GU Flashcards
renal colic- other name
nephrolithiasis (stones)
nephrolithiasis definition (G)
-stones form in the renal pelvis of the kidneys and can be deposited from kidneys down to the ureters
-90% are calcium oxalate (radio-opaque)
other types:
-calcium phosphate
-uric acid (radio-lucent: not seen on X ray)
-struvite (bacterial cause- UTI)
-cysteine
nephrolithiasis epidemiology (G)
very common
men slightly more likely (testosterone increases oxalate)
age 20-40
uncommon in children
nephrolithiasis aetiology/ risk factors (G)
chronic dehydration
obesity
high protein/ salt intake
low urine output
recurrent UTIs
hyperparathyroidism / hypercalcaemia
primary kidney disease
Hx of previous stone
nephrolithiasis pathophysiology (G)
-chronic dehydration results in excess solute
-causes supersaturation of urine which favours crystalisation
-stones cause regular outflow obstruction -(hydronephrosis)
-results in dilation and obstruction of renal pelvis which increases risk of infection
common places for kidney stones to get stuck (G)
-pelvo-uteric junction
-vesico-uteric junction
-pelvic brim (where ureters cross iliac vessels)
nephrolithiasis key presentation (G)
-severe colicky unilateral pain, originating in loin and radiating to groin, in peristaltic waves
-patient may find it hard to sit still
-haematuria, dysuria
nephrolithiasis investigations (G)
1st:
-U+E: if deranged, shows hydronephrosis, can show hypercalcaemia
-urine dipstick: haematuria, leukocytes, nitrates
-FBC: raised CRP
-abdominal X-ray: shows calcium calcium stones- 80% specific
gold:
-non contrast CT of KUB (kidney, ureters, bladder)- 99% specific, diagnostic
-don’t use contrast- kidney would have to excrete = harmful
nephrolithiasis DD (G)
peritonitis, appendicitis, UTI
nephrolithiasis management (G)
symptomatic relief:
fluid
NSAIDs- diclofenac, or IV analgesic if needed
Abx if UTI eg gentamycin for pyelonephritis
anti-emetic
for stones under 5mm:
watch and wait, will pass spontaneously
elective treatment for bigger stones:
ESWL - 6-10mm
PCNL- 10mm+
uretoscopy- pass ureteroscope into ureter to remove stone
nephrolithiasis: use of ESWL vs PCNL (G)
ESWL- extracorporeal sound wave lithotripsy
-break stones with sound waves
-for smaller stones 6-10mm
PCNL: percutaneous nephrolithotomy
-keyhole removal of stone
-larger stones, 20mm+
nephrolithiasis complications (G)
obstruction > AKI
infection > pyelonephritis
recurrent stones are very common
hydronephrosis management
urgent surgical decompression
result of obstruction in nephrolithiasis
-causes prostaglandin release, resulting in natural diuresis
-leading to complications eg AKI
AKI definition (G)
injury in kidney causes a rapid decline in kidney function, manifesting as increased urea and creatinine and decreased urine output
KDIGO classification (G)
classes as an AKI if:
-rise of creatinine >25 mm/l in 48 hours
-rise of creatinine >50% from baseline in 7 days
-urine output <0.5 ml/kg/hr for 6 consecutive hours
pre-renal AKI pathophysiology, aetiology and presentation (G)
decreased blood flow to the kidneys, resulting in inadequate blood volume: hypoperfusion. GFR and creatinine clearance is decreased
-hypotension
-hypovolaemia
-cardiogenic shock
-dehydration
-sepsis
-heart failure
-hypercalcaemia
-drugs eg NSAIDs, ACEi (ACEi cause constriction of afferent arteriole)
-renal arterial blockage/ stenosis
-emboli
presentation:
syncope, hypotension, V+D
intra-renal AKI pathophysiology, aetiology and presentation (G)
-damage to the parenchyma and glomerulus causes decrease in oncotic and hydrostatic pressure, resulting in decrease in GFR
-glomerulonephritis
-acute interstitial nephritis
-acute tubular necrosis
-haemolytic uraemic syndrome
-toxins eg sepsis
-rhabdomyolosis
-drugs eg vancomycin
presentation: signs of infection/ underlying disease
post-renal AKI pathophysiology, aetiology and presentation (G)
obstruction of urinary outflow causes back pressure on the kidney, resulting in decreased hydrostatic pressure, causing reduced GFR
-obstructive uropathy:
-ureter strictures
-BPH
-prostate cancer
-renal stones
-occluded catheter
-neurogenic bladder
-drugs eg CCB
presentation:
LUTS -low urine output
result of reduced GFR (G)
build up of normally excreted substances:
-urea: uraemia, confusion if severe (HE, ammonia as a by product of urea metabolism)
-K+ :arrhythmias
-Creatinine
-fluid: oedema
-H+ :acidosis
what are the top 3 causes of an AKI (G)
-sepsis
-major surgery
-cardiogenic shock
AKI key presentation (G)
low urine output (oliguria), haematuria, proteinuria, high creatinine, hypotension,
due to build up:
urea: confusion, skin manifestations, N+V, pericarditis
fluid overload: peripheral/ pulmonary oedema, cardiogenic shock, orthopnoea
K+: arrhythmias, muscle weakness
AKI investigations (G)
gold/ first:
urea: creatinine
>100:1 =pre renal
<40:1 =intra-renal
40-100:1 =post-renal
U+E:
raised creatinine, urea, potassium
low urine output
urinalysis:
leukocytes and nitrates (infection), proteinuria, haematuria, glucose
other:
renal USS if post renal cause suspected
FBC, CRP
ECG- hyperkalaemia
AKI DD (G)
CKD, renal stones, tubular necrosis
AKI management (G)
1st:
-treat cause (eg hypotension, stones, infection)
-stop nephrotoxic drugs eg NSAIDs, ACEi
-treat complications eg electrolyte imbalances
-adequate fluid intake, prophylactic additional fluids
severe cases:
renal replacement therapy (RRT), haemodialysis
only if acidosis, fluid overload, uraemia, hyperkalaemia (>6.5)
AKI complications
end stage renal failure, CKD, metabolic acidosis, uraemia > encephalopathy, pericarditis
acute tubular necrosis- definition, investigations, management
-most common intrinsic cause of AKI
-damage/ death of epithelial cells of renal tubules occurring due to hypoperfusion
-confirmed by muddy brown casts on urinalysis
-epithelial cells can regenerate so recovery takes 1-3 weeks
pyelonephritis definition (G)
Upper UTI
inflammation of kidneys from renal pelvis (where kidneys meet ureters) to the parenchyma
most commonly caused by transurethral UPEC (uteropathogenic E coli)
UTI epidemiology (G)
women <35
UTI risk factors (G)
female (shorter urethra closer to anus)
urinary stasis (BPH, stones, cancer)
vesicoureteral reflex (urine travels backwards, ureter > bladder > kidneys)
catheters
diabetes
pyelonephritis aeitology (G)
KEEPS
klesbiella
enterococcus
E coli
proteus
s staphyticus
pyelonephritis pathophysiology (G)
complicated UTI
more than ureters and bladder involved as spreads to kidneys
pyelonephritis key presentation (G)
triad:
joint pain
fever
pyuria
dysuria, N+V, urgency, frequency, suprapubic pain
pyelonephritis other signs/ symptoms
renal angle tenderness
loss of appetite
headache
back pain
UTI (both types) investigations
1st line:
urine dipstick
-leukocytes
-nitrites (bacteria convert nitrates to nitrites) (if just nitrites= treat as UTI, just leukocytes= don’t treat as UTI unless clinical evidence)
-possible haematuria
gold:
MSU- microscopy
-confirm UTI, identify pathogen, decide Abx
other:
USS if stones are suspected
pyelonephritis management (G)
1:
analgesia
antibiotics (ciprofloxacin, co-amoxiclav)
pyelonephritis DD (G)
lower UTI, prostatitis
pyelonephritis complications (G)
renal failure
need for catheterisation
renal parenchyma scarring
chronic pyelonephritis presentation
-episodes of recurrent infection in the kidneys
-it scarring of renal parenchyma > CKD > end stage renal failure.
-DMSA scans show damage
what is cystitis (G)
lower urinary tract infection- inflammation of the bladder,
most commonly enteropathogenic E coli
uncomplicated UTI
cystitis aetiology
KEEPS
klesbiella
enterococcus
E.coli
proteus
s.saprophyticus
mostly from faeces, normal intestinal bacteria eg E.coli can get to urethral opening from anus- sexual activity, incontinence, poor hygeine, catheters
cystitis risk factors (G)
female
frequent sexual activity
instrumentation (catheters)
urinary stasis
bladder lining damage
cystitis key presentation (G)
suprapubic pain/ tenderness
dysuria, polyuria, visible haematuria
frequency and urgency
confusion in the elderly
cloudy foul smelling urine
incontinence
cystitis management
1st:
Abx:
trimethoprim (but high rates of bacterial resistance)- inhibits folate synthesis so not in 1st trimester
nitrofurantoin (avoid if eGFR < 45)- not in 3rd trimester (risk of neonatal haemolysis) -amoxicillin, cefalexin used instead
3 day course for women, 7 for men or in pregnancy, 5-10 for women with complications
cystitis complications (G)
renal infection, sepsis
in pregnancy: increased risk of pyelonephritis, premature rupture of membranes, pre-term labour
what is an uncomplicated UTI (Y)
lower UTI in men or non pregnant women who are otherwise healthy
CKD definition (G)
chronic kidney disease- decline in kidney function, progressive and permanent
>3 months
eGFR <60ml/min/1.73m2
or
eGFR <90ml/min/1.73m2 with signs of renal damage eg haematuria, proteinuria, pathological on imaging
or
albuminuria >30mg/34hrs
^more than 3 months
CKD aetiology/ risk factors (G)
main 2:
hypertension, type 2 diabetes
also:
glomerulonephritis
polycystic kidney disease
nephrotoxic drugs eg NSAIDs ACEi
male
increasing age
CKD pathophysiology (G)
-damage to many nephrons, decreasing GFR
-increased burden on other nephrons
-compensatory RAAS system to increase GFR, but there is trans-glomerular shearing pressure and loss of basement membrane permeability, resulting in haematuria and proteinuria
-angiotensin 2 upregulates TGF-B and plasminogen activator-inactivator 1 causing mesangial scarring
CKD presentation (G)
starts asymptomatic (lots of reserve nephrons), then symptomatic due to accumulation of substances and renal damage
key:
haematuria
proteinuria
hypertension
oedema
peripheral neuropathy
pruritis, loss of appetite, nausea, muscle cramps, pallor, fatigue
CKD investigations
1st:
FBC: anaemia of CD
U+E: decreased GFR, creatinine, phosphate, potassium
urinalysis: haematuria, proteinuria,
raised urine albumin (if albumin: creatinine ratio >3mm/mmol -significant proteinuria)
renal USS: bilateral renal atrophy
gold
GFR classification
>60ml/min/1.73m2
or
>90ml/min/1.73m2 with renal signs
CKD staging
U+E to find eGFR:
- > 90 with renal symptoms
- 60-89 with renal symptoms
3a. 45-59
3b. 30-44 - 15-29
- <15
CKD management
aims to slow progression and prevent CVD (biggest mortality)- no cure
CVD:
weight loss,
hypertension-ACEi, CCB
diabetes- metformin, diet
treat complications:
anaemia- ferrous sulphate, erythropoietin
oedema- diuretics
metabolic acidosis- sodium bicarbonate
CKD-mineral bone disease- Vitamin D
CVD- statins
STOP NSAIDS
stage 5:
renal replacement therapy (eGFR < 15)- dialysis
eventually kidney transplant- curative
CKD complications (G)
anaemia (decreased EPO)
CKD-mineral bone disease/ oesteodystrophy (less vit D activation)
neuropathy,
encephalopathy,
CVD
metformin and CKD
metformin is contraindicated when eGFR <30
how to differentiate between Henloch Schoenlein purpura and IgA nephropathy
(Henloch Schoenlein purura is small cell vasculitis)
investigation give same results
only difference:
IgA is only kidney deposition, HSP is systemic- kidney, intestines, liver
nephritic syndrome (glomerulonephritis) definition (G)
group of syndromes that cause inflammation in the kidneys
they cause proteinuria (1-3.5g/day, less than nephrotic) and haematuria (5 RBC/ uL)
Increased permeability of the glomeruli cause RBCs to move into the filtrate
nephritic syndromes conditions (G)
-IgA nephropathy (Berger’s syndrome)- most common cause
-systemic lupus erythematosus (SLE)(autoimmune)
-goodpasture’s (rapidly progressing glomerulonephritis)
-post-streptococcal glomerulonephritis
-Henoch-Schoenlein purpura
-ANCA associated vasculitis
nephritic syndromes epidemiology
general: increased risk with age
IgA: Asian populations, HIV, 20-30
post-streptococcal glomerulonephritis: under 30
SLE nephropathy: female 15-45 with renal impairment
nephritic syndrome pathophysiology (G)
inflammation → reactive tissue proliferation → break in glomerular basement membrane → crescent formation.
Some are associated with anti-glomerular basement membrane antibodies which attack the basement membrane (eg Goodpasture’s)
nephritic syndrome key presentation (G)
-visible haematuria (always, 5 RBC/uL),
-oliguria,
-proteinuria (usually, 1-3.5 g/day) (but less than 3g per 24 hours- higher suggests nephrotic),
-fluid retention: oedema (peripheral/pulmonary), weight gain
-hypertension,
-uraemic signs
IgA presentation (G)
visible haematuria
1-3 days after viral infection eg tonsilitis
post strep GN presentation (G)
visible haematuria
2 weeks after strep infection eg pharyngitis
-inflammatory response following infection results in rapid deterioration of kidney function
rapidly progressing GN presentation (Y)
Goodpastures/ Wegeners:
-fatigue
-SOB
-cough
-haemoptysis
-AKF
SLE presentation (Y)
symptoms of active SLE:
-fatigue
-fever
-rash
-peripheral oedema
-N+V
nephritic syndromes investigations (G)
1st:
urinalysis and microscopy: haematuria, proteinuria, dysmorphic RBCs
24 urine protein collection
bloods: anaemia, elevated AST/ALT, elevated creatinine
serology: anti-GBM (goodpastures), anti double stranded DNA (SLE), antinuclear antibody (SLE), ANCA (Wegener’s vasculitis)
IgA: immunofluorescence microscopy shows IgA complex deposition and mesangial proliferation
rapidly progressive GN: microscopy shows crescent GN
post-strep GN: light microscopy shows hypercellular glomeruli, electron shows subendothelial immune complex deposition
gold: renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)
nephritic syndrome management (G)
general: HTN control, proteinuria (ACEi/ ARB, loop diuretics, prednisolone),
immunosuppression.
Specific:
-post-streptococcal GN- penicillin, normally self limiting
-Goodpasture’s (plasmapheresis, corticosteroid immunosuppression),
-SLE (immunosuppression- rituximab, cyclophosphamide, steroid)
-IgA- non curative, 30% progress to ESRF
-
nephritic syndrome DD(G)
Nephrolithiasis, renal cancer, bladder cancer
nephritic syndrome complications (G)
risk of stroke, retinopathy, MI, AKI, CVD, hypercholesterolaemia
BPH definition (G)
benign prostatic hyperplasia
non-malignant hyperplasia of stromal and epithelial cells of the prostate
causes prostate enlargement and narrowing of the urethra, normal with age
BPH epidemiology (G)
men > 50
BPH aetiology (G)
age related hormonal changes
BPH risk factors (G)
-age
-race (non Asian, Afro-Caribbean as higher testosterone)
-smoking
-FHx
castration is protective
BPH pathophysiology (G)
inner transitional layer of the prostate (muscular, glands) proliferates narrowing the urethra
BPH presentation (G)
LUTS- mainly voiding
voiding:
-incomplete emptying
-terminal dribble
-weak flow/ intermittent stream
-hesitancy
-dysuria
-straining
storage:
-urgency
-frequency
-incontinence
-nocturia
BPH investigations
1:
-digital rectal exam- smooth, enlarged, soft, central sulcus
-prostate specific antigen (PSA) to rule out cancer (always raised in cancer but sometimes raised in BPH so not that useful)
GOLD: DIGITAL RECTAL EXAM
also:
-urine dipstick- rule out infection
-urinary frequency volume chart
-abdo exam- palpable bladder and other abnormalities
-international prostate symptom score
digital rectal exam, BPH vs prostate cancer
BPH
-smooth
-slightly soft
-central sulcus
-symmetrical
-enlarged
prostate cancer
-craggy
-firm
-no central sulcus
-asymmetrical
BPH management (G)
1: alpha blockers eg tamsulosin
-relax smooth muscle in bladder neck and prostate
2: 5 alpha reductase inhibitors eg finasteride
block conversion of testosterone to dihydrotestosterone which decreases prostate size
lifestyle: reduce caffeine and alcohol
TURP- transurethral resection of the prostate
others: transurethral electrovaporisation of the prostate, holmium laser enucleation of the prostate, open prostatectomy
catheter acutely
BPH complications (G)
postural hypotension (tamsulosin)
sexual dysfunction (reduced testosterone from finasteride)
retrograde ejaculation from TURP
