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GU Flashcards

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
Q

AKI management (G)

A

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)

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26
Q

AKI complications

A

end stage renal failure, CKD, metabolic acidosis, uraemia > encephalopathy, pericarditis

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27
Q

acute tubular necrosis- definition, investigations, management

A

-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

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28
Q

pyelonephritis definition (G)

A

Upper UTI
inflammation of kidneys from renal pelvis (where kidneys meet ureters) to the parenchyma
most commonly caused by transurethral UPEC (uteropathogenic E coli)

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29
Q

UTI epidemiology (G)

A

women <35

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30
Q

UTI risk factors (G)

A

female (shorter urethra closer to anus)
urinary stasis (BPH, stones, cancer)
vesicoureteral reflex (urine travels backwards, ureter > bladder > kidneys)
catheters
diabetes

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31
Q

pyelonephritis aeitology (G)

A

KEEPS

klesbiella
enterococcus
E coli
proteus
s staphyticus

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32
Q

pyelonephritis pathophysiology (G)

A

complicated UTI
more than ureters and bladder involved as spreads to kidneys

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33
Q

pyelonephritis key presentation (G)

A

triad:
joint pain
fever
pyuria

dysuria, N+V, urgency, frequency, suprapubic pain

34
Q

pyelonephritis other signs/ symptoms

A

renal angle tenderness
loss of appetite
headache
back pain

35
Q

UTI (both types) investigations

A

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
Q

pyelonephritis management (G)

A

1:
analgesia
antibiotics (ciprofloxacin, co-amoxiclav)

37
Q

pyelonephritis DD (G)

A

lower UTI, prostatitis

38
Q

pyelonephritis complications (G)

A

renal failure
need for catheterisation
renal parenchyma scarring

39
Q

chronic pyelonephritis presentation

A

-episodes of recurrent infection in the kidneys
-it scarring of renal parenchyma > CKD > end stage renal failure.
-DMSA scans show damage

40
Q

what is cystitis (G)

A

lower urinary tract infection- inflammation of the bladder,
most commonly enteropathogenic E coli
uncomplicated UTI

41
Q

cystitis aetiology

A

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
Q

cystitis risk factors (G)

A

female
frequent sexual activity
instrumentation (catheters)
urinary stasis
bladder lining damage

43
Q

cystitis key presentation (G)

A

suprapubic pain/ tenderness
dysuria, polyuria, visible haematuria
frequency and urgency
confusion in the elderly

cloudy foul smelling urine

incontinence

44
Q

cystitis management

A

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
Q

cystitis complications (G)

A

renal infection, sepsis
in pregnancy: increased risk of pyelonephritis, premature rupture of membranes, pre-term labour

46
Q

what is an uncomplicated UTI (Y)

A

lower UTI in men or non pregnant women who are otherwise healthy

47
Q

CKD definition (G)

A

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
Q

CKD aetiology/ risk factors (G)

A

main 2:
hypertension, type 2 diabetes

also:
glomerulonephritis
polycystic kidney disease
nephrotoxic drugs eg NSAIDs ACEi

male
increasing age

49
Q

CKD pathophysiology (G)

A

-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
Q

CKD presentation (G)

A

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
Q

CKD investigations

A

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
Q

CKD staging

A

U+E to find eGFR:

  1. > 90 with renal symptoms
  2. 60-89 with renal symptoms
    3a. 45-59
    3b. 30-44
  3. 15-29
  4. <15
53
Q

CKD management

A

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
Q

CKD complications (G)

A

anaemia (decreased EPO)
CKD-mineral bone disease/ oesteodystrophy (less vit D activation)
neuropathy,
encephalopathy,
CVD

55
Q

metformin and CKD

A

metformin is contraindicated when eGFR <30

56
Q

how to differentiate between Henloch Schoenlein purpura and IgA nephropathy

A

(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
Q

nephritic syndrome (glomerulonephritis) definition (G)

A

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
Q

nephritic syndromes conditions (G)

A

-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
Q

nephritic syndromes epidemiology

A

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
Q

nephritic syndrome pathophysiology (G)

A

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
Q

nephritic syndrome key presentation (G)

A

-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
Q

IgA presentation (G)

A

visible haematuria
1-3 days after viral infection eg tonsilitis

63
Q

post strep GN presentation (G)

A

visible haematuria
2 weeks after strep infection eg pharyngitis
-inflammatory response following infection results in rapid deterioration of kidney function

64
Q

rapidly progressing GN presentation (Y)

A

Goodpastures/ Wegeners:
-fatigue
-SOB
-cough
-haemoptysis
-AKF

65
Q

SLE presentation (Y)

A

symptoms of active SLE:
-fatigue
-fever
-rash
-peripheral oedema
-N+V

66
Q

nephritic syndromes investigations (G)

A

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
Q

nephritic syndrome management (G)

A

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
Q

nephritic syndrome DD(G)

A

Nephrolithiasis, renal cancer, bladder cancer

69
Q

nephritic syndrome complications (G)

A

risk of stroke, retinopathy, MI, AKI, CVD, hypercholesterolaemia

70
Q

BPH definition (G)

A

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
Q

BPH epidemiology (G)

A

men > 50

72
Q

BPH aetiology (G)

A

age related hormonal changes

73
Q

BPH risk factors (G)

A

-age
-race (non Asian, Afro-Caribbean as higher testosterone)
-smoking
-FHx

castration is protective

74
Q

BPH pathophysiology (G)

A

inner transitional layer of the prostate (muscular, glands) proliferates narrowing the urethra

75
Q

BPH presentation (G)

A

LUTS- mainly voiding

voiding:
-incomplete emptying
-terminal dribble
-weak flow/ intermittent stream
-hesitancy
-dysuria
-straining

storage:
-urgency
-frequency
-incontinence
-nocturia

76
Q

BPH investigations

A

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
Q

digital rectal exam, BPH vs prostate cancer

A

BPH
-smooth
-slightly soft
-central sulcus
-symmetrical
-enlarged

prostate cancer
-craggy
-firm
-no central sulcus
-asymmetrical

78
Q

BPH management (G)

A

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
Q

BPH complications (G)

A

postural hypotension (tamsulosin)
sexual dysfunction (reduced testosterone from finasteride)
retrograde ejaculation from TURP

80
Q
A

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