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renal and urology Flashcards

1
Q

stage 5 ckd

A

0-15 eGFR

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2
Q

stage 4 ckd

A

15-30 eGFR

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3
Q

stage 3 ckd

A

3a = 45-60 eGFR
3b = 30-45 eGFR

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4
Q

causes of CKD

A

diabetic nephropathy
chronic glomerulonephritis
chronic pyelonephritis
hypertension
adult polycystic kidney disease

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5
Q

features of renal bone disease

A

osteomalacia
osteoporosis
osteosclerosis

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6
Q

spine x-ray in renal bone disease

A

“rugger jersey” spine
sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)

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7
Q

metabolic probs in ckd

A

low VD
high phosphate
LOW calcium
secondary hyperparathyroidism

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8
Q

ckd bone disease tx

A

reduce dietary phosphate
phosphate binders (sevelamer)
give VD (eg alfacalcidol, calcitriol)
bisphosphonates (alendronic acid)

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9
Q

hypercalcaemia tx

A

Fluids

Calcitonin (reduces serum calcium levels by inhibiting osteoclast activity)

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10
Q

nice criteria for AKI

A

Rise in creatinine of ≥ 25 micromol/L in 48 hours
Rise in creatinine of ≥ 50% in 7 days
Urine output of < 0.5ml/kg/hour for > 6 hours

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11
Q

RFs AKI

A

Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (above 65 years)
Cognitive impairment
Nephrotoxic medications such as NSAIDS and ACE inhibitors
Use of a contrast medium such as during CT scans

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12
Q

pre renal causes AKI

A

inadequate BS:
Dehydration
Hypotension (shock)
Hypovolaemia - D+V
Heart failure
Renal artery stenosis

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13
Q

renal causes AKI

A

Glomerulonephritis
Interstitial nephritis
Acute tubular necrosis (most common)
Rhabdomyolysis
tumour lysis syndrome

drugs - ACEi, NSAIDs, nephrotoxic abx (gentamicin, vancomycin, tetracyclines)

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14
Q

post renal causes AKI

A

obstruction to outflow:
Kidney stones
Masses such as cancer in the abdomen or pelvis
Ureter or uretral strictures
Enlarged prostate or prostate cancer

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15
Q

what drugs to stop in AKI

A

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

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16
Q

eGFR variables

A

CAGE - Creatinine, Age, Gender, Ethnicity

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17
Q

inheritance pattern of PKD

A

autosomal dominant
- more common
- assoc w cerebral haemorrhage

autosomal recessive
- more severe, usually presents antenatally or at birth
- less likely to have FHX

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18
Q

when is contrast CI

A

renal impairment

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19
Q

most signif cause of anaemia in CKD

A

reduced erythropoietin

(carry out iron studies b4 giving EPO)

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20
Q

stages to classify AKI

A

Stage 1 - 1.5-1.9x baseline creatinine - All in the 1’s

Stage 2 - 2-2.9x baseline creatinine - All in the 2’s

Stage 3 - 3x baseline creatinine - All in the 3’s

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21
Q

when to send a urine culture in UTI

A

if pregnant
visible or non-visible haematuria
> 65 yrs
if male

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22
Q

UTI tx non-pregnant women

A

trimethoprim or nitrofurantoin for 3 days

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23
Q

how long to give UTI abx if catheterised

A

7 days

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24
Q

UTI tx males

A

trimethoprim or nitrofurantoin 7 days

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25
Q

Differentiating between IgA nephropathy and post-streptococcal glomerulonephritis

A

post-streptococcal glomerulonephritis presents after 1-2 WEEKS, IgA nephropathy after 1-2 DAYS (post RTI)

post-strep has low complement
post- strep has more proteinuria

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26
Q

prostatitis presentation+ what is a common cause

A

chronic if > 3mths

Prostatitis: perineal or prostatic pain
Lower urinary tract symptoms: dysuria, frequency, urgency
Symptoms of systemic upset: fever, myalgia

E. coli is common cause

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27
Q

prostatitis ix

A

Focussed history
Digital rectal examination: tender, warm, swollen prostate
Midstream sample of urine
Screening for sexually transmitted infections (gonorrhoea can cause prostatitis)

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28
Q

acute prostatitis mx

A

Hospital admission for systemically unwell or septic patients (for bloods, blood cultures and IV antibiotics)

Oral abx 14 days (quinolone) = ciprofloxacin 1st line

(ofloxacin or trimethoprim)

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29
Q

chronic prostatitis mx

A

Alpha-blockers (e.g., tamsulosin)
Analgesia
Psychological treatment
Antibiotics if less than 6 months of symptoms or a history of infection (e.g., trimethoprim or doxycycline for 4-6 weeks)
Laxatives

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30
Q

how to measure proteinuria in CKD

A

albumin:creatinine ratio (ACR)

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31
Q

when to prescribe ACEi in CKD

A

if they have an albumin:creatinine ratio (ACR) > 30 mg/mmol + existing HTN

ACR > 70 regardless

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32
Q

valvular abnormality w PKD

A

Mitral valve prolapse
mitral regurgitation

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33
Q

AKI mx

A

stop nephrotoxic drugs

careful fluid balance
fluid resus espesh if pre-renal cause

tx hyperkalaemia

specialist if cause is not known or is severe

haemodialysis when not responding to med tx of comps

if fluid overload consider
- loop diuretics e.g. furosemide
- adrenaline
- inotrope like dobutamine to increase BP

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34
Q

AKI ix

A

U&Es - sodium
- potassium
- urea
- creatinine - for dx

urine output

urinalysis - blood + protein (nephritic syndrome?)

no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound

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35
Q

when to refer AKI to nephrologist

A

Renal tranplant
ITU patient with unknown cause of AKI
Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma
AKI with no known cause
Inadequate response to treatment
Complications of AKI
Stage 3 AKI (see guideline for details)
CKD stage 4 or 5
Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)

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36
Q

features to differentiate AKI from CKD

A

renal ultrasound in CKD will have bilateral small kidneys
apart from:
AD PKD
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

CKD will have hypocalcaemia due to lack of VD

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37
Q

what can cause hyperkalaemia

A

AKI
CKD (stage 4 or 5)
Rhabdomyolysis
Adrenal insufficiency - addisons
Tumour lysis syndrome

metabolic acidosis disease
massive blood transfusion

drugs*: , ACEis, ARBs, spironolactone (K+ sparing), ciclosporin, heparin
*BBs interfere with K+ transport into cells + can potentially cause hyperkalaemia in renal failure patients - remember beta-agonists, e.g. Salbutamol, are sometimes used as emergency treatment

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38
Q

what foods are high in K+

A

salt substitutes (i.e. Contain potassium rather than sodium)
bananas, oranges, kiwi fruit, avocado, spinach, tomatoes

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39
Q

ECG hyperkalaemia

A

Peaked or ‘tall-tented’ T waves (occurs first)
Loss of P waves
Broad QRS complexes
Prolonged PR interval
Sinusoidal wave pattern (v severe)
Ventricular fibrillation

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40
Q

mx hyperkalaemia below 6.5mmol/L + no ECG changes

A

tx underlying cause
for example, treating acute kidney injury and stopping medications (e.g., spironolactone or ACE inhibitors)

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41
Q

mx hyperkalaemia above 6.5 or w ECG changes

A

IV CALCIUM GLUCONATE + INSULIN WITH DEXTROSE INFUSION

INSULIN drives potassium from the extracellular space to the intracellular space
DEXTROSE is required to prevent hypoglycaemia while on insulin
CALCIUM GLUCONATE stabilises the cardiac muscle cells and reduces the risk of arrhythmias

other options:
Nebulised salbutamol temporarily drives potassium into cells
Oral calcium resonium reduces potassium absorption in the GI tract (this is slow and causes constipation)
Sodium bicarbonate (in acidotic patients on renal advice) drives potassium into cells as it corrects the acidosis
Haemodialysis may be required in severe or persistent cases

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42
Q

what albumin:creatinine ratio means

A

proteinuria
>3 mg/mmol

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43
Q

what albumin:creatinine ratios to refer to a nephrologist

A

> 70 mg/mmol
- unless known to be caused by diabetes + already approp tx

> 30 mg/mmol w persistent haematuria

3-29 mg/mmol w persistent haematuria + other RFs e.g. declining eGFR/CVD

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44
Q

what is rhabdomyolysis

A

skeletal muscle breaking down + releasing various chemicals into the blood. Muscle cells (myocytes) undergo cell death (apoptosis), releasing:
Myoglobin
Potassium
Phosphate
Creatine kinase

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45
Q

complications of rhabdomyolysis

A

hyperkalaemia - arrythmias + arrest
AKI
- myoglobin is toxic in high concs
DIC
compartment syndrome

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46
Q

causes of rhabdomyolysis

A

Anything that causes significant damage to muscle cells:
Prolonged immobility, particularly frail patients who fall + spend time on the floor before being found
Extremely rigorous exercise beyond the person’s fitness level (e.g., endurance events or CrossFit)
Crush injuries
Seizures
Statins

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47
Q

features of rhabdomyolysis

A

Muscle pain
Muscle weakness
Muscle swelling
Reduced urine output (oliguria)
Red-brown urine (myoglobinuria)
Fatigue
Nausea and vomiting
Confusion (particularly in frail patients)

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48
Q

ix rhabdomyolysis

A

Creatine kinase (CK) blood test for dx
- normally <150 U/L. In rhabdomyolysis, it can be 1,000-100,000 U/L
- typically rises in the first 12 hours, then remains elevated for 1-3 days, then gradually falls
- higher the CK, the greater the risk of kidney injury

Myoglobinuria - urine dipstick will test +ve for blood

U&Es for AKI + hyperkalaemia

ECGs- hyperkalaemia

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49
Q

tx rhabdomyolysis

A

IV fluids
hyperkalaemia tx

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50
Q

what is haemolytic uraemic syndrome (HUS)

A

thrombosis in small BVs throughout the body, usually triggered by Shiga toxins from either E. coli O157 or Shigella

Most often affects children following an episode of gastroenteritis. Abx and anti-motility medication (e.g., loperamide) used to treat gastroenteritis caused by E. coli O157 or Shigella increase the risk of HUS.

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51
Q

triad in HUS

A

Microangiopathic haemolytic anaemia (thrombi causes RBCs to ruptures as they pass through small BVs)
AKI
Thrombocytopenia (low platelets) (as they are used to form the thrombus)

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52
Q

HUS presentation

A

E. coli O157 + Shigella cause gastroenteritis. Diarrhoea is the first symptom, which turns bloody within 3 days. Around a week after the onset of diarrhoea, the features of HUS develop:

Fever
Abdominal pain
Lethargy
Pallor
Reduced UO
Haematuria
Hypertension
Bruising
Jaundice (due to haemolysis)
Confusion

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53
Q

mx HUS

A

Medical emergency + requires hospital admission + supportive management:
Hypovolaemia (e.g., IV fluids)
Hypertension
Severe anaemia (e.g., blood transfusions)
Severe renal failure (e.g., haemodialysis)

It is self-limiting, and most patients fully recover with good supportive care.

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54
Q

ix HUS

A

stool culture to establish causative organism

FBC = anaemia - haemoglobin level less than 8 g/dL with a negative Coomb’s test, thrombocytopenia
Fragmented blood film = schistocytes and helmet cells
U&Es = AKI

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55
Q

features of nephritic syndrome

A

Haematuria - microscopic or macroscopic
Oliguria
Proteinuria, <3g per 24 hours (higher protein suggests nephrotic syndrome)
Fluid retention

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56
Q

what is nephritic syndrome

A

a group of features that occurs w nephritis (inflammation of the kidneys)

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57
Q

what is nephrotic syndrome

A

occurs when the basement membrane in the glomerulus becomes highly permeable, resulting in significant proteinuria.

It refers to a group of features without specifying the underlying cause

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58
Q

features of nephrotic syndrome

A

NO blood
Proteinuria (>3kg in 24hr) = FROTHY urine
Low serum albumin (<25g per litre)
Peripheral oedema
Hypercholesterolaemia

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59
Q

what does nephrotic syndrome predispose px to

A

thrombosis
- loss of antithrombin III (a protein that will be lost in urine) - it inhibits coagulation by inhibiting the enzymatic activity of thrombin

hypertension

hyperlipidaemia - due to overproduction in the liver

infection risk - due to urinary immunoglobulin loss

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60
Q

most common cause of nephrotic syndrome

A

minimal change disease

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61
Q

top causes of nephrotic syndrome in adults

+ other causes

A

Membranous nephropathy
Focal segmental glomerulosclerosis

Membranoproliferative glomerulonephritis
Henoch-Schönlein purpura (HSP)
Diabetes
Infection (e.g., HIV)

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62
Q

what is IgA nephropathy (Berger’s disease)

A

commonest cause of primary glomerulonephritis worldwide (nephritic syndrome)

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63
Q

IgA nephropathy presentation

A

young male, recurrent episodes of macroscopic haematuria

typically associated with a recent/current RTI

nephrotic range proteinuria is rare

renal failure is unusual and seen in a minority of patients

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64
Q

histology in IgA nephropathy

A

IgA deposits and glomerular mesangial proliferation

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65
Q

what is membranous nephropathy

A

deposits of immune complexes (IgG + complement) in the glomerular basement membrane -> thickening + malfunctioning of the membrane, proteinuria

usually idiopathic

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66
Q

histology in membranous nephropathy

A

IgG and complement deposits on the basement membrane

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67
Q

histology in Rapidly progressive glomerulonephritis

A

glomerular crescents

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68
Q

what is goodpasture syndrome

A

also known as anti-glomerular basement membrane (anti-GBM) disease

Anti-GBM antibodies attack the glomerulus + pulmonary basement membranes. It causes glomerulonephritis and pulmonary haemorrhage

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69
Q

goodpastures syndrome histology

A

renal biopsy: linear IgG deposits along the basement membrane

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70
Q

goodpastures syndrome presentation

A

patient in their 20s or 60s with acute kidney failure and haemoptysis (coughing up blood)

can be exacerbated by a RTI

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71
Q

systemic diseases that can cause glomerulonephritis

A

Henoch-Schönlein purpura (HSP)
Vasculitis (e.g., microscopic polyangiitis or granulomatosis with polyangiitis)
Lupus nephritis (associated with systemic lupus erythematosus)

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72
Q

what is post-streptococcal glomerulonephritis

A

Occurs 7-14 days following a group A beta-haemolytic Streptococcus infection (Strep pyogenes)
Caused by immune complex (IgG, IgM and C3) deposition in the glomeruli
Usually young children

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73
Q

Membranoproliferative glomerulonephritis

A

It involves immune complex deposits and mesangial proliferation.

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74
Q

post-streptococcal glomerulonephritis sx

A

headache
malaise
visible haematuria
proteinuria (less commonly signif)
this may result in oedema
hypertension
oliguria

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75
Q

ix in post-strep glomerulonephritis

A

bloods
- raised anti-streptolysin O titre are used to confirm the diagnosis of a recent streptococcal infection
- low C3

renal biopsy
- electron microscopy: subepithelial ‘humps’ caused by lumpy immune complex deposits
- immunofluorescence: ‘starry sky’ appearance

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76
Q

significant AKI, haemoptysis + p-ANCA antibodies

A

microscopic polyangiitis

(diff from egwp which is also p-ANCA, similar sx to gwp which is c-ANCA)

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77
Q

significant AKI, haemoptysis + c-ANCA antibodies

A

granulomatosis with polyangiitis

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78
Q

what is tumour lysis syndrome

A

usually triggered by intro of combo chemo

  • occurs from the breakdown of tumour cells -> release of chemicals from the cell -> high potassium and high phosphate level in the presence of a low calcium.

Suspect in any patient presenting with an AKI in the presence of a high phosphate and high uric acid level.

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79
Q

what is serum urea-creatinine ratio used for

A

urea and creatinine both freely filtered at the glomerulus

creatinine is not reabsorbed (it is removed from body entirely by the kidneys therefore v high if kidneys are not working)

urea reabsorbed by tubules (urea absorption increased compared to creatinine in pre-renal)

can be used as an indicator of the likely cause of renal failure

80
Q

high urea-creatinine ratio

A

PRE- RENAL FAILURE
- dehydration
corticosteroids
GI haemorrhage
protein-rich diet
severe catabolic state

81
Q

low urea-creatinine ratio

A

intrinsic renal damage

severe liver dysfunction
malnutrition
pregnancy
low protein diet
SIADH
rhabdomyolysis

82
Q

spironolactone mechanism of action

A

aldosterone antagonist

83
Q

what does renal artery stenosis cause

A

secondary hyperaldosteronism due to disproportionately low BP in the kidneys
-> HTN as excessive renin is released

84
Q

what is renal artery stenosis

A

narrowing of the artery supplying the kidney, usually due to atherosclerosis

85
Q

where do renal stones most commonly get stuck

A

vesico-ureteric junction

86
Q

most common type of kidney stone

A

calcium based
- Calcium oxalate (more common)
- Calcium phosphate

Opaque on XR (can be seen)

87
Q

other types of kidney stone (apart from calcium)

A

Uric acid – these are not visible on x-ray
Struvite – produced by bacteria, therefore, associated with infection (stag horn shape)
Cystine – associated with cystinuria, an autosomal recessive disease (semi-opaque ground glass on XR)

88
Q

what is a staghorn calculus + what is it made from

A

where a renal stone forms in the shape of the renal pelvis - body sits in the renal pelvis with horns extending into the renal calyces

occurs with stones made of struvite

In recurrent URTIs, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite

89
Q

renal stones presentation

A

may be asx

Renal colic is the usual complaint:
- Unilateral loin to groin pain that can be excruciating
- Colicky (fluctuating in severity) as the stone moves and settles

May also be:
- haematuria
- N&V
- reduced urine output
- sx of sepsis if infection present

90
Q

renal stones ix

A

Non-contrast computer tomography (CT) of the kidneys, ureters and bladder (CT KUB) = INITIAL IX OF CHOICE FOR DX, do within 24 hrs pres

US KUB (preg women or children)

urine dipstick = haematuria (but normal does not exclude)
bloods - infection + U&Es, Ca (hypercalcaemia is a cause)
Abdo XR (wld not show uric acid stones, + may not show small stones)

Analyse stone

91
Q

mx renal stones

A

NSAIDs best analgesia = IM diclofenac
Antiemetics = metoclopramide, prochlorperazine or cyclizine
Abx if infection
Watch + wait if < 5mm + uncomplicated
Consider tamsulosin (alpha blocker) to aid spontan passage (only if <10mm)
5-10mm shockwave lithotripsy

Surgical (e.g. ureteroscopy, Percutaneous nephrolithotomy) if >10mm, do not pass spontan or complete obstruction (hydronephrosis shown by dilation of renal pelvis) / infection

92
Q

advice to px who get recurrent renal stones

A

Increase oral fluid intake (2.5 – 3 litres per day)
Add fresh lemon juice to water (citric acid binds to urinary calcium reducing the formation of stones)
Avoid carbonated drinks (cola drinks contain phosphoric acid, which promotes calcium oxalate formation)
Reduce dietary salt intake (less than 6g per day)
Maintain a normal calcium intake (low dietary calcium might increase the risk of kidney stones)

For calcium stones – reduce the intake of oxalate-rich foods (e.g., spinach, beetroot, nuts, rhubarb and black tea)
For uric acid stones – reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)
Limit dietary protein

93
Q

medications for recurrent renal stones

A

POTASSIUM CITRATE in patients with calcium oxalate stones and raised urinary calcium

Thiazide diuretics (e.g., indapamide) in patients with calcium oxalate stones and raised urinary calcium (can increase distal tubular calcium resorption)

94
Q

what is a hydrocele

A

collection of fluid within the tunica vaginalis that surrounds the testes

usually painless and present with a soft scrotal swelling

communicating + non-communicating

95
Q

hydrocele examination

A

The testicle is palpable within the hydrocele
Soft, fluctuant, may be large
Irreducible + has no bowel sounds (distinguishing it from a hernia)
Transilluminated by shining torch through the skin, into the fluid (the testicle floats within the fluid)

96
Q

mx hydrocele

A

exclude serious causes (cancer)

If idiopathic - conservative mx only
if uncertainty/hard to palpate - do an USS

97
Q

what type of hydrocele may you get in newborn males

A

communicating - caused by patency of the processus vaginalis allowing peritoneal fluid to drain down into the scrotum

usually resolve in 1st few mths
so reassure (think about surgical repair if not resolved in 1-2 yrs)

98
Q

what is a varicocele

A

occurs where the veins in the pampiniform plexus become swollen as a result of increased resistance in the testicular vein (incompetent valves / obstruction by tumour?)

99
Q

comps in varicocele

A

can cause impaired fertility - due to disrupting the temperature in the affected testicle

may result in testicular atrophy, reducing the size and function of the testicle

100
Q

what is the pampiniform plexus

A

a venous plexus found in the spermatic cord and drains the testes
(drains into the testicular vein)

plays a role in regulating the temperature of blood entering the testes by absorbing heat from the nearby testicular artery

101
Q

which side do most varicoceles occur on

A

LEFT
due to increased resistance in L testicular vein

(R drains into IVC, L drains into L renal vein)

102
Q

varicocele presentation

A

Throbbing/dull pain or discomfort, worse on standing
A dragging sensation
Sub-fertility or infertility

103
Q

varicocele examination

A

A scrotal mass that feels like a “bag of worms”
More prominent on standing
Disappears when lying down
Asymmetry in testicular size if the varicocele has affected the growth of the testicle

104
Q

when to refer varicocele urgently to urology

A

Varicoceles that do not disappear when lying down - as they raise concerns about retroperitoneal tumours obstructing the drainage of the renal vein

105
Q

varicocele ix

A

Ultrasound with Doppler imaging can be used to confirm the diagnosis
Semen analysis if there are concerns about fertility
Hormonal tests (e.g., FSH and testosterone) if there are concerns about function

106
Q

varicocele tx

A

Uncomplicated cases can be managed conservatively.

Surgery or endovascular embolisation may be indicated for pain, testicular atrophy or infertility.

107
Q

what is an epididymal cyst

A

fluid filled sac that occurs at the head of the epididymis
if it contains sperm it is called a spermatocele

108
Q

epididymal cyst presentation

A

mostly asx
may present having felt a lump, or they may be found incidentally on ultrasound for another indication.

109
Q

epididymal cyst examination

A

Soft, round lump
Typically at the top of the testicle
Associated with the epididymis
Separate from the testicle
May be able to transilluminate large cysts (appearing separate from the testicle)

110
Q

epididymal cyst tx

A

Usually harmless and are not associated with infertility or cancer. They may cause pain or discomfort where removal wld be considered.

111
Q

indications for short-term dialysis

A

A – Acidosis (severe and not responding to treatment)
E – Electrolyte abnormalities (particularly treatment-resistant hyperkalaemia)
I – Intoxication (overdose of certain medications)
O – Oedema (severe and unresponsive pulmonary oedema)
U – Uraemia leading to pericarditis or encephalitis - sx such as seizures or reduced consciousness

112
Q

options for long term dialysis

A

Haemodialysis
for long term access use:
- Tunnelled cuffed catheter
- Arteriovenous fistula
Peritoneal dialysis

113
Q

AV fistula features to examine in OSCE

A

Skin integrity
Aneurysms
Palpable thrill (a fine vibration felt over the anastomosis)
A “machinery murmur” on auscultation over the fistula

114
Q

comps of AV fistula

A

Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High-output heart failure

115
Q

what is STEAL syndrome

A

occurs when there is inadequate blood flow to the limb distal to the fistula. The AV fistula “steals” blood from the rest of the limb.
Blood is diverted away from the part of the limb it was supposed to supply -> ischaemia. Instead, it flows through the fistula and into the venous system.

116
Q

what is high-output heart failure

A

caused by blood flowing quickly from the arterial to the venous system through an A-V fistula.

There is a rapid return of blood to the heart, increasing the pre-load -> hypertrophy of the heart muscle and heart failure.

117
Q

comps of peritoneal dialysis

A

Bacterial peritonitis (infections in the high-sugar environment are common and serious)
Peritoneal sclerosis (thickening and scarring of the peritoneal membrane)
Ultrafiltration failure (the dextrose is absorbed, reducing the filtration gradient, making ultrafiltration less effective)
Weight gain (due to absorption of the dextrose)
Psychosocial implications

118
Q

what does the dialysis solution that goes into peritoneal cavity contain

A

dextrose

119
Q

most common cause of peritonitis secondary to peritoneal dialysis

A

Staphylococcus epidermidis

120
Q

LUTS

A

occur w prostate pathology

Hesitancy – difficult starting and maintaining the flow of urine
Weak flow
Urgency – a sudden pressing urge to pass urine
Frequency – needing to pass urine often, usually with small amounts
Intermittency – flow that starts, stops and varies in rate
Straining to pass urine
Terminal dribbling – dribbling after finishing urination
Incomplete emptying – not being able to fully empty the bladder, with chronic retention
Nocturia – having to wake to pass urine multiple times at night

121
Q

initial assessment of man presenting w LUTS

A

Digital rectal examination (prostate exam) to assess the size, shape and characteristics of the prostate
Abdominal examination to assess for a palpable bladder and other abnormalities
Urinary frequency volume chart, recording 3 days of fluid intake and output
Urine dipstick to assess for infection, haematuria (e.g., due to bladder cancer) and other pathology
Prostate-specific antigen (PSA) for prostate cancer, depending on the patient preference

122
Q

common causes of raised PSA

A

Prostate cancer
Benign prostatic hyperplasia
Prostatitis
Urinary tract infections
Vigorous exercise (notably cycling)
Recent ejaculation or prostate stimulation

123
Q

difference between exam in benign + cancerous prostate

A

A benign prostate feels smooth, symmetrical and slightly soft, with a maintained central sulcus
A cancerous prostate may feel firm/hard, asymmetrical, craggy or irregular, with loss of the central sulcus

124
Q

medical mx of BPH

A

Alpha-blockers (e.g., tamsulosin) relax smooth muscle, with rapid improvement in symptoms (tx of immediate sx)

5-alpha reductase inhibitors (e.g., finasteride) gradually reduce the size of the prostate (tx of the enlargement, takes 6 mths)

125
Q

how long does finasteride take to improve sx in BPH

A

6 mths

126
Q

SE tamsulosin

A

postural hypotension as alpha blocker

127
Q

SE finasteride

A

sexual dysfunction (due to reduced testosterone).

as a 5-alpha reductase inhibitor it stops the conversion testosterone to dihydrotestosterone (DHT) (more potent version)

128
Q

what to monitor in HSP

A

blood pressure and urinanalysis

129
Q

HIV-associated nephropathy (HIVAN) features

A

massive proteinuria resulting in nephrotic syndrome
normal or large kidneys
focal segmental glomerulosclerosis with focal or global capillary collapse on renal biopsy
elevated urea and creatinine
normotension

130
Q

which form of renal impairment is most commonly assoc w hep C

A

Membranoproliferative glomerulonephritis

131
Q

which form of renal impairment is most commonly assoc w HIV

A

focal segmental glomerulosclerosis

132
Q

what can invalidate eGFR

A

Eating red meat the evening before a blood test

133
Q

Rfs for prostate cancer

A

Increasing age
Family history
Black African or Caribbean origin
Tall stature
Anabolic steroids

134
Q

prostate cancer presentation

A

asx

LUTS
Haematuria
Erectile dysfunction
Symptoms of advanced disease or metastasis (e.g., weight loss, bone pain or cauda equina syndrome)

135
Q

first line ix for suspected prostate cancer

A

Multiparametric MRI of prostate

results reported on a Likert scale
1 – very low suspicion
2 – low suspicion
3 – equivocal
4 – probable cancer
5 – definite cancer

136
Q

when to perform a prostate biopsy

A

MRI findings (e.g., Likert 3 or above) and the clinical suspicion (i.e. examination and PSA level)

137
Q

what to do if suspicion of cancer on DRE

A

Refer for 2-week wait appointment and advise urgent multiparametric MRI

138
Q

gleason grading system

A

prostate cancer grading system
based on histology from biopsies

The greater the Gleason score, the more poorly differentiated the tumour is + the worse the prognosis - 1 (closest to normal) to 5 (most abnormal)
made up of 2 nos from different samples

6 is considered low risk
7 is intermediate risk (3 + 4 is lower risk than 4 + 3)
8 or above is deemed to be high risk

139
Q

RFs bladder cancer

A

increased age
smoking
aromatic amines - dye + rubber - transitional cell carcinoma
Schistosomiasis causes squamous cell carcinoma

140
Q

types of bladder cancer

A

Transitional cell carcinoma (90%)
Squamous cell carcinoma (5% – higher in areas of schistosomiasis)

141
Q

bladder cancer key presentation

A

Painless haematuria

142
Q

when to do a 2 week wait referral for bladder cancer

A

> 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI

> 60 with microscopic haematuria
PLUS:
- Dysuria or;
- Raised white blood cells on a full blood count

consider a non-urgent referral in >60 with recurrent unexplained UTIs

143
Q

bladder cancer dx

A

Cystoscopy

144
Q

tx of non-muscle invasive bladder cancer

A

Transurethral resection of bladder tumour (TURBT)
Intravesical chemotherapy is often used after a TURBT procedure to reduce the risk of recurrence.

145
Q

tx for invasive bladder cancer

A

radical cystectomy

146
Q

immunotherapy in bladder cancer

A

Intravesical BCG
Giving the BCG vaccine (the same one as for tuberculosis) into the bladder is thought to stimulate the immune system, which in turn attacks the bladder tumours.

147
Q

most common renal tumour

A

Renal adenocarcinoma

148
Q

Renal Cell Carcinoma presentation

A

haematuria, flank pain and a palpable mass

149
Q

RFs Renal Cell Carcinoma

A

Smoking
Obesity
Hypertension
End-stage renal failure
Von Hippel-Lindau Disease
Tuberous sclerosis

150
Q

when to do 2 week wait for renal cell carcinoma

A

> 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI

151
Q

classic feature of metastatic renal cell carcinoma

A

“Cannonball metastases” in the lungs
- appear as clearly-defined circular opacities scattered throughout the lung fields on a chest x-ray.

152
Q

paraneoplastic features of renal cell carcinoma

A

Polycythaemia – due to secretion of unregulated erythropoietin
Hypercalcaemia – due to secretion of a hormone that mimics the action of parathyroid hormone
Hypertension – due to various factors, including increased renin secretion, polycythaemia and physical compression
Stauffer’s syndrome – abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis

153
Q

types of renal cell adenocarcinoma

A

Clear cell (around 80%)
Papillary (around 15%)
Chromophobe (around 5%)

154
Q

how to calc urea:creatinine ratio

A

plasma urea (mmol/L) / (plasma creatinine (μmol/L) divided by 1000)

155
Q

mx for confined renal cancer

A

a partial or total nephrectomy depending on the tumour size
- patients with a T1 tumour (i.e. < 7cm in size + confined to kidney) are typically offered a partial nephrectomy

156
Q

Alport’s syndrome presentation

A

microscopic haematuria, bilateral sensorineural deafness, and lenticonus

157
Q

drug causes of acute interstitial nephritis

A

PENICILLIN
rifampicin
NSAIDs
allopurinol
furosemide

158
Q

acute interstitial nephritis presentation

A

allergic picture
may have just had penicillin abx

fever, rash, arthralgia
EOSINOPHILIA
mild renal impairment
hypertension

159
Q

ix results in acute interstitial nephritis

A

sterile pyuria
white cell casts in urine

160
Q

what to use in px who have troubling gynaecomastia on spironolactone

A

Eplerenone

161
Q

what cells does testicular cancer usually come from

A

germ cells in the testes

162
Q

2 types of testicular cancer

A

Seminomas
Non-seminomas (mostly teratomas)

163
Q

RFs testicular cancer

A

Undescended testes
Male infertility
Family history
Increased height

164
Q

presentation testicular cancer

A

lump on testicle
- non-tender
- arising from testicle
- hard
- irregular
- non-fluctuant
- no transillumination

rarely can get gynaecomastia - espesh in Leydig cell tumours

165
Q

ix testicular cancer

A

SCROTAL USS initial ix

staging CT scan

166
Q

tumour markers for testicular cancer

A

Alpha-fetoprotein – may be raised in teratomas (not in pure seminomas)
Beta-hCG – may be raised in both teratomas and seminomas
Lactate dehydrogenase (LDH) is a very non-specific tumour marker

167
Q

Royal Marsden Staging System testicular cancer

A

Stage 1 – isolated to the testicle
Stage 2 – spread to the retroperitoneal lymph nodes
Stage 3 – spread to the lymph nodes above the diaphragm
Stage 4 – metastasised to other organs

168
Q

Extra-renal manifestations of PKD

A

berry aneurysms
Hepatic, splenic, pancreatic, ovarian and prostatic cysts (LIVER CYSTS ARE THE MOST COMMON EXTRA THING)
Mitral regurgitation
Colonic diverticula

169
Q

comps of PKD

A

Chronic loin/flank pain
Hypertension
Gross haematuria can occur with cyst rupture (usually resolves within a few days)
Recurrent urinary tract infections
Renal stones
End-stage renal failure occurs at a mean age of 50 years

170
Q

ix PKD

A

Ultrasound and genetic testing are used for diagnosis.

171
Q

mx ADPKD

A

tolvaptan - vasopressin receptor antagonist
- can slow progression of cysts + progression of renal failure

tx HTN
analgesia
abx if infections
drainage if sx
dialysis
renal transplant

172
Q

conservative mx PKD

A

Genetic counselling
Avoiding contact sports due to the risk of cyst rupture
Avoiding NSAIDs and anticoagulants
MR angiography (MRA) can be used to screen for cerebral aneurysms

173
Q

what is pyelonephritis

A

inflammation of the kidney resulting from bacterial infection - affects the renal pelvis (join between kidney and ureter) and parenchyma (tissue)

174
Q

RFs pyelonephritis

A

Female sex
Structural urological abnormalities
Vesico-ureteric reflux (urine refluxing from the bladder to the ureters – usually in children)
Diabetes

175
Q

most common cause pyelonephritis

A

E. coli
- gram-negative, anaerobic, rod-shaped bacteria that are part of the normal lower intestinal microbiome (found in the faeces + can easily spread to bladder)

176
Q

presentation pyelonephritis

A

Lower UTI sx - dysuria, suprapubic discomfort and increased frequency
+
Fever
Loin or back pain (bilateral or unilateral)
Nausea / vomiting

Patients may also have:
Systemic illness
Loss of appetite
Haematuria
Renal angle tenderness on examination

177
Q

ix pyelonephritis

A

Urine dipstick = nitrites, leukocytes, blood.

Midstream urine (MSU) for microscopy, culture and sensitivity testing to establish the causative organism

Raised white blood cells and raised inflammatory markers

ultrasound or CT scan to exclude other things

178
Q

1st line for mx pyelonephritis in community

A

cefalexin for 7-10 days

co-amoxiclav if culture results
trimethoprim if culture results
ciprofloxacin (keep tendon damage and lower seizure threshold in mind)

hx if thinking sepsis!

179
Q

what to use to assess for renal damage in recurrent pyelonephritis

A

Dimercaptosuccinic acid (DMSA) scans

180
Q

what is orchitis

A

inflammation of the testicle

181
Q

what does the epididymis do

A

Sperm mature and are stored in the epididymis (released from testicle into its head). The epididymis drains into the vas deferen

182
Q

causes of epididymo-orchitis

A

Escherichia coli (E. coli)
Chlamydia trachomatis
Neisseria gonorrhoea
Mumps - usually just testicle

183
Q

presentation epididymo-orchitis

A

gradual onset, over minutes to hours, with unilateral:

Testicular pain
Dragging or heavy sensation
Swelling of testicle and epididymis

Tenderness on palpation, particularly over epididymis
- positive Prehn’s sign (relief of pain upon lifting the scrotum)
Presence of the cremasteric reflex (stroking the inner thigh, testicle moves upwards)
- both differentiate from torsion

Urethral discharge (should make you think of chlamydia or gonorrhoea)

Systemic symptoms such as fever and potentially sepsis

184
Q

tx for epididymo-orchitis when it is most likely caused by an enteric organism (e.g., E. coli)

A

Ofloxacin for 14 days
Levofloxacin for 10 days
Co-amoxiclav for 10 days (where quinolones are contraindicated)

185
Q

causes of non-gonococcal urethritis (NGU)

A

Chlamydia trachomatis
Ureaplasma urealyticum
Mycoplasma genitalium

186
Q

tx urethritis

A

either oral doxycycline for 7 days or single dose of oral azithromycin

187
Q

exceptions to the rule that most patients with CKD have bilateral small kidney

A

autosomal dominant polycystic kidney disease
diabetic nephropathy (early stages)
amyloidosis
HIV-associated nephropathy

188
Q

features that suggest CKD rather than AKI

A

bilateral small kidneys (apart from exceptions)
hypocalcaemia (due to lack of vitamin D)

189
Q

what is acute tubular necrosis

A

most common renal cause of an AKI

damage to the tubular cells from prolonged ischaemia/presence of toxins. The kidneys are no longer able to concentrate urine or retain sodium leading to high urinary sodium and low urine osmolality (more dilute).

190
Q

what happens if you correct chronic hypernatraemia too fast

A

cerebral oedema

191
Q

plasma sodium in dehydration

A

high

(however not if there is salt loss eg D+V)

192
Q

acute tubular necrosis presentation

A

AKI with the presence of muddy brown casts in the urine.

193
Q

what can cause acute tubular necrosis

A

Ischaemia due to hypoperfusion (e.g., dehydration, shock or heart failure)
Nephrotoxins (e.g., gentamicin, radiocontrast agents or cisplatin)

194
Q

surgical mx renal stones

A

Treatment
Stone <5mm = expectant treatment
Stone <2cm = lithotripsy (wave to break stone)
Stone <2cm + pregnant = ureteroscopy (camera passed through urethra)
Stone complex = percutaneous nephrolithotomy (invasive, camera passed though kidney from back)
hydronephrosis/infection = nephrostomy (drainage of urine from kidney) as needs urgent decompression

195
Q

pain reliever in renal stones

A

IM Diclofenac

196
Q

comp of radiotherapy of the prostate + how does that comp present

A

proctitis (inflammation in the rectum)

pain, altered bowel habit, rectal bleeding and discharge

(Prednisolone suppositories can help reduce inflammation)

197
Q

tx testicular torsion

A

Emergency bilateral orchidopexy - surgical fixation of both testes to the posterior wall
(need both done to prevent further risk)

finals (27 decks)

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