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1
Q

renal colic- other name

A

nephrolithiasis (stones)

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2
Q

nephrolithiasis definition (G)

A

-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

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3
Q

nephrolithiasis epidemiology (G)

A

very common
men slightly more likely (testosterone increases oxalate)
age 20-40
uncommon in children

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4
Q

nephrolithiasis aetiology/ risk factors (G)

A

chronic dehydration
obesity
high protein/ salt intake
low urine output
recurrent UTIs
hyperparathyroidism / hypercalcaemia
primary kidney disease
Hx of previous stone

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5
Q

nephrolithiasis pathophysiology (G)

A

-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

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6
Q

common places for kidney stones to get stuck (G)

A

-pelvo-uteric junction
-vesico-uteric junction
-pelvic brim (where ureters cross iliac vessels)

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7
Q

nephrolithiasis key presentation (G)

A

-severe colicky unilateral pain, originating in loin and radiating to groin, in peristaltic waves
-patient may find it hard to sit still
-haematuria, dysuria

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8
Q

nephrolithiasis investigations (G)

A

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

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9
Q

nephrolithiasis DD (G)

A

peritonitis, appendicitis, UTI

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10
Q

nephrolithiasis management (G)

A

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

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11
Q

nephrolithiasis: use of ESWL vs PCNL (G)

A

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+

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12
Q

nephrolithiasis complications (G)

A

obstruction > AKI
infection > pyelonephritis

recurrent stones are very common

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13
Q

hydronephrosis management

A

urgent surgical decompression

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14
Q

result of obstruction in nephrolithiasis

A

-causes prostaglandin release, resulting in natural diuresis
-leading to complications eg AKI

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15
Q

AKI definition (G)

A

injury in kidney causes a rapid decline in kidney function, manifesting as increased urea and creatinine and decreased urine output

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16
Q

KDIGO classification (G)

A

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

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17
Q

pre-renal AKI pathophysiology, aetiology and presentation (G)

A

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

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18
Q

intra-renal AKI pathophysiology, aetiology and presentation (G)

A

-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

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19
Q

post-renal AKI pathophysiology, aetiology and presentation (G)

A

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

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20
Q

result of reduced GFR (G)

A

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

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21
Q

what are the top 3 causes of an AKI (G)

A

-sepsis
-major surgery
-cardiogenic shock

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22
Q

AKI key presentation (G)

A

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

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23
Q

AKI investigations (G)

A

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

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24
Q

AKI DD (G)

A

CKD, renal stones, tubular necrosis

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25
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)
26
AKI complications
end stage renal failure, CKD, metabolic acidosis, uraemia > encephalopathy, pericarditis
27
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
28
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)
29
UTI epidemiology (G)
women <35
30
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
31
pyelonephritis aeitology (G)
KEEPS klesbiella enterococcus E coli proteus s staphyticus
32
pyelonephritis pathophysiology (G)
complicated UTI more than ureters and bladder involved as spreads to kidneys
33
pyelonephritis key presentation (G)
triad: joint pain fever pyuria dysuria, N+V, urgency, frequency, suprapubic pain
34
pyelonephritis other signs/ symptoms
renal angle tenderness loss of appetite headache back pain
35
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
36
pyelonephritis management (G)
1: analgesia antibiotics (ciprofloxacin, co-amoxiclav)
37
pyelonephritis DD (G)
lower UTI, prostatitis
38
pyelonephritis complications (G)
renal failure need for catheterisation renal parenchyma scarring
39
chronic pyelonephritis presentation
-episodes of recurrent infection in the kidneys -it scarring of renal parenchyma > CKD > end stage renal failure. -DMSA scans show damage
40
what is cystitis (G)
lower urinary tract infection- inflammation of the bladder, most commonly enteropathogenic E coli uncomplicated UTI
41
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
42
cystitis risk factors (G)
female frequent sexual activity instrumentation (catheters) urinary stasis bladder lining damage
43
cystitis key presentation (G)
suprapubic pain/ tenderness dysuria, polyuria, visible haematuria frequency and urgency confusion in the elderly cloudy foul smelling urine incontinence
44
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
45
cystitis complications (G)
renal infection, sepsis in pregnancy: increased risk of pyelonephritis, premature rupture of membranes, pre-term labour
46
what is an uncomplicated UTI (Y)
lower UTI in men or non pregnant women who are otherwise healthy
47
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
48
CKD aetiology/ risk factors (G)
main 2: hypertension, type 2 diabetes also: glomerulonephritis polycystic kidney disease nephrotoxic drugs eg NSAIDs ACEi male increasing age
49
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
50
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
51
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
52
CKD staging
U+E to find eGFR: 1. >90 with renal symptoms 2. 60-89 with renal symptoms 3a. 45-59 3b. 30-44 4. 15-29 5. <15
53
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
54
CKD complications (G)
anaemia (decreased EPO) CKD-mineral bone disease/ oesteodystrophy (less vit D activation) neuropathy, encephalopathy, CVD
55
metformin and CKD
metformin is contraindicated when eGFR <30
56
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
57
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
58
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
59
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
60
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)
61
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
62
IgA presentation (G)
visible haematuria 1-3 days after viral infection eg tonsilitis
63
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
64
rapidly progressing GN presentation (Y)
Goodpastures/ Wegeners: -fatigue -SOB -cough -haemoptysis -AKF
65
SLE presentation (Y)
symptoms of active SLE: -fatigue -fever -rash -peripheral oedema -N+V
66
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)
67
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 -
68
nephritic syndrome DD(G)
Nephrolithiasis, renal cancer, bladder cancer
69
nephritic syndrome complications (G)
risk of stroke, retinopathy, MI, AKI, CVD, hypercholesterolaemia
70
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
71
BPH epidemiology (G)
men > 50
72
BPH aetiology (G)
age related hormonal changes
73
BPH risk factors (G)
-age -race (non Asian, Afro-Caribbean as higher testosterone) -smoking -FHx castration is protective
74
BPH pathophysiology (G)
inner transitional layer of the prostate (muscular, glands) proliferates narrowing the urethra
75
BPH presentation (G)
LUTS- mainly voiding voiding: -incomplete emptying -terminal dribble -weak flow/ intermittent stream -hesitancy -dysuria -straining storage: -urgency -frequency -incontinence -nocturia
76
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
77
digital rectal exam, BPH vs prostate cancer
BPH -smooth -slightly soft -central sulcus -symmetrical -enlarged prostate cancer -craggy -firm -no central sulcus -asymmetrical
78
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
79
BPH complications (G)
postural hypotension (tamsulosin) sexual dysfunction (reduced testosterone from finasteride) retrograde ejaculation from TURP
80

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