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Finals > Renal and Urology > Flashcards

Renal and Urology Flashcards

1
Q

intrinsic causes of AKI

A
  • glomerulonephritis
  • acute tubular necrosis (ATN)
  • acute interstitial nephritis (AIN), respectively
  • rhabdomyolysis
  • tumour lysis syndrome
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2
Q

what is the criteria for AKI

A
  • any of the following;
    • a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
    • a 50% or greater rise in serum creatinine over past 7 days
    • a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults
    • 25% fall in eGFR in children / young adults in 7 days.
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3
Q

5 types of drug that should be stopped in aki as they may worsen renal function

A
  • NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
  • Aminoglycosides
  • ACE inhibitors
  • Angiotensin II receptor antagonists
  • Diuretics
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4
Q

three drugs that should be stopped in aki since there is increased risk of toxicity (but won’t worsen the aki itself)

A
  • Metformin
  • Lithium
  • Digoxin
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5
Q

what are the causes of acute interstitial nephritis

A
  • drugs are by far the most common cause - particularly antibiotics
    • penicillin
    • rifampicin
    • NSAIDs
    • allopurinol
    • furosemide
  • infection
    • staphylococci
    • Hanta virus
  • systemic illness
    • sjorgen’s
    • sarcoid
    • SLE
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6
Q

What is the histology finding in acute interstitial nephritis

A

marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules

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7
Q

what are the clinical features of acute interstitial nephritis

A
  • fever, rash, arthralgia
  • eosinophilia
  • mild renal impairment
  • hypertension
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8
Q

investigation results in acute interstitial nephritis

A
  • sterile pyuria
  • white cell casts
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9
Q

how do you differentiate between AKI and CKD

A
  • ultrasound
    • most CKD will have bilateral small kidneys apart from
      • autosomal dominant polycystic kidney
      • amyloid
      • early diabetic
  • hypocalcaemia
    • in CKD they are likely to have hypocalcaemia due to lack of vitamin D
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10
Q

what is the most common cause of AKI seen in clinical practice?

A

acute tubular necrosis

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11
Q

what is the cause of acute tubular necrosis

A
  • there are two main causes
    • ischaemia
      • shock
    • nephrotoxins
      • aminoglycosides
      • myoglobin secondary to rhabdomyolysis
      • radiocontrast agents
      • lead
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12
Q

histopathological features of acute tubular necrosis

A
  • tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
  • dilatation of the tubules may occur
  • necrotic cells obstruct the tubule lumen
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13
Q

histopathological features of acute tubular necrosis

A
  • tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
  • dilatation of the tubules may occur
  • necrotic cells obstruct the tubule lumen
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14
Q

what are the phases of acute tubular necrosis?

A
  • oliguric phase
  • polyuric phase
  • recovery phase
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15
Q

what do you find in the urine in acute tubular necrosis

A

brown granular casts

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16
Q

what are the different stages of AKI

A
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17
Q

How do you calculate the anion gap?

A

(sodium + potassium) - (bicarbonate + chloride)

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18
Q

what causes tumour lysis syndrome?

A

It can occur in the absence of chemotherapy but is usually triggered by the introduction of combination chemotherapy. On occasion, it can occur with steroid treatment alone.

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19
Q

what should be suspected in any patient presenting with an acute kidney injury in the presence of a high phosphate and high uric acid level.

A

tumour lysis syndrome

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20
Q

how should you protect against TLS

A

Patients at high risk of TLS should be given IV allopurinol or IV rasburicase immediately prior to and during the first days of chemotherapy.

They should not be given in combination

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21
Q

how do you diagnose tumour lysis syndrome

A
  • Laboratory tumor lysis syndrome: abnormality in two or more of the following, occurring within three days before or seven days after chemotherapy.
    • uric acid 25% increase
    • potassium25% increase
    • phosphate 25% increase
    • calcium 25% decrease
  • clinical tumour lysis syndrome: you need laboratory TLS and one of the following
    • seizure
    • arrhythmia
    • sudden death
    • creatinine 1.5x upper limit of normal
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22
Q

what is the more common type of autosomal dominant polycystic kidney disease, which chromosomes are the mutations on and which presents earlier?

A
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23
Q

what is the method of screening for relatives of patients with ADPKD and what are the criteria

A

Ultrasound diagnostic criteria (in patients with positive family history)

  • two cysts, unilateral or bilateral, if aged < 30 years
  • two cysts in both kidneys if aged 30-59 years
  • four cysts in both kidneys if aged > 60 years
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24
Q

what ethnicities are most likely to get BPH

A

black > white > Asian

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25
Q

What are the LUTS that BPH is likely to present with?

A
  • voiding symptoms (obstructive):
    • weak or intermittent urinary flow
    • straining
    • hesitancy
    • terminal dribbling
    • incomplete emptying
  • storage symptoms (irritative)
    • urgency
    • frequency
    • urgency incontinence
    • nocturia
  • post-micturition
    • dribbling
  • complications
    • urinary tract infection
    • retention
    • obstructive uropathy
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26
Q

how do you classify the severity of BPH

A
  • International Prostate Symptom Score (IPSS)
    • tool for classifying the severity of lower urinary tract symptoms (LUTS) and assessing the impact of LUTS on quality of life
    • Score 20–35: severely symptomatic
    • Score 8–19: moderately symptomatic
    • Score 0–7: mildly symptomatic
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27
Q

what is the ipss

A

international prostate symptom score

then at the end ask them if they were to spend the rest of their life with their currect symptoms how would this make them feel

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28
Q

what are the treatment options for BPH

A
  • watchful waiting
  • for voiding symptoms
    • alpha-1 antagonists (e.g. tamsulosin, alfuzosin)
      • first line
      • relax smooth muscle around prostate and bladder
      • first line if IPSS >8
      • Improve symptoms in 70% of men
    • 5 alpha-reductase inhibitors (e.g. finasteride)
      • block the conversion of testosterone to dihydrotestosterone (DHT)
      • indicated if patient has a particularly large prostate
      • symptoms may not improve for 6 months
      • can increase PSA
    • combination of the above
  • antimuscarinic (e.g. tolterodine) if mixture of storage and voiding symptoms after treatment with alpha-1 antagonist alone
  • TURP
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29
Q

what are the side effects of alpha-1 antagonists and give an example

A

tamsulosin

dizziness, postural hypotension, dry mouth, depression

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30
Q

what are the side effects of 5 alpha-reductase inhibitors and give an example

A

finasteride

erectile dysfunction, reduced libido, ejaculation problems, gynaecomastia

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31
Q

what are the different types of bladder cancer

A
  • Urothelial (transitional cell) carcinoma (>90% of cases)
  • Squamous cell carcinoma ( 1-7% -except in regions affected by schistosomiasis)
  • Adenocarcinoma (2%)
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32
Q

how will most patients with bladder cancer present

A

most will present with macroscopic haematuria

the rest will pick it up as an incidental finding of microscopic haematuria

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33
Q

investigations for bladder cancer

A
  • cystoscopy and biopsies or TURBT provides histological diagnosis and information relating to depth of invasion.
  • Locoregional spread is best determined using pelvic MRI and distant disease CT scanning.
  • Nodes of uncertain significance may be investigated using PET CT.
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34
Q

treatment for bladder cancer

A

TURBT and intravesicular chemotherapy

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35
Q

what is the most important risk factor for bladder cancer

A

smoking

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36
Q

what are the causes of chronic kidney disease

A
  • diabetic nephropathy
  • chronic glomerulonephritis
  • chronic pyelonephritis
  • hypertension
  • adult polycystic kidney disease
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37
Q

what are the different stages of ckd

A
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38
Q

what type of aneamia do you get in CKD

A

normochromic normocytic anaemia caused by a lack of production of epo

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39
Q

what is an important complication of anaemia in ckd

A

it predisposes to the development of left ventricular hypertrophy - associated with a three fold increase in mortality in renal patients

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40
Q

why does ckd cause bone problems

A

low vitamin d leads to low calcium which leads to bone resorption which leads to high phosphate and high parathyroid hormone

this is a secondary hyperparathyroidism

this can all lead to osteoporosis

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41
Q

what albumin creatinine ratio is clinically important proteinuria

A

3 mg/mmol or more

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42
Q

how do you manage proteinuria in CKDCE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria

A

ACE inhibitors (or angiotensin II receptor blockers) are key in the management of proteinuria

  • they should be used first-line in patients with coexistent hypertension and CKD, if the ACR is > 30 mg/mmol
  • if the ACR > 70 mg/mmol they are indicated regardless of the patient’s blood pressure
  • ace inhibitors reduce filtration pressure but a decrease in eGFR of up to 25% is acceptable
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43
Q

how do you manage mineral bone disease in ckd

A
  • The aim is to reduce phosphate and parathyroid hormone levels.
    • reduced dietary intake of phosphate is the first-line management
    • phosphate binders
      • sevelamer binds dietary phosphate and prevents its absorption
    • vitamin D: alfacalcidol, calcitriol
    • parathyroidectomy may be needed in some cases
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44
Q

what is the screening for diabetic nephropathy

A
  • all patients should be screened annually using urinary albumin:creatinine ratio (ACR)
  • should be an early morning specimen
  • ACR > 2.5 = microalbuminuria
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45
Q

what is the management of diabetic nephropathy

A
  • dietary protein restriction
  • tight glycaemic control
  • BP control: aim for < 130/80 mmHg
  • ACE inhibitor or angiotensin-II receptor antagonist
    • should be start if urinary ACR of 3 mg/mmol or more
    • dual therapy with ACE inhibitors and angiotensin-II receptor antagonist should not be started
  • control dyslipidaemia e.g. Statins
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46
Q

what is the most common type of testicular cancer

A

seminoma

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47
Q

what are the risk factors for testicular cancer

A
  • Cryptorchidism
  • Infertility
  • Family history
  • Klinefelter’s syndrome
  • Mumps orchitis
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48
Q

how do you diagnose testicular cancer

A
  • Ultrasound is first-line
  • CT scanning of the chest/ abdomen and pelvis is used for staging
  • Tumour markers (see above) should be measured
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49
Q

which are the two most common causative organisms in epididymo-orchitis

A

Chlamydia trachomatis and Neisseria gonorrhoeae

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50
Q

which drug may cause epididymo-orchitis

A

amiodarone

51
Q

how would you identify a torted testi on examination

A
  • very tender testicle
  • Cremasteric reflex is lost and elevation of the testis does not ease the pain.
52
Q

with a tender swollen testicle which factors would suggest torsion

A

patients < 20 years, severe pain and an acute onset

53
Q

what is the management of epididymo-orchitis

A

ceftriaxone 500mg intramuscularly single dose, plus doxycycline 100mg by mouth twice daily for 10-14 days

54
Q

what is nephrotic syndrome

A
    1. Proteinuria (> 3g/24hr) causing
    1. Hypoalbuminaemia (< 30g/L) and
    1. Oedema
55
Q

what are the complications of nephrotic syndrome and why

A
  • thrombosis
    • due to loss of anti-thrombin in urine
  • hyperlipidaemia
  • ckd
  • infection
    • ig loss in urine
  • hypocalcaemia
    • vitamin D deficiency
56
Q

what is the most common nephrotic syndrome in children

A

minimal change glomerulonephritis

57
Q

what is the commonest type of glomerulonephritis in adults

A

Membranous glomerulonephritis

58
Q

electron microscopy of renal biopsy in membranous glomerulonephritis would show what:

A

basement membrane is thickened with subepithelial electron dense deposits. This creates a ‘spike and dome’ appearance

59
Q

what is the prognosis for membranous glomerulonephritis

A
  • one-third: spontaneous remission
  • one-third: remain proteinuric
  • one-third: develop ESRF
60
Q

what is the management for membranous glomerulonephritis

A
  • all patients should go on an ACE inhibitor and an ARB
  • only patients with severe progressive disease require immunosuppression
    • this is with a corticosteroid and cyclophosphamide in combination
61
Q

focal segmental glomerulosclerosis normally presents in which age group

A

young adults

62
Q

in focal segmental glomerulosclerosis what would you see on a renal biopsy

A
  • focal and segmental sclerosis and hyalinosis on light microscopy
  • effacement of foot processes on electron microscopy
63
Q

what is the managment of focal segmental glomerulosclerosis

A
  • steroids +/- immunosuppressants
64
Q

name 5 causes of nephrotic syndrome

A

minimal change disease (most common in children)

membranous glomerulonephritis (most common in adults)

focal segmental glomerulosclerosis

amyloidosis

diabetic nephropathy

65
Q

what are three causes of rapidly progressive glomerulonephritis

A
  • Goodpasture’s syndrome
  • Wegener’s granulomatosis
  • others: SLE, microscopic polyarteritis
66
Q

what is goodpastures syndrome

A

it is anti GBM nephritic syndrome

is a rare type of small-vessel vasculitis associated with both pulmonary haemorrhage and rapidly progressive glomerulonephritis

67
Q

what would you find on renal biopsy in goodpasture’s syndrome

A

linear IgG deposits along the basement membrane

68
Q

what are the clinical features of goodpastures

A
  • pulmonary haemorrhage
  • rapidly progressive glomerulonephritis
    • this typically results in a rapid onset acute kidney injury
    • nephritis → proteinuria + haematuria
69
Q

what are the treatment options for goodpastures

A
  • plasma exchange (plasmapheresis)
  • steroids
  • cyclophosphamide
70
Q

what is Wegener’s granulomatosis

A

granulomatosis with polyangiitis

autoimmune condition associated with a necrotizing granulomatous vasculitis, affecting both the upper and lower respiratory tract as well as the kidneys.

71
Q

what are the clinical features of granulomatosis with polyangiitis

A
  • upper respiratory tract: epistaxis, sinusitis, nasal crusting
  • lower respiratory tract: dyspnoea, haemoptysis
  • rapidly progressive glomerulonephritis (‘pauci-immune’, 80% of patients)
  • saddle-shape nose deformity
  • also: vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions
72
Q

what investigations should you do for granulomatosis with polyangiitis and what would the findings be

A
  • cANCA positive in > 90%, pANCA positive in 25%
  • chest x-ray: wide variety of presentations, including cavitating lesions
  • renal biopsy: epithelial crescents in Bowman’s capsule
73
Q

what is the treatment for granulomatosis with polyangiitis

A
  • steroids
  • cyclophosphamide
  • plasma exchange
  • median survival = 8-9 years
74
Q

what is IgA nephropathy AKA

A

Berger’s disease

75
Q

what is the most common cause of glomerulonephritis worldwide?

A

IgA nephropathy

76
Q

what is the classic presentation of IgA nephropathy

A

macroscopic haematuria in young people following an upper respiratory tract infection

proteinuria is rare

renal failure is unusual and seen in a minority of patients

77
Q

what is the histology finding for IgA nephropathy

A

mesangial hypercellularity, positive immunofluorescence for IgA & C3

78
Q

how would you differentiate between IgA nephropathy and post-streptococcal glomerulonephritis

A
79
Q

name 9 important glomerulonephritides and how they typically present

A
80
Q

how is alport’s syndrome inherited?

A

usually in an X linked dominant way

10% of cases are autosomal recessive

there are rare autosomal recessive versions

81
Q

what happens in alport syndrome

A
  • they have a mutation in type iv collagen so they produce an abnormal glomerular basement membrane
  • this means if they get a renal transplant they may produce anti gbm antibodies in a goodpastures syndrome like picture
82
Q

how does alport’s syndrome present

A
  • microscopic haematuria
  • progressive renal failure
  • bilateral sensorineural deafness
  • lenticonus: protrusion of the lens surface into the anterior chamber
  • retinitis pigmentosa
83
Q

what would you see on renal biopsy in alport’s syndrome

A
  • longitudinal splitting of lamina densa of the glomerular basement membrane, resulting in a ‘basket-weave’ appearance seen on electron microscopy
84
Q

what renal complication can SLE cause and what would biopsy show

A
  • diffuse proliferative glomerulonephritis
    • glomeruli shows endothelial and mesangial proliferation, ‘wire-loop’ appearance
    • if severe, the capillary wall may be thickened secondary to immune complex deposition
    • electron microscopy shows subendothelial immune complex deposits
    • granular appearance on immunofluorescence
85
Q

what bacteria normally causes post-streptococcal glomerulonephritis

A

Post-streptococcal glomerulonephritis typically occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (usually Streptococcus pyogenes)

86
Q

post-streptococcal glomerulonephritis normally affects which age group?

A

young children

87
Q

what are the renal biopsy features of post-streptococcal glomerulonephritis

A
  • endothelial proliferation with neutrophils
  • electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
  • immunofluorescence: granular or ‘starry sky’ appearance
88
Q

investigations for renal calculi

A
  • urine dipstick and culture
  • serum creatinine and electrolytes: check renal function
  • FBC / CRP: look for associated infection
  • calcium/urate: look for underlying causes
  • also: clotting if percutaneous intervention planned and blood cultures if pyrexial or other signs of sepsis
  • CT KUB within 14 hours of admission
89
Q

renal calculi of what diameter will typically pass spontaneously

how long does this normally take

A

less than 5mm

they typically pass within 4 weeks of symptom onset

90
Q

what is the management of renal calculi

A
  • less than 5mm and no complicating features
    • normally pass spontaneously within 4 weeks
    • analgesia → parenteral nsaid such as IM diclofenac
  • if there is ureteric obstruction and infection due to stones
    • surgical emergency → nephrostomy tube placement or insertion of ureteric catheters or ureteric stent placement
  • non-emergency setting
    • see table
91
Q

therapeutic selection of techniques for renal calculi management in the non-emergency setting

A
92
Q

if urge incontinence is the predominant cause of incontinence then what is the management

A
  • 6 weeks bladder retraining
  • bladder stabilising drugs: antimuscarinics are first-line
    • e.g. oxybutynin, tolterodine
    • Immediate release oxybutynin should, however, be avoided in ‘frail older women’
  • mirabegron (a beta-3 agonist) may be useful if there is concern about anticholinergic side-effects in frail elderly patients
93
Q

if stress incontinence is the predominant picture in incontinence then what is the management

A
  • pelvic floor muscle training
    • for a minimum of 3 months
  • surgical procedures: e.g. retropubic mid-urethral tape procedures
  • duloxetine may be offered to women if they decline surgical procedures
    • a combined noradrenaline and serotonin reuptake inhibitor
    • mechanism of action: increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction
94
Q

how frequently is chlamydia asymptomatic in women and men

A

asymptomatic in 70% of women and 50% of men

95
Q

what are the symptoms of chlamydia trachomatis in women and men

A
  • women: cervicitis (discharge, bleeding), dysuria
  • men: urethral discharge, dysuria
96
Q

management of chlamydia

A

7 day course of doxycycline

if pregnant then azithromycin, erythromycin or amoxicillin may be used

97
Q

who needs to be contacted if someone has a positive chlamydia result

A
  • for men with urethral symptoms: all contacts since, and in the four weeks prior to, the onset of symptoms
  • for women and asymptomatic men: all partners from the last six months should be contacted
98
Q

how does Neisseria gonorrhoeae appear down the microscope

A

gram negative diplococci

99
Q

what are the symptoms of gonorrhoea

A
  • males: urethral discharge, dysuria
  • females: cervicitis e.g. leading to vaginal discharge
  • rectal and pharyngeal infection is usually asymptomatic
100
Q

what is the treatment for gonorrhoea

A
  • a single dose of IM ceftriaxone 1g
  • if needle phobic then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used
  • If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given
101
Q

what is the most common cause of septic arthritis in young adults

A

neisseria gonorrhoea

102
Q

what bacteria causes syphillis

A

the spirochaeteTreponema pallidum.

103
Q

what is the incubation period of syphilis

A

9-90 days

104
Q

what are the primary features of syphilis

A
  • chancre - painless ulcer at the site of sexual contact
  • local non-tender lymphadenopathy
  • often not seen in women (the lesion may be on the cervix)
105
Q

when do secondary features of syphilis occur

A

6-10 weeks after the primary infection

106
Q

what are the secondary features of syphillis

A
  • systemic symptoms: fevers, lymphadenopathy
  • rash on trunk, palms and soles
  • buccal ‘snail track’ ulcers (30%)
  • condylomata lata (painless, warty lesions on the genitalia )
107
Q

what are the tertiary features of syphillis

A
  • gummas (granulomatous lesions of the skin and bones)
  • ascending aortic aneurysms
  • general paralysis of the insane
  • tabes dorsalis
  • Argyll-Robertson pupil
    • accomodate but don’t react
108
Q

what are the features of congenital syphilis

A
  • blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
  • rhagades (linear scars at the angle of the mouth)
  • keratitis
  • saber shins
  • saddle nose
  • deafness
109
Q

what is a varicocele

A
  • Varicosities of the pampiniform plexus
  • Typically occur on left (because testicular vein drains into renal vein)
  • May be presenting feature of renal cell carcinoma
  • Affected testis may be smaller and bilateral varicoceles may affect fertility
110
Q

what is the management of testicular torsion

A

The treatment is prompt surgical exploration and testicular fixation of both testis

111
Q

what is a hydrocele

A
  • Non painful, soft fluctuant swelling
  • Often possible to ‘get above it’ on examination
  • Usually contain clear fluid
  • Will often transilluminate
  • May be presenting feature of testicular cancer in young men
112
Q

what is an epididymal cyst

A

Single or multiple cysts
May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Painless
Lie above and behind testis
It is usually possible to ‘get above the lump’ on examination

113
Q

what investigation if you suspect testicular cancer

A

USS scrotum and serum AFP and β HCG required

114
Q

how does inguinal hernia present

A
  • If inguinoscrotal swelling; cannot ‘get above it’ on examination
  • Cough impulse may be present
  • May be reducible
115
Q

what is the treatment for testicular cancer

A

orchidectomy via an inguinal approach

high ligation of the testicular vessels which avoids exposure of another lymphatic field to the tumour

116
Q

what is the management of a varicocele

A

usually managed conservatively. If there are concerns about testicular function or infertility then surgery can be considered.

117
Q

what is the management of an epididymal cyst

A
  • usually supportive
  • Epididymal cysts can be excised using a scrotal approach if they’re large
118
Q

how are hydroceles managed

A
  • Hydroceles are managed differently in children where the underlying pathology is a patent processus vaginalis and therefore an inguinal approach is used in children so that the processus can be ligated.
  • In adults a scrotal approach is preferred and the hydrocele sac excised or plicated.
119
Q

abx for acute pyelonephritis

A

Broad-spectrum cephalosporin or quinolone

120
Q

abx for acute prostatitis

A

Quinolone or trimethoprim

121
Q

management of gonorrhoea

A

Intramuscular ceftriaxone

122
Q

management of pelvic inflammatory disease

A

Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole

123
Q

management of syphilis

A

Benzathine benzylpenicillin or doxycycline or erythromycin

Finals (19 decks)

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