Renal medicine Flashcards
1
Q
what is bacteriuria
A
bacteria in the urine - may be asymptomatic or symptomatic
2
Q
what is lower UTI
A
uretheritis
cystitis
prostatitis
3
Q
what is upper UTI
A
renal pelvis - pyelonephritis
4
Q
what are risk factors for UTI
A
female
sexual intercourse
exposure to spermicide in females (by diaphragms or condoms)
pregnancy
menopause
reduced defence host -
immunosuppression, DM
urinary tract - obstruction, stones, catheter, malformation
5
Q
UTI in catheterised patients - tx?
A
no treatment unless symptomatic.
6
Q
main organism(s) causing UTI
A
E.coli
proteus mirabilis
klebsiella pneumonia
staphylococcus saprophyticus
7
Q
symptoms of cystitis
A
frequency dysuria urgency haematuria suprapubic pain
8
Q
symptoms of acute pyelonpehritis
A
high fevers rigors vomiting loin pain tenderness oliguria
9
Q
symptoms of prostatitis
A
flu-like symptoms
low backache
few urinary symptoms
swollen or tender prostate on PR
10
Q
signs of UTI
A
fever
abdo pain or loin tenderness
foul-smelling urine
occasionally distended bladder, enlarged prostate
11
Q
investigations for a UTI
A
DIPSTICK THE URINE
if dipstick negative but patient symptomatic -> send a MSU sample for lab MC&S to confirm this.
Send a lab MC&S anyway if
- child (do USS)
- MALE
- pregnant
- immunosuppressed
- ill
MC&S - pure growth of >10 organisms/ml is diagnostic.
12
Q
causes of a sterile pyuria
A
TB treated UTI <2 weeks prior inadequately treated UTI appendicitis calculi; prostatitis bladder tumour polycystic kidney
13
Q
bloods for UTI
A
FBC
U+E
CRP
blood cultures
14
Q
imaging for UTI
A
consider ultrasound referral to urology for assessment (CTKUB, cystoscopy, urodynamics) for UTI: - in children - men - if failure to respond to treatment - recurrent UTI (>2/year) - pyelonephritis - unusual organisms - persistent haematuria
15
Q
prevention of UTI
A
drink more water
antibiotic prophylaxis, continuously or post-coital
drinking 200-750ml of cranberry or lingo berry juice a day - reduces risk of symptomatic recurrent infection in women by 10-20%. (Avoid if on warfarin)
16
Q
management of UTI - non-pregnant women ≥16 years old
A
drink plenty of fluids; urinate often
Trimethoprim or nitrofurantoin (eGFR ≥45) for 3 days.
2nd line
- nitrofurantoin if not used first line
- fosfomycin
- pivmecillinam
17
Q
management of UTI - pregnant women
A
nitrofurantoin (eGFR ≥45) for 7 days (AVOID AT TERM).
2nd line
- Amoxicillin for 7 days
- Cefalexin for 7 days
18
Q
management of UTI - men ≥16y
A
trimethoprim or nitrofurantoin (eGFR ≥45) for 7 days.
2nd line
- consider pyelonephritis or prostatitis
19
Q
management of prostatitis
A
1st line
- ciprofloxacin
or ofloxacin
(alt if unable to take fluoroquinolone - trimethoprim)
2nd line (on specialist advice) - levofloxacin or co-trimoxazole
20
Q
management of pyelonephritis
A
ORAL cefalexin or ciprofloxacin
(if sensitivity known - co-amoxiclav or trimethoprim)
IV first line if severely unwell or unable to take oral treatment: ceftriaxone cefuroxime ciprofloxacin gentamicin
21
Q
management of pyelonephritis - pregnant women
A
oral first line - cefalexin
IV first line - cefuroxime
22
Q
features of genitourinary TB
A
have a high suspicion in sterile pyuria and those with risk factors (esp HIV +ve), look for high ESR/CRP, ask about past lung TB
dysuria flank pain perineal pain scrotal fistula sterile pyuria - leucocytes in urine haematuria
23
Q
criteria for diagnosing AKI - stage 1
A
rise in creatinine >26 in 48h or increase in creatinine >1.5x baseline
urine output <0.5ml/kg/h for >6 consecutive hours
24
Q
criteria for diagnosing AKI - stage 2
A
increase in creatinine 2-2.9x baseline
<0.5ml/kg/h for >12h consecutive hours UO
25
criteria for diagnosing AKI - stage 3
increase in creatinine >3x baseline or >354 or commenced on RRT irrespective of stage
<0.3ml/kg/h for >24h or anuria for 12h
26
risk factors for developing AKI
```
age >75
CKD
HF
peripheral vascular disease
chronic liver disease
DM
drugs
sepsis
poor fluid intake/increased losses
history of urinary sx
```
27
pre-renal causes of AKI
renal hypoperfusion - hypotension (any cause, inc hypovolaemia, sepsis), renal artery stenosis ± ACEi
28
renal causes of AKI
acute tubular necrosis - commonest intrinsic renal cause of AKI - due to drugs e.g. ahminoglycosides, radiological contrast or myoglobinuria in rhabdomyolysis.
glomerular - autoimmune such as SLE, HSP, drugs, infections, primary glomerulonephritides
interstitial - drugs, infiltration with e..g lymphoma, infection, tumour lysis syndrome
vascular - vasculitis, malignant high BP, thrombus or emboli from angiography, HUS/TTP, dissection.
29
post-renal causes of AKI
caused by urinary tract obstruction
- luminal: stones, clots, sloughed papillae
- mural: malignancy (ureteric, bladder, prostate), BPH, strictures
- extrinsic compression - malignancy (e.g. pelvic), retroperitoneal fibrosis
30
assessment of a patient with an AKI
ABCDE
- check fluid status - check BP, JVP, skin turgor, CRT <2sec, UO (catheterise)
- check an urgent K on a venous blood specimen and an ECG to check for life-threatening hyperkalaemia
31
bedside tests for AKI
DIPSTICK URINE ALWAYS
- infection or glomerular disease
- microscopy for casts, crystals, cells
- culture for infection
- consider Bence Jones Proteins
32
bloods for AKI
U+E, FBC, LFT, CLOTTING, CK, ESR, CRP
consider ABG for acid-base assessment
blood cultures if signs of infection
consider blood film and renal immunology if systemic cause suspected
- immunoglobulins and paraprotein electrophoresis
- complement (c3/4), autoantibodies (ANA, ANCA, anti-GBM)
- ASOT
33
imaging for AKI
renal ultrasound
- distinguishes obstruction and hydronephrosis, and look for abnormalities such as:
- --- cysts
- --- small kidneys
- --- masses
- --- corticomedullary differentiation
- Complete anuria is unusual in AKI and suggests an obstruction
o In elderly men – prostate should be considered – often relieved by catheterisation.
- If catheterization does not resolve anuria and you suspect obstruction above the prostate, get an URGENT USS TO CHECK FOR HYDRONEPHROSIS AND CONSIDER AN URGENT CTKUB (no contrast required), which can show OBSTRUCTING MASSES OR CALCULI.
34
parameters suggesting CKD
small kidneys
anaemia
low calcium
high phosphate
35
indications for dialysis
refractory pulmonary oedema
persistent hyperkalaemia
severe metabolic acidosis (ph <7.2)
uraemia complications such as encephalopathy or uraemic pericarditis
drug overdose - BLAST: barbiturates, lithium, alcohol, salicylates, theophylline
36
management of AKI
assess volume status
- low urine output
- non-visible JVP
- poor tissue turgor
- low BP
- high pulse
signs of fluid overload
- high BP
- high JVP
- lung crepitations
- peripheral oedema
- gallop rhythm on cardiac auscultation
STOP NEPHROTOXIC DRUGS e.g. NSAIDs, ACEi, gentamicin, amphotericin. stop metformin if creatinine >150.
monitor observations hourly.
daily u+e
daily fluid balance and daily weight
treat underlying cause
- pre-renal: iv fluids, treat sepsis with iv abx.
- intra-renal: refer to nephrology early
post-renal: catheterise and consider CTKUB if obstruction likely
RRT - haemodilaysis/ haemofiltration
37
complications of AKI
hyperkalaemia
pulmonary oedema
uraemia
acidaemia
38
ECG changes in hyperkalaemia
Tall Tented T waves
Widened QRS complex
Increased PR interval
small or absent P wave
39
immediate treatment of hyperkalaemia
Do ECG + if ECG changes:
10ml of 10% calcium gluconate
IV insulin and glucose - 10 units of act rapid in 100ml of 20% glucose over 30 mins.
salbutamol nebuliser
IV sodium bicarbonate if patient is acidotic.
40
treatment of pulmonary oedema
sit the patient up
give high flow oxygen
IV furosemide 40mg
diamorphine 2.5mg IV (+anti-emetic e.g. cyclizine)
if no response, haemodialysis or haemofiltration is needed.
consider CPAP
41
prevention of AKI (sick day rules)
```
review drugs
withhold/avoid
- diuretics
- NSAIDs
- ACEi
- Metformin
- abx - gentamicin, nitrofurantoin
```
use opiates with caution as they accumulate in renal failure. oxycodone is better in renal impairment.
radiological contrast
- ensure patient is well hydrated - 1L 0.9% saline over 12 hours pre and post-procedure
42
CKD - definition
Impaired renal function for >3 months based on abnormal structure or function,
OR GFR <60ml/min/1.73m2 for 3 months with or without evidence of kidney damage.
43
stages of CKD
```
stage 1 - >90*
stage 2 - 60-89*
stage 3a - 45-59
stage 3b - 30-44
stage 4 - 15-29
stage 5 - <15
```
*stages 1+2 (eGFR >60) - must have other evidence of renal damage e.g. proteinuria, haematuria, evidence of abnormal anatomy
44
causes of CKD
```
diabetes
hypertension or renovascular disease
glomerulonephritis - IgA nephropathy
Unknown
pyelonephritis and reflux nephropathy
```
45
risk factors for developing ESRF
```
deteriorating function
proteinuria ≥3mg/mmol
haematuria
high BP
young age
```
46
commonest inherited cause of CKD
adult polycystic kidney disease
rare - Alpert's syndrome: CKD, hearing loss, minor eye problems
47
symptoms of uraemia
```
anorexia
vomiting
restless legs
fatigue
weakness
pruritis
bone pain
```
48
causes of rapid decline in renal function
```
infection
dehydration
uncontrolled high BP
metabolic disturbance e.g. high Ca
obstruction
nephrotoxins
```
49
chief cause of death in renal failure
cardiovascular disease
| - falling GFR is an independent risk factor for CVD
50
investigations for CKD
creatinine-based estimate of eGFR (eGFRcreatinine) - advise patient not to eat meat in the 12h before having this blood test.
o Interpret with caution – reduced muscle mass will give an overestimate and increased muscle mass may give an underestimate.
- Cystatin C-based estimate of GFR (eGFRcystatinC), use if:
o An eGFRcreatinine of 45-59, sustained for 90d AND
o No proteinuria (ACR <3)
- early morning urine sample to test for urinary albumin:creatinine ratio (ACR)
- <3 - no proteinuria. no action.
- ≥3-70 - suggests proteinuria, REPEAT TEST WITHIN 3 MONTHS.
- if ≥70 - don't repeat
transient increases in urine ACR may be seen with menstruation, urinary tract infection (UTI), strenuous exercise, and upright posture ('orthostatic proteinuria').
Make a diagnosis of CKD if there is a persistent reduction in renal function (eGFR is <60 mL/min/1.73 m2) and/or proteinuria (urinary ACR is ≥3 mg/mmol) lasting for at least three months.
Check the person's nutritional status, body mass index (BMI), blood pressure, and serum HbA1c and lipid profile to assess for cardiovascular risk factors
51
for which indications should patients with CKD be referred early to a nephrologist.
CKD stage 4+5
moderate proteinuria (ACR ≥70) unless due to DM and already treated.
proteinuria (ACR ≥30) with haematuria
rapidly falling egfr (>15 in 1year or >10 in 5years)
high BP poorly controlled despite ≥4 antihypertensives
known or suspected rare or genetic cause of CKD
suspected renal artery stenosis
52
management of CKD
1. Investigation - identify and treat reversible causes - relieve obstruction, stop nephrotoxic drugs, deal with high Ca, and cardiovascular risk (stop smoking, healthy weight), tight glucose control in DM.
2. Limit progression
- BP (target <140/90). treat with ACEi or ARB in diabetic kidney disease even if normal BP.
- Renal bone disease: low vitamin D, high phosphate, low calcium
- Secondary hyperparathyroidism - due to low calcium, high phosphate and low vitaminD. can cause a Brown tumour in bones.
severe clinical manifestations
- osteitis fibrosa cystica (hyperparathyroid bone disease)
- osteomalacia - due to low vit D
- osteoporosis
- osteosclerosis
phosphate rises in CKD, which increases PTH further, also precipitates in the kidney and vasculature.
- restrict diet, give binders (e.g. Calcichew) to reduce gut absorption.
- vitamin D
offer colecalciferol or ergocalciferol to treat vit D deficiency first.
- if vit D deficiency has corrected but sx of CKD mineral and bone disease persist --> vitamin D analogues (e.g. calcitriol) to people with GFR ≤30.
offer bisphosphonates to prevent and treat osteoporosis in its with GFR ≥30.
cardiovascular modification - give stains and aspirin.
diet - healthy, moderate protein diet, K restriction if hyperkalaemic, avoidance of high phosphate foods (milk, cheese, eggs)
53
symptom control in CKD
ANAEMIA
o Most significant reason is REDUCED ERYTHROPOIETIN LEVELS.
Gives a normocytic normochromic anaemia
Becomes apparent when GFR <35ml/min
Anaemia in CKD predisposes to the development of LEFT VENTRICULAR HYPERTROPHY – associated with a three fold increase in mortality in renal patients.
o Check haematinics and replace iron/b12/folate if necessary
o if still anaemic, consider recombinant EPO
ACIDOSIS
- consider sodium bicarbonate supplements
OEDEMA
- high doses of loop diuretics may be needed (e.g. furosemide + metalozone each morning) and restriction of fluid and sodium intake.
RESTLESS LEGS/CRAMPS
- clonazepam or gabapentin
or
dopamine agonists
54
types of dialysis
haemodialysis
haemofiltration
peritoneal dialysis - risk of PF peritonitis (due to s. epidermidis/aureus)
55
indications for emergency dialysis
AEIOU
- Acidosis
- Electrolytes (refractory K)
- Intoxicants (lithium)
- Overload (fluid) when diuresis isn’t working (refractory)
- Uraemia (pericarditis, encephalitis)
56
absolute c/i to renal transplant
active infection
cancer
severe co-morbidity
57
triple therapy used to maintain immunosuppression in transplant patients
tacrolimus/ciclosporin
azathioprine/mycophenolate
prednisolone
58
complications of transplants
surgical - bleed, thrombosis, infection, urinary leaks, lymphocyte, hernia
delayed graft function - acute tubular necrosis in graft due to ischaemic-perfusion injury.
rejection
drug toxicity
infection - HSV, candida, pneumocystis jerovecii, CMV
malignancy
cardiovascular disease - leading cause of death in transplant patients.
59
important bloods to check before biopsy (renal)
FBC
CLOTTING
G+S
stop anticoagulants
- aspirin 1 week before
- warfarin 2-3d before
- LMWH - 24h before
60
indications for renal biopsy
- unexplained AKI/CKD
- acute nephritic syndromes
- unexplained proteinuria and haematuria
- systemic diseases associated with kidney dysfunction
- suspected transplant rejection
- to guide treatment
61
what is glomerulonephritis
inflammation of the glomeruli and nephrons
62
what are the consequences of inflammation
damage to the glomerulus restricts blood flow, leading to compensatory high BP (activation of renin-angiotensin system).
damage to the filtration mechanism allows protein and blood to enter the urine.
loss of usual filtration capacity leads to AKI
63
presentation of nephrotic syndrome
hypoalbuminaemia
proteinuria
oedema
hyperlipidaemia
64
presentation of nephritic syndrome
haematuria
proteinuria
hypertension
oliguria
65
causes of nephrotic syndrome
membranous nephropathy
minimal change disease
focal segmental glomerulosclerosis
mesangiocapillary GN
66
causes of nephritic syndrome
```
IgA nephropathy
post-streptococcal nephropathy
vasculitis
SLE
anti-GBM disease
cryoglobulinaemia
```
mesangiocapillary GN
67
investigations for glomerulonephritis
bloods - FBC, U+E, LFT, ESR, CRP, IgA, electrophoresis, complement
autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM
blood culture
ASOT
HBsAg
anti-HCV
urine
- RBC casts
- MC&S
- bence jones protein
- ACR
imaging
- CXR
- renal ultrasound
RENAL BIOPSY - gold standard for glomerulonephritis.
68
general management of glomerulonephritis
early referral to a nephrologist.
keep BP <130/80 or <125/75 if proteinuria >1g/d
include an ACEi or ARB - reduce proteinuria and preserving renal function.
69
what is IgA nephropathy
most present with macroscopic or microscopic haematuria - occasionally nephritic syndrome.
typical patient - young man with episodic macroscopic haematuria, recovery is often rapid between attacks.
increased IgA possibly due to infection, which forms immune complexes and deposits in mesangial cells.
occurs DURING OR STRAIGHT AFTER a streptococcal infection.
70
what would you find on renal biopsy for IgA nephropathy
mesangial proliferation, immunofluorescence shows deposits of IgA and C3
high serum IgA
normal C3
71
treatment of IgA nephropathy
BP control with ACEi.
| immunosuppression may slow decline of renal function.
72
What is Henoch-Schönlein purpura
it is similar to IgA nephropathy but has a systemic picture.
causes a small vessel vasculitis.
73
features of HSP
features
- Purpuric rash on extensor surfaces (legs, buttocks)
- fitting polyarthritis
- abdominal pain - GI bleeding (maleana, haematemesis)
- Nephritis
74
diagnosis of HSP
clinical.
| confirmed with positive IF for IgA and C3 in skin or renal biopsy.
75
treatment of HSP
BP control with ACEi
Ibuprofen - for joint pain
Steroid treatment for bowel symptoms in children.
Skin rash - dapsone
76
what is Goodpasture's disease
anti-glomerular basement membrane disease
caused by autoantibodies to type IV collagen.
type IV collagen is found in the kidneys and lungs.
77
presentation of good pasture's syndrome
```
haematuria/nephritic syndrome
pulmonary haemorrhage (haemoptysis)
```
78
treatment of good pasture's syndrome
plasma exchange
steroids
± cytotoxics
79
what is post-streptococcal GN
Occurs MANY WEEKS AFTER A SORE THROAT OR SKIN INFECTION.
streptococcal antigen is deposited on the glomerulus, causing a host reaction and immune complex deposition.
80
presentation of post-streptococcal GN
nephritic syndrome
81
investigation for post-streptococcal GN
high ASOT
| Low C3
82
treatment for streptococcal GN
supportive
83
what forms rapidly progressive GN
1. immune complex deposition e.g. post-infectious GN, SLE, IgA/HSP
2. pauci-immune disease (80-90% ANCA +ve) - granulomatosis with polyangiitis: c-ANCA +ve,
microscopic polyangiitis (p-ANCA +ve),
churg-strauss syndrome
3. anti-GBM disease
84
presentation of patients with rapidly progressive GN
AKI
| fever, myalgia, weight loss, haemoptysis.
85
commonest reason for death in rapidly progressive GN
pulmonary haemorrhage
86
treatment of rapidly progressive GN
aggressive immunosuppression with high-dose IV steroids and cyclophosphamide
± plasma exchange
87
which type of GN is caused by hepatitis B/C
membranous nephropathy (hep B)
mesangiocapillary GN (hep C)
88
which type of GN is caused by SLE
class V lupus nephritis causes membranous nephropathy
89
in diabetic nephropathy, which specific nodules are found on biopsy
Kimmelstein-Wilson nodules
90
in amyloidosis, what is found on biopsy specifically
apple green birefringence (nodular)
91
which drugs can cause nephrotic syndrome
NSAIDs
penicillamine
anti-TNF
gold
92
pathophysiology of nephrotic syndrome
injury to the podocyte - effacement of the foot processes and loss of podocytes causes heavy protein loss
93
presentation of nephrotic syndrome
patients present with pitting oedema (ankles, shins, periorbitally)
94
investigations of nephrotic syndrome
urine dip: protein ++++
albumin low on LFT
?renal biopsy
95
ddx of nephrotic syndrome
CCF - high JVP, pulmonary oedema, mild proteinuria
liver disease - low albumin
96
management of minimal change disease
STEROIDS - common in children.
97
complications of nephrotic syndrome
susceptibility to infection e.g. cellulitis, strep infections and SBP.
thromboembolism (40%) - hypercoagulable state due to high clotting factors and platelet abnormalities.
hyperlipidaemia - hepatic lipoprotein synthesis in response to low oncotic pressure.
98
treatment of nephrotic syndrome
reduce oedema - loop diuretics e.g. furosemide.
- daily weights and daily U+Es
- fluid restrict to 1L/d and salt restrict while giving diuretics.
reduce proteinuria
- ACEi/ARB
reduce risk of complications
- anticoagulate if nephrotic range proteinuria
- statin to reduce cholesterol
- treat infections promptly and vaccinate
treat underlying cause
99
minimal change disease biopsy
normal under light microscopy
electron microscopy - effacement of the podocyte foot processes.
rx
- 90% children and 70% adults undergo remission with steroids.
(if relapsing and steroid-dependent) - cyclophosphamide or ciclosporin/tacrolimus
100
associations of membranous nephropathy
malignancy
hep B
drugs (gold, pencillamine, NSAIDs)
autoimmune disease (thyroid, SLE)
101
biopsy of membranous nephropathy
diffusely thickened GBM with IgG and C3 sub epithelial deposits on immunofluorescence.
102
treatment of membranous nephropathy
secondary - treat underlying cause
| idiopathic - ACEi/ARB and diuretics
103
associations of focal segmental glomerulosclerosis (FSGS)
```
primary - idiopathic
secondary
- vesicoureteric reflux
- IgA nephropathy
- Alport syndrome
- Vasculitis
- SCD
- Heroin use
- HIV
```
104
presentation of FSGS
nephrotic syndrome or proteinuria
105
treatment of FSGS
responds to corticosteroids in 30%
| cyclophosphamide or ciclosporin - if steroid resistant
106
associations of mesangiocapillary GN
Immune complex mediated - hepatitis C, SLE, monoclonal gammopathies.
107
treatment of mesangiocapillary GN
underlying cause as priority
| ACEi/ARB
108
where do loop diuretics act on the kidney
Na/K/2Cl co-transporter on the thick ascending loop of Henle
cause hypokalaemia, hyponatraemia, alkalosis (H+ excretion increased), hypocalcaemia.
can be ototoxic in high doses
109
where do thiazide diuretics act
inhibit NaCl transporter in the DISTAL CONVOLUTED TUBULE
cause
- hypokalaemia
- hyponatraemia
- hypomagnesaemia
- high uric acid (gout)
- reduce urinary calcium
110
k-sparing diuretics SEs
hyperkalaemia
metabolic acidosis (reduced H excretion)
gynaecomastia
111
where do carbonic anhydrase inhibitors act
proximal convoluted tubule
112
where do k-sparing diuretics act
cortical collecting tubule
113
another name for IgA nephropathy
Berger's disease
114
presentation of granulomatosis with polyangiitis (Wegener's )
upper respiratory tract: epistaxis, sinusitis, nasal crusting.
lower respiratory tract:
- dyspnoea
- haemoptysis
rapidly progressive GN (pauci-immune)
saddle-shaped nose deformity
also - vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
c-ANCA positive
115
test for microscopic polyangiitis
p-ANCA
116
presentation of churg strauss syndrome
present with asthma, allergic rhinitis, purpura, peripheral neuropathy.
p-ANCA positive
peripheral eosinophilia
117
inheritance of aport syndrome
x-linked (affects males usually)
118
presentation of alport syndrome
microhaematuria persistent with intermittent gross haematuria.
hearing loss
eye abnormalities
119
drug that causes SLE + nephritic syndrome
Infliximab
120
presentation of SLE
A RASH POINTs MD
arthritis
renal disease (proteinuria, cellular casts)
ANA +ve
serositis (pleurisy or pericarditis)
haematological disorders (haemolytic aneamia/leucopenia/thrombocytopenia)
photosensitivity
oral ulcers
immunological disorder (anti-dsDNA, anti-Sm)
neurological disorders (seizures or psychosis)
malar rash
discoid rash
121
rapidly progressive GN biopsy findings
CRESCENT FORMATION
monocytes
macrophages
122
urinalysis findings of nephritic syndrome
haematuria
RBC casts
proteinuria
123
management of nephritic syndrome
low-sodium diet
water restriction
proteinuria and/or HTN - ACEi or ARBs
severe HTN and/or oedema - diuretics
severe kidney failure - RRT
124
look at this summary of nephrotic syndrome causes
- Minimal change = children/young people. steroid responsive.
- Membranous disease = common in lupus, malignancy, HEP B
- FSGS = heroin use and HIV
125
look at this summary of nephritic syndrome causes
- IgA nephropathy – occurs during or straight after viral infection. ACEi effective.
- Post-strep nephropathy – occurs many weeks after viral infection. self-limiting, spontaneous and remission within 6-8 weeks.
- vasculitic (ANCA) – patients will mention nose bleeding, feeling of congestion and generalized myalgia.
o Wegeners – c-ANCA
- Anti-GBM: usually causes renal disease and pulmonary haemorrhage (haemoptysis)
- SLE – butterfly rash, nephritis, low c3/c4, low hb, low plt, anti-dsdna, ANA
- Alport syndrome – ADPKD (renal disease) + ocular problems + hearing loss
126
what is cryoglobulinaemia
form of vasculitis
presence of cryoglobulins (proteins) that clump together at cold temp, restricting blood flow and causing damage to the skin.
high platelets
high C3/C4
ANCA negative
elderly patients
associated with HEPATITIS C
127
cause of acute interstitial nephritis
immune reaction drugs, infections or autoimmune disorders.
drugs
- NSAIDs
- Abx - penicillins
- diuretics - furosemide
- allopurinol
- omeprazole
- phenytoin
infections
- staph
- streps
- brucella
- leptospira
immune causes
- SLE
- sarcoid
128
features of acute interstitial nephritis
'allergic' picture - fever, rash, peripheral eosinophilia.
fever, rash, arthralgia, hypertension
mild renal impairment
129
investigation of acute interstitial nephritis
sterile pyuria
| white cell casts
130
treatment of acute interstitial nephritis
stop/treat causative agent
| if renal function doesn't improve within a week -> trial of prednisolone for 4 weeks may improve prognosis.
131
common cause of chronic tubulointerstitial nephritis
analgesic nephropathy
132
what is analgesic nephropathy
history is of chronic, heavy analgesic use, usually NSAIDs
commoner in pain
133
presentation of analgesic nephropathy
loin pain (papillary necrosis) but is often silent until late CKD
134
cause of urate nephropathy
AKI due to uric acid precipitation within the tubules.
most often due to tumour lysis syndrome, seen in haematological malignancies after chemotherapy, which leads to overproduction of uric acid.
the renal parenchyma appears bright on USS.
plasma urate is often markedly raised with urinary birefringent crystals on microscopy.
rx
- keep well hydrated
- oral allopurinol before chemotherapy
- urinary alkalinisation with sodium bicarbonate (increased solubility of uric acid).
135
treatment of hypercalcaemia
rehydration with iv fluids
| pamidronate (iv bisphosphonates)
136
drugs toxic to the kidney - cause AKI usually by direct acute tubular necrosis, or by causing interstitial nephritis
NSAIDs
Antimicrobials - gentamicin, rifampicin, sulphonamides, penicillins
anticonvulsants - lamotrigine, valproate, phenytoin
other drugs - omeprazole, furosemide, thiazides, ACEi/ARBs, cimetidine, lithium, iron, cisplatin.
radiocontrast
137
radio contrast nephropathy - cause and treatment
iatrogenic AKI with iv contrast
tx
- stop nephrotoxic drugs
- pre-hydrate with iv 0.9% saline
- then give saline after imaging - 0.9% saline iv
138
what is rhabdomyolysis
results from skeletal muscle breakdown with release of its contents into the circulation, including myoglobin, K, phosphate, urate and CK.
139
complications of rhabdomyolysis
hyperkalaemia
AKI
myoglobin is filtered by the glomeruli and precipitates, obstructing renal tubules.
140
causes of rhabdomyolysis
post-ischaemia e.g. embolism, clamp on artery during surgery.
trauma
prolonged immobilisation
e.g. falling in elderly
burns
crash injury
excessive exercise
uncontrolled seizures
drugs and toxins - statins, alcohol, ecstasy, heroin, snake bite, carbon monoxide, neuroleptic malignant syndrome.
infections - coxsackie, EBV, influenza
metabolic - low K, low phosphate, myositis, malignant hyperpyrexia
inherited muscle disorders e.g. McArdle's disease, Duchenne's muscular dystrophy.
141
clinical features of rhabdomyolysis
muscle pain
swelling
tenderness
red-brown urine (myoglobinuria)
142
tests for rhabdomyolysis
plasma CK >1000
exclude MI as a cause (troponin negative)
visible myoglobinuria (tea or cola coloured urine)
others
- high phosphate
- high potassium
- low calcium (enters muscles)
- high urate
AKI develops 12-24h later and DIC is associated
143
treatment of rhabdomyolysis
urgent treatment for hyperkalaemia
IV fluid rehydration is a priority to prevent AKI - maintain urine output at 300ml/h until myoglobinuria has ceased, initially up to 1.5l fluid/h may be needed.
iv sodium bicarbonate - to alkalinise urine to ph >6.5.
dialysis may be needed.
ideally manage pt in HDU/ICU setting to allow early detection of deterioration and regular bloods and monitoring.
144
what is renovascular disease
defined as stenosis of the renal artery or one of its branches.
145
causes of renovascular disease
atherosclerosis (80%) - co-existing IHD, stroke or PVD
fibromuscular dysplasia (10%) - younger males
rarer causes
- takayasu's arteritis
- antiphospholipid syndrome
- post-renal transplant
- thromboembolism
- external compression
146
signs of renovascular disease
high BP resistant to treatment,
worsening renal function after ACEi/ARB in bilateral renal artery stenosis
'flash' PULMONARY OEDEMA (sudden onset - no LV impairment on echo)
weak leg pulses can be found
147
investigation for renovascular disease
ultrasound - renal size asymmetry (affected side smaller)
doppler USS - disturbance in renal blood flow
CT/MR angiography - more sensitive
RENAL ANGIOGRAPHY - GOLD STANDARD (done after CT)
148
treatment of renovascular disease
comprehensive antihypertensive regimens.
transluminal angioplasty ± stent placement or revascularisation surgery.
149
what is haemolytic uraemic syndrome
characterised by microangiopathic haemolytic anaemia (MAHA) - intravascular haemolytic + red cell fragmentation.
endothelial damage triggers thrombosis, platelet consumption and fibrin strand deposition, mainly in renal microvasculature.
strands cause mechanical destruction of passing RBCs
thrombocytopenia and AKI result.
150
causes of HUS
E.coli O157 - produces a verotoxin that attacks endothelial cells.
typically affects young children in outbreaks after eating undercooked contaminated meat.
151
signs of HUS
abdominal pain
bloody diarrhoea
AKI
152
tests for HUS
```
haematuria/proteinuria
blood film - SCHISTOCYTES (fragmented RBC)
low platelets
low Hb
clotting tests normal
```
153
treatment of HUS
seek expert advice
dialysis for AKI may be needed
plasma exchange used in severe disease
154
what is thrombotic thrombocytopenic purpura (TTP)
HAEMATOLOGICAL EMERGENCY
all patients have a MAHA (severe with jaundice) an LOW PLATELETS.
155
5 cardinal symptoms of TTP
```
Fever
MAHA
AKI
Low platelets
Neuro symptoms (seizures, hemiparesis, reduced vision, low GCS)
```
156
pathophysiology of TTP
genetic or acquired deficiency of a protease (ADAMTS13) that normally cleaves multimeters of vWF.
o Large vWF multimers form, causing platelet aggregation and fibrin deposition in small vessels, leading to microthrombi
157
causes of TTP
idiopathic (40%)
```
autoimmune - SLE
cancer
pregnancy
drugs - quinine
bloody diarrhoea (childhood HUS)
```
158
investigations for TTP
```
haematuria/proteinuria
blood film - schistocytes
low platelets
low Hb
clotting normal
```
159
treatment for TTP
URGENT PLASMA EXCHANGE
steroids for non-responders
eculizumab
- the unexplained occurrence of thrombocytopniea and anaemia should prompt immediate consideration of the diagnosis and evaluation of a peripheral blood smear for evidence of maha.
160
what is important control in patients with diabetes to prevent end-organ damage
BLOOD PRESSURE
| + good BM control
161
screening for nephropathy in DM
ACR - for microalbuminuria
162
treatment of microalbuminuria in DM
ACEi or ARB (IRRESPECTIVE OF BP)
Manage cardiovascular risk factors - stop smoking, reduce cholesterol, consider aspirin
163
symptoms of cholesterol emboli
fever, uncontrolled high BP, lived reticularis, oliguria, AKI, gangrene
164
what is renal tubular acidosis
- Metabolic acidosis due to impaired acid secretion by the kidney
- HYPERCHOLARAEMIC METABOLIC ACIDOSIS WITH A NORMAL ANION GAP.
165
what is type 1 renal tubular acidosis
inability to excrete H and generate acidic urine in the distal tubule, even in states of metabolic acidosis.
166
causes of type 1 renal tubular acidosis
idiopathic
connective tissue disease - marfans, ehlers danlos
autoimmune - SLE, Sjogrens (commonest cause)
nephrocalcinosis (e.g. hypercalcaemia)
tubulointerstitial disease e.g. chronic pyelonephritis, chronic interstitial nephritis
drugs - lithium
167
features of type 1 renal tubular acidosis
rickets (+growth failure) or osteomalacia, due to buffering of H with calcium in bone.
NEPHROCALCINOSIS WITH RENAL CALCULI, leading to recurrent UTIs --> combination of hypercalciuria, low urinary citrate and alkaline urine (all favour calcium phosphate stone formation).
168
treatment of type 1 renal tubular acidosis
oral sodium bicarbonate or citrate
169
difference between type 1 and type 2 RTA
type 1 is linked with renal calculi
170
what is type 2 RTA
- ‘Bicarbonate leak’: a defect in HCO3- reabsorption in the proximal tubule resulting in excess HCO3- in the urine (pH <5.5) leading to a metabolic acidosis
171
causes of type 2 RTA
o Idiopathic
o Fanconi syndrome
o Tubulointersitial disease e.g. myeloma, interstitial nephritis
o Drugs (e.g. lead or other heavy metals, acetazolamide, out-of-date tetracycline)
172
electrolyte imbalance in type 2 RTA
hypokalaemia
173
treatment of type 2 RTA
high doses of bicarbonate
174
what is type 4 RTA
due to hypoaldosteronism - causes hyperkalaemia and acidosis
175
causes of type 4 RTA
addisons
diabetic nephropathy
o INTERSTITIAL NEPHRITIS (SLE, chronic obstruction)
o DRUGS (K-sparing diuretics, beta-blockers, NSAIDs, ciclosporin)
176
treatment of type 4 RTA
remove cause
fludrocortisone 0.1mg
calcium resonium - to control K
177
what is fanconi syndrome
proximal tubular dysfunction leading to loss of amino acids, glucose, phosphate and HCO3 in urine.
178
features of fanconi syndrome
dehydration
metabolic acidosis
osteomalacia/rickets
electrolyte abnormalities
179
congenital causes of fanconi syndrome
```
idiopathic
cysteinosis
wilsons disease
tyrosinaemia
lowe syndrome
```
180
acquired causes of fanconi syndrome
Heavy metal poisoning (lead, mercury, cadmium, platinum, uranium)
Drugs (gentamicin, cisplatin, ifosfamide)
Light chains (Myeloma, amyloid)
Sjogrens
181
treatment of fanconi syndrome
o REMOVE ANY CAUSE
o REPLACE LOSSES
o K, HCO3-, PHOSPHATE AND VITAMIN D SUPPLEMENTS
182
what is bartter syndrome
hereditary hypokalaemic tubulopathies
- Low K
- metabolic alkalosis
- hypercalciuria
183
causes of bartter syndrome
inherited mutation in the co-transporter targeted by LOOP DIURETICS
184
treatment of bartter syndrome
```
replace K
give indomethacin (prostaglandin synthesis inhibitor)
```
185
what is gitelman syndrome
hereditary hypokalaemic tubulopathies
- Low K
- metabolic alkalosis
- hypocalciuria
- Low Mg
186
cause of gitelman syndrome
o Inherited mutation in the co-transporter targeted by THIAZIDE DIURETICS
187
treatment of gitelman syndrome
replace Mg + K
188
which genes are affected in ADPKD
PKD1 - 85% (chromosome 16)
| PKD2 - 15% (chromosome 4)
189
signs of ADPKD
renal enlargement with cysts
abdo pain/flank pain/chest pain/back pain
haematuria
cyst infection (e.coli, staph aureus)
renal calculi
high BP (ACEi/ARB first line)
progressive renal failure
190
extra-renal manifestations of ADPKD
```
liver cysts - 70%
intra-cranial aneurysms (SAH)
mitral valve prolapse
ovarian, pancreatic and spleen cysts.
diverticular disease
```
191
investigation for ADPKD
CT abdomen to diagnose
192
screening for ADPKD
abdominal USS
≥2 cysts, unilateral or bilateral if aged <30y
≥2 cysts in both kidneys if aged 30-59y
≥4 cysts in both kidneys if aged ≥60y
193
treatment of ADPKD
monitor U+E
high BP - treat aggressively with ACEi/ARB (target <130/80)
treat infections, dialysis or transplant for ESRF, genetic counselling.
selected patients - TOLVAPTAN (vasopressin receptor 2 antagonist) may be an option - slows progression of cyst development.
194
what is autosomal recessive PKD associated with
childhood - renal cysts and hepatic fibrosis
195
what is medullary cystic disease
inherited disorder with tubular loss and medullary cyst formation.
juvenile - autosomal recessive (10-20% of ESRF in children)
adult - AD is rare
196
signs of medullary cystic disease
shrunken kidneys
cysts restricted to renal medulla
salt wasting
```
polyuria
polydipsia
enuresis
failure to thrive
ESRF
```
197
extra-renal features of medullary cystic disease
```
retinal degeneration
retinitis pigmentosa
skeletal changes
cerebellar ataxia
liver fibrosis
```
198
signs of tuberous sclerosis
autosomal dominant disorder
signs
- 'ash leaf' macules
- shagreen patches
- angiofibromas
- periungual fibroma
- adenoma sebaceum
- low IQ
- epilepsy
- infantile spasms
199
what is von hippel landeau syndrome
chief cause of inherited renal cancers.
other cancers its associated with:
- eyes
- spinal cord
- brain
- phaeochromocytoma
- pancreas
200
what is alport syndrome
x-linked inherited disorder
201
signs of alport syndrome
renal - haematuria, proteinuria, progressive renal failure
ears - sensorineural deafness
eyes - ocular defects
202
biopsy signs of alport syndrome
thickened GBM with 'splitting'
203
what are the different stages of diabetic nephropathy
1. GFR elevated - renal blood flow increases, increasing the GFR and leading to microalbuminuria.
2. Glomerular hyperfiltration
- in the next 5-10y, mesangial expansion gradually occurs and hyper filtration at the glomerulus seen without microalbuminuria.
3. Microalbuminuria
- indicates progression of disease.
4. Nephropathy
- GFR declines and proteinuria increases
204
what is the pathgnomic finding in myeloma
bence jone proteins in the urine
| myeloma kidney is due to blockage of tubules by CASTS, consisting of light chains.
205
features of kidney myeloma
AKI
CKD
amyloidosis
hypercalcaemic nephropathy
206
treatment of kidney myeloma
FLUID INTAKE 3litres/d to prevent further impairment.
dialysis may be required in AKI
207
clinical features of hypercalcaemia
'bones, stones, groans, psychic moans'
```
abdominal pain
vomiting
constipation
polyuria
polydipsia
```
```
depression
anorexia
weight loss
tiredness
weakness
```
painful bones - osteitis fibrosa cystica
hypertension
confusion
pyrexia
renal stones
renal failure
ectopic calcification e.g. cornea
cardiac arrest
reduced QT interval
208
where do renal calculi most commonly deposit in the renal tract
```
pelviureteric junction (PUJ)
pelvic brim
vesicoureteric junction (VUJ)
```
209
types of renal calculi
```
calcium oxalate/phosphate
magnesium ammonium phosphate (struvite)
urate
cystine
mixed
```
210
presentation of renal colic
excruciating ureteric spasms 'loin to groin' pain
nausea and vomiting
often cannot sit/lie still
LUTS - dysuria, frequency, urgency
or pyelonephritis sx (fever, rigors, loin pain, nausea, vomiting)
haematuria
211
tests for renal calculi
BLOODS - FBC, U+E, CALCIUM, GLUCOSE, BICARBONATE, URATE
urine dipstick - blood +++ (gross or microscopic haematuria)
urine ph
>7 - urea splitting organisms and struvite stones
<5 - uric acid stones
```
urine microscopy (may detect crystals)
- dumbbell-shaped or octahedron-shaped crystals - calcium oxalate
```
- rhomboid/needle-shaped crystals - uric acid stones
- rectangular prisms - struvite stones
MSU - MC&S
212
imaging for renal calculi
NON-CONTRAST CT KUB
KUB XR
- x-ray positive (radio-opaque) - calcium-containing stones
- x-ray negative (radiolucent) - uric acid stones
ULTRASOUND
- to look for hydronephrosis or hydroureter
- done in patients in whom radiation exposure should be minimised - pregnant, children, recurrent stone formers.
213
initial management of renal calculi
ANALGESIA e.g. diclofenac 75mg IV/IM
- offer iv paracetamol to adults, children and young people if NSAIDs C/I or are not giving sufficient pain relief.
- consider opiates next in line if still in pain.
IV FLUIDS
antibiotics (cefuroxime or gentamicin) if infection
214
management - ureteric/renal stones <5mm
90-95% pass spontaneously
watchful waiting
increase fluid intake
215
management - ureteric stone 5-10mm
offer medical expulsive therapy first if distal - alpha blocker (tamsulosin) or nifedipine.
if still persistnet
1. ESWL
2. URS
216
management - ureteric stone >10mm
1st line - Ureteroscopy
2nd line - Extracorporeal shockwave lithotripsy (ESWL)
217
management - kidney stones 5-10mm
1st line - Extracorporeal shockwave lithotripsy (ESWL)
2nd line - Ureteroscopy (URS)
218
management - kidney stone 10-20mm
1st line - ESWL or URS
2nd line - PCNL (PERCUTANEOUS NEPHROLITHOTOMY)
219
management - kidney stone >20mm (inc staghorn)
1st line - PCNL (PERCUTANEOUS NEPHROLITHOTOMY)
2nd line - URS
220
management - sepsis/anuria in an obstructed kidney
1st line - Abx and ureteric stenting
or
Abx + percutaneous NEPHROSTOMY
221
indications for urgent intervention
presence of infection and obstruction - a percutaneous nephrostomy or ureteric stent may be needed to relieve obstruction.
```
urosepsis
intractable pain or vomiting
impending acute renal failure
obstruction in a solitary kidney
bilateral obstructing stones
```
222
prevention of renal calculi
DRINK PLENTY OF FLUIDS
normal dietary calcium
reduce salt intake to <6g
calcium stones - in hypercalciuria, a thiazide diuretic is used to reduce calcium excretion.
oxalate - reduce oxalate intake. pyridoxine may be used.
struvite - treat infection promptly. common in UTIs. PROTEUS causes alkaline urine and calcium precipitation and ammonium salt formation.
urate - allopurinol - urine alkalisation may also help, as urate is more soluble at ph >6 (with potassium citrate or sodium bicarbonate).
cystine - vigorous hydration to keep urine output >3L/d and urinary alkalinisation. d-penicillinamine is used to chelate cystine, given with pyridoxine to prevent vitamin B6 deficiency.
223
cause of calcium phosphate stones
hyperparathyroidism
| type 1 renal tubular acidosis
224
cause of struvite stones
PROTEUS
recurrent UTIs
formed of Mg, ammonium and phosphate
225
cause of urate stones
low urine pH
hyperuricaemia, gout, hyperuricosuria
RADIOLUCENT (requires CTKUB)
226
cause of cystine stones
inherited recessive disorder - renal tubular defect
227
which medications precipitate renal stones
```
diuretics
antacids
acetazolamide
corticosteroids
theophylline
aspirin
allopurinol
vit C and D
indinavir
```
228
predisposing factors of renal calculi - urinary tract abnormalities
```
pelviureteric junction obstruction
hydronephrosis
horseshoe kidney
vesicoureteric reflux
medullary sponge kidney
```
229
cause of urinary tract obstruction
luminal
- stones
- blood clot
- sloughed papilla
- tumour - renal, ureteric, bladder
mural
- congenital or acquired stricture
- neuromuscular dysfunction
- schistosomiasis
extra-mural
- abdominal or pelvic mass/tumour
- retroperitoneal fibrosis
- iatrogenic - post-surgery
230
features of acute upper urinary tract obstruction
loin to groin pain
± superimposed infection
± loin tenderness or an enlarged kidney
231
features of chronic upper tract obstruction
flank pain
renal failure
superimposed infection
polyuria - impaired urinary conc
232
features of acute lower urinary tract obstruction
acute urinary retention
severe suprapubic pain
distended, palpable bladder, dull to percussion
233
features of chronic lower urinary tract obstruction
sx - urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence.
signs - distended, palpable bladder
234
tests for urinary tract obstruction
ULTRASOUND
if there is hydronephrosis or hydroureter --> arrange a CT KUB
235
treatment of upper urinary tract obstruction
NEPHROSTOMY OR URETERIC STENT (hydronephrosis)
236
treatment of lower urinary tract obstruction
URETHRAL OR SUPRAPUBIC CATHETER
beware a large diuresis after relief of obstruction - temporary salt-losing nephropathy may occur resulting in the loss of several litres of fluid a day
(monitor weight, fluid balance and U+E closely)
237
what is periaortitis
retroperitoneal fibrosis
Chronic periaortitis is inflammation caused by advanced atherosclerosis (affecting the infrarenal portion of the abdominal aorta).
causes ureteric obstruction resulting in renal failure.
risk of AAA rupture
238
causes of periaortitis
idiopathic retroperitoneal fibrosis (IRF)
inflammatory AAA
perianeurysmal RF
239
consequences of idiopathic retroperitoneal fibrosis
ureters get embedded in dense, fibrous tissue resulting in progressive bilateral ureteric obstruction.
240
presenting features of periaortitis
middle aged male
vague loin, back or abdo pain
high BP
unilateral or bilateral hydronephrosis and consequent renal insufficiency
241
tests for periaortitis
bloods - high urea and creatinine, high ESR, high CRP, anaemia.
ultrasound - dilated ureters (hydronephrosis)
CT/MRI - periaortic mass
242
treatment of periaortitis
retrograde stent placement to relieve obstruction
± ureterolysis
immunosuppression with low dose steroids
243
causes of acute retention
```
prostatic obstruction
urethral strictures
anticholinergics
alcohol
constipation
post-op
infection
cauda-equina syndrome
carcinoma
```
244
examination for acute retention
abdominal exam
DRE of prostate
perianal sensation
245
tests for acute retention
```
MSU
U+E
FBC
PSA
renal ultrasound if renal impairment
```
246
conservative measures to aid voiding in acute urinary retention
```
analgesia
privacy on hospital wards
ambulation
standing to void
voiding to the sound of running tap
```
247
management of acute retention
catheterise and start an alpha-blocker (tamsulosin)
if in clot retention --> 3-way catheter and bladder washout.
if >1L residual check U+E and monitor for post-obstructive diuresis.
after 2-3days trial without catheter (TWOC) may work
248
prevention of acute retention
in males - finasteride to reduce prostate size
249
presentation of chronic urinary retention
overflow incontinence
acute on chronic retention
lower abdominal mass
UTI or renal failure
250
causes of chronic urinary retention
prostatic enlargement common
pelvic malignancy
rectal surgery
DIABETES
251
management of chronic urinary retention
- ONLY CATHETERISE PATIENT IF THERE IS PAIN, URINARY INFECTION, OR RENAL IMPAIRMENT.
- Institute definitive treatment promptly
- Intermittent self-catheterisation is sometimes required
252
what is benign prostatic hyperplasia
benign nodular or diffuse proliferation of musculofibroid and glandular layers of the prostate.
Inner (transitional) zone enlarges in contrast to peripheral layer expansion seen in prostate carcinoma.
253
features of BPH
LUTS
- nocturia
- frequency
- urgency
- post-micturition dribbling
- poor stream/flow
- hesitancy
- overflow incontinence
- haematuria
- bladder stones
- UTI
254
investigation for BPH
digital rectal examination - symmetrically enlarged, smooth, firm, non-tender prostate with rubbery texture.
MSU
U+E
USS (hydronephrosis)
PSA ± transrectal USS + biopsy
255
lifestyle advice for mx of BPH
avoid caffeine/alcohol
relax when voiding
void twice in a row to aid emptying
control urgency by practising distraction methods.
train the bladder by 'holding on' to increase between voiding.
256
pharmacological therapy for BPH
alpha blocker - tamsulosin
(reduces smooth muscle tone of prostate and bladder)
SE - drowsiness, dry mouth, weight gain, depression, hypotension
5-alpha reductase inhibitors e.g. finasteride
(reduce testosterone conversion to dihydrotestosterone)
- excreted in semen - so warn to use condoms.
SE - impotence, reduced libido.
257
surgery for BPH
transurethral resection of prostate (TURP)
- crossmatch 2units
- beware bleeding, clot retention and TUR syndrome
transurethral incision of prostate (TUIP)
- best for small glands <30g
retropubic prostatectomy
- open operation (if large prostate)
258
risks of TURP
```
haemorrhage
haematospermia
hypothermia
urethral trauma/stricture
post-op TURP syndrome (hypothermia, hyponatraemia)
infection - prostatitis
ED
incontinence
retrograde ejaculation
```
259
post-op advice for BPH (TURP)
- Avoid driving for 2 weeks after the operation
- Avoid sex for 2 weeks after surgery. Amount of ejaculate produced will be reduced (as it flows back into bladder – harmless, but may cloud urine).
- Expect to pass blood in urine for the first 2 weeks. Don’t be alarmed.
- At first, you may need to urinate frequently than before. In 6 weeks things should be much better – but operation cannot be guaranteed to work (8% fail and lasting incontinence is a problem in 6%)
- If feverish or if urination hurts, take a sample of urine to doctor.
260
Consequences of chronic urinary retention
```
hyperkalaemia
metabolic acidosis
post-obstructive diuresis
sodium-and bicarbonate losing nephropathy
infection
```
261
common location of renal cell carcinoma
proximal renal tubular epithelium
262
features of renal cell carcinoma
50% found incidentally
```
haematuria
loin pain
abdo mass
anorexia
weight loss
malaise
```
varicocele - invasion of left renal vein compresses left testicular vein
263
tests for RCC
```
high BP
bloods
- FBC (polycythaemia due to high EPO)
- ESR
- U+E
- ALP (?bone mets)
```
urine
- RBCs
- cytology
imaging
- USS
- CT/MRI KUB
- CXR (cannon ball mets in lungs)
264
metastases of RCC
bone
liver
lung
265
treatment of RCC
radical nephrectomy
if unresectable or metastatic disease --> biologics e.g. sunitinib, sorafenib
266
what score is used in RCC to predict survival, tumour size etc
MAYO PROGNOSTIC RISK SCORE
267
transitional cell carcinoma of kidney risk factors
chemicals in the textile
rubber
plastic industry
268
presentation of transitional cell carcinoma of kidney
```
painless visible haematuria
frequency
urgency
dysuria
urinary tract obstruction
```
269
what is a nephroblastoma
childhood tumour of primitive renal tubules and mesenchymal cells.
chief abdominal malignancy in children.
present with an abdominal mass and haematuria.
270
associations with prostate cancer
positive family history
| increased testosterone
271
where do prostate cancers commonly arise
adenocarcinomas arising in PERIPHERAL PROSTATE
272
metastasis of prostate cancer
local - seminal vesicles, bladder, rectum (spread via lymph)
haematogenous - sclerotic bony lesions
273
which system is used to grade prostate cancer
GLEASON GRADING SYSTEM
274
symptoms of prostate cancer
asymptomatic
```
hesitancy
poor stream
terminal dribbling
obstruction
weight loss
± BONE PAIN (METS)
```
275
investigation of prostate cancer
digital rectal examination of prostate - hard, irregular prostate.
high PSA - false negatives in prostatitis, UTI, BPH, vigorous DRE.
transrectal ultrasound + biopsy
(recent guidelines suggest a multiparametric MRI first line)
X-rays
bone scan
CT/MRI with contrast - for staging
276
treatment of prostate cancer
radical prostatectomy if <70y
radical radiotherapy - external beam or brachytherapy.
hormone therapy e.g. goserelin:
- considered in elderly unfit patients with high-risk disease.
- if the cancer has spread too far to be cured by surgery or radiation or cannot have these treatments.
- along with radiation therapy as the initial tx, if at high risk of the cancer coming back after treatment (based on high gleason score, high PSA level and mets)
277
management of metastatic disease in prostate cancer patients
orchidectomy bilateral (most of the androgens made here) - causes prostate cancer to shrink or stop growing over time.
LHRH agonists/GnRH agonists
- lower the amount of testosterone made by testes.
- e.g. goserelin
- when LHRH are first given, causes A FLARE because testosterone levels go up briefly before falling to very low levels. (can cause back pain, bone pain). so to avoid this:
- ----> give ANTI-ANDROGENS e.g. flutamide for a few weeks when starting treatment with LHRH agonists.
LHRH antagonists
- e.g. degarelix
- lowers testosterone very quickly
- doesn't cause tumour flare
- used to treat advanced prostate cancer. better in mets.
SE of above tx
- reduced libido
- ED
- hot flashes
- gynaecomastia
- osteoporosis
- anaemia
- fatigue
- weight gain
- depression
- loss of muscle mass
278
screening for prostate cancer
DRE of prostate
transrectal ultrasound
PSA
279
what type of cancers are bladder tumours
transitional cell carcinomas (>90%)
280
presentation of bladder cancer
PAINLESS HAEMATURIA
recent UTIs
voiding irritability
281
associations of bladder cancer
SMOKING
AROMATIC AMINES - RUBBER
SCHISTOSOMIASIS - increased risk of squamous cell carcinoma
chronic cystitis
pelvic irradiation
282
tests for bladder cancer
CYSTOSCOPY WITH BIOPSY
urine: microscopy/cytology (sterile pyuria)
CT urogram - for staging
bimanual exam under anaesthesia (EUA) helps assess spread.
283
TNM staging of bladder cancer
Tis – carcinoma in situ [Not felt at EUA]
Ta – tumour confined to epithelium [Not felt at EUA]
T1 – Tumour in lamina propria [Not felt at EUA]
T2 – Superficial muscle involved [Rubbery thickening at EUA]
T3 – Deep muscle involved [EUA: mobile mass]
T4 – Invasion beyond bladder [EUA: fixed mass]
284
treatment of bladder cancer
Tis/Ta/T1 - diathermy via transurethral cystoscopy. or Transurethral resection of the bladder tumour (TURBT)
Consider chemotherapy.
T2-3
- radical cystectomy - gold standard
- radiotherapy
- post-op chemo (M-VAC: methotrexate - vinblastine, adriamycin, cisplatin.
T4
- usually palliative chemo/radiotherapy
285
metastasis of bladder cancer
local - pelvic structures
lymphatic - iliac and para-aortic nodes.
haematogenous - LIVER AND LUNGS
286
complications of cystectomy
sexual and urinary malfunction
| massive bladder haemorrhage
