltrate add enormously to solute drag - especially for the larger “middle molecule” solute classes
different types of PD
continuous (2L x 4times per day) vs automated (overnight)
types of renal transplant
Deceased Heart Beating Donors (Brain stem death (DBD))
Non-Heart Beating Donors (DCD)
Live Donation (altruistic)
Lifelong immunosuppression for kidney transplant
Induction
Consolidation
Maintenance
Transplant rejection types
- Hyperacute - preformed antibodies
- Acute rejection: cellular or antibody mediated, treated with immunosuppression
- Chronic rejection: antibody mediated slowly progressive decline in renal function.
CMV infection - transplant
1st 3 months
- Prophylactic PO valganciclovir in higher risk patients
- IV ganciclovir if evidence of infection
Nephritic syndrome
Haematuria oliguria Proteinuria (<3g) Oedema Hypertension affect endothelial cells (proliferative process)
Nephrotic syndrome
Peripheral oedema Proteinuria >3g Hypoalbuminemia (<25g/L) Hypercholesterolaemia affects podocytes (non-proliferative process)
Minimal change disease
usually idiopathic, most common nephrotic syndrome in children, secondary to hodgkins lymphoma, leukaemia and a virus
EM: foot fusion
1st line: steroids
2nd line: cyclophosphamide
Focal segmental glomerulosclerosis
small sections of each glomerulus (filter), and only a limited number of glomeruli are damaged at first.
Commonest cause of nephrotic syndrome in adults (35%)
primary (more common) or secondary (HIV/Heroin use/Obesity/ Reflux nephropathy)
Focal segmental glomerulosclerosis diagnosis and management
Small areas of mesangial collapse and sclerosis
steroids
Membranous glomerulonephritis
2nd commonest cause of nephrotic syndrome in adults (15-30%)
- idiopathic (majority)
- Infections (Hep B), malignancies, Connective tissue diseases and drugs (gold/penicillamine)
Membranous glomerulonephritis diagnosis
Renal biopsy: subepithelial immune complex deposition in the basement membrane
Anti PLA2r antibody: forms immune complex stuck between podocytes and basement membrane (blood)
LM: Diffuse thickening of GBM. “spikes” with special silver stains
IF: “IgG and complement (C3) deposits on the basement membrane”
EM: Electron dense sub-epithelial deposits
Membranous glomerulonephritis Mx
immunosuppression e.g. Steroids/Alkylating agents/B cell monoclonal Ab (rituximab: stop antibody production and therefore damage)
• 30% progress to end stage renal failure in 10 years
IgA nephropathy
Commonest GN in the world (Nephritis)
IgA nephropathy signs/symptoms
Asymptomatic microhaematuria non-nephrotic range proteinuria
Macroscopic haematuria after resp/GI infection
Young adult and tonsillitis
AKI (red cells clogging tubes up)/CKD
Associated with Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)
IgA nephropathy Ix and management
LM: Diffuse mesangial IgA deposition
IF: IgA and C3 deposition
EM: Electron dense deposits in mesangium
- BP control/ ACE inhibitors & ARBs/ Fish oil
- Corticosteroids if persistent proteinuria >1g 3-6 months of ACE-i/ARB and GFR>50
Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
Skin or throat infection: 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
Strep endocarditis: immune complex (bacterial antigen and antibody) – circulates and lodges into the kidney
They develop a nephritic syndrome
Can cause rapid decline unlike IgA
Complement levels are lower in this but normal in IgA nephropathy
Post streptococcal glomerulonephritis Ix
Evidence of strep infection: increase ASOT, anti-DNAse B or decrease C3
CRP (less in IgA) and more in raise in this
Fever, AKI, CRP, low complement
Echo: for endocarditis
Mesangiocapillary glomerulonephritis
Idiopathic
Secondary to Autoimmune e.g. SLE, RA, Cancer
Mixed nephrotic/ nephritic syndrome
Mesangiocapillary glomerulonephritis diagnosis
LM: Mesangial proliferation, neutrophils and monocytes, thickened capillary walls. “tram track” GBM
IF: Granular deposits of C3
EM: Electron dense sub-endothelial deposits +/- sub-epithelial +/- mesangial
Mesangiocapillary glomerulonephritis management
ACE-i/ARB and BP control
Treat underlying cause
Trial of immunosuppression if no underlying cause is found and progressive decline in function
Rapidly progressive glomerulonephritis
ANCA-Positive: Systemic Vasculitis, Wegener’s granulomatosis (Granulomatosis with polyangiitis) and Microscopic polyangiitis
ANCA-Negative: Goodpasture’s disease-Anti-GBM, Henoch Scholein Purpura HSP/IgA, IgA & membranous (transforms into this) and Systemic Lupus Erythematosus SLE
crescentic glomerulonephritis
Rapidly progressive glomerulonephritis signs/symptoms
Rapid deterioration in renal function over days/weeks
Active urinary sediment (RBC’s, RBC & Granular Casts)
It presents with a very acute illness with sick patients but it responds well to treatment
Rapidly progressive glomerulonephritis management
• Immunosuppression
- Steroids (IV Methylprednisolone / Oral Prednisolone)
- Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine
- dialysis
Goodpasture Syndrome
Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes due to type IV collagen
Goodpasture Syndrome Mx
Imunosuppression
- Steroids (IV Methylprednisolone / Oral Prednisolone)
- Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine
- dialysis
Diabetic nephropathy
chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis. Haemodynamic changes – increased GFR and initial decrease in creatinine – afferent arteriolar vasodilation mediated by range of vasoactive mediators.
Renal hypertrophy due to raised plasma glucose which stimulates growth factors, renin-angiotensin aldosterone activation, production of advanced glycation products and oxidative stress
Diabetic nephropathy screening
albumin: creatinine ratio and U&Es.
Overt diabetic nephropathy is characterised by persistent albuminuria
(300mg/24 hours on at least 2 occasions separated by 3-6 months)
Diabetic nephropathy management
optimising blood sugar levels (Hb1Ac below 53 mmol to reduce microvascular complications) and blood pressure (ACE inhibitors)
Lipid control: statins
Myeloma
Cancer of plasma cells: a type of WBC normally responsible for producing antibodies
Excess production of immunoglobins (proteins)
Collections of abnormal plasma cells accumulate in the bone marrow
Myeloma diagnosis
FBC, U&Es, LFTS
Bloods: Serum Protein Electrophoresis and Serum Free light chains
Urine: Bence Jones Protein
Bone Marrow Biopsy
Myeloma management
Stop nephrotoxic medication e.g. NSAIDs – don’t give for the back pain
Diuretics in view of risk increasing cast formation – flush calcium out as well
Manage hypercalcaemia (saline +/- bisphosphonates [inhibit osteoclasts] )
- Chemotherapy to reduce tumour load
- High dose dexamethasone may help reduce tumour load
- Thalidomide/bortezomib: monoclonal antibodies
- Stem cell transplant
Amyloidosis
extracellular amyloid (insoluble protein fibrils) in tissues or organs
Occurs due to abnormal folding of proteins which aggregate and become insoluble
Amyloidosis types
- Primary / Light chain (AL)
- Secondary / Systemic / Inflammatory (AA)
- Dialysis (Aβ2M)
- Hereditary and old age (ATTR)
Amyloidosis complications
Renal – (nephrotic range) proteinuria +/- impaired renal function
Cardiac – Restrictive Cardiomyopathy
Nerves – peripheral or autonomic neuropathy
Hepatomegaly / Splenomegaly
GI – malabsorption
Amyloidosis Iv
Urinalysis + uPCR (urine protein creatinine ratio)
Blood tests – renal function, markers of inflammation, protein electrophoresis, SFLC (Serum free light-chain measurement)
Renal Biopsy: Congo red staining (apple green under polarised light)
[Other biopsy - abdominal fat pad or rectal biopsy]
SAP scan – Scintigraphy with radiolabelled serum amyloid – shows extent of disease
Vasculitis Mx
Corticosteroids
Cyclophosphamide/Rituximab
Azathioprine/Methotrexate used for maintenance
Plasma Exchange – dialysis machine
SLE diagnosis
High index of suspicion: young lady with non-specific symptoms
Blood: Raised inflammatory markers, Immunology – ANA +ve, anti-dsDNA ab (~70%) and Complement – low levels
Urinalysis: protein: ACR >30 and PCR>50
Renal biopsy:
Interstitial nephritis
inflammation of the space between cells and tubules (the interstitium) within the kidney.
Acute interstitial nephritis
presents with AKI and hypertension
acute inflammation of tubules and interstitium
hypersensitivity reaction to:
- drugs (NSAIDs or antibiotics)
- Infection e.g. strep
- autoimmune
Acute interstitial nephritis other signs/symptoms
o Rash o Fever o Eosinophilia on blood test o Arthralgia AKI + hypertension
Acute interstitial nephritis management
treat underlying cause
steroids
Chronic Tubulointerstitial Nephritis
chronic inflammation of the tubules and interstitium. Presents as CKD.
Autoimmune, infectious, iatrogenic and granulomatous disease causes
Chronic Tubulointerstitial Nephritis management
ACEi/ARB (BP control), glucose control and lipids (statins)
steroids
Acute tubular necrosis
damage and death (necrosis) of the epithelial cells of the renal tubules. Most common cause of AKI
Cause: ischaemia or toxins
reversible: regenerates after 7-21 days
Acute tubular necrosis Iv
- Urinalysis: “Muddy brown casts”
- renal tubular epithelial cells in urine
Acute tubular necrosis management
Same as AKI supportive IV fluids stop nephrotoxins treat complications
Renal tubular acidosis
metabolic acidosis due to pathology in the tubules of the kidney.
Type 1 renal tubular acidosis
pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions that cause acidosis
- hyperventilate to compensate for metabolic acidosis (blow CO2)
Type 1 renal tubular acidosis Ix + Mx
Hypokalaemia, metabolic acidosis and high urinary pH
Mx: Oral bicarbonate
Type 2 renal tubular acidosis
The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood.
Excessive bicarbonate is excreted in the urine leads to acidosis in the blood due bicarbonate normally lowers pH
Fanconi’s syndrome is the main cause
Type 2 renal tubular acidosis Ix + Mx
Hypokalaemia
Metabolic acidosis
High urinary pH
Mx: oral bicarbonate and K+ replacement
Type 3 RTA
Type 3 renal tubular acidosis is a combination of type 1 and type 2 with pathology in the proximal and distal tubule.
Type 4 Renal Tubular Acidosis
Reduced aldosterone (stimulates sodium absorption and excretion of K+ and H+) and affects the distal tubule. Lower levels of K+ and H+ becomes excreted in the urine from the blood leading to hyperkalaemic renal tubule acidosis
Causes: adrenal insufficiency, ACEi, spironolactone, SLE, diabetes or HIV
Type 4 Renal Tubular Acidosis Ix and Mx
- Hyperkalaemia – how to distinguish between type 1 and 4
- High chloride
- Metabolic acidosis
- Low urinary pH – reduced ammonia (suppressed by K+ -normally counter balances H+ acidity) production and less in urine
Mx:
- Fludrocortisone – synthetic corticosteroid medication that works similar to aldosterone
- Sodium bicarbonate
- Treatment of the hyperkalaemia may also be required
Haemolytic Uraemic Syndrome
thrombosis (blood clots) in small blood vessels throughout the body (especially glomerulus capillaries).
- Haemolytic anaemia
- AKI (haematuria and proteinuria)
- Low platelet count
HUS signs/symptoms
Reduced urine output – due to AKI Haematuria or dark brown urine Abdominal pain Lethargy & irritability Confusion Hypertension Bruising
HUS management
anti-hypertensives
blood transfusions
dialysis
Rhabdomyolysis
skeletal muscle tissue breaks down and releases breakdown products into the blood.
Myocytes undergo apoptosis
- myoglobin, K+, P+, CK
Causes of Rhabdomyolysis
Prolonged immobility
Extremely rigorous exercise
Crush injuries
Seizures
signs/symptoms of Rhabdomyolysis
Muscle aches & pain Oedema Fatigue Confusion Red-brown urine
Rhabdomyolysis Ix and Mx
CK blood test
Myoglobinuria
U&Es
ECG
Mx
IV fluids: rehydrate and encourage filtration
IV NaCl (reduce myoglobin toxicity)
IV mannitol
Causes of hyperkalaemia
Acute kidney injury Chronic kidney disease Rhabdomyolysis Adrenal insufficiency Tumour lysis syndrome Medications a lot
hyperkalaemia ECG results
Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes
Hyperkalaemia management
calcium gluconate 10mls 10% - stabilise myocardium
Insulin (actrapid) and dextrose (50mls of 50%)
Nebulised salbutamol IV fluids Oral calcium resonium Sodium bicarbonate Dialysis
Polycystic Kidney Disease chromosomes
PKD-1: chromosome 16
PKD-2: chromosome 4
Polycystic Kidney Disease extra renal manifestations
Cerebral aneurysms
Hepatic cysts: SOB, ankle swelling and pain
Cardiac valve disease (aortic/mitral regurgitation/Aortic root dilatation)
Colonic diverticula and colonic perforation-
Abdominal and inguinal hernias
Polycystic Kidney Disease management
Tolvaptan: slow the development of cysts and renal failure Antihypertensives Hydration Analgesia Antibiotics Dialysis Renal transplant
Autosomal recessive polycystic kidney disease (ARPKD) chromosome
6
Young children and constantly associated with hepatic lesions
renal: bilateral and symmetrical
small cysts appearing from collecting duct system
Autosomal recessive polycystic kidney disease (ARPKD) signs/symptoms
Kidneys always palpable
Hypertension
Recurrent Urinary Tract Infections
Slow Decline in GFR -less than 1/3 reach dialysis
It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine.
They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge.
Autosomal recessive polycystic kidney disease (ARPKD) management
dialysis in the first few days
tolvaptan
ALPORTS SYNDROME (HEREDITARY NEPHRITIS)
genetically heterogeneous disorder characterized by nephritic syndrome
X linked inheritance (85%)
Disorder of Type IV collagen matrix
Mutation (COL4A5 gene) leads to deficient collagenous matrix
ALPORTS SYNDROME signs/symptoms
Haematuria - characteristic feature.
Proteinuria seen later but confers bad prognosis
Sensorineural deafness
Ocular defects
Leiomyomatosis of oesophagus/genitalia-rare
Suspect in haematuria and hearing loss
ANDERSON FABRYS DISEASE
Uncommon Inborn error of Glycosphingolipid metabolism (deficiency of a-galactosidase A)
X linked disease lysosomal storage disease
Look for angiokeratomas
ANDERSON FABRYS diagnosis and Mx
Plasma /Leukocyte: a-GAL activity in blood
Enzyme replacement - Fabryzyme
MEDULLARY CYSTIC KIDNEY
Autosomal Dominant inheritance
Morphologically abnormal renal tubules leading to fibrosis
Cysts are in the corticomedullary junction/medulla - not essential for diagnosis
Oncocytoma: benign tumour
Spherical, capsulated, brown/tan colored
CT scan: Spoke wheel pattern (Has got central scar (stellate): strands come out from the center. Necrosis in the middle – can’t revascularize)
Angiomyolipoma (AML)
Blood vessels, muscle and fats: typical hamartoma
associated with TS
Angiomyolipoma (AML) Mx
4 cm is considered cut off: rough guide
Elective: Embolization/Partial nephrectomy
Emergency: Embolization / emergency nephrectomy: usually the whole
Renal cell carcinoma
adenocarcinoma of renal cortex (arise from proximal convoluted tube)
Types of RCC
Clear cell: loss of VHL Papillary Chromophobe Collecting duct Medullary cell
RCC signs/symptoms
Haematuria, vague loin pain and mass (3 together: less than 10% in cases)
Non-specific symptoms of cancer (e.g. weight loss, fatigue, anorexia, night sweats)
Pyrexia of unknown origin (8-9 %)
Varicocoele: causing pressure on left gonadal vein. Left gonadal vein drains in left renal vein. Left sided renal tumours can cause these
Paraneoplastic syndrome (30%): weight loss, anaemia, HT and hypercalcemia
RCC Ix
USS
CT: Chest, abdo and pelvis
FBC: Hb
RCC Mx
small tumours 3-4cm:
- surveillance (elderly)
- ablation
- partial nephrectomy
> 3-4cm
- surveillance (elderly)
- ablation
- partial nephrectomy
- Radical Nephrectomy
> 7cm
- radical nephrectomy
RCC adjuvant therapy
TKI (Tyrosine kinase inhibitors) e.g. Sunitinib
- Reduces neovascularisation
RCC paraneoplastic syndromes
Polycythaemia (RCC secretes unregulated erythropoietin)
Hypercalcaemia (RCC secretes a hormone that mimics the action of PTH)
Wilms tumour
- Under 5
- Mass in the abdomen (parents noticed or presenting with signs/symptoms)
- Abdominal pain
- Haematuria
- Lethargy
- Fever
- Hypertension
- Weight loss
Prostate cancer pathology
adenocarcinomas originating in peripheral zone
local extension through the prostatic capsule, to the urethra, bladder base and seminal vesicles and with perineural invasion along autonomic nerves.
pelvic lymph nodes
Prostate cancer sign/symptoms
Majority asymptomatic
Lower urinary tract symptoms:
bladder outflow obstruction: hesitancy, poor stream, terminal dribbling, frequency, nocturia, urinary retention or obstruction
Hematuria/Haematospermia
Bone pain, Anorexia, Weight loss and fatigue
ED
Prostate cancer diagnosis
PSA PR exam Prostate biopsy TMN: T1-4 - Gleason grading system (1-5)
Prostate cancer management
Organ confined
- watchful waiting
- active surveillance
- Radical prostatectomy
- Radical radiotherapy
Locally advanced
- radiotherapy
- watchful waiting
- hormonal therapy
Metastatic disease
- GNRH analogues e.g. Goserelin
- Anti-androgens
- Steroidal: cyproterone acetate
- Non-steroidal: nilutamide and bicalutamide
- bilateral subcapsular orchidectomy
- maximal androgen blockade
Cytotoxic chemotherapy with docetaxel
Abiraterone (androgen synthesis inhibitor)
Bladder cancer
arise from the endothelial lining (urothelium)
- transitional cell carcinoma (papillary 80% and non papillary 20%)
- squamous cell carcinomas
Urachal
Bladder cancer risk factors
- smoking
- hair dyes
- ## schistosomiasis
Bladder cancer signs/symptoms
painless haematuria
bladder mass and palpable kidney
bladder cancer diagnosis
Cystoscopy and biopsy (transurethral resection of bladder tumour)
Urine cytology
During a CT urogram
Retrograde pyelogram
Bladder cancer Mx
Not invading the muscle
- Superficial bladder – resected endoscopically with repeated cystoscopic surveillance to detect surveillance to detect recurrence
- Transurethral Resection of a Bladder Tumour (TURBT)
- Chemo into bladder after surgery (use barrier contraception afterwards)
- Weekly treatments for 6 weeks with BCG vaccine squirted into the bladder via catheter, then every six months for 3 years.
Muscle-invasive bladder cancer
- Radical cystectomy with ileal conduit+/- removal of other pelvic contents
- Radiotherapy (as neoadjuvant, primary treatment or palliative)
- IV chemotherapy as neoadjuvant or palliative
Testicular cancer risk factors
previous TC
Cryptorchidism
HIV
FH
Types of TC
Seminoma Non-seminomatous - Teratoma - Yolk sac - Choriocarcinoma
Testicular Cancer signs/symptoms
Asymmetry or slight scrotal discoloration
o Hard without flatulence or transillumination, non-tender, irregular mass mostly intratesticular
o Assess involvement of epididymis, spermatic cord and scrotal skin.
o Secondary hydrocoele
o Abdominal mass – advanced disease
TC bloods
Alpha-fetoprotein: teratomas and yolk sac
Beta-hCG - choriocarcinoma
TC mx
Orchidectomy
- radicular inguinal orchidectomy
- chemo/radio
Penile cancer
Squamous cell carcinoma
Kaposi sarcoma
BCC
Penile cancer risk factors
Age: 5-6 th decade Pre-malignant conditions in 40% cases Phimosis (unable to retract foreskin): Chronic inflammation Geography: Asia, Africa, South America Human Papilloma virus: Types 16 and 18 Smoking Immunocompromised patients
Squamous carcinoma in situ Mx
Circumcision: if prepuce alone (foreskin)
Topical 5 fluorouracil
Invasive Squamous carcinoma Mx
Prepucial lesions: Circumcision
Glans lesions
- Superficial: Glans resurfacing
- Deep: Glansectomy
More advanced disease:
- Total penile amputation with formation of perineal urethrostomy
- Inguinal lymphadenectomy
- If involved lymph nodes. Also in high risk penile cancer cases even when not involved.
Upper Urinary Obstructive Uropathy
Loin to groin/flank pain on affected side (stretching/irritation of ureter and kidney)
pain on affected side (stretching/irritation of ureter and kidney)
Reduced / no urine output
Non-specific symptoms (e.g. vomiting)
Reduced renal function on bloods
Lower Urinary Tract Obstruction (i.e. bladder / urethra)
Acute urinary retention (unable to pass urine and increasingly full bladder)
Lower urinary tract symptoms (e.g. poor flow, difficulty initiating urination, terminal dribbling)
Reduced renal function on bloods
Benign Prostatic Hyperplasia
hyperplasia of the stromal and epithelial cells of the prostate
BPH key questions
Storage
- Urgency: If you are watching your favourite TV Programme, and get the feeling of wanting to pass urine, can you delay until the programme is finished?
- Frequency: How often do you pass urine from the time you wake up in the morning until the time you go to sleep at night?
- Nocturia: How many times, on average are you woken from sleep because you need to pass urine?
Voiding
- Hesitancy
- Poor flow
- Intermittency
- Straining to void
- Terminal dribbling
- Incomplete emptying
Red flags in urinary tract obstruction
- haematuria
- bedwetting (high pressure chronic retention)
- suprapubic pain
- recurrent urinary tract infections
- back pain and neurological symptoms
BPH Ix
Urine dipstick PSA Rectal exam IPSSS Serum creatinine Frequency - volume chart USS Cystoscopy
BPH Mx
- Alpha blockers (relax smooth muscle; e.g. tamsulosin 400 mcg once daily)
- 5-alpha reductase inhibitors (block testosterone and reduce the size of the prostate; e.g. finasteride)
- Anticholinergic (Inhibits bladder smooth muscle contraction)
- Beta agonist (Inhibits bladder smooth muscle contraction)
Surgery
- Transurethral resection of the prostate (TURP)
Acute Urinary Retention
complication of BPH, prostate cancer and urethral stricture (women: pelvic prolapse, mass or post surgery for stress incontinence)
- spontaneous vs precipitated
- painful (acute) vs painless (chronic)
Acute Urinary Retention Ix
FBC, renal functions (usually normal in acute urinary retention)
urine dipstick
DRE: Prostate and pelvic mass: anal tone & perianal sensation (S2-3): Cauda equina
Acute Urinary Retention Mx
catheter and record residual volume
treat cause
Chronic retention signs/symptoms
Painless and may not feel any difficulty: renal impairment in high pressure chronic retention
Nocturnal enuresis
Sometimes smell slightly like urine due to leakage
Tense, palpable bladder, hypertension, and progressive renal impairment associated with bilateral hydronephrosis and hydroureter commonly leading to uraemia and death
Chronic retention Mx
Admit cathertise , monitor post obstruction diuresis (>200ml/hr for 2 consecutive hours or >3L/24h)
Definitive: LTC/ISC/Surgery (after at least 6 weeks)
Renal stones signs/symptoms
asymptomatic and never cause an issue
Renal colic
Excruciating loin to groin pain
Colicky (fluctuating in severity) as the stone moves and settles
May have haematuria, nausea, vomiting and oliguria
May have symptoms of sepsis if infection present (i.e. fever)
Renal stones diagnosis
Urine dipstick: haematuria and infection
Bloods: FBC, U&Es, CRP, urate and calcium
CT KUB
Renal stones Mx
NSAIDs e.g. PR diclofenac+/- anti-opiate Antiemetic Fluids Antibiotics if infection
- No pain, no sepsis or AKI = manage conservatively (watchful waiting and Tamsulosin to aid passage)
- Surgical Interventions
if stone has not passed in one month and AKI/sepsis/refractory pain: aim to decompress kidney in immediate management
Indications to treat urgently: Pain unrelieved, Pyrexia, Persistent nausea/vomiting and High-grade obstruction
- Extracorporeal Shock Wave Lithotripsy
- Ureteroscopy and Laser Lithotripsy
- Percutaneous Nephrolithotomy (under GA in theatre)
- Open Surgery
Testicular torsion signs/symptoms
Acute/sudden onset of unilateral testicular pain
- nausea/vomiting
- May be referral of pain to lower abdomen
- Acutely tender testicle (often difficult to examine due to extent of tenderness)
- Firm testicle
- Absent cremasteric reflex
- Abnormal lie and Horizontal lie
- Rotated so that epididymis is not in normal posterior position
- Elevated (retracted) testicle
- Acute hydrocoele + oedema may obliterate landmarks
Testicular torsion Mx
Immediate surgical scrotal exploration
- orchiplexy and possible orchiectomy if delayed surgery
Torsion of appendage
twisting of a vestigial appendage that is located along the testicle. This appendage has no function, yet more than half of all boys are born with one
Torsion of appendage
very similar to torsion
seen early, may have localised tenderness at superior pole and “blue dot” sign
Testis should be mobile and cremasteric reflex present
Paraphimosis
Painful swelling of the foreskin distal to a phimotic ring
Paraphimosis Mx
Iced glove, granulated sugar for 1-2hrs (facilitates manual reduction – osmotic gradient), multiple punctures in oedematous skin
Manual compression of glans with distal traction on oedematous foreskin
Dorsal slit (relieve strangulation of the glans)
Priapism
• Prolonged erection (> 4hrs), often painful and not associated with sexual arousal
Priapism classification
Ischaemic (Vascular stasis in penis and decreased venous outflow)
Non-ischaemic (arterial or high-flow)
Priapism Mx
Ischaemic
- Aspiration +/- irrigation with saline
- Injection of alpha-agonist, e.g. phenylephrine 100-200ug every 5-10 mins up to max 1000ug after aspiration: reduce blood flow to penis
- Surgical shunt
Non-ischaemic
- Observe, may resolve spontaneously
- Selective arterial embolization with non-permanent materials
Fournier’s gangrene
necrotizing fasciitis occurring about the male genitalia
Emphysematous pyelonephritis
acute necrotizing parenchymal and perirenal infection caused by gas-forming uropathogens, usually E coli
Bladder injury
Commonly associated with pelvic fracture
- Suprapubic/abdominal pain + inability to void
- Suprapubic tenderness, lower abdominal bruising, guarding/rigidity, diminished bowel sounds
Bladder injury Mx
Large-bore catheter
Antibiotics
Urethral injury
Posterior urethral injury often associated with fracture of pubic rami
Post. urethra fixed at urogenital diaphragm and puboprostatic ligaments, so bulbomembranous junction most vulnerable
Penile fracture
Typically happens during intercourse – buckling injury when penis slips out of vagina and strikes pubis
Complicated UTI
- systemic symptoms (infection goes into the bloodstream) or
- urinary structural abnormality /stones
Common organisms of UTI
Escherichia coli is the most common cause
Klebsiella
Proteus: struvite stones – calculi: Produces urease which breaks down urea to form ammonia, which increases urinary pH - precipitation of salts (swarming cultures)
Enterococcus: hospital acquired infections
Pseudomonas: associated with catheters and instrumentation – needs ciprofloxacin
UTI diagnosis
> 105 - probale UTI
<103 - not significant UTI
104 - contamianed? infection? repeat?
Empirical antibiotic treatment for UTI Female
Nitrofurantoin or trimethoprim orally (3 days)
Empirical antibiotic treatment for UTI Uncatheterised male UTI
nitrofurantoin or trimethoprim orally (7 days)
Complicated UTI or pyelonephritis (GP) Mx
com-amox or co-trimoxazole (14 days)
Complicated UTI or pyelonephritis (Hospital)
Amoxicillin (enterococci) and gentamicin (coliforms) IV for 3 days
- (co-trimoxazole and gentamicin if penicillin allergy), stepdown as guided by antibiotic sensitivities
Abacterial cystitis/Urethral syndrome + Mx
• Pus cells present in urine, but no significant growth on culture
- alkalinising urine and stop the thing causing it
Asymptomatic bacteriuria
Patient is asymptomatic, therefore condition is detected incidentally
Significant bacteriuria (>105 orgs/mL) No pus cells in urine
Asymptomatic bacteriuria Mx
treat in pregnancy
UTI in catheterised patients
Catheterised patients with >105 orgs/mL should ONLY be given antibiotics if there is supporting evidence of UTI (fever, symptoms etc.)
Unnecessary antibiotics result in the catheter becoming colonised with increasingly resistant organisms
Pyelonephritis
Infection in the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
Pyelonephritis Ix
- Specimen collection – mid stream as first stream most likely to be contaminated
- Blood cultures
- Urine dipstick
- CT scan
- USS
- DMSA scans
Pyelonephritis Mx
Broad spectrum: IV amoxicillin + Gentamicin (IV Co-trimoxazole + Gentamicin)
adimt, iV fluids, analgesia and antipyretics
