renal and urology Flashcards
stage 5 ckd
0-15 eGFR
stage 4 ckd
15-30 eGFR
stage 3 ckd
3a = 45-60 eGFR
3b = 30-45 eGFR
causes of CKD
diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease
features of renal bone disease
osteomalacia
osteoporosis
osteosclerosis
spine x-ray in renal bone disease
“rugger jersey” spine
sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)
metabolic probs in ckd
low VD
high phosphate
LOW calcium
secondary hyperparathyroidism
ckd bone disease tx
reduce dietary phosphate
phosphate binders (sevelamer)
give VD (eg alfacalcidol, calcitriol)
bisphosphonates (alendronic acid)
hypercalcaemia tx
Fluids
Calcitonin (reduces serum calcium levels by inhibiting osteoclast activity)
nice criteria for AKI
Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours
RFs AKI
Chronic kidney disease
Heart failure
Diabetes
Liver 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 causes AKI
inadequate BS:
Dehydration
Hypotension (shock)
Hypovolaemia - D+V
Heart failure
Renal artery stenosis
renal causes AKI
Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis (most common)
Rhabdomyolysis
tumour lysis syndrome
drugs - ACEi, NSAIDs, nephrotoxic abx (gentamicin, vancomycin, tetracyclines)
post renal causes AKI
obstruction to outflow:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer
what drugs to stop in AKI
NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
* Aminoglycosides
* ACE inhibitors
* Angiotensin II receptor antagonists
* Diuretics
eGFR variables
CAGE - Creatinine, Age, Gender, Ethnicity
inheritance pattern of PKD
autosomal dominant
- more common
- assoc w cerebral haemorrhage
autosomal recessive
- more severe, usually presents antenatally or at birth
- less likely to have FHX
when is contrast CI
renal impairment
most signif cause of anaemia in CKD
reduced erythropoietin
(carry out iron studies b4 giving EPO)
stages to classify AKI
Stage 1 - 1.5-1.9x baseline creatinine - All in the 1’s
Stage 2 - 2-2.9x baseline creatinine - All in the 2’s
Stage 3 - 3x baseline creatinine - All in the 3’s
when to send a urine culture in UTI
if pregnant
visible or non-visible haematuria
> 65 yrs
if male
UTI tx non-pregnant women
trimethoprim or nitrofurantoin for 3 days
how long to give UTI abx if catheterised
7 days
UTI tx males
trimethoprim or nitrofurantoin 7 days
Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis
post-streptococcal glomerulonephritis presents after 1-2 WEEKS, IgA nephropathy after 1-2 DAYS (post RTI)
post-strep has low complement
post- strep has more proteinuria
prostatitis presentation+ what is a common cause
chronic if > 3mths
Prostatitis: perineal or prostatic pain
Lower urinary tract symptoms: dysuria, frequency, urgency
Symptoms of systemic upset: fever, myalgia
E. coli is common cause
prostatitis ix
Focussed history
Digital rectal examination: tender, warm, swollen prostate
Midstream sample of urine
Screening for sexually transmitted infections (gonorrhoea can cause prostatitis)
acute prostatitis mx
Hospital admission for systemically unwell or septic patients (for bloods, blood cultures and IV antibiotics)
Oral abx 14 days (quinolone) = ciprofloxacin 1st line
(ofloxacin or trimethoprim)
chronic prostatitis mx
Alpha-blockers (e.g., tamsulosin)
Analgesia
Psychological treatment
Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
Laxatives
how to measure proteinuria in CKD
albumin:creatinine ratio (ACR)
when to prescribe ACEi in CKD
if they have an albumin:creatinine ratio (ACR) > 30 mg/mmol + existing HTN
ACR > 70 regardless
valvular abnormality w PKD
Mitral valve prolapse
mitral regurgitation
AKI mx
stop nephrotoxic drugs
careful fluid balance
fluid resus espesh if pre-renal cause
tx hyperkalaemia
specialist if cause is not known or is severe
haemodialysis when not responding to med tx of comps
if fluid overload consider
- loop diuretics e.g. furosemide
- adrenaline
- inotrope like dobutamine to increase BP
AKI ix
U&Es - sodium
- potassium
- urea
- creatinine - for dx
urine output
urinalysis - blood + protein (nephritic syndrome?)
no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound
when to refer AKI to nephrologist
Renal tranplant
ITU patient with unknown cause of AKI
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
features to differentiate AKI from CKD
renal ultrasound in CKD will have bilateral small kidneys
apart from:
AD PKD
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy
CKD will have hypocalcaemia due to lack of VD
what can cause hyperkalaemia
AKI
CKD (stage 4 or 5)
Rhabdomyolysis
Adrenal insufficiency - addisons
Tumour lysis syndrome
metabolic acidosis disease
massive blood transfusion
drugs*: , ACEis, ARBs, spironolactone (K+ sparing), ciclosporin, heparin
*BBs interfere with K+ transport into cells + can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment
what foods are high in K+
salt substitutes (i.e. Contain potassium rather than sodium)
bananas, oranges, kiwi fruit, avocado, spinach, tomatoes
ECG hyperkalaemia
Peaked or ‘tall-tented’ T waves (occurs first)
Loss of P waves
Broad QRS complexes
Prolonged PR interval
Sinusoidal wave pattern (v severe)
Ventricular fibrillation
mx hyperkalaemia below 6.5mmol/L + no ECG changes
tx underlying cause
for example, treating acute kidney injury and stopping medications (e.g., spironolactone or ACE inhibitors)
mx hyperkalaemia above 6.5 or w ECG changes
IV CALCIUM GLUCONATE + INSULIN WITH DEXTROSE INFUSION
INSULIN drives potassium from the extracellular space to the intracellular space
DEXTROSE is required to prevent hypoglycaemia while on insulin
CALCIUM GLUCONATE stabilises the cardiac muscle cells and reduces the risk of arrhythmias
other options:
Nebulised salbutamol temporarily drives potassium into cells
Oral calcium resonium reduces potassium absorption in the GI tract (this is slow and causes constipation)
Sodium bicarbonate (in acidotic patients on renal advice) drives potassium into cells as it corrects the acidosis
Haemodialysis may be required in severe or persistent cases
what albumin:creatinine ratio means
proteinuria
>3 mg/mmol
what albumin:creatinine ratios to refer to a nephrologist
> 70 mg/mmol
- unless known to be caused by diabetes + already approp tx
> 30 mg/mmol w persistent haematuria
3-29 mg/mmol w persistent haematuria + other RFs e.g. declining eGFR/CVD
what is rhabdomyolysis
skeletal muscle breaking down + releasing various chemicals into the blood. Muscle cells (myocytes) undergo cell death (apoptosis), releasing:
Myoglobin
Potassium
Phosphate
Creatine kinase
complications of rhabdomyolysis
hyperkalaemia - arrythmias + arrest
AKI
- myoglobin is toxic in high concs
DIC
compartment syndrome
causes of rhabdomyolysis
Anything that causes significant damage to muscle cells:
Prolonged immobility, particularly frail patients who fall + spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins
features of rhabdomyolysis
Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)
ix rhabdomyolysis
Creatine kinase (CK) blood test for dx
- normally <150 U/L. In rhabdomyolysis, it can be 1,000-100,000 U/L
- typically rises in the first 12 hours, then remains elevated for 1-3 days, then gradually falls
- higher the CK, the greater the risk of kidney injury
Myoglobinuria - urine dipstick will test +ve for blood
U&Es for AKI + hyperkalaemia
ECGs- hyperkalaemia
tx rhabdomyolysis
IV fluids
hyperkalaemia tx
what is haemolytic uraemic syndrome (HUS)
thrombosis in small BVs throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella
Most often affects children following an episode of gastroenteritis. Abx and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS.
triad in HUS
Microangiopathic haemolytic anaemia (thrombi causes RBCs to ruptures as they pass through small BVs)
AKI
Thrombocytopenia (low platelets) (as they are used to form the thrombus)
HUS presentation
E. coli O157 + Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:
Fever
Abdominal pain
Lethargy
Pallor
Reduced UO
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion
mx HUS
Medical emergency + requires hospital admission + supportive management:
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)
It is self-limiting, and most patients fully recover with good supportive care.
ix HUS
stool culture to establish causative organism
FBC = anaemia - haemoglobin level less than 8 g/dL with a negative Coomb’s test, thrombocytopenia
Fragmented blood film = schistocytes and helmet cells
U&Es = AKI
features of nephritic syndrome
Haematuria - microscopic or macroscopic
Oliguria
Proteinuria, <3g per 24 hours (higher protein suggests nephrotic syndrome)
Fluid retention
what is nephritic syndrome
a group of features that occurs w nephritis (inflammation of the kidneys)
what is nephrotic syndrome
occurs when the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria.
It refers to a group of features without specifying the underlying cause
features of nephrotic syndrome
NO blood
Proteinuria (>3kg in 24hr) = FROTHY urine
Low serum albumin (<25g per litre)
Peripheral oedema
Hypercholesterolaemia
what does nephrotic syndrome predispose px to
thrombosis
- loss of antithrombin III (a protein that will be lost in urine) - it inhibits coagulation by inhibiting the enzymatic activity of thrombin
hypertension
hyperlipidaemia - due to overproduction in the liver
infection risk - due to urinary immunoglobulin loss
most common cause of nephrotic syndrome
minimal change disease
top causes of nephrotic syndrome in adults
+ other causes
Membranous nephropathy
Focal segmental glomerulosclerosis
Membranoproliferative glomerulonephritis
Henoch-Schönlein purpura (HSP)
Diabetes
Infection (e.g., HIV)
what is IgA nephropathy (Berger’s disease)
commonest cause of primary glomerulonephritis worldwide (nephritic syndrome)
IgA nephropathy presentation
young male, recurrent episodes of macroscopic haematuria
typically associated with a recent/current RTI
nephrotic range proteinuria is rare
renal failure is unusual and seen in a minority of patients
histology in IgA nephropathy
IgA deposits and glomerular mesangial proliferation
what is membranous nephropathy
deposits of immune complexes (IgG + complement) in the glomerular basement membrane -> thickening + malfunctioning of the membrane, proteinuria
usually idiopathic
histology in membranous nephropathy
IgG and complement deposits on the basement membrane
histology in Rapidly progressive glomerulonephritis
glomerular crescents
what is goodpasture syndrome
also known as anti-glomerular basement membrane (anti-GBM) disease
Anti-GBM antibodies attack the glomerulus + pulmonary basement membranes. It causes glomerulonephritis and pulmonary haemorrhage
goodpastures syndrome histology
renal biopsy: linear IgG deposits along the basement membrane
goodpastures syndrome presentation
patient in their 20s or 60s with acute kidney failure and haemoptysis (coughing up blood)
can be exacerbated by a RTI
systemic diseases that can cause glomerulonephritis
Henoch-Schönlein purpura (HSP)
Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis)
Lupus nephritis (associated with systemic lupus erythematosus)
what is post-streptococcal glomerulonephritis
Occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (Strep pyogenes)
Caused by immune complex (IgG, IgM and C3) deposition in the glomeruli
Usually young children
Membranoproliferative glomerulonephritis
It involves immune complex deposits and mesangial proliferation.
post-streptococcal glomerulonephritis sx
headache
malaise
visible haematuria
proteinuria (less commonly signif)
this may result in oedema
hypertension
oliguria
ix in post-strep glomerulonephritis
bloods
- raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
- low C3
renal biopsy
- electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
- immunofluorescence: ‘starry sky’ appearance
significant AKI, haemoptysis + p-ANCA antibodies
microscopic polyangiitis
(diff from egwp which is also p-ANCA, similar sx to gwp which is c-ANCA)
significant AKI, haemoptysis + c-ANCA antibodies
granulomatosis with polyangiitis
what is tumour lysis syndrome
usually triggered by intro of combo chemo
- occurs from the breakdown of tumour cells -> release of chemicals from the cell -> high potassium and high phosphate level in the presence of a low calcium.
Suspect in any patient presenting with an AKI in the presence of a high phosphate and high uric acid level.
what is serum urea-creatinine ratio used for
urea and creatinine both freely filtered at the glomerulus
creatinine is not reabsorbed (it is removed from body entirely by the kidneys therefore v high if kidneys are not working)
urea reabsorbed by tubules (urea absorption increased compared to creatinine in pre-renal)
can be used as an indicator of the likely cause of renal failure
high urea-creatinine ratio
PRE- RENAL FAILURE
- dehydration
corticosteroids
GI haemorrhage
protein-rich diet
severe catabolic state
low urea-creatinine ratio
intrinsic renal damage
severe liver dysfunction
malnutrition
pregnancy
low protein diet
SIADH
rhabdomyolysis
spironolactone mechanism of action
aldosterone antagonist
what does renal artery stenosis cause
secondary hyperaldosteronism due to disproportionately low BP in the kidneys
-> HTN as excessive renin is released
what is renal artery stenosis
narrowing of the artery supplying the kidney, usually due to atherosclerosis
where do renal stones most commonly get stuck
vesico-ureteric junction
most common type of kidney stone
calcium based
- Calcium oxalate (more common)
- Calcium phosphate
Opaque on XR (can be seen)
other types of kidney stone (apart from calcium)
Uric acid – these are not visible on x-ray
Struvite – produced by bacteria, therefore, associated with infection (stag horn shape)
Cystine – associated with cystinuria, an autosomal recessive disease (semi-opaque ground glass on XR)
what is a staghorn calculus + what is it made from
where a renal stone forms in the shape of the renal pelvis - body sits in the renal pelvis with horns extending into the renal calyces
occurs with stones made of struvite
In recurrent URTIs, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite
renal stones presentation
may be asx
Renal colic is the usual complaint:
- Unilateral loin to groin pain that can be excruciating
- Colicky (fluctuating in severity) as the stone moves and settles
May also be:
- haematuria
- N&V
- reduced urine output
- sx of sepsis if infection present
renal stones ix
Non-contrast computer tomography (CT) of the kidneys, ureters and bladder (CT KUB) = INITIAL IX OF CHOICE FOR DX, do within 24 hrs pres
US KUB (preg women or children)
urine dipstick = haematuria (but normal does not exclude)
bloods - infection + U&Es, Ca (hypercalcaemia is a cause)
Abdo XR (wld not show uric acid stones, + may not show small stones)
Analyse stone
mx renal stones
NSAIDs best analgesia = IM diclofenac
Antiemetics = metoclopramide, prochlorperazine or cyclizine
Abx if infection
Watch + wait if < 5mm + uncomplicated
Consider tamsulosin (alpha blocker) to aid spontan passage (only if <10mm)
5-10mm shockwave lithotripsy
Surgical (e.g. ureteroscopy, Percutaneous nephrolithotomy) if >10mm, do not pass spontan or complete obstruction (hydronephrosis shown by dilation of renal pelvis) / infection
advice to px who get recurrent renal stones
Increase oral fluid intake (2.5 – 3 litres per day)
Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones)
Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation)
Reduce dietary salt intake (less than 6g per day)
Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones)
For calcium stones – reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea)
For uric acid stones – reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)
Limit dietary protein
medications for recurrent renal stones
POTASSIUM CITRATE in patients with calcium oxalate stones and raised urinary calcium
Thiazide diuretics (e.g., indapamide) in patients with calcium oxalate stones and raised urinary calcium (can increase distal tubular calcium resorption)
what is a hydrocele
collection of fluid within the tunica vaginalis that surrounds the testes
usually painless and present with a soft scrotal swelling
communicating + non-communicating
hydrocele examination
The testicle is palpable within the hydrocele
Soft, fluctuant, may be large
Irreducible + has no bowel sounds (distinguishing it from a hernia)
Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)
mx hydrocele
exclude serious causes (cancer)
If idiopathic - conservative mx only
if uncertainty/hard to palpate - do an USS
what type of hydrocele may you get in newborn males
communicating - caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum
usually resolve in 1st few mths
so reassure (think about surgical repair if not resolved in 1-2 yrs)
what is a varicocele
occurs where the veins in the pampiniform plexus become swollen as a result of increased resistance in the testicular vein (incompetent valves / obstruction by tumour?)
comps in varicocele
can cause impaired fertility - due to disrupting the temperature in the affected testicle
may result in testicular atrophy, reducing the size and function of the testicle
what is the pampiniform plexus
a venous plexus found in the spermatic cord and drains the testes
(drains into the testicular vein)
plays a role in regulating the temperature of blood entering the testes by absorbing heat from the nearby testicular artery
which side do most varicoceles occur on
LEFT
due to increased resistance in L testicular vein
(R drains into IVC, L drains into L renal vein)
varicocele presentation
Throbbing/dull pain or discomfort, worse on standing
A dragging sensation
Sub-fertility or infertility
varicocele examination
A scrotal mass that feels like a “bag of worms”
More prominent on standing
Disappears when lying down
Asymmetry in testicular size if the varicocele has affected the growth of the testicle
when to refer varicocele urgently to urology
Varicoceles that do not disappear when lying down - as they raise concerns about retroperitoneal tumours obstructing the drainage of the renal vein
varicocele ix
Ultrasound with Doppler imaging can be used to confirm the diagnosis
Semen analysis if there are concerns about fertility
Hormonal tests (e.g., FSH and testosterone) if there are concerns about function
varicocele tx
Uncomplicated cases can be managed conservatively.
Surgery or endovascular embolisation may be indicated for pain, testicular atrophy or infertility.
what is an epididymal cyst
fluid filled sac that occurs at the head of the epididymis
if it contains sperm it is called a spermatocele
epididymal cyst presentation
mostly asx
may present having felt a lump, or they may be found incidentally on ultrasound for another indication.
epididymal cyst examination
Soft, round lump
Typically at the top of the testicle
Associated with the epididymis
Separate from the testicle
May be able to transilluminate large cysts (appearing separate from the testicle)
epididymal cyst tx
Usually harmless and are not associated with infertility or cancer. They may cause pain or discomfort where removal wld be considered.
indications for short-term dialysis
A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia leading to pericarditis or encephalitis - sx such as seizures or reduced consciousness
options for long term dialysis
Haemodialysis
for long term access use:
- Tunnelled cuffed catheter
- Arteriovenous fistula
Peritoneal dialysis
AV fistula features to examine in OSCE
Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
A “machinery murmur” on auscultation over the fistula
comps of AV fistula
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure
what is STEAL syndrome
occurs when there is inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb.
Blood is diverted away from the part of the limb it was supposed to supply -> ischaemia. Instead, it flows through the fistula and into the venous system.
what is high-output heart failure
caused by blood flowing quickly from the arterial to the venous system through an A-V fistula.
There is a rapid return of blood to the heart, increasing the pre-load -> hypertrophy of the heart muscle and heart failure.
comps of peritoneal dialysis
Bacterial peritonitis (infections in the high-sugar environment are common and serious)
Peritoneal sclerosis (thickening and scarring of the peritoneal membrane)
Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)
Weight gain (due to absorption of the dextrose)
Psychosocial implications
what does the dialysis solution that goes into peritoneal cavity contain
dextrose
most common cause of peritonitis secondary to peritoneal dialysis
Staphylococcus epidermidis
LUTS
occur w prostate pathology
Hesitancy – difficult starting and maintaining the flow of urine
Weak flow
Urgency – a sudden pressing urge to pass urine
Frequency – needing to pass urine often, usually with small amounts
Intermittency – flow that starts, stops and varies in rate
Straining to pass urine
Terminal dribbling – dribbling after finishing urination
Incomplete emptying – not being able to fully empty the bladder, with chronic retention
Nocturia – having to wake to pass urine multiple times at night
initial assessment of man presenting w LUTS
Digital rectal examination (prostate exam) to assess the size, shape and characteristics of the prostate
Abdominal examination to assess for a palpable bladder and other abnormalities
Urinary frequency volume chart, recording 3 days of fluid intake and output
Urine dipstick to assess for infection, haematuria (e.g., due to bladder cancer) and other pathology
Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference
common causes of raised PSA
Prostate cancer
Benign prostatic hyperplasia
Prostatitis
Urinary tract infections
Vigorous exercise (notably cycling)
Recent ejaculation or prostate stimulation
difference between exam in benign + cancerous prostate
A benign prostate feels smooth, symmetrical and slightly soft, with a maintained central sulcus
A cancerous prostate may feel firm/hard, asymmetrical, craggy or irregular, with loss of the central sulcus
medical mx of BPH
Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms (tx of immediate sx)
5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate (tx of the enlargement, takes 6 mths)
how long does finasteride take to improve sx in BPH
6 mths
SE tamsulosin
postural hypotension as alpha blocker
SE finasteride
sexual dysfunction (due to reduced testosterone).
as a 5-alpha reductase inhibitor it stops the conversion testosterone to dihydrotestosterone (DHT) (more potent version)
what to monitor in HSP
blood pressure and urinanalysis
HIV-associated nephropathy (HIVAN) features
massive proteinuria resulting in nephrotic syndrome
normal or large kidneys
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
elevated urea and creatinine
normotension
which form of renal impairment is most commonly assoc w hep C
Membranoproliferative glomerulonephritis
which form of renal impairment is most commonly assoc w HIV
focal segmental glomerulosclerosis
what can invalidate eGFR
Eating red meat the evening before a blood test
Rfs for prostate cancer
Increasing age
Family history
Black African or Caribbean origin
Tall stature
Anabolic steroids
prostate cancer presentation
asx
LUTS
Haematuria
Erectile dysfunction
Symptoms of advanced disease or metastasis (e.g., weight loss, bone pain or cauda equina syndrome)
first line ix for suspected prostate cancer
Multiparametric MRI of prostate
results reported on a Likert scale
1 – very low suspicion
2 – low suspicion
3 – equivocal
4 – probable cancer
5 – definite cancer
when to perform a prostate biopsy
MRI findings (e.g., Likert 3 or above) and the clinical suspicion (i.e. examination and PSA level)
what to do if suspicion of cancer on DRE
Refer for 2-week wait appointment and advise urgent multiparametric MRI
gleason grading system
prostate cancer grading system
based on histology from biopsies
The greater the Gleason score, the more poorly differentiated the tumour is + the worse the prognosis - 1 (closest to normal) to 5 (most abnormal)
made up of 2 nos from different samples
6 is considered low risk
7 is intermediate risk (3 + 4 is lower risk than 4 + 3)
8 or above is deemed to be high risk
RFs bladder cancer
increased age
smoking
aromatic amines - dye + rubber - transitional cell carcinoma
Schistosomiasis causes squamous cell carcinoma
types of bladder cancer
Transitional cell carcinoma (90%)
Squamous cell carcinoma (5% – higher in areas of schistosomiasis)
bladder cancer key presentation
Painless haematuria
when to do a 2 week wait referral for bladder cancer
> 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI
> 60 with microscopic haematuria
PLUS:
- Dysuria or;
- Raised white blood cells on a full blood count
consider a non-urgent referral in >60 with recurrent unexplained UTIs
bladder cancer dx
Cystoscopy
tx of non-muscle invasive bladder cancer
Transurethral resection of bladder tumour (TURBT)
Intravesical chemotherapy is often used after a TURBT procedure to reduce the risk of recurrence.
tx for invasive bladder cancer
radical cystectomy
immunotherapy in bladder cancer
Intravesical BCG
Giving the BCG vaccine (the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours.
most common renal tumour
Renal adenocarcinoma
Renal Cell Carcinoma presentation
haematuria, flank pain and a palpable mass
RFs Renal Cell Carcinoma
Smoking
Obesity
Hypertension
End-stage renal failure
Von Hippel-Lindau Disease
Tuberous sclerosis
when to do 2 week wait for renal cell carcinoma
> 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI
classic feature of metastatic renal cell carcinoma
“Cannonball metastases” in the lungs
- appear as clearly-defined circular opacities scattered throughout the lung fields on a chest x-ray.
paraneoplastic features of renal cell carcinoma
Polycythaemia – due to secretion of unregulated erythropoietin
Hypercalcaemia – due to secretion of a hormone that mimics the action of parathyroid hormone
Hypertension – due to various factors, including increased renin secretion, polycythaemia and physical compression
Stauffer’s syndrome – abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis
types of renal cell adenocarcinoma
Clear cell (around 80%)
Papillary (around 15%)
Chromophobe (around 5%)
how to calc urea:creatinine ratio
plasma urea (mmol/L) / (plasma creatinine (μmol/L) divided by 1000)
mx for confined renal cancer
a partial or total nephrectomy depending on the tumour size
- patients with a T1 tumour (i.e. < 7cm in size + confined to kidney) are typically offered a partial nephrectomy
Alport’s syndrome presentation
microscopic haematuria, bilateral sensorineural deafness, and lenticonus
drug causes of acute interstitial nephritis
PENICILLIN
rifampicin
NSAIDs
allopurinol
furosemide
acute interstitial nephritis presentation
allergic picture
may have just had penicillin abx
fever, rash, arthralgia
EOSINOPHILIA
mild renal impairment
hypertension
ix results in acute interstitial nephritis
sterile pyuria
white cell casts in urine
what to use in px who have troubling gynaecomastia on spironolactone
Eplerenone
what cells does testicular cancer usually come from
germ cells in the testes
2 types of testicular cancer
Seminomas
Non-seminomas (mostly teratomas)
RFs testicular cancer
Undescended testes
Male infertility
Family history
Increased height
presentation testicular cancer
lump on testicle
- non-tender
- arising from testicle
- hard
- irregular
- non-fluctuant
- no transillumination
rarely can get gynaecomastia - espesh in Leydig cell tumours
ix testicular cancer
SCROTAL USS initial ix
staging CT scan
tumour markers for testicular cancer
Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas)
Beta-hCG – may be raised in both teratomas and seminomas
Lactate dehydrogenase (LDH) is a very non-specific tumour marker
Royal Marsden Staging System testicular cancer
Stage 1 – isolated to the testicle
Stage 2 – spread to the retroperitoneal lymph nodes
Stage 3 – spread to the lymph nodes above the diaphragm
Stage 4 – metastasised to other organs
Extra-renal manifestations of PKD
berry aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts (LIVER CYSTS ARE THE MOST COMMON EXTRA THING)
Mitral regurgitation
Colonic diverticula
comps of PKD
Chronic loin/flank pain
Hypertension
Gross haematuria can occur with cyst rupture (usually resolves within a few days)
Recurrent urinary tract infections
Renal stones
End-stage renal failure occurs at a mean age of 50 years
ix PKD
Ultrasound and genetic testing are used for diagnosis.
mx ADPKD
tolvaptan - vasopressin receptor antagonist
- can slow progression of cysts + progression of renal failure
tx HTN
analgesia
abx if infections
drainage if sx
dialysis
renal transplant
conservative mx PKD
Genetic counselling
Avoiding contact sports due to the risk of cyst rupture
Avoiding NSAIDs and anticoagulants
MR angiography (MRA) can be used to screen for cerebral aneurysms
what is pyelonephritis
inflammation of the kidney resulting from bacterial infection - affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue)
RFs pyelonephritis
Female sex
Structural urological abnormalities
Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children)
Diabetes
most common cause pyelonephritis
E. coli
- gram-negative, anaerobic, rod-shaped bacteria that are part of the normal lower intestinal microbiome (found in the faeces + can easily spread to bladder)
presentation pyelonephritis
Lower UTI sx - dysuria, suprapubic discomfort and increased frequency
+
Fever
Loin or back pain (bilateral or unilateral)
Nausea / vomiting
Patients may also have:
Systemic illness
Loss of appetite
Haematuria
Renal angle tenderness on examination
ix pyelonephritis
Urine dipstick = nitrites, leukocytes, blood.
Midstream urine (MSU) for microscopy, culture and sensitivity testing to establish the causative organism
Raised white blood cells and raised inflammatory markers
ultrasound or CT scan to exclude other things
1st line for mx pyelonephritis in community
cefalexin for 7-10 days
co-amoxiclav if culture results
trimethoprim if culture results
ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
hx if thinking sepsis!
what to use to assess for renal damage in recurrent pyelonephritis
Dimercaptosuccinic acid (DMSA) scans
what is orchitis
inflammation of the testicle
what does the epididymis do
Sperm mature and are stored in the epididymis (released from testicle into its head). The epididymis drains into the vas deferen
causes of epididymo-orchitis
Escherichia coli (E. coli)
Chlamydia trachomatis
Neisseria gonorrhoea
Mumps - usually just testicle
presentation epididymo-orchitis
gradual onset, over minutes to hours, with unilateral:
Testicular pain
Dragging or heavy sensation
Swelling of testicle and epididymis
Tenderness on palpation, particularly over epididymis
- positive Prehn’s sign (relief of pain upon lifting the scrotum)
Presence of the cremasteric reflex (stroking the inner thigh, testicle moves upwards)
- both differentiate from torsion
Urethral discharge (should make you think of chlamydia or gonorrhoea)
Systemic symptoms such as fever and potentially sepsis
tx for epididymo-orchitis when it is most likely caused by an enteric organism (e.g., E. coli)
Ofloxacin for 14 days
Levofloxacin for 10 days
Co-amoxiclav for 10 days (where quinolones are contraindicated)
causes of non-gonococcal urethritis (NGU)
Chlamydia trachomatis
Ureaplasma urealyticum
Mycoplasma genitalium
tx urethritis
either oral doxycycline for 7 days or single dose of oral azithromycin
exceptions to the rule that most patients with CKD have bilateral small kidney
autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy
features that suggest CKD rather than AKI
bilateral small kidneys (apart from exceptions)
hypocalcaemia (due to lack of vitamin D)
what is acute tubular necrosis
most common renal cause of an AKI
damage to the tubular cells from prolonged ischaemia/presence of toxins. The kidneys are no longer able to concentrate urine or retain sodium leading to high urinary sodium and low urine osmolality (more dilute).
what happens if you correct chronic hypernatraemia too fast
cerebral oedema
plasma sodium in dehydration
high
(however not if there is salt loss eg D+V)
acute tubular necrosis presentation
AKI with the presence of muddy brown casts in the urine.
what can cause acute tubular necrosis
Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)
surgical mx renal stones
Treatment
Stone <5mm = expectant treatment
Stone <2cm = lithotripsy (wave to break stone)
Stone <2cm + pregnant = ureteroscopy (camera passed through urethra)
Stone complex = percutaneous nephrolithotomy (invasive, camera passed though kidney from back)
hydronephrosis/infection = nephrostomy (drainage of urine from kidney) as needs urgent decompression
pain reliever in renal stones
IM Diclofenac
comp of radiotherapy of the prostate + how does that comp present
proctitis (inflammation in the rectum)
pain, altered bowel habit, rectal bleeding and discharge
(Prednisolone suppositories can help reduce inflammation)
tx testicular torsion
Emergency bilateral orchidopexy - surgical fixation of both testes to the posterior wall
(need both done to prevent further risk)
