Breast, Renal & Urology Flashcards
Breast cancer
most common cancer in women, 2nd most common cause of cancer death in the UK
incidence ↑ with age
Risk factors fro breast cancer
↑age personal history of breast cancer family history of breast cancer obesity nulliparity 1st pregnancy age >30yrs early menarche / late menopause COCP HRT ionising radiation
Genetics:
- BRCA 1
- BRAC2
- p53 gene mutation
Types of breast cancer
Invasive ductal carcinoma
- most common
- may be quite aggressive
- usually unilateral & unifocal
Invasive lobular carcinoma
- less aggressive
- often multifocal
Ductal carcinoma in situ (DCIS)
Lobular carcinoma in situ (DCIS)
Medullary breast cancer
- most common type associated with BRCA1
- often triple +ve cancer
Mucinous carcinoma
Pagets disease of the nipple
-eczematous changes of the nipple associated with underlying malignancy
Presentation of breast cancer
palpable mass
-often non tender, firm
nipple discharge
-bloody discharge is associated strongly with ductal carcinoma
nipple retraction, scaling of the nipple
axillae lymphadenopathy, skin changes e.g. discolouration, dimpling, Peau d’orange, oedema of the arm
NB mastalgia (breast pain) is an uncommon presentation of breast cancer
Screening for breast cancer
NHS screening programme for women aged 50-70yrs, who are offered mammography every 3yrs, after age 70 pts are encouraged to make their own mammography appointments
if ↑ breast cancer risk due to FH screening may be offered at younger agre
-e.g. if one 1st degree relative diagnosed at <40y/o or 1st degree male relative diagnosed, or if one 1st degree relative with bilateral cancer at age <50yrs
NB first invitation should be sent to all women before age 53yrs
Investigations for breast cancer
mammography
- bilateral
- preferred if pt >30y/o
USS of breast + regional lymph nodes
- often with a biopsy
- preferred if <30y/o due to denser breast tissue in younger pts
Biopsy
- fine needle aspration
- core biopsy (preferred)
Human epithelial growth factor receptor 2 (HER2) status
Hormon receptor testing
-progesterone & oestrogen
genetic testing for BRCA1/BRCA2
-for all women <50y/o with triple -ve breast cancer
NB generally pts will have triple assessment of examination, imaging & biopsy at the breast clinic
Referral for breast cancer pathway
age ≥30yrs with unexplained breast lump ± pain
age ≥50yrs with discharge/retraction/other change of one nipple
consider referral if skin changes suggestive of breast cancer or age ≥30yrs with unexplained lump in axilla
NB if <30y/o with unexplained breast lump consider non urgent referral
Management of breast cancer
Surgical
- offered to majority of pts
- mastectomy ± axillary lymph node clearance
- if lymph spread suggested = sentinel node biopsy to asses spread during surgery
- usually also offered breast reconstruction
Radiotherapy
-whole breast radiotherapy is offered to most pts
Hormonal therapy
- offered as adjuvant therapy if hormone receptor +ve
- pre-menopause = tamoxifen
- post-menopause = anastrozole
Biologicals
- Trastuzumab for HER2 +ve cancer
- also known as herceptin
- contraindicated if pt has heart problems
chemotherapy
- used pre/post op
- FEC-D is used
Hormonal treatment of breast cancer
offered as adjuvant therapy if hormone receptor +ve
pre-menopause = tamoxifen
- ↑ risk of VTE
- ↑ risk of endometrial cancer
- NB also used in males
post-menopausal = aromatase inhibitors e.g. anastrozole
Fibroadenoma
a benign breast tumour typically seen in women aged <35 (peak incidence 25-35) accounts for ~10% of all breast masses
presents as highly mobile, firm, smooth & non-tender breast lump (also called a breast mouse)
no ↑ risk of malignancy
generally gets smaller over time, but if >3cm is usually excised
Breast cyst
usually seen in women aged 35-50yrs
presents as solitary cyst, usually a discrete small lump that may fluctuate in size
should be referred for imaging at breast clinic
may require aspiration
Fat necrosis
usually seen in larger, fatty breasts in overweight women
often after trauma
lump is painless, skin may be red/bruised/dimpled
may require biopsy to confirm diagnosis but then no further management is needed
Ductal papilloma
benign warty lesion usually located behind the areola that may cause sticky nipple discharge (discharge is usually from a single duct)
requires triple assessment to rule out cancer
Phyllodes tumour
rare tumour that is hard to distinguish from a fibroadenoma but usually occurs in older women
i.e. mobile, small, firm breast lump
treated with wide excision & follow-up
Sclerosis adenosis
sclerosis within the lobules causing a lump/pain
can be hard to distinguish from malignancy so biopsy is advised but no ↑ risk of malignancy
Cyclical mastalgia
common cause of benign breast pain in young females
breast pain that varies in intensity according to the phases of the menstrual cycle
- pain rapidly resolves with the start of menstruation
- pain generally diffuse & bilateral
management includes supportive bras, topical/oral analgesia (NSAIDs/paracetamol)
consider referral if no improvement after 3 months, specialists may consider danazol or bromocriptine
Puerperal mastitis
inflammation of the breast, often secondary to nipple fissures, affecting ~10% of breast feeding mothers
presents with ≥1 week postpartum in one breast with painful/tender, red, hot breast with pain during breastfeeding, fever and malaise
women should be encouraged to continue breast feeding
give Abx (flucloxacillin, 10-14days) if systemically unwell / nipple fissure / symptoms not improving 12-24h post effective milk removal
NB if untreated may cause breast abscess
Breast abscess
may be a consequence of untreated Puerperal mastitis or mammary duct ectasia
presents with purulent nipple discharge, a fluctuating mass, pain and fever
Non lactational mastitis
usually seen in smokers or those with nipple rings usually are of reproductive age
mammary duct ectasia
due to dilation of breast ducts, usually seen in perimenopausal women (age 40-50yrs)
presents as tender lump around areola with green nipple discharge ± blood
usually no treatment needed unless recurrent/persistent then may need surgical excision
may progress to breast abscess
Testicular cancer
most common malignancy in men aged 20-30yrs
95% are germ cell tumours e.g. seminomas or non seminomas (e.g. embryonal, teratoma)
Risk factors for testicular cancer
infertility cryptorchidism Fh of testicular cancer mumps orchitis Klinefelters syndrome
Presentation, investigations & management of testicular cancer
Presentation:
- painless testicular lump
- hydrocele
- gynaecomastia
- NB pain is a rare symptom
Investigations:
- testicular USS (1st line)
- Tumour markers
- Seminomas = ↑hCG
- non-seminomas = ↑AFP / beta-hCG
- germ cell tumours = ↑LDH
Management:
-orchidectomy ± chemo/radiotherapy
Hydrocele
presents as a fluctuating, painless transilluminating mass, usually possible to get above the mass on examination
investigated with USS in younger men to exclude cancer
Varicocele
abnormal enlargement of pampiniform plexus, most common cause of scrotal enlargement
generally presents as painless enlargement or with dull aching pain of hemiscortum
-most commonly left sided
feels like bag of worms on palpation, with negative transillumination
diagnosed with USS
management is generally conservative but surgery may be required if painful
NB there is an increased risk of subfertility/infertility
Bening prostatic hyperplasia (BPH)
a non-neoplastic glandular & stromal hyperplasia of the transition zone to the prostate
common enough to be considered normal with increasing age
~50% of 50y/o mean have evidence of BPH, but unusual before age 45
Presentation of Bening prostatic hyperplasia (BPH)
lower urinary tract symptoms (LUTS)
- urinary frequency
- urinary urgency
- hesitancy
- incomplete emptying
- weak/intermittent stream
- straining
- terminal dribble
- nocturia
PR examination
-symmetrically enlarged, smooth, firm, non tender prostate
Assessment of Bening prostatic hyperplasia (BPH)
International prostate symptom score (IPSS)
- used to assess the severity of LUTS
- assess impact on QoL
Investigations for Bening prostatic hyperplasia (BPH)
Prostate specific antigen (PSA)
- indicated if pt is worried about prostate cancer
- usually ↑
Prostate USS
-done pre surgery
Urinalysis (normal usually) post-void residual bladder scan urinary frequency - volume chart uroflowmetry U&Es, FBC, LFTs
Management of Bening prostatic hyperplasia (BPH)
Minimal symptoms
-watchful waiting
Pharmacological (trialed before surgery)
- Alpha-1 antagonist (1st line)
- e.g. Tamsulosin or alfuzosin
- improve symptoms in ~70% of men
- ↓ muscle tone of prostate & bladder
- side effects: dizziness, hypotension, dry mouth
- 5-alpha reductase inhibitors (2nd line)
- e.g. finasteride
- block conversion of testosterone→dihydrotestosterone
- ↓ prostate volume
- side effects: erectile/ejaculation dysfunction, ↓ libido
- can be combine with Alpha-1 antagonist if severe BPH
Surgery (2nd line)
- generally only after failed medical treatment
- transurethral resection of prostate (TURP) = procedure of choice
- may consider UroLift system
Prostatitis
an inflammation of the prostate gland that may be of infectious or non infectious
infectious causes are commonly due to E.coli (may also be STI causes e.g. Chlamydia/Gonorrhoea especially in <35y/o men, while non infectious may be inflammatory response post UTI
presents generally with fever, malaise, dysuria / frequency / urgency (due to bladder irritation, with pain radiating to lower back, perineum, rectum or penis
DRE may reveal a tender, boggy prostate gland
treatment includes STI screening and a 14day course of quinones if bacterial, and NSAIDs
Pharmacological treatment of Benign prostatic hyperplasia (BPH)
1st line = Alpha-1 antagonist
- e.g. Tamsulosin or alfuzosin
- improve symptoms in ~70% of men
- ↓ muscle tone of prostate & bladder
- side effects: dizziness, hypotension, dry mouth
2nd line = 5-alpha reductase inhibitors
- e.g. finasteride
- block conversion of testosterone→dihydrotestosterone
- ↓ prostate volume
- side effects: erectile/ejaculation dysfunction, ↓ libido
If severe symptoms then both drug types can be combined
Prostate cancer
a malignant tumour of glandular origin situated in the prostate, most commonly adenocarcinomas arising in the peripheral zone of the prostate
most common site of metastasis = bones & lymph nodes
most common cancer in men (~27% of all male cancer)
especially common in black males
usually seen at age >50yrs
Location of prostate lesions
Prostate cancer:
-peripheral zone
BPH
-transitional zone
Epidemiology & Risk factors for Prostate cancer
most common cancer in men (~27% of all male cancer)
especially common in black males
least common in asian men
usually seen at age >50yrs
2nd most common cause of cancer death in males
Risk factors:
- ↑ age
- afro-carribbean origin
- afro-american origin
- Family history
Presentation of prostate cancer
typically asymptomatic
LUTS (hesitancy, weak stream, incomplete emptying, frequency) haematuria flank pain weight loss ↓ appetite Bone pain (if metastasis)
PR examination
- may remain normal even in advanced disease
- hard irregular prostate with lobar asymmetry
DRE examination findings for prostate pathology
Prostate cancer
- may remain normal even in advanced disease
- hard irregular prostate with lobar asymmetry
BPH
-symmetrically enlarged, smooth, firm, non tender prostate
Prostatitis
-tender, boggy prostate gland
Investigations for prostate cancer
Prostate specific antigen (PSA) ↑
multi parametric MRI*
-1st line imagine now
transurethral ultrasound guided biopsy
- biopsy is grade with Gleason scale
- Gleason scale goes from 1-10
- used as prognostic indicator
Management of prostate cancer
Localised prostate cancer
- active monitoring
- watchful waiting
Locally advanced cancer
- radical prostatectomy
- commonly causes erectile dysfunction
- radiotherapy
- external beam & brachytherapy
Metastatic prostate cancer
- hormonal therapy with anti androgen therapy
- GnRH agonist e.g. goserelin*
- bicalutamide (non steroidal anti androgen)
- cryptoterone acetate, abiraterone
- enzalutamide (NICE recommended)
- bilateral orchidectomy
Bladder cancer
most common malignancy of the urinary tract
Types:
- transitional cell (urothelial) carcinoma (~90% of cases)
- squamous cell carcinoma (~8% of cases)
- adenocarcinoma (~2% of cases)
NB these can occur anywhere in the urinary tract but bladder is most common place
Risk factors for bladder cancer
smoking
exposure to aniline dyes e.g. 2-naphthylamine
rubber manufacturing
cyclophosphamide
Risk factor for squamous cell bladder cancer
Indwelling catheters
schistosomiasis**
Presentation of bladder cancer
painless macroscopic haematuria
dysuria
urinary frequency
other voiding symptoms
NB painless haematuria is cancer until proven otherwise
Investigations for bladder cancer
Urinalysis
- haematuria
- may show pyuria
cystoscopy ± biopsy
urine cytology
CT/MRI chest/abdo/pelvis
U&Es, FBC
NB incidental microscopic haematuria is still associated with bladder cancer and should be treated as such especially in those aged >60
Management of bladder cancer
Non-invasive
-transurethral resection of bladder tumour (TURBT)
Invasive cancer
- neo-adjuvant chemotherapy
- radical cystectomy
Metastatic disease
-treated with cisplatin based chemo
NB pts should be followed up post TURBT with cystoscopy every 3 months as superficial transitional cell carcinoma may recur in ~80% of pts
Renal cell carcinoma (RCC)
also known as hypernephroma
a renal malignancy arising from the renal parenchyma/cortex (usually proximal tubular epithelium) accounting for ~90% of renal cancers
Most common kidney cancer in adults (NB in children Wilm’s tumour is most common)
~85% are clear cell carcinomas
usually seen in males, aged 60-70yrs
Risk factors for Renal cell carcinoma (RCC)
smoking
obesity
HTN
also associated with von Hippel-Lindau syndrome & tuberous sclerosis
Presentation of Renal cell carcinoma (RCC)
Triad of
-haematuria
-loin pain
-loin/abdo mass
plus
fatigue, weight loss, varicocele (L sided usually), pyrexia of unknown origin, oedema
~25% of pts have metastatic disease
- haemoptysis
- bone pain
- pathological fractures
NB paraneoplastic features e.g. hepatic dysfunction or polycythaemia (↑EPO production) may be present
Investigations for Renal cell carcinoma (RCC)
FBC
-Hb ↓
urinalysis
-haematuria ± proteinuria
CT kidney with contrast MRI/USS kidney U&Es (usually normal) LFTs (may be abnormal) Urine MC&S CT/MRI chest/abdo/pelvis
Management of Renal cell carcinoma (RCC)
confined disease
-partial/total nephrectomy depending on tumour size
if <7cm = partial
advanced/metastatic disease
- receptor kinase inhibitors (1st line)
- e.g. surafenib / sutinib - alpha-interferon & interleukin 2
- help ↓ tumour size
Nephrolithiasis (renal stones)
encompasses te formation of all types of urinary calculi in the kidney / urinary system
- ~80% of stones are calcium containing - calcium oxalate stones are most common type
very common condition, usually age 40-60yrs
more common in men (3:1 male:female ratio)
most common in white people
Epidemiology of Nephrolithiasis (renal stones)
very common condition
more common in men (3:1 male:female ratio)
most common in white people
peak age 40-60yrs
calcium oxalate are the most common stones
Risk factors for Nephrolithiasis (renal stones)
dehydration ↑ Ca2+ hyperparathyrodisim renal tubular acidosis FH of urinary tract stones cystinuria diet high in urate/calcium/sodium/animal protein gout (RF for urate stones) Drugs (generally ↑ Ca2+ excretion) -loop diuretics, steroids, acetazolamide, theophylline
Presentation of Nephrolithiasis (renal stones)
Renal colic
- sudden severe flank pain radiating to ipsilateral groin
- often intermittent
- pain recedes to dull ache in between attacks
rigours, fever
dysuria, haematuria, urinary retention
nausea & vomiting
NB pt generally unable to lie/sit still and frequently moves i.e. writhing in pain
Investigations for Nephrolithiasis (renal stones)
Urinalysis
- haematuria
- leukocytosis
- nitrates
- pH <5 suggestive of uric acid stones
non enchanted CT
- imaging of choice
- non contrast CT KUB should be done within 14h of admission
USS
-imaging of choice in children/young adults/pregnant women
FBC, U&Es Ca2+
CRP, coagulation
Management of Nephrolithiasis (renal stones)
Pain relief
-NSAIDs e.g. diclofenac = 1st line
-Stones <5mm generally pass spontaneously
- ureteric obstruction + infection = requires urgent surgical decompression
- nephrostomy tubes or ureteric stent
Non emergency management:
- shock wave lithotripsy, ureteroscopy, percutaneous nephrolithotomy
- stone <2cm = lithotripsy
- stone <2cm & pregnant = ureteroscopy
- complex stone/staghorn calculi = percutaneous nephrolithotomy
Prevention
-if ↑Ca2+ thiazide diuretics & good fluid intake can reduce reoccurrence
Urinary tract infection (UTI)
an inflammatory reaction of the urinary tract epithelium in response to infection
very common especially in women
men are much less likely to get UTIs but if they do its more serious
Aetiology of Urinary tract infection (UTI)
E. Coli (most common)
staph saprophyticus, proteus mirabilis, klebsiella
NB non E.coli infection more often seen in pts with underlying pathologies, immunosuppression or those who are catheterised
Risk factors of Urinary tract infection (UTI)
↑ age recent instrumentation of the renal tract renal tract abnormalities sexual activity diabetes institutionisation catheterisation pregnancy immune suppression
Presentation of Urinary tract infection (UTI)
dysuria (burning/stinging on urination) urinary frequency urinary urgency cloudy/offensive smelling urine fever (often low grade) malaise suprapubic / loin pain rigors
in elderly pts UTIs may present as an acute confusional state / delirium
Investigations for Urinary tract infection (UTI)
Urinalysis
- nitrates +
- leukocytes +
- sufficient to diagnose UTI in healthy women
- NB this is not used to diagnose UTI in catheterised pts
urine MC&S
- shows organism + sensitivity
- should be done for all men, pregnant pts, immunosuppressed pts, or if empirical treatment fails
Management of Urinary tract infection (UTI)
Non pregnant women
-3 days of trimethoprim / nitrofurantoin
Pregnant women
- Symptomatic:
- 1st line = nitrofurantoin
- 2nd line = amoxicillin / cefalexin
- Asymptomatic bacteriuria
- 7 days of nitrofurantoin + follow up culture as evidence of cure
Men
-offer 7 days of trimethoprim or nitrofurantoin
catheterised pts
- DO NOT treat asymptomatic bactiuria
- if symptomatic = 7 days of Abx
Management of Urinary tract infection (UTI) in non pregnant women
3 days pf trimethoprim / nitrofurantoin
NB send cultures if age >65yrs or macro.microscopic haematuria
Management of Urinary tract infection (UTI) in pregnant women
Symptomatic:
- 1st line = nitrofurantoin
- 2nd line = amoxicillin / cefalexin
Asymptomatic bacteriuria
-7 days of nitrofurantoin + follow up culture as evidence of cure
NB trimethoprim is contraindicated in pregnancy but used instead of nitrofurantoin in breastfeeding women
Management of Urinary tract infection (UTI) in men
offer 7 days of trimethoprim or nitrofurantoin
Management of Urinary tract infection (UTI) in catheterised pts
DO NOT treat asymptomatic bactiuria
if symptomatic = 7 days of Abx
Acute kidney injury (AKI)
an acute deterioration in kidney function leading to ↑ serum creatinine, and/or ↓ urine output
causes may be pre-renal (most common), intrinsic renal or post-renal
Pre-renal causes of Acute kidney injury (AKI)
Most common, account for ~90% of cases)
Volume depletion
-haemorrhage, burns, D&V, dehydration
Hypotension
-sepsis, cardiogenic shock
oedematous state
-HF, cirrhosis, nephrotic syndrome
renal hypoperfusion
-Renal artery stenosis, NSAIDs, ACE-I/ARBs
Intrinsic renal causes of Acute kidney injury (AKI)
2nd most common
glomerulonephritis, HUS, acute tubular necrosis following prolonged ischaemia, nephrotoxins (e.g. NSAIDs, infection), vasculitis, malignant hypertension, polyarteritis nodosa, eclampsia
Post-renal causes of Acute kidney injury (AKI)
Least common causes
calculi papillary necrosis urethral stricture BPH/Prostate cancer bladder tumour radiation fibrosis
Risk factors for Acute kidney injury (AKI)
↑ age (especially >65yrs) CKD (especially eGFR <40) history of AKI co-existing illness e.g. HF, liver disease, diabetes neurological impairment reliance on carers use of NSAIDs use of ACE-Is/ARBs use of diuretics
Presentation of Acute kidney injury (AKI)
Often asymptomatic
↓ urine output pulmonary & peripheral oedema oliguria/anuria dyspnoea uraemia (anorexia, nausea, encephalopathy, asterix, pericarditis) fatigue confusion lethargy
Investigations for Acute kidney injury (AKI)
U&Es
- ↑ creatinine
- ↑ urea
- ↑ K+
FBC, CRP, Coagulation urinalysis urine output measurement urine MC&S ABG/VBG CXR ECG
Staging of Acute kidney injury (AKI)
Staged via KDIGO criteria
Stage I
- ↑ creatinine to 1.5-1.9x baseline or
- ↑ creatinine by ≥26.5 µmol/L, or
- ↓ urine output to <0.5 mL/kg/hour for ≥ 6 hours
Stage II
- ↑ creatinine to 2.0 to 2.9 times baseline, or
- ↓ urine output to <0.5 mL/kg/hour for ≥12 hours
Stage III
- ↑ creatinine to ≥ 3.0 times baseline, or
- ↑ creatinine to ≥353.6 µmol/L or
- ↓ urine output to <0.3 mL/kg/hour for ≥24 hours or
- initiation of kidney replacement therapy or,
- patients <18 years, ↓ eGFR to <35 mL/min/1.73 m2
Management of Acute kidney injury (AKI)
management is largely supportive
Stop medications
- NSAIDs, ahminoglycosides, ACE-Is/ARBs, diuretics
- Also stop lithium, metformin, digoxin due to ↑ risk of toxicity
monitor K+, Na+, Ca2+, glucose
optimise fluid balance
-e.g. with IV fluids
nephrology referral to treat underlying cause or if considering renal replacement therapy
Chronic kidney disease (CKD)
an abnormality in kidney structure or function persisting >3 months
accelerated progression of CKD = sustained ↓ in GFR ≥25% or ↓ in GFR of >15 per year
common causes include diabetic nephropathy, hypertension, chronic glomerulonephritis/pyelonephritis and adult PKD
Staging of Chronic kidney disease (CKD)
Stage I
-GFR >90ml/min with some signs of kidney damage on other tests
Stage II
-GFR 60-90ml/min with some signs of kidney damage
Stage III
- a = GFR 45-59ml/min
- b = GFR 30-44ml/min
Stage IV
-GFR 15-29ml/min
Stage V
-GFR <15ml/min
NB if all kidney tests are normal there is no CKD
Staging of Chronic kidney disease (CKD)
Stage I
-GFR >90ml/min with some signs of kidney damage on other tests
Stage II
-GFR 60-90ml/min with some signs of kidney damage
Stage III
- a = GFR 45-59ml/min
- b = GFR 30-44ml/min
Stage IV
-GFR 15-29ml/min
Stage V
-GFR <15ml/min
NB if all kidney tests are normal there is no CKD
Presentation of Chronic kidney disease (CKD)
often asymptomatic
oedema polyuria lethargy pruritis anorexia insomnia hypertension sexual dysfunction
Investigations for Chronic kidney disease (CKD)
renal ultrasound
-small kidneys on USS are indicative of CKD
U&Es
- often severely deranged
- pts often tolerate this due to chronicity
FBC
- anaemia usually
- if not anaemic points more to AKI
eGFR ↓ Ca2+ (usually ↓) urinalysis urine albumin glucose
Management of Chronic kidney disease (CKD)
annual CVD assessment nutrition & exercise adjustment Vit D & Calcium supplements 20mg statin consider oral anticoagulant
control BP
- target 130/80, requires ≥2 meds mostly
- use ACE-Is
- if eGFR <45 consider furosemide
If severe = renal replacement therapy (RRT)
Monitoring of Chronic kidney disease (CKD)
monitored with eGFR & creatinine as well as ACR
frequency determined by severity of CKD
Complications of Chronic kidney disease (CKD)
anaemia (↓EPO) hypetension secondary hyperparathyroidism coagulopathy fluid overload
Renal replacement therapy (RRT)
RRT is indicated when kidneys transiently or persistently lose function to remove toxins, metabolites and water from the body
~10% of CKD pts develop renal failure (GFR <15ml/min)
Types:
- haemodialysis
- peritoneal dialysis
- renal transplant
Haemodialysis
most common form of RRT
involves haemofiltration at hospital ~3x per week for 3-5h
requires formation of arteriovenous fistula at least 8 weeks before
Peritoneal dialysis (PD)
filtration occurs in via pts peritoneum with dialysis solution injected into abdominal cavity via a permanent catheter
can be continuous PD (CAPD) where fluid is exchanged every 48h OR automated PD (APD) where dialysis machine performs 3-5 exchanges as pt sleeps
Renal transplant
kidney can be from live or deceased donor, average wait list is ~3years
donated kidney usually transplanted into the groin & the vessel connected to external iliac arteries with the failing kidneys left in place
lifespan of donated kidney is 10-12yrs from deceased donor & 12-15yrs from live donor
pt on lifelong immunosuppression e.g. Tacrolimus, Cyclosporine, Mycophenolate
Indications for acute dialysis
Hyperkalaemia pulmonary oedema pericarditis symptomatic uraemia severe acidosis
(obviously pt also has to be in renal failure)
Nephrotic syndrome
A collection of signs & symptoms indicating damage to the glomerular filtration barrier
characterised by:
- Proteinuria >3.5g/24h
- Hypoalbuminaemia ≤30g/L (≤3g/dL)
- Oedema
Key features of nephrotic syndrome
Proteinuria >3.5g/24h
Hypoalbuminaemia ≤30g/L (≤3g/dL)
Oedema
Aetiology of Nephrotic syndrome
Focal segmental glomerulosclerosis = most common cause in adults
Minimal change disease = most common cause in children
Other causes
-membranoproliferative glomerulonephritis, membranous nephropathy
Secondary causes
-diabetic nephropathy, lupus nephritis, amyloid nephropathy
Presentation of Nephrotic syndrome
Peripheral oedema
-in children often starts with periorbital oedema
frothy urine
leukonychia
SOB
dyspnoea
hypercoaguability
-e.g. DVT, PE
Investigations for Nephrotic syndrome
Urinalysis
- proteinuria +++
- haematuria may be +
serum albumin
- ≤30g/L
24h urine protein
->3.5g
lipid profile
-commonly shows hyperlipidaemia
renal biopsy
-shows definitive cause often
FBC, U&Es, LFts, glucose, CRO
urine MC&S
Management of Nephrotic syndrome
Dietary sodium restriction
fluid restriction
high dose diuretics
- 1st line furosemide ± spironolactone
- can also consider other loop diuretics e.g. bumetanide
In children:
- corticosteroids
- ~80% of children have relapses so consider cyclophosphamide when relapsing
- most are initially steroid sensitive
consider ACE-Is in adults
Nephritic syndrome
characterised by glomerular capillary damage leading to
- haematuria*
- pyuria
- water retention
- hypertension*
- oedema
Aetiology of Nephritic syndrome
IgA nephropathy (burgers disease) -most common cause
post-streptococcal glomerulonephritis
-usually seen in children ~1-2 weeks post strep throat/skin infections
small vessel vasculitis e.g. WEgners / Churg strauss
Goodpastures disease (anti-GBM antibodies)
Alport syndrome
rapidly progressing glomerulonephritis (RPGN)
Presentation of Nephritic syndrome
intermittent gross haematuria
-cola-coloured urine
hypertension
pitting oedema
oliguria
Investigations for Nephritic syndrome
Urinalysis
- blood ++
- protein <3.5g/24h
urinary sediment
- red cell casts
- sterile pyuria
U&Es
- ↓eGFR
- ↑ creatinine
Renal biopsy
Management of Nephritic syndrome
low sodium diet
water restriction
ACE-Is/ARBs
-for HTN & proteinuria
Plasmapheresis
-for anti-GBM & RPGN
acute streptococcal glomerulonephritis in children is usually self limiting and doesn’t require treatment
Glomerulonephritis
denotes glomerular injury and applies to a group of diseases that are generally charcterised by inflammatory changes in the glomerular capillaries & glomerular basement membrane
can cause both nephrotic or nephritic syndromes
IgA nephropathy (Bergers disease)
Most common cause of glomerulonephritis world wide
classically presents 1-2 days post URTI/GI infection in young people (especially men) with recurring episodes of macroscopic haematuria + flank pain ± nephritic syndrome
diagnostic include ↑IgA levels, normal C3/C4 complement levels & renal biopsy (showing mesangial IgA deposition)
management includes ARBs/ACE-Is for BP control and steroids
Post-streptococcal glomerulonephritis
typically occurs 1-2 weeks post group A strep infection (strep progenes), especially in young children
due to immune complex (IgG, IgM, C3 complement) deposition in the glomeruli
presents with proteinuria, haematuria, HTN and oedema
Investigations include ↓C3/C4 complement levels, ↑ASO titre & biopsy (often not required but shows starry-sky appearance)
usually self limiting with good prognosis
Anti-glomerular basement membrane disease (Goodpastures disease)
a type of small vessel vasculitis associated with pulmonary haemorrhage & rapidly progressing glomerulonephritis caused by anti-GBM antibodies
presents with pulmonary haemorrhage & nephritic syndrome
diagnostics include normal ESR (normally ↑ in vasculitis), +ve anti-GBM antibodies, CXR, renal biopsy (showing linear IgG deposits along basement membrane)
managed with plasma exchange, steroids and cyclophosphamide
Focal segmental glomerulosclerosis (FSGS)
most common cause of nephrotic syndrome in adults, due to injury of podocytes
often idiopathic but may be due to HIV, heroin use or sickle cell
presents wit nephrotic syndrome (proteinuria, oedema)
diagnostics include renal biopsy showing focal & segmental sclerosis with podocyte effacement
managed with steroids ± immunosuppressants
NB noted to have high reoccurrence rate in renal transplants)
Membranous glomerulonephritis
most common cause of nephrotic syndrome in european & middle easter ppl
usually presents with nephrotic syndrome
diagnostics include renal biopsy, showing thickened basement membrane (spike & dome appearance), and if idiopathic may have +ve anti-phospholipase A2 antibodies
managed with ACE-Is/ARBs, immunosuppression (steroids + cyclophosphamide)
poor prognosis with 1/3 pts progressing to end stage renal failure
Minimal change disease
most common cause of nephrotic syndrome in children
generally idiopathic
presents with nephrotic syndrome (proteinuria, hypoalbuminaemia, oedema)
diagnosis include renal biopsy (normal appearance on light microscopy with podocyte fusion & effacement on electron microscopy)
managed with steroids (~80% of cases are steroid sensitive) or cyclophosphamide if steroid resistant
Membranoproliferazive glomerulonephritis (mesangiocapillary glomerulonephritis)
uncommmon
associated with ↓C3 levels
generally treated with ACE-Is/ARBs
Rapidly progressive gvomerulonpoehritis
rapid ↓ renal function associated with formation of epithelia crescents
causes include good pastures, Wegners, SLE
presents with nephritic syndrome (HTN, haematuria)
& features of underlying cause
generally treated with steroids & cyclophosphamide
Alport Syndrome
most common inherited nephritis
X-linked recessive condition usually presenting in childhood
presents with progressive renal failure & bilateral sensorineural hearing loss/deafness
no definitive treatment available
Diuretics
a group of drugs that ↑ urine production, they are generally categorised by what renal structures they affect
Types:
- Loop diuretics e.g. furosemide/bumetanide
- Thiazide diuretics e.g. bendroflumathiazide
- Thiazide-like diuretics e.g. indapamide/chlortalidone
- Aldosterone antagonist e.g. spironolcatone/epleronone
- epithelial Na+ channel blockers e.g. amiloride
- Osmotic diuretics e.g. mannitol
- Carbonic anhydrase inhibitors e.g. acetazolamide
Carbonic anhydrase inhibitors
Examples:
-acetazolamide
MOA:
-inhibits carbonic anhydrase in kidney, eyes and brain
Indications:
- acute glaucoma
- altitude sickness
- Idiopathic intracranial hypertension (IIH)
Osmotic diuretics
Examples:
-mannitol, urea
MOA:
-↑osmolality of tubular fluid = ↑ urine production
Indications:
- ↑ICP e.g. in cerebral oedma
- acute glaucoma
NB can lead to dehydration
Loop diuretics
Examples:
-Furosemide, Bumetanide
MOA:
-inhibit Na-K-Cl cotransporter in the thick ascending loop of Henle
Indications:
- HF
- resistant hypertension (especially in pts with renal impairment)
- fluid retention in CKD
- Oedema
Side effects:
- ↓ Na+
- ↓ K+
- ↓ Ca2+
- hypochloraemic alkalosis
- gout
Thiazide diuretics
Examples:
- bendroflumathiazide
- Thiazide like diuretics e.g. Indapamide / Chlortalidone are now preferred
MOA:
-inhibit thiazide sensitive Na+-Cl- symporters in distal convoluted tubules
Indications:
- hypertension
- severe HF in combination with loop diuretics
Side effects:
- ↓ Na+
- ↓ K+
- ↓ Ca2+
- postural hypotension
- impotence
- impaired glucose tolerance
Potassium sparing diuretics
2 subtypes
- Aldosterone antagonist e.g. spironolcatone/epleronone
- epithelial Na+ channel blockers e.g. amiloride
Side effects:
-↑K+
Aldosterone antagonist (a type of Potassium sparing diuretic)
Examples:
-spironolcatone, epleronone
Indications:
- ascites (large doses of 100-200mg)
- HF (if ↓K+)
- Hypertension (if ↓K+)
- nephrotic syndrome
- conns syndrome
Side effects:
- ↑K+
- spironolactone can cause endocrine disturbances e.g. gynaecomastia, amenorrhoea, erectile dysfunction
NB epleronone does not cause frequently cause endocrine disturbances so can be used instead of spironolactone
Epithelial Na+ channel blockers (a type of Potassium sparing diuretic)
Examples:
-amiloride
Indications:
-used with other diuretics as alternative to K+ supplements
Side effects:
-↑K+
Polycystic kidney disease (PKD)
a heterogenous group of disorders characterised by renal cysts and numerous system & extra renal manifestation
Types:
- Autosomal dominant PKD (ADPKD)
- most common form
- onset usually age >30yrs
- Autosomal recessive PKD (ARPKD)
- more likely to present in childhood
NB ADPKD is the most common inherited serious renal disease, and is responsible for ~10% of end stage renal failure
Types of Polycystic kidney disease (PKD)
Autosomal dominant PKD (ADPKD)
- most common form
- onset usually age >30yrs
Autosomal recessive PKD (ARPKD)
-more likely to present in childhood
Presentation of Polycystic kidney disease (PKD)
hypertension recurrent UTIs abdo pain renal stones haematuria CKD flank pain / loin pain palpable enlarged kidneys
hepatomegaly
-due to bening liver cysts
cerebral berry aneurysms
-can cause SAH
Screening for Polycystic kidney disease (PKD)
In relatives of pts with PKD using renal USS
Diagnostic criteria in pt with +ve family history
- 2 cysts, unilateral/bilateral if age <30yrs
- 2 cysts in both kidneys if age 30-59yrs
- 4 cysts in both kidneys if age >60yrs
Investigations for Polycystic kidney disease (PKD)
FBC
-may be ↑Hb due to ↑ EPO secretion
Renal USS
- diagnostic method of choice
- shows renal cysts
Urinalysis Urine MC&S U&Es Bone profile genetic testing
Management of Polycystic kidney disease (PKD)
screening family members
pt & relative education
Tolvaptan
- used in selected pts
- usually CKD stage 1-3 with rapid progression
ACE-Is/ARBs
- for HTN
- target BP 130/80
Pyelonephritis
an infection of the renal pelvis & parenchyma that is usually associated with an ascending UTI, generally more common in women (in neonates more common in boys)
Causes usually same as UTIs
-E.coli*, Klebsiella, proteus, enterococcus
NB repeated episodes of acute pyelonephritis can lead to chronic pyelonephritis which involves destruction & scarring of renal tissue due to repeated inflammation and can lead to CKD
Risk factors for Pyelonephritis
structural renal abnormalities
-e.g. vesicoureteric reflux (VUR
calculi urinary catheterisation stents pregnancy diabetes
Presentation of Pyelonephritis
Fever, chills, rigors flank pain / loin pain dysuria, weakness costovertebral angle tenderness suprapubic tenderness nausea & vomiting tachycardia, hypotension
Investigations for Pyelonephritis
Urinalysis
- leukocytes +
- nitrites +
- WCC casts
- haematuria
FBC
- WCC ↑
- neutrophilia
Renal USS
-if blood in urine or urine unclear
CRP/ESR (↑)
Contrast enhanced CT
Urine MC&S
Blood cultures
Management of Pyelonephritis
Supportive
- IV fluids
- Analgesia
Empirical Abx
-1st line = co-amoxiclav or ciprofloxacin for 7days
Surgery
-may be needed to drain renal abscesses or perinephric abscesses
NB in children 1st line = co-amoxiclav and 2nd line is cefixime
Prophylaxis for Pyelonephritis
usually in women with ≥3 episodes in a year
usually with trimethoprim
