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Phase2a > urology > Flashcards

urology Flashcards

1
Q

what are the stages of CKD

A
  1. kidney damage with normal or increased GFR >90
  2. 60-89
    3a 45-59
    3b 30-44
  3. 15-29
  4. <15 = kidney failure
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2
Q

what are the three sites a kidney stone is likely to get stuck

A
  • ureteric junction of renal pelvis - pelvourteric junction
  • as the ureter passes over the iliac vessels
  • where the ureter enters the bladder - vesouteric junction
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3
Q

what is the surface anatomy of the kidneys

A

T11-L3

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4
Q

what is the blood supply of the kidney

A

Renal artery branch of aorta at L1

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5
Q

what is the path of the ureters

A
  • run over psoas muscle
  • cross iliac vessels at pelvic brim
  • insert into trigone of bladder (smooth area - no rugae)
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6
Q

what the nervous control of the bladder

A
  1. parasympathetic - pelvic nerve
    - S2 - S4 (keep the urine off the floor)
    - Ach neurotransmitter
    - involuntary control
    - detrusor muscle stimulated during voiding
  2. sympathetic - hypogastric plexus
    - T11 - L2
    - noradrenaline
    - involuntary
    - internal urethral sphincter stimulated during storage
  3. somatic nerve - pedunal nerve
    - s2 -s4
    - onuf’s nucleus - guarding reflex tells inappropriate to void
    - Ach
    - external urethral sphincter stimulated during storage
    - can control this (context decides)
  4. afferent pelvic nerve
    - sensory nerve
    - signals from detrusor muscle on how bladder full
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7
Q

which part of the brain controls micturition

A

pontine micturition centre

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8
Q

explain the physiology of micturition

A

storage phase
-as volume increases pressure remains low due to receptive relaxation due to muscle compliance of detrusor muscle

filling phase

  • afferent pelvic nerve sends slow firing signals to pons
  • SNS stimulation/PSNS inhibition maintains detrusor relaxation
  • somatic stimulation (pudendal) maintains urethral contraction

voiding phase

  • micturition reflex autonomic spinal reflex
  • sacral micturition centre receives fast signals via afferent pelvic nerve
  • PSNS stimulated so detrusor contracts
  • SNS inhibited so IUS relaxes
  • somatic inhibited so EUS relaxes
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9
Q

what are the symptoms or storage and voiding disorders

A 
storage 
- frequency 
-nocturia 
-urgency 
- incontinence 
voiding 
- hesitancy 
- straining
- poor/intermittent stream 
post micturition dribbling 
- incomplete emptying 
- haematuria 
-dysuria - painful
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10
Q

what is the difference between BPH and BPE

A

BPH - benign prostatic hyperplasia - is a histological diagnosis based on increased number of cells in the prostrate
- increase in epithelial and stroll cell numbers in periurethral area of prostrate due to increased production or decreased apoptosis (transitional area)

BPE - is a clinically diagnosis based on increased physical size of prostrate found on a PR exam

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11
Q

what are the symptoms of BPH

A

LUTS (lower urinary tract symptoms)

  • nocturnia
  • urgency
  • frequency
  • post micturition dribbling
  • poor stream/flow - hesitancy
  • haematuria
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12
Q

what are the tests for BPH

A
  • U+E
  • US
  • PR exam
  • MSU
  • biopsy
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13
Q

what is the management of BPH

A

lifestyle

  • avoid caffeine and alcohol to reduce the frequency
  • drink less in evening - to decrease nocturnia
  • double voiding - fully emptied bladder
  • bladder training - aim to try and increase time between urination

drugs

  • alpha blocker - decrease smooth muscle tone in prostrate and bladder making it easier to pass urine e.g tamsulosin
  • anticholinergics to relax an overactive bladder
  • 5 alpha reductase inhibitors e.g finasteride decrease prostrate size - inhibits testosterone —> dihydrotestosterone
  • desmopressins slow down urine production for at night

surgery

  • Transurethral resection of prostrate (TURP) - removal of part of prostrate with a tube that passes through urethra
  • cytoplasty - increase size of bladder by adding piece of intestine - helps men whose bladder contracts before its full
  • open prostectomy - removal of prostrate if very large
  • urinary diversion - stoma for urine outside of body
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14
Q

what are the complications of BPH

A
  • symptom progression
  • infections
  • stones
  • haematuria
  • acute retention
  • chronic retention
  • interactive obstructive uropathy
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15
Q

what are the features of acute retention of urine

A
  • painful
  • relieved by catheterisation
  • 600-1L residual urine]
  • normal U+E’s
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16
Q

what is interactive obstructive uropathy

A
  • functional or anatomic obstruction of urine flow at any level of the urine tract
  • residual up to 4L
  • causes nocturnal enuresis (bed wetting)
  • can cause kidney failure during diuresis when catheterised
  • do lying and standing BP to assess likelihood of this
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17
Q

What are the indications for surgery with LUTS

A

mnemonic

Retention
UTI's
Stones
Haematuria
Elevated creatinine due to bladder outflow obstruction
Symptom deterioration
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18
Q

what is hydronephrosis

A
  • dilation of the renal pelvis of calyces causing urinary tract obstruction
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19
Q

what is the difference between supra vesicle and infra vesicle urinary tract obstruction

A

supravesicle - above level of bladder - drain with stent or nephrostomy

infravesicle - below the level of bladder e.g BPE

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20
Q

what are the causes of urinary tract obstruction in the renal tract, ureter and bladder/urethral

A

renal

  • congenital e.g polycystic kidney disease
  • neoplastic
  • inflammatory e.g TB
  • metabolic - calculi/stones

ureter

  • congenital - stricture
  • neoplastic - pressing on ureter
  • inflammatory - TB

Bladder/urethral

  • congenital - urethral valve
  • neoplastic
  • inflammation
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21
Q

what is the definiton of UTI

A

a pure growth of more than 10^5 organisms per ml collected from a fresh clean catch sample

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22
Q

why might patients get renal stones

A 
anatomical 
- congenital (horseshoe, duplex, spina difada, PUJO - pelvouretic junction obstruction)
- aquired (obstuction, trauma, reflux)
urinary 
- dehydration 
- calcium, oxalate, urate, cysteine
- metastable urine
infection
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23
Q

what are the four types of renal stones/what are they made of

A
  • Calcium - oxalate, phosphate
  • uric acid - lucent on KUB XR
  • struvite - infection stones
  • cysteine - congenital (COLA)
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24
Q

What are the prevention methods for urinary stones

A
  • overhydration - 2.5/3L per day urine output
  • low salt/sodium diet - can increase calcium in urine
  • normal dairy intake
  • healthy protein intake (inc uric acid levels)
  • reduce BMI
  • active lifestyle
  • for uric acid stones - alkanization of urine as uric acid stones only form in acidic urine - use sodium bicarbonate or potassium citrate
  • for cysteine stones - excessive overhydration, alkanization and cysteine binders - e.g penicillamine
  • calcium stones - in hypercalcuria use thiazide to decrease calcium excretion
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25
Q

what are the symptoms of urinary stones

A
  • pain loin to groin with nausea and vomiting ‘renal colic’
  • UTI symptoms - dysuria, strangulation, urgency, frequency
  • haematuria
  • proteinuria
    -sterile pyuria (pus)
    -anuria
    -
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26
Q

what are the tests for urinary stones

A
  • FBC, U+E, Ca2+, phosphate, glucose, bicarb, urate
  • dipstick positive for haematuria
  • if urinalysis positive, MSU
  • PH of urine
  • calcium, oxalate, urate, citrate, sodium
  • imaging - non contrast Ct for imaging stones, KUB XR
  • NCCT KUB - non contrast computerised tomography - 99% sensitive for stones 90%specific
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27
Q

what are the differential diagnosis of urinary stones

A
  • vascular accident e.g ruptured AAA >50years
  • bowel pathology - diverticulitis, appendicitis
  • gynae - ectopic pregnancy, ovarian torsion
  • testicular torsion
  • MSK pain
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28
Q

what is the management of urinary stones

A

analgesia
- NSAID suppository
- opiates
antiemetics
IV fluids
medical expulsive therapy if do not pass naturally
- nifedipine (CCB)
- alpha blockers (tamsulosin)
urgent intervention if infection or obstruction
-percutaneous nephrostomy or ureteric stent -Extracorporeal shock wave lithotripsy (ESWL)

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29
Q

what is the pathology and epidemiology of prostrate cancer

A
  • mean diagnosis 72
  • family history 5-10%
  • 12-16% LIFETIME RISK
  • adenocarcinoma of the peripheral zone of prostrate
  • 85% multifocal
  • spreads locally through prostrate capsule
  • metastasis to lymph nodes and bone (sclerotic)
  • androgen sensitive - fusing of gene and onco gene - upregulation of oncogene when androgen fuses
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30
Q

what are the tests for prostrate cancer

A
  • serum PSA (prostrate specific antigen)
  • tissue
  • urine - PCA3 and gene fusion products
  • CT/MRI, US, biopsy, bone scan
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31
Q

what is PSA and the problems with prostrate cancer diagnosis because of it

A
  • prostrate specific antigen
  • not cancer specific
  • can be elevated due to other causes - but most commonly cancer
  • e,g BPE, UTI, prostatitis
  • 70% of men with a raised PSA will not have prostrate cancer
  • 6% of men with a normal PSA will have prostrate cancer
  • with PSA there is an earlier age of presentation (lead time bias) and more confined prostate cancer diagnosed
  • can cause over diagnosis and over treatment - often prostrate wouldn’t be diagnosed
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32
Q

which grading is used for prostrate cancer

A

gleason grading

- histological diagnosis due to appearance of tissue (1-5, 5 being poor)

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33
Q

what is the staging of prostrate cancer

A

T1 - not palpable
T2 - palpable confined to prostrate
T3 - extends beyond prostrate

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34
Q

what are the symptoms of prostrate cancer

A
  • nocturia
  • hesitancy
  • poor stream
  • terminal dribbling
  • obstruction
  • weight loss bone pain = metastases
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35
Q

what is the treatment of prostrate cancer

A

localised disease
- surgery - radical prostectomy - open, laproscopic, robotic
- radiotherapy - external beam or bracytherapy (placed in/near area)
-observation - active monitoring
- hormone therapy
advanced
locally
- radiotherapy
- radical prostectomy
metastasic
- surgical castration - remission of advanced disease
- androgen deprivation therapy - LHRH antagonists blocks release of testosterone

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36
Q

what are the benefits and risk of prostrate cancer screening

A 
benefits 
- early diagnosis of localised disease
- early treatment of advanced disease
risk 
- increased anxiety 
- costs 
-harm caused by investigation/treatment 
- over diagnosis of insignificant disease
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37
Q

what are the differential diagnosis of haematuria

A
  • infection - UTI, pyelonephritis, TB
  • malignancy - anywhere in tract
  • trauma - penetrating vs blunt
  • stones - bladder, kidney, ureteric
  • nephrological - diabetes, nephropathy
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38
Q

what are the criteria for a 2 week wait for bladder cancer

A
  • aged 45 and over and have - unexplained visible haematuria without UTI or visible haematuria persisting after successful UTI treatment
  • aged 60 and over with unexplained non visible haematuria and either dysuria or increased WCC
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39
Q

what are the investigations for bladder/renal/testes cancer

A
  • FBC, U+E, PSA, glucose
  • MSU/dip: microscopy, culture, sensitivity
  • cytology - direct look at cells
  • USS, CTU
  • cystoscopy - tube up bladder with biospy
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40
Q

what is the presentation of bladder cancer

A
  • painless VH
  • recurrent UTI’s
  • irritative voiding
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41
Q

what are the risk factors for bladder cancer

A
  • smoking - urinary excretion of inhaled carcinogens
  • aromatic amines
  • chronic cystitis
  • pelvic irradiation
  • paraplegia -catheters - irritation causing squamous tumour
  • drugs
  • stones - squamous
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42
Q

what is the pathology of bladder cancer

A
  • 90% transitional cell carcinoma (TCC)
  • 5% squamous - related to inflammation e.g parasitic infection (SCC)
  • 1% adenocarcinoma
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43
Q

what is the grading of bladder cancer

A

1- differentiated (original cell) only through lamina propria not muscle
2. intermediate
3 - poorly differentiated

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44
Q

what is the treatment of bladder cancer

A 
grade 1 
- transurethral resection of bladder tumour (turbt) scope removal of tumour
- BCG intravesicle treatment through catheter - stmulates non specific immune response 
grade 2+3
- radial cystectomy - bladder removal
-chemo
4
- palliative chemo/radio
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45
Q

what are the main types of renal cancer

A
  • 95% RCC

- 5% TCC - transitional cell carcinoma

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46
Q

what is the presentation of renal cancer

A
  • haematuria
  • loin pain
  • adbo mass
  • weight loss
  • malaise
  • anorexia
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47
Q

what is the staging of renal cancer

A

1 - <7cm limited to kidney - remove kidney or partial neprectomy
2- >7cm (limited to kidney)
3- tumour in major veins or adrenal gland - radical nephrectomy + adrenalectomy
4- tumour beyond Gerotus fascia, distant metastases - nephrectomy (cytoreductive), systemic treatment

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48
Q

what is the distuingishing feature of a true testicular mass

A

you are able to get above it when examining

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49
Q

what should you think of when a patient has acutely painful testis

A

testicular torsion until proven otherwise

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50
Q

what is epididymitis

A
  • swollen epididymis due to spread of ecoli or chlamydia from prostatic urethra and seminal vesicles
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51
Q

what is a hydrocele

A

excessive fluid in tunica vaginalis

- primary in young boys, secondary = pathology - tumours, infections

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52
Q

what is the testicular appendix

A

remnant of the Mullerian duct

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53
Q

what is a varicocele

A

dilated veins of the pampiniform plexus

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54
Q

what are the risk factors for developing a testicular tumour

A
  • cryptochidism (undescended testes)
  • infant hernia
  • infertility
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55
Q

what is the presentation of a testicular tumour

A 
- painless lump in testes
can be felt above
- hard
-does transilluminate
- hydrocele
- pain unexplained
- metastases e.g lung, abdo, cervical nodes
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56
Q

what are the tests for a testicular tumour

A
  • USS
  • B-HCG marker, AFp
  • CXR -resp symptoms
  • CT - staging
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57
Q

what is the management of testicular tumour

A
  • radical orchidectomy - testes and spermatic cord
  • seminomas very radiosensitive (slow growing)
  • teratomas - cytotoxic chemo
  • treatment causes sterility - collect sperm
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58
Q

what are the layers of the glomerulus filtration barrier

A

capillary - endothelium - BM - podocyte foot processes - bowmans space

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59
Q

what determines if a molecule can cross the filtration barrier

A
  1. size of molecule
  2. charge of molecule - BM is negative
  3. binding to plasma proteins
  4. rate of blood flow
  5. pressure gradient
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60
Q

how much blood does each kidney recieve per min

A

1 litre of 5litres cardiac output

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61
Q

how is eGFR predicted

A

from age, gender, race (creatinine generation)

  • require steady state
  • may be misleading in high muscle mass
  • creatinine also secreted by the kidney
  • inhibitors of this will cause increased serum creatinine and make function look worse e.g trimethoprim
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62
Q

what is fanconi syndrome and what are the symptoms

A
  • proximal tubular insult
  • glycosuria
  • acidosis
  • phosphate wasting - rickets/osteomalacia
  • aminoacid uria
  • caused by wilsons, cystinosis, glycogen storage disease
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63
Q

what is the action of aldosterone on the kidney

A

increases transcription of ENac channels in the collecting duct
causes influx of Na and efflux of K

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64
Q

what is the action of ADH on the kidney

A

ADH acts on principal cells by acting on V2R receptor, causing aquaporin 2 insertion into the apical membrane
increased water permeability
also a direct vasoconstrictor

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65
Q

where is aldosterone released from

A

zona glomerulosa of adrenal cortex

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66
Q

what does renal artery stenosis cause

A
  • increased systemic BP due to decreased delivery of Na to macula densa, even though body Na levels are normal
  • can be treated by stenting
  • flash pulmonary oedema
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67
Q

how do NSAIDS damage the kidney

A
  • prostaglandins cause afferent vasodilation
  • NSAIDS block PG production
  • causes afferent vasoconstriction
  • decreased GFR
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68
Q

which molecule is responsible for constriction of the efferent arteriole

A

angiotensin II

- this is why ACE I and ARB are contraindicated in acute kidney insults and renovascular disease

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69
Q

what drives cellular K+ uptake in the short and long term

A

short term
-insulin and catecholamines
long term
- aldosterone and Na

70
Q

what does increased vit D cause

A
  • increased calcidiol formation in liver
  • increased calcitriol formation in kidneys
  • which causes decreased calcium excretion at kidneys, increased calcium release from bone, and increased calcium absorption in the small intestine
  • leading to increased serum calcium
71
Q

which channel transports calcium in the small intestine

A

plasma membrane calcium pump ATPase

72
Q

what is renal anaemia

A
  • deficiency of EPO in advanced kidney disease leads to decreased haemopoesis and anaemia
  • exacerbated by functional iron deficiency in renal disease
  • seldom seen until eGFR below 30
73
Q

what is the definition of acute kidney injury

A
  • rise in creatinine >26micromol/L in 48 hours (above baseline)
  • rise in creatinine > 50% (best figure in last 6 months)
  • urine output <0.5ml/kg/hr for >6 consecutive hours
    1 out of 3 needed
74
Q

what are the pre renal causes of AKI

A
  • decreased vascular volume - haemorrhage, D+V, pancreatitis
  • decreased CO - cardiogenic shock, MI
  • systemic vasodilation - sepsis, drugs
  • renal vasoconstriction - NSAIDS, ACEI, ARB
75
Q

what are the renal causes of AKI

A
  • glomerular - glomerulonephritis, ATN
  • interstitial - drug reaction, infection, infiltration
  • vascular - vasculitis, DIC, TT, HUS
76
Q

what are the post renal causes of AKI

A
  • extrinsic compression - pelvic malignancy, prostratic hypertrophy, retroperitoneal fibrosis
  • within renal tract - stone, renal tract malignancy, stricture, clot
77
Q

give two life threatening complications of AKI

A
  • pulmonary oedema - furosemide

- hyperkalaemia - treat if >6.5mmol/L or ECG changes (insulin and dextrose, calcium gluconate, IV fluid, salbutamol)

78
Q

what are the investigations of AKI

A
  • dipstick and quantification of proteinuria (haematuria/proteinuria may suggest intrinsic disease)
  • USS within 24 hours - small kidneys suggest CKD, asymmetry suggests renal vascular disease
  • liver function - hepatorenal disease
  • platelets (HUS/TTP)
79
Q

what is the management of AKI

A
  • monitor - fluids/balance, K+, vitals, lactate if sepsis
  • treat hypovolaemia
  • treat sepsis
  • stop nephrotoxic medication - NSAIDS, ACEI, ARB
  • stop drugs that may increase complications e.g diuretics
  • check drug doses
  • dialysis
80
Q

what are the indications for dialysis in AKI

A
  • pulmonary oedema
  • persistant hyperkalaemia
  • metabolic acidosis
  • uraemia encephalopathy or pericarditis
  • drug overdose
81
Q

what are the types of RRT + describe

A

haemodialysis
- blood is passed over a semi permeable membrane against dialysis fluid flowing in the opposite direction
- diffusion of solutes occurs down the concentration gradient
- a hydrostatic gradient is used to clear excess fluid as required
- access via arteriovenous fistula
-HD needed 3 times a week or more - time consuming
Peritoneal dialysis
- uses the peritoneum as a semi permeable membrane
- a catheter is inserted into the peritoneal cavity and fluid infused
- fluid diffuses slowly across
- continuous and performed at home
- can get infection of catheter
- loss of membrane function over time

82
Q

what is chronic kidney disease

A
  • abnormal kidney structure or function, present for >3 months with implications for health
  • GFR < 60ml/min/1.73^2 on at least 2 occasions 90 days apart
  • markers of kidney damage
83
Q

what are the stages of CKD by GFR

A 
G1 >90 - if other evidence of kidney damage: protein/haematuria 
G2 60-89
G3a 45-59
G3b 30-44
G4 15-29
G5 <15
84
Q

what are the stages of CKD by albuminuria

A

stage albumin ACR (albumin:creatinine)
A1 <30mg <3
A2 30-300 3-30
A3 >300 >30

85
Q

What are the causes of CKD

A
  • diabetes - inc glucose can decrease NO (vasodilator) causing increase renal bp
  • glomerulonephritis
  • Inc BP/renovascular disease
  • high cholesterol
  • infections
  • polycystic kidney disease
  • long term use of NSAIDS
  • blockage in urine flow e.g recurrent stones
86
Q

what are the tests for CKD

A
  • eGFR
  • dipstick: ACR and other proteins
  • U+E, Hb, Ca2+ decrease, phosphate increase, PTH increase, ANA, ANCA (for intrinsic renal disease)
  • USS for site, symmetry, exclude obstruction
  • biopsy
87
Q

how should CKD be monitored

A
  • GFR and ACR at least annually
  • if high risk - every 6 months - high risk:
    • G3b+
    • A2 + G3a
    • A3
  • if very high every 3-4 months
  • small fluctuations are common but a decrease of 25% is significant
88
Q

what is the management of CKD

A
  • appropriate referral to nephrology
  • treatment to slow renal disease progression
  • treatment for renal and other complications of CKD
  • preparation for renal replacement therapy
89
Q

when should you refer a renal CKD patient to nephrology

A
  • stage G4 +G5
  • ACR > 70mg or 30mg with haematuria
  • declining GFR of >25%
  • BP poorly controlled despite >4 antihypertensives at therapeutic dose
  • known or suspected rare or genetic causes of CKD
90
Q

what is the treatment use to slow renal progression in CKD

A
  • ARB or ACE - don’t combine due to risk of hyperkalaemia
  • glycemic control
  • lifestyle - exercise, healthy weight, smoking cessation, decreased salt intake
  • BP targets 140/90 or if ACR >70 130/80
91
Q

what is the treatment of renal + other complications in CKD

A
  • anaemia
  • acidosis - sodium bicarbonate
  • oedema - restrict Na + fluid intake, loop diuretic/thiazide
  • CKD bone mineral disorders

other
- inc CV disease risk - anti platelets, atorvostatin

92
Q

describe preparation for RRT

A
  • should begin in progressive CKD when risk of kidney failure is 10-20% within a year
  • listed for a deceased donor transplant 6 months before RRT scheduled
  • efforts made to find a preemptive living donor
93
Q

what are the contraindications for renal transplant

A
  • absolute: cancer with metastases
  • temporary: active infection, HIV, unstable CVD
  • relative: congestive heart failure, CVD
94
Q

describe the different types of kidney donation

A
  • living donor: best graft function and survival, especially if HLA matched
  • deceased donor - 1 donor after brain death, 2. expanded criteria donor (older kidney) 3. donor after cardiac death
95
Q

wha are the different means of immunosuppression

A
  • glucocorticosteroids - decrease transcription of inflammatory cytokines, SE: BP, hyperlipidaemia, osteoporosis, diabetes mellitus, impaired wound healing, skin fragility, cataracts
  • monoclonal antibodies e.g daclizumab (selectively block activated T cells via CD25)
  • antimetabolites
  • calcineurin - inhibit T cell activation and proliferation
96
Q

what is the management of a patient who has had a renal transplant

A
  • infection risk especially opportunistic
  • increased malignancy risk
  • rejection - acute (antibody mediated or cellular) or chronic (causes increased loss of function of the graft)
  • no vaccinations with live organisms
  • good personal hygiene must be upheld
  • avoid foods with high risk of food poisoning
97
Q

what is glomerulonephritis

A
  • a number of conditions which are caused by pathology in the glomerulus
  • present with haematuria, proteinuria or both
  • are diagnosed on renal biopsy
  • cause CKD
  • can progress to kidney failure
  • exist on a spectrum from nephrotic (proteinuria due to podocyte pathology) to nephritic (haematuria due to inflammatory damage)
98
Q

what are the investigations for glomerulonephritis

A
  • dipstick: protein, ACR
  • blood: FBC, U+E, LFT, CRP, Ig, electrophoresis, autoantibodies
  • CXR (pulmonary haemorrhage), RUS
  • renal biopsy - for diagnosis
99
Q

what is the management of glomerulonephritis

A
  • general as for CKD including BP control and inhibition of renin angiotensin axis
  • steroids
  • statin
  • antithrombotics
  • other treatment depends on diagnosis
100
Q

what are the features of a nephritic glomerulonephritis

A
  • haematuria
  • cola coloured urine
  • inflammation of the glomeruli
  • red cell casts on blood film
101
Q

describe IgA nephropathy

A
  • commonest GN
  • diffuse mesangial IgA deposits
  • asymptomatic NHV or episodic VH
  • slow disease, progressing to renal failure over 30 years
  • ACEI/ARB reduce proteinuria and protect against further renal decline
  • corticosteroids and fish oil if persistent proteinuria
  • lower cholesterol
102
Q

list some nephritic GN

A
  • small cell vasculitis
  • IgA nephropathy
  • lupus nephritis
  • post streptococcal GN
  • antiglomerular basement membrane anti GBM (autoantibodies to type IV collagen)
103
Q

what is lupus nephritis

A
  • when SLE effects kidneys
  • ISPN classification from 1-6 with 6 being the worst
  • immunosuppression and supportive care
104
Q

what is post streptococcal GN

A
  • after throat infection
  • streptococcal antigen resides in glomerulus
  • immune complex formation and inflammation
105
Q

describe nephrotic GN

A
  • proteinuria >3g/24hours
  • hypoalbuminaemia
  • oedema
  • hyper coagulability
  • hyperlipidaemia
  • podocyte pathology
106
Q

give two nephrotic GN

A
  • membranous nephropathy

- minimal change disease

107
Q

describe membranous nephropathy

A
  • thickening of glomerular capillary wall
  • IgG, complement deposit in sub epithelial surface causing leaky glomeruli
  • primary or secondary to malignancy, autoimmune disease e.g RA, SLE, infection e.g hepB/C, drugs
    primary: glomerular podocyte membrane PLA2R is target in 70-80% (autoantibody)
  • treat with ACEI/ARB + BP control
  • control of oedema, hypertension, hyperlipidaemia and proteinuria
108
Q

what is urge incontinence/overactive bladder

A
  • urgency with frequency, with or without nocturia, appearing in the absence of local pathology
109
Q

what is the management of overactive bladder

A
  • behavioural therapy - bladder training, frequency volume chart, decreased caffeine and alcohol
  • antimuscarinic agents - decreased PSNS activity by blocking M2/3, SE - dry mouth
  • B3 agonists - increase SNS in bladder
  • Botox - blocks neuromuscular junction for Ach release SE - incomplete bladder emptying and need to catheterise in 15%
  • sacral neuromodulation - insertion of electrode to S3 nerve root to modulate afferent signals from bladder
  • surgery - augmentation cytoplasty
110
Q

what is stress incontinence

A

due to weakening of the pelvic floor

often secondary to birth trauma - due to denervation of the pelvic and urethral and weakening of fascial support of bladder and urethra

  • congenital
  • neurogenic
111
Q

what is the management of stress incontinence

A

pelvic floor physio

surgery - sling, bulking agents, duloxetine

112
Q

what are the parameters of bladder diaries

A 
frequency day/night 
volume day/night
nocturnal volume
functional capacity
incontience/day
113
Q

what is the physiology of an erection

A
  • release of NO
  • Ca2+ and cGMP hyper polarises this
  • relaxes sm cells
  • allows engorgement
114
Q

which enzyme returns a penis to the flaccid state

A

phosphodiesterase

115
Q

which nerves cause erection and return to flaccid

A

erection - S2-S4 PSNS
flaccid - T11-L2 sympathetic
(both carried in cavernous nerve)

116
Q

what is the anatomy of the penis

A
  • 2 corpus cavernosa covered by tunica albuginea
  • contains spongy vascular erectile tissue
  • corpus spongiosum contains urethra
  • supplied by pudendal artery of internal iliac
117
Q

what is erectile dysfunction

A

the persistent inability to attain and sustain an erection sufficient to permit satisfactory sexual performance

118
Q

what are the causes of ED

A
  • smoking
  • alcohol
  • diabetes
  • endocrine - hypogonadism hyperthyroidism
  • neuro cord lesions, MS
  • pelvic surgery - prostate
  • psychological - indicators - sudden onset, good nocturnal and early morning erections, situational ED, younger patient
119
Q

what are the tests for ED

A
  • sexual history
  • testosterone
  • examine genitalia
  • prostrate
  • hypogonadism - small testes
  • lipids
  • glucose
120
Q

what is the treatment of ED

A
  • of underlying condition
  • decrease risk factors
  • weight loss
  • exercise
  • 1st line- phosphodiesterase inhibitors e.g sildenafil/viagra (requires sexual stimulation)
  • 2nd line- vacuum devices and other drugs such as intracavernosal injection
  • 3rd line -penile prosthesis implant
121
Q

what are the classifications of UTI

A

complicated

  • structural/functional abnormality of GU tract
  • pregnant
  • men
  • catheter
  • recurrent
  • immunocompromised
  • urosepsis

uncomplicated
- normal renal tract structure and function

asymptomatic bacteriuria

122
Q

what are the risk factors for UTI

A
  • increased bacterial occupation: sexual activity, urinary incontinence, faecal incontinence, constipation
  • increased binding of uropathogenic bacteria: spermicide use, decreased oestrogen, menopause
  • decreased urine flow: dehydration, obstructed urinary tract
  • increased bacteria growth: DM, immunosuppression, obstruction, stones, catheter, pregnancy
123
Q

what are the symptoms of cystitis

A
  • dysuria
  • frequency
  • urgency
  • suprapubic pain
  • haematuria
  • polyuria
124
Q

what are the symptoms of pyelonephritis

A 
diagnostic
-loin tenderness
-fever
-pyuria
others
- rigor
-costovertebral pain
-septic shock
-cystitis symptoms
125
Q

what are the symptoms of prostatitis

A
  • pain - perineum, rectum, scrotum, penis, bladder, lower back
  • fever
  • malaise
  • nausea
  • urinary symptoms
  • swollen or tender prostate on PR
126
Q

What are the tests for UTI

A
  • dipstick in non pregnant women - shows pyuria (leukocytes in urine), blood and positive for nitrites
  • MSU culture
  • blood tests: FBC, U+E, CRP, culture
  • imaging: USS and referral to urology in men with upper UTI, failure to respond to treatment, recurrent UTI, pyelonephritis, unusual organism, persistant haematuria
127
Q

what are the main organisms causing UTI

A
  • e.coli >50%
  • pseudomonas aeruginosa - recurrent UTI/underlying pathology
  • staphylococcus saprophyticus (commensal of skin) in young women
  • proteus - renal stone associated
  • klebsiella - hospital/catheterised
128
Q

what is the management of UTI

A

uncomplicated

  • empirical treatment with 3 day course of trimethoprim or nitrofurantoin if eGFR >30 or if pregnant
  • if fails culture urine and treat according to antibiotic sensitivity
complicated 
- get expert health
- preterm birth in pregnancy and intrauterine growth restriction
-nitrofurantoin 
men
- lower - nitrofurantoin
- prostatitis - fluoroquinolone
129
Q

what are the symptoms of chlamydia trachomatous

A 
often asymptomatic or:
- dysuria 
-vaginal discharge
- intermenstrual bleeding
male 
-dysuria
-urethral discharge
130
Q

what is the treatment of chlamydia

A
  • azithromycin or doxycycline

- erythromycin in pregnancy

131
Q

what are the symptoms of a Neisseria Gonorrhoea infection

A

urethral/vaginal discharge

dysuria

132
Q

what is the treatment with gonorrhoea

A

ceftriaxone and azithromycin

133
Q

list some causes of urethritis

A
  • gonorrhoea
  • chlamydia
  • non gonococcal urethritis (NGU)
  • bacterial vaginosis
  • genital candidiasis
134
Q

what are the symptoms of genital candida and treatment

A
  • dyspareunia - difficult or painful sex
  • genital itch
  • cottage cheese like discharge
  • treat with azoles
135
Q

what are the symptoms and treatment of bacterial vaginosis

A

-fishy
-thin
-white
discharge
-oral or PV metronidazole

136
Q

what are the symptoms and treatment of NGU

A
  • urethral discharge
  • dysuria
  • urethral discomfort
  • treat with doxycycline
137
Q

describe autosomal dominant polycystic kidney disease

A
  • 1 in 400-1000
  • 85% have mutations in PKD1 (chromosome 16)
    -reach end stage kidney failure by 50’s
  • or PKD2 (chromosome 4)
  • slower to reach ESRF by 70’s
    may be clinically silent or: loin pain, visible haematuria, cyst infection, hypertension, renal caliculi, liver cysts
  • USS test of choice
  • treatment
  • water intake 3-4L per day may suppress cyst growth
  • BP management
  • treat infection
    -plan for RRT
138
Q

describe autosomal recessive polycystic kidney disease

A
  • chromosome 6
  • presents antenatally with renal cysts, congenital hepatic fibrosis —> portal hypertension
  • no specific therapy
139
Q

what is the pathogenesis of UTI

A 
colonic flora
colonisation of vagina
colonisation of urethral meatus
ascent of bacteria - bacteriuria 
UTI
140
Q

What are the host factors that cause UTI

A
  • ureteric reflex
  • female shorter urethra
  • stasis of urine due to BPH, stones, stasis in pregnancy, low urinary volume
  • catheter
  • loss of oestrogenisation - post menopause PH in the vagina rises and the vagina becomes more colonised by colonic flora, decreased vaginal mucus and increased mucosal receptivity to UPEC
141
Q

what is the most likely pathogen to cause a UTI

A 
Uropathogenic E.coli (UPEC)
- virulence 
pili and fimbrae for adherence
deployment of toxins - tissue damage 
antimicrobial resistance
142
Q

what would be found on a dipstick test for UTI

A
  • haematuria
  • proteinuria
  • altered PH
  • glucose - diabetics more prone to UTI
  • leukocytes and nitrites specific for UTI
143
Q

what would be found on microscopy for UTI

A
  • white blood cells >10^4wbc/ml (pyuria)
  • casts - renal pathology e.g glomerulonephritis
  • bacteria - counts > 10^4 indicative of infection
  • epithelial cells - poorly taken specimen
144
Q

how is a UTI identified by culture

A

it is achromogenic - colour of culture decides what organism it is

145
Q

describe catheter associated UTI

A
  • insertion may carry bacteria
  • at risk up to 24 hours post removal
  • form biofilms (prosthetic material)
  • hospitable environment
  • incomplete voiding
146
Q

when should asymptomatic bacteriauria be treat

A

in pregnancy

not in elderly

147
Q

what are the three types of prostatitis

A
  1. acute bacteria
    - systemically unwell, fever, rigors, significant voiding LUTS, pelvic pain, tender prostrate
  2. chronic bacterial
    - symptoms >3 months, recurrent UTI, pelvic pain, voiding LUTS, uropathogens in urine with or without blood
  3. CPPS (chronic pelvic pain syndrome)
    - chronic pelvic pain +/- LUTS+/- UTI
148
Q

what is the pathology of prostatitis

A
  • ascending infection from urinary tract
  • haematogenous spread
  • gram -ve organisms
149
Q

what is the treatment of prostatitis

A

quinolone for 28 days
pain relief
stool softener
alpha blocker

150
Q

what are the causes of epididymorchitis (sexual and non sexual)

A 
sexually transmitted 
- chylamidia 
-gonorrhoea
- gram -ve
non sexually transmitted 
- mumps
-TB
-candida
151
Q

what are the symptoms and signs of epididymorchitis

A
  • acute onset unilateral scrotal pain +/- swelling, urethritis +UTI symptoms

signs

  • tenderness
  • oedema (scrotal)
  • erythema
  • pyrexia
  • urethral discharge
  • hydrocele
152
Q

what features suggest scrotal pain may be due to testicular torsion

A
  • short pain duration
  • nausea and abdo pain
  • previous short duration orchalgia
153
Q

what are the tests for epididymorchitis

A
  • urethral smear
  • dipstick
  • swab
  • FPU
  • MSU:MC&S
  • CRP+ESR
154
Q

What is the treatment of epididymorchitis

A
  • analgesia
  • antibiotics - doxycline (STI) ofoxacicin/quinolone (non STI)
  • sexual abstinence
  • supportive underwear
  • contact tracing
155
Q

what are the complications of STI

A
  • PID
  • tubal factor infertility
  • ectopic pregnancy
  • chronic pelvic pain
  • neonatal transmutation
  • Fitz Hugh curtis syndrome
156
Q

how is chlamydia diagnosed

A 
- nucleic acid amplification tests 
female
-self collected vaginal swab
-endocervical swab
-first void urine
male 
-first void urine
157
Q

how is gonorrhoea diagnoses

A
  • near patient test
    microscope of gram stained smear of genital secretions looking for gram -ve diplococci within cytoplasms of polymorphs
  • culture
    -NAAT
158
Q

which organism causes syphilis

A
  • treponema pallidum
159
Q

what are the stages of a syphilis infection

A
  • primary chancre - 95% genital skin, incubation 9-90days, macule - papule- ulcer
  • secondary (primary may be present concurrently) - mucous membrane lesions, generalised lymphadenopathy, alopecia, hoarseness, bone pain, hepatitis, nephrotic syndrome, deafness, meningitis, cranial nerve palsies
  • tertiary - 20-40 years post infection
160
Q

how is syphilis diagnosed

A
  • early moist lessons, may be able to identify motile spirochetes on wet mount using dark ground microscopy
  • serology usually positivee if ulcer present
161
Q

what is the treatment of syphilis

A

penicillin by injection

partner notification

162
Q

which organism is most likely to cause pyelonephritis and what is the treatment

A
  • e.coli

- IV coamoxiclav, ciprofloxacin/cephalosporin

163
Q

what are the symptoms and signs of AKI

A

symptoms

  • low urine output
  • confusion
  • nausea and vomiting

signs

  • hypertension
  • distended bladder
  • pericardial rub
  • pallor
  • rash
  • bruising
164
Q

who are the high risk patients for AKI

A
  • elderly
  • ckd
  • DM
  • in patients (15%)
  • CCF
  • myeloma
165
Q

presence of c-ANCA and antiPR3 is suggestive of which disease

A

Wegeners/granulomatosis with polyangiitis

166
Q

presence of antiGBM is suggestive of which disease

A
  • goodpastures/ anti glomerular basement membrane antibody

type 4 collagen

167
Q

what is the presentation of CKD

A
  • fatigue
  • weakness
  • lethargy
  • restless legs
  • insomnia
  • muscle cramps
  • pulmonary oedema
  • polyuria
  • headache
168
Q

what are the complications of PKD

A
  • hypertension
  • SAH
  • mitral valve prolapse
169
Q

what are the secondary causes of nephrotic syndrome

A
  • DM
  • SLE
  • amyloidosis
  • NSAIDS
  • myeloma
170
Q

what are the secondary causes of nephritic syndrome

A
  • goodpastures
  • SLE
  • vasculitis
  • post strep throat

Phase2a (10 decks)

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