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Finals > Renal medicine > Flashcards

Renal medicine Flashcards

1
Q

what is bacteriuria

A

bacteria in the urine - may be asymptomatic or symptomatic

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2
Q

what is lower UTI

A

uretheritis
cystitis
prostatitis

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3
Q

what is upper UTI

A

renal pelvis - pyelonephritis

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4
Q

what are risk factors for UTI

A

female

sexual intercourse

exposure to spermicide in females (by diaphragms or condoms)

pregnancy

menopause

reduced defence host -

immunosuppression, DM

urinary tract - obstruction, stones, catheter, malformation

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5
Q

UTI in catheterised patients - tx?

A

no treatment unless symptomatic.

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6
Q

main organism(s) causing UTI

A

E.coli

proteus mirabilis
klebsiella pneumonia
staphylococcus saprophyticus

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7
Q

symptoms of cystitis

A 
frequency
dysuria
urgency
haematuria
suprapubic pain
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8
Q

symptoms of acute pyelonpehritis

A 
high fevers
rigors
vomiting
loin pain
tenderness
oliguria
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9
Q

symptoms of prostatitis

A

flu-like symptoms
low backache
few urinary symptoms
swollen or tender prostate on PR

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10
Q

signs of UTI

A

fever
abdo pain or loin tenderness
foul-smelling urine
occasionally distended bladder, enlarged prostate

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11
Q

investigations for a UTI

A

DIPSTICK THE URINE

if dipstick negative but patient symptomatic -> send a MSU sample for lab MC&S to confirm this.

Send a lab MC&S anyway if

  • child (do USS)
  • MALE
  • pregnant
  • immunosuppressed
  • ill

MC&S - pure growth of >10 organisms/ml is diagnostic.

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12
Q

causes of a sterile pyuria

A 
TB
treated UTI <2 weeks prior
inadequately treated UTI
appendicitis
calculi; prostatitis
bladder tumour
polycystic kidney
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13
Q

bloods for UTI

A

FBC
U+E
CRP
blood cultures

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14
Q

imaging for UTI

A 
consider ultrasound
referral to urology for assessment (CTKUB, cystoscopy, urodynamics) for UTI:
- in children
- men
- if failure to respond to treatment 
- recurrent UTI (>2/year)
- pyelonephritis
- unusual organisms
- persistent haematuria
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15
Q

prevention of UTI

A

drink more water

antibiotic prophylaxis, continuously or post-coital

drinking 200-750ml of cranberry or lingo berry juice a day - reduces risk of symptomatic recurrent infection in women by 10-20%. (Avoid if on warfarin)

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16
Q

management of UTI - non-pregnant women ≥16 years old

A

drink plenty of fluids; urinate often

Trimethoprim or nitrofurantoin (eGFR ≥45) for 3 days.

2nd line

  • nitrofurantoin if not used first line
  • fosfomycin
  • pivmecillinam
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17
Q

management of UTI - pregnant women

A

nitrofurantoin (eGFR ≥45) for 7 days (AVOID AT TERM).

2nd line

  • Amoxicillin for 7 days
  • Cefalexin for 7 days
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18
Q

management of UTI - men ≥16y

A

trimethoprim or nitrofurantoin (eGFR ≥45) for 7 days.

2nd line
- consider pyelonephritis or prostatitis

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19
Q

management of prostatitis

A

1st line
- ciprofloxacin
or ofloxacin
(alt if unable to take fluoroquinolone - trimethoprim)

2nd line (on specialist advice)
- levofloxacin or co-trimoxazole
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20
Q

management of pyelonephritis

A

ORAL cefalexin or ciprofloxacin

(if sensitivity known - co-amoxiclav or trimethoprim)

IV first line if severely unwell or unable to take oral treatment:
ceftriaxone 
cefuroxime
ciprofloxacin
gentamicin
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21
Q

management of pyelonephritis - pregnant women

A

oral first line - cefalexin

IV first line - cefuroxime

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22
Q

features of genitourinary TB

A

have a high suspicion in sterile pyuria and those with risk factors (esp HIV +ve), look for high ESR/CRP, ask about past lung TB

dysuria
flank pain
perineal pain
scrotal fistula
sterile pyuria - leucocytes in urine
haematuria
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23
Q

criteria for diagnosing AKI - stage 1

A

rise in creatinine >26 in 48h or increase in creatinine >1.5x baseline

urine output <0.5ml/kg/h for >6 consecutive hours

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24
Q

criteria for diagnosing AKI - stage 2

A

increase in creatinine 2-2.9x baseline

<0.5ml/kg/h for >12h consecutive hours UO

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25
Q

criteria for diagnosing AKI - stage 3

A

increase in creatinine >3x baseline or >354 or commenced on RRT irrespective of stage

<0.3ml/kg/h for >24h or anuria for 12h

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26
Q

risk factors for developing AKI

A 
age >75
CKD
HF
peripheral vascular disease
chronic liver disease
DM
drugs 
sepsis
poor fluid intake/increased losses
history of urinary sx
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27
Q

pre-renal causes of AKI

A

renal hypoperfusion - hypotension (any cause, inc hypovolaemia, sepsis), renal artery stenosis ± ACEi

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28
Q

renal causes of AKI

A

acute tubular necrosis - commonest intrinsic renal cause of AKI - due to drugs e.g. ahminoglycosides, radiological contrast or myoglobinuria in rhabdomyolysis.

glomerular - autoimmune such as SLE, HSP, drugs, infections, primary glomerulonephritides

interstitial - drugs, infiltration with e..g lymphoma, infection, tumour lysis syndrome

vascular - vasculitis, malignant high BP, thrombus or emboli from angiography, HUS/TTP, dissection.

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29
Q

post-renal causes of AKI

A

caused by urinary tract obstruction
- luminal: stones, clots, sloughed papillae

  • mural: malignancy (ureteric, bladder, prostate), BPH, strictures
  • extrinsic compression - malignancy (e.g. pelvic), retroperitoneal fibrosis
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30
Q

assessment of a patient with an AKI

A

ABCDE
- check fluid status - check BP, JVP, skin turgor, CRT <2sec, UO (catheterise)

  • check an urgent K on a venous blood specimen and an ECG to check for life-threatening hyperkalaemia
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31
Q

bedside tests for AKI

A

DIPSTICK URINE ALWAYS

  • infection or glomerular disease
  • microscopy for casts, crystals, cells
  • culture for infection
  • consider Bence Jones Proteins
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32
Q

bloods for AKI

A

U+E, FBC, LFT, CLOTTING, CK, ESR, CRP

consider ABG for acid-base assessment

blood cultures if signs of infection

consider blood film and renal immunology if systemic cause suspected

  • immunoglobulins and paraprotein electrophoresis
  • complement (c3/4), autoantibodies (ANA, ANCA, anti-GBM)
  • ASOT
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33
Q

imaging for AKI

A

renal ultrasound

  • distinguishes obstruction and hydronephrosis, and look for abnormalities such as:
  • — cysts
  • — small kidneys
  • — masses
  • — corticomedullary differentiation
  • Complete anuria is unusual in AKI and suggests an obstruction
    o In elderly men – prostate should be considered – often relieved by catheterisation.
  • If catheterization does not resolve anuria and you suspect obstruction above the prostate, get an URGENT USS TO CHECK FOR HYDRONEPHROSIS AND CONSIDER AN URGENT CTKUB (no contrast required), which can show OBSTRUCTING MASSES OR CALCULI.
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34
Q

parameters suggesting CKD

A

small kidneys
anaemia
low calcium
high phosphate

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35
Q

indications for dialysis

A

refractory pulmonary oedema

persistent hyperkalaemia

severe metabolic acidosis (ph <7.2)

uraemia complications such as encephalopathy or uraemic pericarditis

drug overdose - BLAST: barbiturates, lithium, alcohol, salicylates, theophylline

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36
Q

management of AKI

A

assess volume status

  • low urine output
  • non-visible JVP
  • poor tissue turgor
  • low BP
  • high pulse

signs of fluid overload

  • high BP
  • high JVP
  • lung crepitations
  • peripheral oedema
  • gallop rhythm on cardiac auscultation

STOP NEPHROTOXIC DRUGS e.g. NSAIDs, ACEi, gentamicin, amphotericin. stop metformin if creatinine >150.

monitor observations hourly.
daily u+e
daily fluid balance and daily weight

treat underlying cause
- pre-renal: iv fluids, treat sepsis with iv abx.

  • intra-renal: refer to nephrology early

post-renal: catheterise and consider CTKUB if obstruction likely

RRT - haemodilaysis/ haemofiltration

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37
Q

complications of AKI

A

hyperkalaemia
pulmonary oedema
uraemia
acidaemia

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38
Q

ECG changes in hyperkalaemia

A

Tall Tented T waves
Widened QRS complex
Increased PR interval
small or absent P wave

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39
Q

immediate treatment of hyperkalaemia

A

Do ECG + if ECG changes:
10ml of 10% calcium gluconate

IV insulin and glucose - 10 units of act rapid in 100ml of 20% glucose over 30 mins.

salbutamol nebuliser

IV sodium bicarbonate if patient is acidotic.

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40
Q

treatment of pulmonary oedema

A

sit the patient up
give high flow oxygen
IV furosemide 40mg
diamorphine 2.5mg IV (+anti-emetic e.g. cyclizine)

if no response, haemodialysis or haemofiltration is needed.

consider CPAP

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41
Q

prevention of AKI (sick day rules)

A 
review drugs
withhold/avoid
- diuretics
- NSAIDs
- ACEi
- Metformin 
- abx - gentamicin, nitrofurantoin

use opiates with caution as they accumulate in renal failure. oxycodone is better in renal impairment.

radiological contrast
- ensure patient is well hydrated - 1L 0.9% saline over 12 hours pre and post-procedure

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42
Q

CKD - definition

A

Impaired renal function for >3 months based on abnormal structure or function,

OR GFR <60ml/min/1.73m2 for 3 months with or without evidence of kidney damage.

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43
Q

stages of CKD

A 
stage 1 - >90*
stage 2 - 60-89*
stage 3a - 45-59
stage 3b - 30-44
stage 4 - 15-29
stage 5 - <15

*stages 1+2 (eGFR >60) - must have other evidence of renal damage e.g. proteinuria, haematuria, evidence of abnormal anatomy

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44
Q

causes of CKD

A 
diabetes
hypertension or renovascular disease
glomerulonephritis - IgA nephropathy
Unknown
pyelonephritis and reflux nephropathy
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45
Q

risk factors for developing ESRF

A 
deteriorating function
proteinuria ≥3mg/mmol
haematuria
high BP
young age
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46
Q

commonest inherited cause of CKD

A

adult polycystic kidney disease

rare - Alpert’s syndrome: CKD, hearing loss, minor eye problems

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47
Q

symptoms of uraemia

A 
anorexia
vomiting
restless legs
fatigue
weakness
pruritis
bone pain
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48
Q

causes of rapid decline in renal function

A 
infection
dehydration
uncontrolled high BP
metabolic disturbance e.g. high Ca
obstruction
nephrotoxins
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49
Q

chief cause of death in renal failure

A

cardiovascular disease

- falling GFR is an independent risk factor for CVD

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50
Q

investigations for CKD

A

creatinine-based estimate of eGFR (eGFRcreatinine) - advise patient not to eat meat in the 12h before having this blood test.
o Interpret with caution – reduced muscle mass will give an overestimate and increased muscle mass may give an underestimate.

  • Cystatin C-based estimate of GFR (eGFRcystatinC), use if:
    o An eGFRcreatinine of 45-59, sustained for 90d AND
    o No proteinuria (ACR <3)
  • early morning urine sample to test for urinary albumin:creatinine ratio (ACR)
  • <3 - no proteinuria. no action.
  • ≥3-70 - suggests proteinuria, REPEAT TEST WITHIN 3 MONTHS.
  • if ≥70 - don’t repeat

transient increases in urine ACR may be seen with menstruation, urinary tract infection (UTI), strenuous exercise, and upright posture (‘orthostatic proteinuria’).

Make a diagnosis of CKD if there is a persistent reduction in renal function (eGFR is <60 mL/min/1.73 m2) and/or proteinuria (urinary ACR is ≥3 mg/mmol) lasting for at least three months.

Check the person’s nutritional status, body mass index (BMI), blood pressure, and serum HbA1c and lipid profile to assess for cardiovascular risk factors

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51
Q

for which indications should patients with CKD be referred early to a nephrologist.

A

CKD stage 4+5
moderate proteinuria (ACR ≥70) unless due to DM and already treated.
proteinuria (ACR ≥30) with haematuria

rapidly falling egfr (>15 in 1year or >10 in 5years)
high BP poorly controlled despite ≥4 antihypertensives
known or suspected rare or genetic cause of CKD
suspected renal artery stenosis

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52
Q

management of CKD

A
  1. Investigation - identify and treat reversible causes - relieve obstruction, stop nephrotoxic drugs, deal with high Ca, and cardiovascular risk (stop smoking, healthy weight), tight glucose control in DM.
  2. Limit progression
    - BP (target <140/90). treat with ACEi or ARB in diabetic kidney disease even if normal BP.
  • Renal bone disease: low vitamin D, high phosphate, low calcium
  • Secondary hyperparathyroidism - due to low calcium, high phosphate and low vitaminD. can cause a Brown tumour in bones.

severe clinical manifestations

  • osteitis fibrosa cystica (hyperparathyroid bone disease)
  • osteomalacia - due to low vit D
  • osteoporosis
  • osteosclerosis

phosphate rises in CKD, which increases PTH further, also precipitates in the kidney and vasculature.

  • restrict diet, give binders (e.g. Calcichew) to reduce gut absorption.
  • vitamin D

offer colecalciferol or ergocalciferol to treat vit D deficiency first.
- if vit D deficiency has corrected but sx of CKD mineral and bone disease persist –> vitamin D analogues (e.g. calcitriol) to people with GFR ≤30.

offer bisphosphonates to prevent and treat osteoporosis in its with GFR ≥30.

cardiovascular modification - give stains and aspirin.

diet - healthy, moderate protein diet, K restriction if hyperkalaemic, avoidance of high phosphate foods (milk, cheese, eggs)

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53
Q

symptom control in CKD

A

ANAEMIA
o Most significant reason is REDUCED ERYTHROPOIETIN LEVELS.
 Gives a normocytic normochromic anaemia
 Becomes apparent when GFR <35ml/min
 Anaemia in CKD predisposes to the development of LEFT VENTRICULAR HYPERTROPHY – associated with a three fold increase in mortality in renal patients.
o Check haematinics and replace iron/b12/folate if necessary
o if still anaemic, consider recombinant EPO

ACIDOSIS
- consider sodium bicarbonate supplements

OEDEMA
- high doses of loop diuretics may be needed (e.g. furosemide + metalozone each morning) and restriction of fluid and sodium intake.

RESTLESS LEGS/CRAMPS
- clonazepam or gabapentin
or
dopamine agonists

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54
Q

types of dialysis

A

haemodialysis
haemofiltration
peritoneal dialysis - risk of PF peritonitis (due to s. epidermidis/aureus)

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55
Q

indications for emergency dialysis

A

AEIOU

  • Acidosis
  • Electrolytes (refractory K)
  • Intoxicants (lithium)
  • Overload (fluid) when diuresis isn’t working (refractory)
  • Uraemia (pericarditis, encephalitis)
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56
Q

absolute c/i to renal transplant

A

active infection
cancer
severe co-morbidity

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57
Q

triple therapy used to maintain immunosuppression in transplant patients

A

tacrolimus/ciclosporin
azathioprine/mycophenolate
prednisolone

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58
Q

complications of transplants

A

surgical - bleed, thrombosis, infection, urinary leaks, lymphocyte, hernia

delayed graft function - acute tubular necrosis in graft due to ischaemic-perfusion injury.

rejection

drug toxicity

infection - HSV, candida, pneumocystis jerovecii, CMV

malignancy

cardiovascular disease - leading cause of death in transplant patients.

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59
Q

important bloods to check before biopsy (renal)

A

FBC
CLOTTING
G+S

stop anticoagulants

  • aspirin 1 week before
  • warfarin 2-3d before
  • LMWH - 24h before
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60
Q

indications for renal biopsy

A
  • unexplained AKI/CKD
  • acute nephritic syndromes
  • unexplained proteinuria and haematuria
  • systemic diseases associated with kidney dysfunction
  • suspected transplant rejection
  • to guide treatment
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61
Q

what is glomerulonephritis

A

inflammation of the glomeruli and nephrons

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62
Q

what are the consequences of inflammation

A

damage to the glomerulus restricts blood flow, leading to compensatory high BP (activation of renin-angiotensin system).

damage to the filtration mechanism allows protein and blood to enter the urine.

loss of usual filtration capacity leads to AKI

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63
Q

presentation of nephrotic syndrome

A

hypoalbuminaemia
proteinuria
oedema
hyperlipidaemia

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64
Q

presentation of nephritic syndrome

A

haematuria
proteinuria
hypertension
oliguria

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65
Q

causes of nephrotic syndrome

A

membranous nephropathy
minimal change disease
focal segmental glomerulosclerosis

mesangiocapillary GN

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66
Q

causes of nephritic syndrome

A 
IgA nephropathy
post-streptococcal nephropathy
vasculitis
SLE
anti-GBM disease
cryoglobulinaemia

mesangiocapillary GN

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67
Q

investigations for glomerulonephritis

A

bloods - FBC, U+E, LFT, ESR, CRP, IgA, electrophoresis, complement

autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM

blood culture
ASOT
HBsAg
anti-HCV

urine

  • RBC casts
  • MC&S
  • bence jones protein
  • ACR

imaging

  • CXR
  • renal ultrasound

RENAL BIOPSY - gold standard for glomerulonephritis.

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68
Q

general management of glomerulonephritis

A

early referral to a nephrologist.

keep BP <130/80 or <125/75 if proteinuria >1g/d

include an ACEi or ARB - reduce proteinuria and preserving renal function.

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69
Q

what is IgA nephropathy

A

most present with macroscopic or microscopic haematuria - occasionally nephritic syndrome.

typical patient - young man with episodic macroscopic haematuria, recovery is often rapid between attacks.

increased IgA possibly due to infection, which forms immune complexes and deposits in mesangial cells.

occurs DURING OR STRAIGHT AFTER a streptococcal infection.

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70
Q

what would you find on renal biopsy for IgA nephropathy

A

mesangial proliferation, immunofluorescence shows deposits of IgA and C3

high serum IgA
normal C3

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71
Q

treatment of IgA nephropathy

A

BP control with ACEi.

immunosuppression may slow decline of renal function.

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72
Q

What is Henoch-Schönlein purpura

A

it is similar to IgA nephropathy but has a systemic picture.

causes a small vessel vasculitis.

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73
Q

features of HSP

A

features

  • Purpuric rash on extensor surfaces (legs, buttocks)
  • fitting polyarthritis
  • abdominal pain - GI bleeding (maleana, haematemesis)
  • Nephritis
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74
Q

diagnosis of HSP

A

clinical.

confirmed with positive IF for IgA and C3 in skin or renal biopsy.

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75
Q

treatment of HSP

A

BP control with ACEi
Ibuprofen - for joint pain
Steroid treatment for bowel symptoms in children.
Skin rash - dapsone

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76
Q

what is Goodpasture’s disease

A

anti-glomerular basement membrane disease

caused by autoantibodies to type IV collagen.

type IV collagen is found in the kidneys and lungs.

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77
Q

presentation of good pasture’s syndrome

A 
haematuria/nephritic syndrome
pulmonary haemorrhage (haemoptysis)
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78
Q

treatment of good pasture’s syndrome

A

plasma exchange
steroids
± cytotoxics

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79
Q

what is post-streptococcal GN

A

Occurs MANY WEEKS AFTER A SORE THROAT OR SKIN INFECTION.

streptococcal antigen is deposited on the glomerulus, causing a host reaction and immune complex deposition.

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80
Q

presentation of post-streptococcal GN

A

nephritic syndrome

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81
Q

investigation for post-streptococcal GN

A

high ASOT

Low C3

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82
Q

treatment for streptococcal GN

A

supportive

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83
Q

what forms rapidly progressive GN

A
  1. immune complex deposition e.g. post-infectious GN, SLE, IgA/HSP
  2. pauci-immune disease (80-90% ANCA +ve) - granulomatosis with polyangiitis: c-ANCA +ve,

microscopic polyangiitis (p-ANCA +ve),

churg-strauss syndrome

  1. anti-GBM disease
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84
Q

presentation of patients with rapidly progressive GN

A

AKI

fever, myalgia, weight loss, haemoptysis.

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85
Q

commonest reason for death in rapidly progressive GN

A

pulmonary haemorrhage

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86
Q

treatment of rapidly progressive GN

A

aggressive immunosuppression with high-dose IV steroids and cyclophosphamide
± plasma exchange

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87
Q

which type of GN is caused by hepatitis B/C

A

membranous nephropathy (hep B)

mesangiocapillary GN (hep C)

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88
Q

which type of GN is caused by SLE

A

class V lupus nephritis causes membranous nephropathy

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89
Q

in diabetic nephropathy, which specific nodules are found on biopsy

A

Kimmelstein-Wilson nodules

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90
Q

in amyloidosis, what is found on biopsy specifically

A

apple green birefringence (nodular)

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91
Q

which drugs can cause nephrotic syndrome

A

NSAIDs
penicillamine
anti-TNF
gold

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92
Q

pathophysiology of nephrotic syndrome

A

injury to the podocyte - effacement of the foot processes and loss of podocytes causes heavy protein loss

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93
Q

presentation of nephrotic syndrome

A

patients present with pitting oedema (ankles, shins, periorbitally)

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94
Q

investigations of nephrotic syndrome

A

urine dip: protein ++++
albumin low on LFT
?renal biopsy

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95
Q

ddx of nephrotic syndrome

A

CCF - high JVP, pulmonary oedema, mild proteinuria

liver disease - low albumin

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96
Q

management of minimal change disease

A

STEROIDS - common in children.

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97
Q

complications of nephrotic syndrome

A

susceptibility to infection e.g. cellulitis, strep infections and SBP.

thromboembolism (40%) - hypercoagulable state due to high clotting factors and platelet abnormalities.

hyperlipidaemia - hepatic lipoprotein synthesis in response to low oncotic pressure.

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98
Q

treatment of nephrotic syndrome

A

reduce oedema - loop diuretics e.g. furosemide.

  • daily weights and daily U+Es
  • fluid restrict to 1L/d and salt restrict while giving diuretics.

reduce proteinuria
- ACEi/ARB

reduce risk of complications

  • anticoagulate if nephrotic range proteinuria
  • statin to reduce cholesterol
  • treat infections promptly and vaccinate

treat underlying cause

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99
Q

minimal change disease biopsy

A

normal under light microscopy

electron microscopy - effacement of the podocyte foot processes.

rx
- 90% children and 70% adults undergo remission with steroids.
(if relapsing and steroid-dependent) - cyclophosphamide or ciclosporin/tacrolimus

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100
Q

associations of membranous nephropathy

A

malignancy
hep B
drugs (gold, pencillamine, NSAIDs)
autoimmune disease (thyroid, SLE)

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101
Q

biopsy of membranous nephropathy

A

diffusely thickened GBM with IgG and C3 sub epithelial deposits on immunofluorescence.

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102
Q

treatment of membranous nephropathy

A

secondary - treat underlying cause

idiopathic - ACEi/ARB and diuretics

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103
Q

associations of focal segmental glomerulosclerosis (FSGS)

A 
primary - idiopathic
secondary
- vesicoureteric reflux
- IgA nephropathy
- Alport syndrome
- Vasculitis
- SCD
- Heroin use
- HIV
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104
Q

presentation of FSGS

A

nephrotic syndrome or proteinuria

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105
Q

treatment of FSGS

A

responds to corticosteroids in 30%

cyclophosphamide or ciclosporin - if steroid resistant

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106
Q

associations of mesangiocapillary GN

A

Immune complex mediated - hepatitis C, SLE, monoclonal gammopathies.

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107
Q

treatment of mesangiocapillary GN

A

underlying cause as priority

ACEi/ARB

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108
Q

where do loop diuretics act on the kidney

A

Na/K/2Cl co-transporter on the thick ascending loop of Henle

cause hypokalaemia, hyponatraemia, alkalosis (H+ excretion increased), hypocalcaemia.

can be ototoxic in high doses

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109
Q

where do thiazide diuretics act

A

inhibit NaCl transporter in the DISTAL CONVOLUTED TUBULE

cause

  • hypokalaemia
  • hyponatraemia
  • hypomagnesaemia
  • high uric acid (gout)
  • reduce urinary calcium
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110
Q

k-sparing diuretics SEs

A

hyperkalaemia
metabolic acidosis (reduced H excretion)
gynaecomastia

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111
Q

where do carbonic anhydrase inhibitors act

A

proximal convoluted tubule

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112
Q

where do k-sparing diuretics act

A

cortical collecting tubule

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113
Q

another name for IgA nephropathy

A

Berger’s disease

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114
Q

presentation of granulomatosis with polyangiitis (Wegener’s )

A

upper respiratory tract: epistaxis, sinusitis, nasal crusting.

lower respiratory tract:

  • dyspnoea
  • haemoptysis

rapidly progressive GN (pauci-immune)

saddle-shaped nose deformity

also - vasculitic rash, eye involvement (e.g. proptosis), cranial nerve lesions

c-ANCA positive

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115
Q

test for microscopic polyangiitis

A

p-ANCA

116
Q

presentation of churg strauss syndrome

A

present with asthma, allergic rhinitis, purpura, peripheral neuropathy.

p-ANCA positive
peripheral eosinophilia

117
Q

inheritance of aport syndrome

A

x-linked (affects males usually)

118
Q

presentation of alport syndrome

A

microhaematuria persistent with intermittent gross haematuria.

hearing loss
eye abnormalities

119
Q

drug that causes SLE + nephritic syndrome

A

Infliximab

120
Q

presentation of SLE

A

A RASH POINTs MD

arthritis

renal disease (proteinuria, cellular casts)
ANA +ve
serositis (pleurisy or pericarditis)
haematological disorders (haemolytic aneamia/leucopenia/thrombocytopenia)

photosensitivity
oral ulcers
immunological disorder (anti-dsDNA, anti-Sm)
neurological disorders (seizures or psychosis)

malar rash
discoid rash

121
Q

rapidly progressive GN biopsy findings

A

CRESCENT FORMATION
monocytes
macrophages

122
Q

urinalysis findings of nephritic syndrome

A

haematuria
RBC casts
proteinuria

123
Q

management of nephritic syndrome

A

low-sodium diet
water restriction

proteinuria and/or HTN - ACEi or ARBs

severe HTN and/or oedema - diuretics

severe kidney failure - RRT

124
Q

look at this summary of nephrotic syndrome causes

A
  • Minimal change = children/young people. steroid responsive.
  • Membranous disease = common in lupus, malignancy, HEP B
  • FSGS = heroin use and HIV
125
Q

look at this summary of nephritic syndrome causes

A
  • IgA nephropathy – occurs during or straight after viral infection. ACEi effective.
  • Post-strep nephropathy – occurs many weeks after viral infection. self-limiting, spontaneous and remission within 6-8 weeks.
  • vasculitic (ANCA) – patients will mention nose bleeding, feeling of congestion and generalized myalgia.
    o Wegeners – c-ANCA
  • Anti-GBM: usually causes renal disease and pulmonary haemorrhage (haemoptysis)
  • SLE – butterfly rash, nephritis, low c3/c4, low hb, low plt, anti-dsdna, ANA
  • Alport syndrome – ADPKD (renal disease) + ocular problems + hearing loss
126
Q

what is cryoglobulinaemia

A

form of vasculitis

presence of cryoglobulins (proteins) that clump together at cold temp, restricting blood flow and causing damage to the skin.

high platelets
high C3/C4

ANCA negative

elderly patients

associated with HEPATITIS C

127
Q

cause of acute interstitial nephritis

A

immune reaction drugs, infections or autoimmune disorders.

drugs

  • NSAIDs
  • Abx - penicillins
  • diuretics - furosemide
  • allopurinol
  • omeprazole
  • phenytoin

infections

  • staph
  • streps
  • brucella
  • leptospira

immune causes

  • SLE
  • sarcoid
128
Q

features of acute interstitial nephritis

A

‘allergic’ picture - fever, rash, peripheral eosinophilia.

fever, rash, arthralgia, hypertension

mild renal impairment

129
Q

investigation of acute interstitial nephritis

A

sterile pyuria

white cell casts

130
Q

treatment of acute interstitial nephritis

A

stop/treat causative agent

if renal function doesn’t improve within a week -> trial of prednisolone for 4 weeks may improve prognosis.

131
Q

common cause of chronic tubulointerstitial nephritis

A

analgesic nephropathy

132
Q

what is analgesic nephropathy

A

history is of chronic, heavy analgesic use, usually NSAIDs

commoner in pain

133
Q

presentation of analgesic nephropathy

A

loin pain (papillary necrosis) but is often silent until late CKD

134
Q

cause of urate nephropathy

A

AKI due to uric acid precipitation within the tubules.

most often due to tumour lysis syndrome, seen in haematological malignancies after chemotherapy, which leads to overproduction of uric acid.

the renal parenchyma appears bright on USS.

plasma urate is often markedly raised with urinary birefringent crystals on microscopy.

rx

  • keep well hydrated
  • oral allopurinol before chemotherapy
  • urinary alkalinisation with sodium bicarbonate (increased solubility of uric acid).
135
Q

treatment of hypercalcaemia

A

rehydration with iv fluids

pamidronate (iv bisphosphonates)

136
Q

drugs toxic to the kidney - cause AKI usually by direct acute tubular necrosis, or by causing interstitial nephritis

A

NSAIDs

Antimicrobials - gentamicin, rifampicin, sulphonamides, penicillins

anticonvulsants - lamotrigine, valproate, phenytoin

other drugs - omeprazole, furosemide, thiazides, ACEi/ARBs, cimetidine, lithium, iron, cisplatin.

radiocontrast

137
Q

radio contrast nephropathy - cause and treatment

A

iatrogenic AKI with iv contrast

tx

  • stop nephrotoxic drugs
  • pre-hydrate with iv 0.9% saline
  • then give saline after imaging - 0.9% saline iv
138
Q

what is rhabdomyolysis

A

results from skeletal muscle breakdown with release of its contents into the circulation, including myoglobin, K, phosphate, urate and CK.

139
Q

complications of rhabdomyolysis

A

hyperkalaemia
AKI

myoglobin is filtered by the glomeruli and precipitates, obstructing renal tubules.

140
Q

causes of rhabdomyolysis

A

post-ischaemia e.g. embolism, clamp on artery during surgery.

trauma

prolonged immobilisation
e.g. falling in elderly

burns

crash injury

excessive exercise

uncontrolled seizures

drugs and toxins - statins, alcohol, ecstasy, heroin, snake bite, carbon monoxide, neuroleptic malignant syndrome.

infections - coxsackie, EBV, influenza

metabolic - low K, low phosphate, myositis, malignant hyperpyrexia

inherited muscle disorders e.g. McArdle’s disease, Duchenne’s muscular dystrophy.

141
Q

clinical features of rhabdomyolysis

A

muscle pain
swelling
tenderness
red-brown urine (myoglobinuria)

142
Q

tests for rhabdomyolysis

A

plasma CK >1000

exclude MI as a cause (troponin negative)

visible myoglobinuria (tea or cola coloured urine)

others

  • high phosphate
  • high potassium
  • low calcium (enters muscles)
  • high urate

AKI develops 12-24h later and DIC is associated

143
Q

treatment of rhabdomyolysis

A

urgent treatment for hyperkalaemia

IV fluid rehydration is a priority to prevent AKI - maintain urine output at 300ml/h until myoglobinuria has ceased, initially up to 1.5l fluid/h may be needed.

iv sodium bicarbonate - to alkalinise urine to ph >6.5.

dialysis may be needed.

ideally manage pt in HDU/ICU setting to allow early detection of deterioration and regular bloods and monitoring.

144
Q

what is renovascular disease

A

defined as stenosis of the renal artery or one of its branches.

145
Q

causes of renovascular disease

A

atherosclerosis (80%) - co-existing IHD, stroke or PVD

fibromuscular dysplasia (10%) - younger males

rarer causes

  • takayasu’s arteritis
  • antiphospholipid syndrome
  • post-renal transplant
  • thromboembolism
  • external compression
146
Q

signs of renovascular disease

A

high BP resistant to treatment,

worsening renal function after ACEi/ARB in bilateral renal artery stenosis

‘flash’ PULMONARY OEDEMA (sudden onset - no LV impairment on echo)

weak leg pulses can be found

147
Q

investigation for renovascular disease

A

ultrasound - renal size asymmetry (affected side smaller)

doppler USS - disturbance in renal blood flow

CT/MR angiography - more sensitive

RENAL ANGIOGRAPHY - GOLD STANDARD (done after CT)

148
Q

treatment of renovascular disease

A

comprehensive antihypertensive regimens.

transluminal angioplasty ± stent placement or revascularisation surgery.

149
Q

what is haemolytic uraemic syndrome

A

characterised by microangiopathic haemolytic anaemia (MAHA) - intravascular haemolytic + red cell fragmentation.

endothelial damage triggers thrombosis, platelet consumption and fibrin strand deposition, mainly in renal microvasculature.

strands cause mechanical destruction of passing RBCs

thrombocytopenia and AKI result.

150
Q

causes of HUS

A

E.coli O157 - produces a verotoxin that attacks endothelial cells.

typically affects young children in outbreaks after eating undercooked contaminated meat.

151
Q

signs of HUS

A

abdominal pain
bloody diarrhoea
AKI

152
Q

tests for HUS

A 
haematuria/proteinuria
blood film - SCHISTOCYTES (fragmented RBC)
low platelets
low Hb
clotting tests normal
153
Q

treatment of HUS

A

seek expert advice
dialysis for AKI may be needed
plasma exchange used in severe disease

154
Q

what is thrombotic thrombocytopenic purpura (TTP)

A

HAEMATOLOGICAL EMERGENCY

all patients have a MAHA (severe with jaundice) an LOW PLATELETS.

155
Q

5 cardinal symptoms of TTP

A 
Fever
MAHA
AKI
Low platelets
Neuro symptoms (seizures, hemiparesis, reduced vision, low GCS)
156
Q

pathophysiology of TTP

A

genetic or acquired deficiency of a protease (ADAMTS13) that normally cleaves multimeters of vWF.

o Large vWF multimers form, causing platelet aggregation and fibrin deposition in small vessels, leading to microthrombi

157
Q

causes of TTP

A

idiopathic (40%)

autoimmune - SLE
cancer
pregnancy
drugs - quinine
bloody diarrhoea (childhood HUS)
158
Q

investigations for TTP

A 
haematuria/proteinuria
blood film - schistocytes
low platelets
low Hb
clotting normal
159
Q

treatment for TTP

A

URGENT PLASMA EXCHANGE
steroids for non-responders
eculizumab

  • the unexplained occurrence of thrombocytopniea and anaemia should prompt immediate consideration of the diagnosis and evaluation of a peripheral blood smear for evidence of maha.
160
Q

what is important control in patients with diabetes to prevent end-organ damage

A

BLOOD PRESSURE

+ good BM control

161
Q

screening for nephropathy in DM

A

ACR - for microalbuminuria

162
Q

treatment of microalbuminuria in DM

A

ACEi or ARB (IRRESPECTIVE OF BP)

Manage cardiovascular risk factors - stop smoking, reduce cholesterol, consider aspirin

163
Q

symptoms of cholesterol emboli

A

fever, uncontrolled high BP, lived reticularis, oliguria, AKI, gangrene

164
Q

what is renal tubular acidosis

A
  • Metabolic acidosis due to impaired acid secretion by the kidney
  • HYPERCHOLARAEMIC METABOLIC ACIDOSIS WITH A NORMAL ANION GAP.
165
Q

what is type 1 renal tubular acidosis

A

inability to excrete H and generate acidic urine in the distal tubule, even in states of metabolic acidosis.

166
Q

causes of type 1 renal tubular acidosis

A

idiopathic

connective tissue disease - marfans, ehlers danlos

autoimmune - SLE, Sjogrens (commonest cause)

nephrocalcinosis (e.g. hypercalcaemia)

tubulointerstitial disease e.g. chronic pyelonephritis, chronic interstitial nephritis

drugs - lithium

167
Q

features of type 1 renal tubular acidosis

A

rickets (+growth failure) or osteomalacia, due to buffering of H with calcium in bone.

NEPHROCALCINOSIS WITH RENAL CALCULI, leading to recurrent UTIs –> combination of hypercalciuria, low urinary citrate and alkaline urine (all favour calcium phosphate stone formation).

168
Q

treatment of type 1 renal tubular acidosis

A

oral sodium bicarbonate or citrate

169
Q

difference between type 1 and type 2 RTA

A

type 1 is linked with renal calculi

170
Q

what is type 2 RTA

A
  • ‘Bicarbonate leak’: a defect in HCO3- reabsorption in the proximal tubule resulting in excess HCO3- in the urine (pH <5.5) leading to a metabolic acidosis
171
Q

causes of type 2 RTA

A

o Idiopathic
o Fanconi syndrome
o Tubulointersitial disease e.g. myeloma, interstitial nephritis
o Drugs (e.g. lead or other heavy metals, acetazolamide, out-of-date tetracycline)

172
Q

electrolyte imbalance in type 2 RTA

A

hypokalaemia

173
Q

treatment of type 2 RTA

A

high doses of bicarbonate

174
Q

what is type 4 RTA

A

due to hypoaldosteronism - causes hyperkalaemia and acidosis

175
Q

causes of type 4 RTA

A

addisons
diabetic nephropathy
o INTERSTITIAL NEPHRITIS (SLE, chronic obstruction)
o DRUGS (K-sparing diuretics, beta-blockers, NSAIDs, ciclosporin)

176
Q

treatment of type 4 RTA

A

remove cause
fludrocortisone 0.1mg
calcium resonium - to control K

177
Q

what is fanconi syndrome

A

proximal tubular dysfunction leading to loss of amino acids, glucose, phosphate and HCO3 in urine.

178
Q

features of fanconi syndrome

A

dehydration
metabolic acidosis
osteomalacia/rickets
electrolyte abnormalities

179
Q

congenital causes of fanconi syndrome

A 
idiopathic
cysteinosis
wilsons disease
tyrosinaemia
lowe syndrome
180
Q

acquired causes of fanconi syndrome

A

 Heavy metal poisoning (lead, mercury, cadmium, platinum, uranium)
 Drugs (gentamicin, cisplatin, ifosfamide)
 Light chains (Myeloma, amyloid)
 Sjogrens

181
Q

treatment of fanconi syndrome

A

o REMOVE ANY CAUSE
o REPLACE LOSSES
o K, HCO3-, PHOSPHATE AND VITAMIN D SUPPLEMENTS

182
Q

what is bartter syndrome

A

hereditary hypokalaemic tubulopathies

  • Low K
  • metabolic alkalosis
  • hypercalciuria
183
Q

causes of bartter syndrome

A

inherited mutation in the co-transporter targeted by LOOP DIURETICS

184
Q

treatment of bartter syndrome

A 
replace K
give indomethacin (prostaglandin synthesis inhibitor)
185
Q

what is gitelman syndrome

A

hereditary hypokalaemic tubulopathies

  • Low K
  • metabolic alkalosis
  • hypocalciuria
  • Low Mg
186
Q

cause of gitelman syndrome

A

o Inherited mutation in the co-transporter targeted by THIAZIDE DIURETICS

187
Q

treatment of gitelman syndrome

A

replace Mg + K

188
Q

which genes are affected in ADPKD

A

PKD1 - 85% (chromosome 16)

PKD2 - 15% (chromosome 4)

189
Q

signs of ADPKD

A

renal enlargement with cysts
abdo pain/flank pain/chest pain/back pain

haematuria
cyst infection (e.coli, staph aureus)
renal calculi

high BP (ACEi/ARB first line)

progressive renal failure

190
Q

extra-renal manifestations of ADPKD

A 
liver cysts - 70%
intra-cranial aneurysms (SAH) 
mitral valve prolapse 
ovarian, pancreatic and spleen cysts.
diverticular disease
191
Q

investigation for ADPKD

A

CT abdomen to diagnose

192
Q

screening for ADPKD

A

abdominal USS
 ≥2 cysts, unilateral or bilateral if aged <30y
 ≥2 cysts in both kidneys if aged 30-59y
 ≥4 cysts in both kidneys if aged ≥60y

193
Q

treatment of ADPKD

A

monitor U+E
high BP - treat aggressively with ACEi/ARB (target <130/80)

treat infections, dialysis or transplant for ESRF, genetic counselling.

selected patients - TOLVAPTAN (vasopressin receptor 2 antagonist) may be an option - slows progression of cyst development.

194
Q

what is autosomal recessive PKD associated with

A

childhood - renal cysts and hepatic fibrosis

195
Q

what is medullary cystic disease

A

inherited disorder with tubular loss and medullary cyst formation.

juvenile - autosomal recessive (10-20% of ESRF in children)

adult - AD is rare

196
Q

signs of medullary cystic disease

A

shrunken kidneys
cysts restricted to renal medulla
salt wasting

polyuria
polydipsia
enuresis
failure to thrive
ESRF
197
Q

extra-renal features of medullary cystic disease

A 
retinal degeneration
retinitis pigmentosa
skeletal changes
cerebellar ataxia
liver fibrosis
198
Q

signs of tuberous sclerosis

A

autosomal dominant disorder

signs

  • ‘ash leaf’ macules
  • shagreen patches
  • angiofibromas
  • periungual fibroma
  • adenoma sebaceum
  • low IQ
  • epilepsy
  • infantile spasms
199
Q

what is von hippel landeau syndrome

A

chief cause of inherited renal cancers.

other cancers its associated with:

  • eyes
  • spinal cord
  • brain
  • phaeochromocytoma
  • pancreas
200
Q

what is alport syndrome

A

x-linked inherited disorder

201
Q

signs of alport syndrome

A

renal - haematuria, proteinuria, progressive renal failure

ears - sensorineural deafness

eyes - ocular defects

202
Q

biopsy signs of alport syndrome

A

thickened GBM with ‘splitting’

203
Q

what are the different stages of diabetic nephropathy

A
  1. GFR elevated - renal blood flow increases, increasing the GFR and leading to microalbuminuria.
  2. Glomerular hyperfiltration
    - in the next 5-10y, mesangial expansion gradually occurs and hyper filtration at the glomerulus seen without microalbuminuria.
  3. Microalbuminuria
    - indicates progression of disease.
  4. Nephropathy
    - GFR declines and proteinuria increases
204
Q

what is the pathgnomic finding in myeloma

A

bence jone proteins in the urine

myeloma kidney is due to blockage of tubules by CASTS, consisting of light chains.

205
Q

features of kidney myeloma

A

AKI
CKD
amyloidosis
hypercalcaemic nephropathy

206
Q

treatment of kidney myeloma

A

FLUID INTAKE 3litres/d to prevent further impairment.

dialysis may be required in AKI

207
Q

clinical features of hypercalcaemia

A

‘bones, stones, groans, psychic moans’

abdominal pain
vomiting
constipation
polyuria
polydipsia
depression
anorexia
weight loss
tiredness
weakness

painful bones - osteitis fibrosa cystica

hypertension
confusion
pyrexia

renal stones
renal failure

ectopic calcification e.g. cornea

cardiac arrest
reduced QT interval

208
Q

where do renal calculi most commonly deposit in the renal tract

A 
pelviureteric junction (PUJ)
pelvic brim
vesicoureteric junction (VUJ)
209
Q

types of renal calculi

A 
calcium oxalate/phosphate
magnesium ammonium phosphate (struvite)
urate 
cystine
mixed
210
Q

presentation of renal colic

A

excruciating ureteric spasms ‘loin to groin’ pain

nausea and vomiting

often cannot sit/lie still

LUTS - dysuria, frequency, urgency
or pyelonephritis sx (fever, rigors, loin pain, nausea, vomiting)

haematuria

211
Q

tests for renal calculi

A

BLOODS - FBC, U+E, CALCIUM, GLUCOSE, BICARBONATE, URATE

urine dipstick - blood +++ (gross or microscopic haematuria)

urine ph
>7 - urea splitting organisms and struvite stones
<5 - uric acid stones

urine microscopy (may detect crystals)
- dumbbell-shaped or octahedron-shaped crystals - calcium oxalate
  • rhomboid/needle-shaped crystals - uric acid stones
  • rectangular prisms - struvite stones

MSU - MC&S

212
Q

imaging for renal calculi

A

NON-CONTRAST CT KUB

KUB XR

  • x-ray positive (radio-opaque) - calcium-containing stones
  • x-ray negative (radiolucent) - uric acid stones

ULTRASOUND

  • to look for hydronephrosis or hydroureter
  • done in patients in whom radiation exposure should be minimised - pregnant, children, recurrent stone formers.
213
Q

initial management of renal calculi

A

ANALGESIA e.g. diclofenac 75mg IV/IM

  • offer iv paracetamol to adults, children and young people if NSAIDs C/I or are not giving sufficient pain relief.
  • consider opiates next in line if still in pain.

IV FLUIDS
antibiotics (cefuroxime or gentamicin) if infection

214
Q

management - ureteric/renal stones <5mm

A

90-95% pass spontaneously
watchful waiting
increase fluid intake

215
Q

management - ureteric stone 5-10mm

A

offer medical expulsive therapy first if distal - alpha blocker (tamsulosin) or nifedipine.
if still persistnet
1. ESWL
2. URS

216
Q

management - ureteric stone >10mm

A

1st line - Ureteroscopy

2nd line - Extracorporeal shockwave lithotripsy (ESWL)

217
Q

management - kidney stones 5-10mm

A

1st line - Extracorporeal shockwave lithotripsy (ESWL)

2nd line - Ureteroscopy (URS)

218
Q

management - kidney stone 10-20mm

A

1st line - ESWL or URS

2nd line - PCNL (PERCUTANEOUS NEPHROLITHOTOMY)

219
Q

management - kidney stone >20mm (inc staghorn)

A

1st line - PCNL (PERCUTANEOUS NEPHROLITHOTOMY)

2nd line - URS

220
Q

management - sepsis/anuria in an obstructed kidney

A

1st line - Abx and ureteric stenting

or

Abx + percutaneous NEPHROSTOMY

221
Q

indications for urgent intervention

A

presence of infection and obstruction - a percutaneous nephrostomy or ureteric stent may be needed to relieve obstruction.

urosepsis
intractable pain or vomiting
impending acute renal failure
obstruction in a solitary kidney
bilateral obstructing stones
222
Q

prevention of renal calculi

A

DRINK PLENTY OF FLUIDS
normal dietary calcium
reduce salt intake to <6g

calcium stones - in hypercalciuria, a thiazide diuretic is used to reduce calcium excretion.

oxalate - reduce oxalate intake. pyridoxine may be used.

struvite - treat infection promptly. common in UTIs. PROTEUS causes alkaline urine and calcium precipitation and ammonium salt formation.

urate - allopurinol - urine alkalisation may also help, as urate is more soluble at ph >6 (with potassium citrate or sodium bicarbonate).

cystine - vigorous hydration to keep urine output >3L/d and urinary alkalinisation. d-penicillinamine is used to chelate cystine, given with pyridoxine to prevent vitamin B6 deficiency.

223
Q

cause of calcium phosphate stones

A

hyperparathyroidism

type 1 renal tubular acidosis

224
Q

cause of struvite stones

A

PROTEUS
recurrent UTIs

formed of Mg, ammonium and phosphate

225
Q

cause of urate stones

A

low urine pH
hyperuricaemia, gout, hyperuricosuria

RADIOLUCENT (requires CTKUB)

226
Q

cause of cystine stones

A

inherited recessive disorder - renal tubular defect

227
Q

which medications precipitate renal stones

A 
diuretics
antacids
acetazolamide
corticosteroids
theophylline
aspirin
allopurinol
vit C and D
indinavir
228
Q

predisposing factors of renal calculi - urinary tract abnormalities

A 
pelviureteric junction obstruction
hydronephrosis
horseshoe kidney
vesicoureteric reflux
medullary sponge kidney
229
Q

cause of urinary tract obstruction

A

luminal

  • stones
  • blood clot
  • sloughed papilla
  • tumour - renal, ureteric, bladder

mural

  • congenital or acquired stricture
  • neuromuscular dysfunction
  • schistosomiasis

extra-mural

  • abdominal or pelvic mass/tumour
  • retroperitoneal fibrosis
  • iatrogenic - post-surgery
230
Q

features of acute upper urinary tract obstruction

A

loin to groin pain
± superimposed infection
± loin tenderness or an enlarged kidney

231
Q

features of chronic upper tract obstruction

A

flank pain
renal failure
superimposed infection
polyuria - impaired urinary conc

232
Q

features of acute lower urinary tract obstruction

A

acute urinary retention
severe suprapubic pain
distended, palpable bladder, dull to percussion

233
Q

features of chronic lower urinary tract obstruction

A

sx - urinary frequency, hesitancy, poor stream, terminal dribbling, overflow incontinence.

signs - distended, palpable bladder

234
Q

tests for urinary tract obstruction

A

ULTRASOUND

if there is hydronephrosis or hydroureter –> arrange a CT KUB

235
Q

treatment of upper urinary tract obstruction

A

NEPHROSTOMY OR URETERIC STENT (hydronephrosis)

236
Q

treatment of lower urinary tract obstruction

A

URETHRAL OR SUPRAPUBIC CATHETER

beware a large diuresis after relief of obstruction - temporary salt-losing nephropathy may occur resulting in the loss of several litres of fluid a day
(monitor weight, fluid balance and U+E closely)

237
Q

what is periaortitis

A

retroperitoneal fibrosis

Chronic periaortitis is inflammation caused by advanced atherosclerosis (affecting the infrarenal portion of the abdominal aorta).

causes ureteric obstruction resulting in renal failure.

risk of AAA rupture

238
Q

causes of periaortitis

A

idiopathic retroperitoneal fibrosis (IRF)

inflammatory AAA

perianeurysmal RF

239
Q

consequences of idiopathic retroperitoneal fibrosis

A

ureters get embedded in dense, fibrous tissue resulting in progressive bilateral ureteric obstruction.

240
Q

presenting features of periaortitis

A

middle aged male
vague loin, back or abdo pain
high BP
unilateral or bilateral hydronephrosis and consequent renal insufficiency

241
Q

tests for periaortitis

A

bloods - high urea and creatinine, high ESR, high CRP, anaemia.

ultrasound - dilated ureters (hydronephrosis)

CT/MRI - periaortic mass

242
Q

treatment of periaortitis

A

retrograde stent placement to relieve obstruction

± ureterolysis

immunosuppression with low dose steroids

243
Q

causes of acute retention

A 
prostatic obstruction 
urethral strictures
anticholinergics
alcohol
constipation
post-op
infection
cauda-equina syndrome
carcinoma
244
Q

examination for acute retention

A

abdominal exam
DRE of prostate
perianal sensation

245
Q

tests for acute retention

A 
MSU
U+E
FBC
PSA
renal ultrasound if renal impairment
246
Q

conservative measures to aid voiding in acute urinary retention

A 
analgesia
privacy on hospital wards
ambulation
standing to void
voiding to the sound of running tap
247
Q

management of acute retention

A

catheterise and start an alpha-blocker (tamsulosin)

if in clot retention –> 3-way catheter and bladder washout.

if >1L residual check U+E and monitor for post-obstructive diuresis.

after 2-3days trial without catheter (TWOC) may work

248
Q

prevention of acute retention

A

in males - finasteride to reduce prostate size

249
Q

presentation of chronic urinary retention

A

overflow incontinence
acute on chronic retention
lower abdominal mass
UTI or renal failure

250
Q

causes of chronic urinary retention

A

prostatic enlargement common
pelvic malignancy
rectal surgery
DIABETES

251
Q

management of chronic urinary retention

A
  • ONLY CATHETERISE PATIENT IF THERE IS PAIN, URINARY INFECTION, OR RENAL IMPAIRMENT.
  • Institute definitive treatment promptly
  • Intermittent self-catheterisation is sometimes required
252
Q

what is benign prostatic hyperplasia

A

benign nodular or diffuse proliferation of musculofibroid and glandular layers of the prostate.

Inner (transitional) zone enlarges in contrast to peripheral layer expansion seen in prostate carcinoma.

253
Q

features of BPH

A

LUTS

  • nocturia
  • frequency
  • urgency
  • post-micturition dribbling
  • poor stream/flow
  • hesitancy
  • overflow incontinence
  • haematuria
  • bladder stones
  • UTI
254
Q

investigation for BPH

A

digital rectal examination - symmetrically enlarged, smooth, firm, non-tender prostate with rubbery texture.

MSU
U+E
USS (hydronephrosis)

PSA ± transrectal USS + biopsy

255
Q

lifestyle advice for mx of BPH

A

avoid caffeine/alcohol
relax when voiding
void twice in a row to aid emptying
control urgency by practising distraction methods.
train the bladder by ‘holding on’ to increase between voiding.

256
Q

pharmacological therapy for BPH

A

alpha blocker - tamsulosin
(reduces smooth muscle tone of prostate and bladder)
SE - drowsiness, dry mouth, weight gain, depression, hypotension

5-alpha reductase inhibitors e.g. finasteride
(reduce testosterone conversion to dihydrotestosterone)
- excreted in semen - so warn to use condoms.
SE - impotence, reduced libido.

257
Q

surgery for BPH

A

transurethral resection of prostate (TURP)

  • crossmatch 2units
  • beware bleeding, clot retention and TUR syndrome

transurethral incision of prostate (TUIP)
- best for small glands <30g

retropubic prostatectomy
- open operation (if large prostate)

258
Q

risks of TURP

A 
haemorrhage
haematospermia
hypothermia
urethral trauma/stricture
post-op TURP syndrome (hypothermia, hyponatraemia)
infection - prostatitis
ED
incontinence 
retrograde ejaculation
259
Q

post-op advice for BPH (TURP)

A
  • Avoid driving for 2 weeks after the operation
  • Avoid sex for 2 weeks after surgery. Amount of ejaculate produced will be reduced (as it flows back into bladder – harmless, but may cloud urine).
  • Expect to pass blood in urine for the first 2 weeks. Don’t be alarmed.
  • At first, you may need to urinate frequently than before. In 6 weeks things should be much better – but operation cannot be guaranteed to work (8% fail and lasting incontinence is a problem in 6%)
  • If feverish or if urination hurts, take a sample of urine to doctor.
260
Q

Consequences of chronic urinary retention

A 
hyperkalaemia
metabolic acidosis 
post-obstructive diuresis 
sodium-and bicarbonate losing nephropathy
infection
261
Q

common location of renal cell carcinoma

A

proximal renal tubular epithelium

262
Q

features of renal cell carcinoma

A

50% found incidentally

haematuria
loin pain
abdo mass
anorexia
weight loss
malaise

varicocele - invasion of left renal vein compresses left testicular vein

263
Q

tests for RCC

A 
high BP
bloods
- FBC (polycythaemia due to high EPO)
- ESR
- U+E
- ALP (?bone mets)

urine

  • RBCs
  • cytology

imaging

  • USS
  • CT/MRI KUB
  • CXR (cannon ball mets in lungs)
264
Q

metastases of RCC

A

bone
liver
lung

265
Q

treatment of RCC

A

radical nephrectomy

if unresectable or metastatic disease –> biologics e.g. sunitinib, sorafenib

266
Q

what score is used in RCC to predict survival, tumour size etc

A

MAYO PROGNOSTIC RISK SCORE

267
Q

transitional cell carcinoma of kidney risk factors

A

chemicals in the textile
rubber
plastic industry

268
Q

presentation of transitional cell carcinoma of kidney

A 
painless visible haematuria
frequency
urgency
dysuria
urinary tract obstruction
269
Q

what is a nephroblastoma

A

childhood tumour of primitive renal tubules and mesenchymal cells.

chief abdominal malignancy in children.

present with an abdominal mass and haematuria.

270
Q

associations with prostate cancer

A

positive family history

increased testosterone

271
Q

where do prostate cancers commonly arise

A

adenocarcinomas arising in PERIPHERAL PROSTATE

272
Q

metastasis of prostate cancer

A

local - seminal vesicles, bladder, rectum (spread via lymph)

haematogenous - sclerotic bony lesions

273
Q

which system is used to grade prostate cancer

A

GLEASON GRADING SYSTEM

274
Q

symptoms of prostate cancer

A

asymptomatic

hesitancy
poor stream
terminal dribbling
obstruction
weight loss
± BONE PAIN (METS)
275
Q

investigation of prostate cancer

A

digital rectal examination of prostate - hard, irregular prostate.

high PSA - false negatives in prostatitis, UTI, BPH, vigorous DRE.

transrectal ultrasound + biopsy
(recent guidelines suggest a multiparametric MRI first line)

X-rays
bone scan
CT/MRI with contrast - for staging

276
Q

treatment of prostate cancer

A

radical prostatectomy if <70y

radical radiotherapy - external beam or brachytherapy.

hormone therapy e.g. goserelin:

  • considered in elderly unfit patients with high-risk disease.
  • if the cancer has spread too far to be cured by surgery or radiation or cannot have these treatments.
  • along with radiation therapy as the initial tx, if at high risk of the cancer coming back after treatment (based on high gleason score, high PSA level and mets)
277
Q

management of metastatic disease in prostate cancer patients

A

orchidectomy bilateral (most of the androgens made here) - causes prostate cancer to shrink or stop growing over time.

LHRH agonists/GnRH agonists

  • lower the amount of testosterone made by testes.
  • e.g. goserelin
  • when LHRH are first given, causes A FLARE because testosterone levels go up briefly before falling to very low levels. (can cause back pain, bone pain). so to avoid this:
  • —-> give ANTI-ANDROGENS e.g. flutamide for a few weeks when starting treatment with LHRH agonists.

LHRH antagonists

  • e.g. degarelix
  • lowers testosterone very quickly
  • doesn’t cause tumour flare
  • used to treat advanced prostate cancer. better in mets.

SE of above tx

  • reduced libido
  • ED
  • hot flashes
  • gynaecomastia
  • osteoporosis
  • anaemia
  • fatigue
  • weight gain
  • depression
  • loss of muscle mass
278
Q

screening for prostate cancer

A

DRE of prostate
transrectal ultrasound
PSA

279
Q

what type of cancers are bladder tumours

A

transitional cell carcinomas (>90%)

280
Q

presentation of bladder cancer

A

PAINLESS HAEMATURIA
recent UTIs
voiding irritability

281
Q

associations of bladder cancer

A

SMOKING

AROMATIC AMINES - RUBBER

SCHISTOSOMIASIS - increased risk of squamous cell carcinoma

chronic cystitis

pelvic irradiation

282
Q

tests for bladder cancer

A

CYSTOSCOPY WITH BIOPSY

urine: microscopy/cytology (sterile pyuria)

CT urogram - for staging

bimanual exam under anaesthesia (EUA) helps assess spread.

283
Q

TNM staging of bladder cancer

A

Tis – carcinoma in situ [Not felt at EUA]
Ta – tumour confined to epithelium [Not felt at EUA]
T1 – Tumour in lamina propria [Not felt at EUA]
T2 – Superficial muscle involved [Rubbery thickening at EUA]
T3 – Deep muscle involved [EUA: mobile mass]
T4 – Invasion beyond bladder [EUA: fixed mass]

284
Q

treatment of bladder cancer

A

Tis/Ta/T1 - diathermy via transurethral cystoscopy. or Transurethral resection of the bladder tumour (TURBT)
Consider chemotherapy.

T2-3

  • radical cystectomy - gold standard
  • radiotherapy
  • post-op chemo (M-VAC: methotrexate - vinblastine, adriamycin, cisplatin.

T4
- usually palliative chemo/radiotherapy

285
Q

metastasis of bladder cancer

A

local - pelvic structures
lymphatic - iliac and para-aortic nodes.
haematogenous - LIVER AND LUNGS

286
Q

complications of cystectomy

A

sexual and urinary malfunction

massive bladder haemorrhage

Finals (4 decks)

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