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Renal Flashcards

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USMLE® Step 1 flashcards
1
Q

AKI

A

defined as an acute drop in kidney function (under 48 hours). It is diagnosed by measuring the serum creatinine.

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2
Q

AKI criteria

A
  1. Rise in creatinine of ≥ 26.4 micromol/L in 48 hours (>1.5-1.9 x reference) or <0.5ml/kg/hr for >6 hours
  2. Rise in creatinine of ≥ 50% (>2-2.9 x reference) in 7 days or Urine output of < 0.5ml/kg/hour for > 12 hours
  3. Increase >3 x reference SCr or increase to >354 and <0.3ml/Kg/hr for >24 hours
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3
Q

risk factors for AKI

A
  1. CKD
  2. Heart failure
  3. Diabetes
  4. Liver disease
  5. Previous AKI
  6. Peripheral vascular disease
  7. Older age (above 65 years)
  8. Cognitive impairment
  9. Nephrotoxic medications such as NSAIDS and ACE inhibitors
  10. Use of a contrast medium such as during CT scans
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4
Q

Pre-renal (inadequate supply of blood to kidneys reducing filtration of blood)

A
  1. Hypovolaemia: Haemorrhage, volume depletion (e.g. D&V, burns and dehydration)
  2. Hypotension: cardiogenic shock and distributive shock (sepsis or anaphylaxis)
  3. Renal Hypoperfusion: Heart failure, NSAIDs/ACEi/ARBs/hepatorenal syndrome
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5
Q

Renal causes of AKI

A
  1. Glomerulonephritis
  2. Interstitial nephritis: Drugs (NSAIDs, antibiotics, PPI), Infection (TB) and systemic (sarcoidosis)
  3. Tubular injury: Ischaemia, drugs (gentamicin), contrast and rhabdomyolysis
  4. Acute tubular necrosis
  5. Vasculitis/renovascular
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6
Q

Post renal causes (obstruction to outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function)

A
  1. Kidney stones
  2. Ureter or urethral strictures
  3. Enlarged prostate or prostate cancer
  4. Masses such as cancer in the abdomen or pelvis
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7
Q

sign/symptoms of AKI

A
  1. Constitutional symptoms e.g. Anorexia, weight loss, fatigue, lethargy
  2. Nausea & Vomiting
  3. Itch
  4. Fluid overload: Oedema, SOB

Signs

  1. Fluid overload incl hypertension, Oedema, Pul oedema, effusions (pleural & pulmonary)
  2. Uraemia incl itch, pericarditis
  3. Oliguria
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8
Q

AKI Iv

A

Urinalysis: protein, blood, nitrites, glucose, WCC

U&E

FBC and coagulation screen

immunology: ANA, ANCA, GBM

protein electrophoresis and BJP

USS

biopsy

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9
Q

Management of AKI

A
  1. assess for hydration: BP, HR, UO, JVP, CRT, Oedema
  2. IV Fluid hydration (fluid challenge for hypovolaemia) - crystalloid (0.9% NaCl) or colloid: not 5% dextrose
    - bolus of fluid, if >1000mls and no improvement, seek help
    - heart failure: fluid overload be careful
  3. Stop nephrotoxic medications e.g. NSAIDS and ACEi
  4. Relive obstruction in post renal AKI
  5. Dialysis: anuria or uraemia
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10
Q

AKI complications

A

Hyperkalaemia
fluid overload, heart failure and pulmonary oedema
metabolic acidosis, uraemia (encephalopathy or pericarditis)

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11
Q

CKD

A

abnormal kidney function and/or structure

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12
Q

CKD risk factor

A 
AKI
CVD disease
diabetes 
hypertension
Glomerulonephritis
Polycystic kidney disease 
age related decline
Medication: NSAIDs, ACEi/ARBs and lithium 
Smoking 
Untreated urinary outflow tract obstruction 
proteinuria
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13
Q

CKD Iv

A

U&Es and eGFR (2 tests + 3 months apart)

Proteinuria (ACR) and Haematuria (dipstick)

renal USS

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14
Q

ACR stages

A

A1: <3
A2: 3-30
A3: >30

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15
Q

CKD stages

A 
G1: >90
G2: 60-89
G3a: 45-59
G3b: 30-44
G4: 15-29
G5: <15`
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16
Q

Accelerated CKD

A

sustained decrease in GFR of 25% or more and a change in GFR category within 12 months

Or

a sustained decrease in GFR of 15 ml/min/1.73m2 per year

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17
Q

Renal consequences of CKD

A
  • Local – pain/ haemorrhage/ infection
  • Urinary – haematuria/ proteinuria
  • Impaired salt and water handling
  • Hypertension
  • Electrolyte abnormalities
  • Acid-base disturbance → ESRD (End stage renal disease)
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18
Q

slowing CKD management

A
  1. ACEi - Reduce proteinuria
  2. Treat glomerulonephritis
  3. Exercise, maintain a healthy weight and stop smoking
  4. Special dietary advice about phosphate, sodium, potassium and water intake
  5. Offer atorvastatin 20mg
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19
Q

Anaemia of CKD

A

Target 100-120Hb, exclude B12 and folate, check ferritin (>100) and TSats > 20%

  1. Oral iron - IV iron - EPO
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20
Q

Bone disease of CKD

A
  1. Osteomalacia occurs due to increased turnover of bones without adequate calcium supply.
    Osteosclerosis occurs when the osteoblasts respond by increasing their activity to match the osteoclasts by creating new tissue in the bone, however due to the low calcium level this new tissue is not properly mineralised.
  2. Osteoporosis can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.
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21
Q

CKD: Bone disease management

A
  1. Active forms of vitamin D (alfacalcidol and calcitriol) – don’t need activation by kidneys
  2. Phosphate binders
  3. Salt reduction, K+ and fluid restriction
  4. Bisphosphonates
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22
Q

Dialysis 3 main purposes

A

excess fluid, solutes and waste products.

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23
Q

Dialysis based on

A
  1. Diffusion e.g. urea, K+, Na+ and infusion of HCO3-
  2. Convection: water across semipermeable membrane
  3. Adsorption: atoms, ions or molecules from a substance
    adhere to a surface of the adsorbent
    e.g. plasma proteins
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24
Q

Dialysis indications

A

A – Acidosis (severe and not responding to treatment)

E – Electrolyte abnormalities (severe and unresponsive hyperkalaemia)

I – Intoxication (overdose of certain medications)

O – Oedema (severe and unresponsive pulmonary oedema)

U – Uraemia symptoms such as seizures or reduced consciousness

eGFR < 7ml/min

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25
Q

Haemodiafiltration (HDF)

A

haemodialysis is primarily diffusive, haemodiafiltration is increasingly convective, in nature. greater the convective force, the greater will be the generated volume of the pressure-driven ‘ultrafiltrate’. • Large volumes of ultrafiltrate add enormously to solute drag - especially for the larger “middle molecule” solute classes

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26
Q

different types of PD

A

continuous (2L x 4times per day) vs automated (overnight)

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27
Q

types of renal transplant

A

Deceased Heart Beating Donors (Brain stem death (DBD))

Non-Heart Beating Donors (DCD)

Live Donation (altruistic)

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28
Q

Lifelong immunosuppression for kidney transplant

A

Induction
Consolidation
Maintenance

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29
Q

Transplant rejection types

A
  1. Hyperacute - preformed antibodies
  2. Acute rejection: cellular or antibody mediated, treated with immunosuppression
  3. Chronic rejection: antibody mediated slowly progressive decline in renal function.
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30
Q

CMV infection - transplant

A

1st 3 months

  • Prophylactic PO valganciclovir in higher risk patients
  • IV ganciclovir if evidence of infection
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31
Q

Nephritic syndrome

A 
Haematuria 
oliguria 
Proteinuria (<3g)
Oedema 
Hypertension 
affect endothelial cells (proliferative process)
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32
Q

Nephrotic syndrome

A 
Peripheral oedema
Proteinuria >3g
Hypoalbuminemia (<25g/L)
Hypercholesterolaemia 
affects podocytes (non-proliferative process)
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33
Q

Minimal change disease

A

usually idiopathic, most common nephrotic syndrome in children, secondary to hodgkins lymphoma, leukaemia and a virus

EM: foot fusion

1st line: steroids
2nd line: cyclophosphamide

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34
Q

Focal segmental glomerulosclerosis

A

small sections of each glomerulus (filter), and only a limited number of glomeruli are damaged at first.

Commonest cause of nephrotic syndrome in adults (35%)

primary (more common) or secondary (HIV/Heroin use/Obesity/ Reflux nephropathy)

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35
Q

Focal segmental glomerulosclerosis diagnosis and management

A

Small areas of mesangial collapse and sclerosis

steroids

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36
Q

Membranous glomerulonephritis

A

2nd commonest cause of nephrotic syndrome in adults (15-30%)

  1. idiopathic (majority)
  2. Infections (Hep B), malignancies, Connective tissue diseases and drugs (gold/penicillamine)
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37
Q

Membranous glomerulonephritis diagnosis

A

Renal biopsy: subepithelial immune complex deposition in the basement membrane

Anti PLA2r antibody: forms immune complex stuck between podocytes and basement membrane (blood)

LM: Diffuse thickening of GBM. “spikes” with special silver stains
IF: “IgG and complement (C3) deposits on the basement membrane”
EM: Electron dense sub-epithelial deposits

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38
Q

Membranous glomerulonephritis Mx

A

immunosuppression e.g. Steroids/Alkylating agents/B cell monoclonal Ab (rituximab: stop antibody production and therefore damage)
• 30% progress to end stage renal failure in 10 years

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39
Q

IgA nephropathy

A

Commonest GN in the world (Nephritis)

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40
Q

IgA nephropathy signs/symptoms

A

Asymptomatic microhaematuria  non-nephrotic range proteinuria

Macroscopic haematuria after resp/GI infection

Young adult and tonsillitis

AKI (red cells clogging tubes up)/CKD

Associated with Henoch-Schonlein Purpura (HSP) (arthritis/colitis/ purpuric skin rash)

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41
Q

IgA nephropathy Ix and management

A

LM: Diffuse mesangial IgA deposition
IF: IgA and C3 deposition
EM: Electron dense deposits in mesangium

  • BP control/ ACE inhibitors & ARBs/ Fish oil
  • Corticosteroids if persistent proteinuria >1g 3-6 months of ACE-i/ARB and GFR>50
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42
Q

Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)

A

Skin or throat infection: 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
Strep endocarditis: immune complex (bacterial antigen and antibody) – circulates and lodges into the kidney
They develop a nephritic syndrome
Can cause rapid decline unlike IgA
Complement levels are lower in this but normal in IgA nephropathy

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43
Q

Post streptococcal glomerulonephritis Ix

A

Evidence of strep infection: increase ASOT, anti-DNAse B or decrease C3

CRP (less in IgA) and more in raise in this

Fever, AKI, CRP, low complement

Echo: for endocarditis

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44
Q

Mesangiocapillary glomerulonephritis

A

Idiopathic

Secondary to Autoimmune e.g. SLE, RA, Cancer

Mixed nephrotic/ nephritic syndrome

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45
Q

Mesangiocapillary glomerulonephritis diagnosis

A

LM: Mesangial proliferation, neutrophils and monocytes, thickened capillary walls. “tram track” GBM
IF: Granular deposits of C3
EM: Electron dense sub-endothelial deposits +/- sub-epithelial +/- mesangial

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46
Q

Mesangiocapillary glomerulonephritis management

A

ACE-i/ARB and BP control
Treat underlying cause
Trial of immunosuppression if no underlying cause is found and progressive decline in function

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47
Q

Rapidly progressive glomerulonephritis

A

ANCA-Positive: Systemic Vasculitis, Wegener’s granulomatosis (Granulomatosis with polyangiitis) and Microscopic polyangiitis

ANCA-Negative: Goodpasture’s disease-Anti-GBM, Henoch Scholein Purpura HSP/IgA, IgA & membranous (transforms into this) and Systemic Lupus Erythematosus SLE

crescentic glomerulonephritis

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48
Q

Rapidly progressive glomerulonephritis signs/symptoms

A

Rapid deterioration in renal function over days/weeks

Active urinary sediment (RBC’s, RBC & Granular Casts)

It presents with a very acute illness with sick patients but it responds well to treatment

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49
Q

Rapidly progressive glomerulonephritis management

A

• Immunosuppression

  • Steroids (IV Methylprednisolone / Oral Prednisolone)
  • Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine
  • dialysis
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50
Q

Goodpasture Syndrome

A

Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes due to type IV collagen

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51
Q

Goodpasture Syndrome Mx

A

Imunosuppression

  • Steroids (IV Methylprednisolone / Oral Prednisolone)
  • Cytotoxic (Cyclophosphamide/ Mycophenolate/ Azathioprine
  • dialysis
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52
Q

Diabetic nephropathy

A

chronic high level of glucose passing through the glomerulus causes scarring. This is called glomerulosclerosis. Haemodynamic changes – increased GFR and initial decrease in creatinine – afferent arteriolar vasodilation mediated by range of vasoactive mediators.

Renal hypertrophy due to raised plasma glucose which stimulates growth factors, renin-angiotensin aldosterone activation, production of advanced glycation products and oxidative stress

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53
Q

Diabetic nephropathy screening

A

albumin: creatinine ratio and U&Es.

Overt diabetic nephropathy is characterised by persistent albuminuria
(300mg/24 hours on at least 2 occasions separated by 3-6 months)

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54
Q

Diabetic nephropathy management

A

optimising blood sugar levels (Hb1Ac below 53 mmol to reduce microvascular complications) and blood pressure (ACE inhibitors)

Lipid control: statins

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55
Q

Myeloma

A

Cancer of plasma cells: a type of WBC normally responsible for producing antibodies

Excess production of immunoglobins (proteins)

Collections of abnormal plasma cells accumulate in the bone marrow

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56
Q

Myeloma diagnosis

A

FBC, U&Es, LFTS

Bloods: Serum Protein Electrophoresis and Serum Free light chains

Urine: Bence Jones Protein

Bone Marrow Biopsy

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57
Q

Myeloma management

A

Stop nephrotoxic medication e.g. NSAIDs – don’t give for the back pain

Diuretics in view of risk increasing cast formation – flush calcium out as well

Manage hypercalcaemia (saline +/- bisphosphonates [inhibit osteoclasts] )

  • Chemotherapy to reduce tumour load
  • High dose dexamethasone may help reduce tumour load
  • Thalidomide/bortezomib: monoclonal antibodies
  • Stem cell transplant
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58
Q

Amyloidosis

A

extracellular amyloid (insoluble protein fibrils) in tissues or organs

Occurs due to abnormal folding of proteins which aggregate and become insoluble

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59
Q

Amyloidosis types

A
  1. Primary / Light chain (AL)
  2. Secondary / Systemic / Inflammatory (AA)
  3. Dialysis (Aβ2M)
  4. Hereditary and old age (ATTR)
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60
Q

Amyloidosis complications

A

Renal – (nephrotic range) proteinuria +/- impaired renal function

Cardiac – Restrictive Cardiomyopathy

Nerves – peripheral or autonomic neuropathy

Hepatomegaly / Splenomegaly

GI – malabsorption

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61
Q

Amyloidosis Iv

A

Urinalysis + uPCR (urine protein creatinine ratio)

Blood tests – renal function, markers of inflammation, protein electrophoresis, SFLC (Serum free light-chain measurement)

Renal Biopsy: Congo red staining (apple green under polarised light)

[Other biopsy - abdominal fat pad or rectal biopsy]

SAP scan – Scintigraphy with radiolabelled serum amyloid – shows extent of disease

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62
Q

Vasculitis Mx

A

Corticosteroids
Cyclophosphamide/Rituximab
Azathioprine/Methotrexate used for maintenance
Plasma Exchange – dialysis machine

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63
Q

SLE diagnosis

A

High index of suspicion: young lady with non-specific symptoms
Blood: Raised inflammatory markers, Immunology – ANA +ve, anti-dsDNA ab (~70%) and Complement – low levels

Urinalysis: protein: ACR >30 and PCR>50

Renal biopsy:

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64
Q

Interstitial nephritis

A

inflammation of the space between cells and tubules (the interstitium) within the kidney.

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65
Q

Acute interstitial nephritis

A

presents with AKI and hypertension

acute inflammation of tubules and interstitium

hypersensitivity reaction to:

  • drugs (NSAIDs or antibiotics)
  • Infection e.g. strep
  • autoimmune
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66
Q

Acute interstitial nephritis other signs/symptoms

A 
o	Rash
o	Fever
o	Eosinophilia on blood test 
o	Arthralgia 
AKI + hypertension
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67
Q

Acute interstitial nephritis management

A

treat underlying cause

steroids

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68
Q

Chronic Tubulointerstitial Nephritis

A

chronic inflammation of the tubules and interstitium. Presents as CKD.

Autoimmune, infectious, iatrogenic and granulomatous disease causes

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69
Q

Chronic Tubulointerstitial Nephritis management

A

ACEi/ARB (BP control), glucose control and lipids (statins)

steroids

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70
Q

Acute tubular necrosis

A

damage and death (necrosis) of the epithelial cells of the renal tubules. Most common cause of AKI

Cause: ischaemia or toxins

reversible: regenerates after 7-21 days

71
Q

Acute tubular necrosis Iv

A
  • Urinalysis: “Muddy brown casts”

- renal tubular epithelial cells in urine

72
Q

Acute tubular necrosis management

A 
Same as AKI
supportive 
IV fluids 
stop nephrotoxins 
treat complications
73
Q

Renal tubular acidosis

A

metabolic acidosis due to pathology in the tubules of the kidney.

74
Q

Type 1 renal tubular acidosis

A

pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions that cause acidosis

  • hyperventilate to compensate for metabolic acidosis (blow CO2)
75
Q

Type 1 renal tubular acidosis Ix + Mx

A

Hypokalaemia, metabolic acidosis and high urinary pH

Mx: Oral bicarbonate

76
Q

Type 2 renal tubular acidosis

A

The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood.

Excessive bicarbonate is excreted in the urine leads to acidosis in the blood due bicarbonate normally lowers pH

Fanconi’s syndrome is the main cause

77
Q

Type 2 renal tubular acidosis Ix + Mx

A

Hypokalaemia
Metabolic acidosis
High urinary pH

Mx: oral bicarbonate and K+ replacement

78
Q

Type 3 RTA

A

Type 3 renal tubular acidosis is a combination of type 1 and type 2 with pathology in the proximal and distal tubule.

79
Q

Type 4 Renal Tubular Acidosis

A

Reduced aldosterone (stimulates sodium absorption and excretion of K+ and H+) and affects the distal tubule. Lower levels of K+ and H+ becomes excreted in the urine from the blood leading to hyperkalaemic renal tubule acidosis

Causes: adrenal insufficiency, ACEi, spironolactone, SLE, diabetes or HIV

80
Q

Type 4 Renal Tubular Acidosis Ix and Mx

A
  • Hyperkalaemia – how to distinguish between type 1 and 4
  • High chloride
  • Metabolic acidosis
  • Low urinary pH – reduced ammonia (suppressed by K+ -normally counter balances H+ acidity) production and less in urine

Mx:

  • Fludrocortisone – synthetic corticosteroid medication that works similar to aldosterone
  • Sodium bicarbonate
  • Treatment of the hyperkalaemia may also be required
81
Q

Haemolytic Uraemic Syndrome

A

thrombosis (blood clots) in small blood vessels throughout the body (especially glomerulus capillaries).

  1. Haemolytic anaemia
  2. AKI (haematuria and proteinuria)
  3. Low platelet count
82
Q

HUS signs/symptoms

A 
Reduced urine output – due to AKI 
Haematuria or dark brown urine
Abdominal pain
Lethargy & irritability
Confusion
Hypertension
Bruising
83
Q

HUS management

A

anti-hypertensives
blood transfusions
dialysis

84
Q

Rhabdomyolysis

A

skeletal muscle tissue breaks down and releases breakdown products into the blood.

Myocytes undergo apoptosis
- myoglobin, K+, P+, CK

85
Q

Causes of Rhabdomyolysis

A

Prolonged immobility
Extremely rigorous exercise
Crush injuries
Seizures

86
Q

signs/symptoms of Rhabdomyolysis

A 
Muscle aches & pain
Oedema
Fatigue
Confusion 
Red-brown urine
87
Q

Rhabdomyolysis Ix and Mx

A

CK blood test
Myoglobinuria
U&Es
ECG

Mx
IV fluids: rehydrate and encourage filtration
IV NaCl (reduce myoglobin toxicity)
IV mannitol

88
Q

Causes of hyperkalaemia

A 
Acute kidney injury
Chronic kidney disease
Rhabdomyolysis
Adrenal insufficiency
Tumour lysis syndrome
Medications a lot
89
Q

hyperkalaemia ECG results

A

Tall peaked T waves
Flattening or absence of P waves
Broad QRS complexes

90
Q

Hyperkalaemia management

A

calcium gluconate 10mls 10% - stabilise myocardium

Insulin (actrapid) and dextrose (50mls of 50%)

Nebulised salbutamol 
IV fluids 
Oral calcium resonium 
Sodium bicarbonate 
Dialysis
91
Q

Polycystic Kidney Disease chromosomes

A

PKD-1: chromosome 16

PKD-2: chromosome 4

92
Q

Polycystic Kidney Disease extra renal manifestations

A

Cerebral aneurysms
Hepatic cysts: SOB, ankle swelling and pain
Cardiac valve disease (aortic/mitral regurgitation/Aortic root dilatation)
Colonic diverticula and colonic perforation-
Abdominal and inguinal hernias

93
Q

Polycystic Kidney Disease management

A 
Tolvaptan: slow the development of cysts and renal failure
Antihypertensives 
Hydration 
Analgesia 
Antibiotics 
Dialysis 
Renal transplant
94
Q

Autosomal recessive polycystic kidney disease (ARPKD) chromosome

A

6
Young children and constantly associated with hepatic lesions
renal: bilateral and symmetrical
small cysts appearing from collecting duct system

95
Q

Autosomal recessive polycystic kidney disease (ARPKD) signs/symptoms

A

Kidneys always palpable
Hypertension
Recurrent Urinary Tract Infections
Slow Decline in GFR -less than 1/3 reach dialysis
It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine.
They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge.

96
Q

Autosomal recessive polycystic kidney disease (ARPKD) management

A

dialysis in the first few days

tolvaptan

97
Q

ALPORTS SYNDROME (HEREDITARY NEPHRITIS)

A

genetically heterogeneous disorder characterized by nephritic syndrome

X linked inheritance (85%)

Disorder of Type IV collagen matrix

Mutation (COL4A5 gene) leads to deficient collagenous matrix

98
Q

ALPORTS SYNDROME signs/symptoms

A

Haematuria - characteristic feature.
Proteinuria seen later but confers bad prognosis
Sensorineural deafness
Ocular defects
Leiomyomatosis of oesophagus/genitalia-rare

Suspect in haematuria and hearing loss

99
Q

ANDERSON FABRYS DISEASE

A

Uncommon Inborn error of Glycosphingolipid metabolism (deficiency of a-galactosidase A)

X linked disease lysosomal storage disease

Look for angiokeratomas

100
Q

ANDERSON FABRYS diagnosis and Mx

A

Plasma /Leukocyte: a-GAL activity in blood

Enzyme replacement - Fabryzyme

101
Q

MEDULLARY CYSTIC KIDNEY

A

Autosomal Dominant inheritance

Morphologically abnormal renal tubules leading to fibrosis

Cysts are in the corticomedullary junction/medulla - not essential for diagnosis

102
Q

Oncocytoma: benign tumour

A

Spherical, capsulated, brown/tan colored

CT scan: Spoke wheel pattern (Has got central scar (stellate): strands come out from the center. Necrosis in the middle – can’t revascularize)

103
Q

Angiomyolipoma (AML)

A

Blood vessels, muscle and fats: typical hamartoma

associated with TS

104
Q

Angiomyolipoma (AML) Mx

A

4 cm is considered cut off: rough guide

Elective: Embolization/Partial nephrectomy

Emergency: Embolization / emergency nephrectomy: usually the whole

105
Q

Renal cell carcinoma

A

adenocarcinoma of renal cortex (arise from proximal convoluted tube)

106
Q

Types of RCC

A 
Clear cell: loss of VHL
Papillary 
Chromophobe 
Collecting duct 
Medullary cell
107
Q

RCC signs/symptoms

A

Haematuria, vague loin pain and mass (3 together: less than 10% in cases)

Non-specific symptoms of cancer (e.g. weight loss, fatigue, anorexia, night sweats)

Pyrexia of unknown origin (8-9 %)

Varicocoele: causing pressure on left gonadal vein. Left gonadal vein drains in left renal vein. Left sided renal tumours can cause these

Paraneoplastic syndrome (30%): weight loss, anaemia, HT and hypercalcemia

108
Q

RCC Ix

A

USS
CT: Chest, abdo and pelvis
FBC: Hb

109
Q

RCC Mx

A

small tumours 3-4cm:

  • surveillance (elderly)
  • ablation
  • partial nephrectomy

> 3-4cm

  • surveillance (elderly)
  • ablation
  • partial nephrectomy
  • Radical Nephrectomy

> 7cm
- radical nephrectomy

110
Q

RCC adjuvant therapy

A

TKI (Tyrosine kinase inhibitors) e.g. Sunitinib

- Reduces neovascularisation

111
Q

RCC paraneoplastic syndromes

A

Polycythaemia (RCC secretes unregulated erythropoietin)

Hypercalcaemia (RCC secretes a hormone that mimics the action of PTH)

112
Q

Wilms tumour

A
  • Under 5
  • Mass in the abdomen (parents noticed or presenting with signs/symptoms)
  • Abdominal pain
  • Haematuria
  • Lethargy
  • Fever
  • Hypertension
  • Weight loss
113
Q

Prostate cancer pathology

A

adenocarcinomas originating in peripheral zone
local extension through the prostatic capsule, to the urethra, bladder base and seminal vesicles and with perineural invasion along autonomic nerves.
pelvic lymph nodes

114
Q

Prostate cancer sign/symptoms

A

Majority asymptomatic

Lower urinary tract symptoms:

bladder outflow obstruction: hesitancy, poor stream, terminal dribbling, frequency, nocturia, urinary retention or obstruction
Hematuria/Haematospermia

Bone pain, Anorexia, Weight loss and fatigue

ED

115
Q

Prostate cancer diagnosis

A 
PSA
PR exam
Prostate biopsy
TMN: T1-4
 - Gleason grading system  (1-5)
116
Q

Prostate cancer management

A

Organ confined

  • watchful waiting
  • active surveillance
  • Radical prostatectomy
  • Radical radiotherapy

Locally advanced

  • radiotherapy
  • watchful waiting
  • hormonal therapy

Metastatic disease

  • GNRH analogues e.g. Goserelin
  • Anti-androgens
    • Steroidal: cyproterone acetate
    • Non-steroidal: nilutamide and bicalutamide
  • bilateral subcapsular orchidectomy
  • maximal androgen blockade

Cytotoxic chemotherapy with docetaxel

Abiraterone (androgen synthesis inhibitor)

117
Q

Bladder cancer

A

arise from the endothelial lining (urothelium)

  • transitional cell carcinoma (papillary 80% and non papillary 20%)
  • squamous cell carcinomas
    Urachal
118
Q

Bladder cancer risk factors

A
  • smoking
  • hair dyes
  • ## schistosomiasis
119
Q

Bladder cancer signs/symptoms

A

painless haematuria

bladder mass and palpable kidney

120
Q

bladder cancer diagnosis

A

Cystoscopy and biopsy (transurethral resection of bladder tumour)

Urine cytology

During a CT urogram
Retrograde pyelogram

121
Q

Bladder cancer Mx

A

Not invading the muscle

  • Superficial bladder – resected endoscopically with repeated cystoscopic surveillance to detect surveillance to detect recurrence
  • Transurethral Resection of a Bladder Tumour (TURBT)
  • Chemo into bladder after surgery (use barrier contraception afterwards)
  • Weekly treatments for 6 weeks with BCG vaccine squirted into the bladder via catheter, then every six months for 3 years.

Muscle-invasive bladder cancer

  • Radical cystectomy with ileal conduit+/- removal of other pelvic contents
  • Radiotherapy (as neoadjuvant, primary treatment or palliative)
  • IV chemotherapy as neoadjuvant or palliative
122
Q

Testicular cancer risk factors

A

previous TC
Cryptorchidism
HIV
FH

123
Q

Types of TC

A 
Seminoma 
Non-seminomatous 
 - Teratoma 
- Yolk sac
- Choriocarcinoma
124
Q

Testicular Cancer signs/symptoms

A

Asymmetry or slight scrotal discoloration
o Hard without flatulence or transillumination, non-tender, irregular mass mostly intratesticular
o Assess involvement of epididymis, spermatic cord and scrotal skin.
o Secondary hydrocoele
o Abdominal mass – advanced disease

125
Q

TC bloods

A

Alpha-fetoprotein: teratomas and yolk sac

Beta-hCG - choriocarcinoma

126
Q

TC mx

A

Orchidectomy

  • radicular inguinal orchidectomy
  • chemo/radio
127
Q

Penile cancer

A

Squamous cell carcinoma
Kaposi sarcoma
BCC

128
Q

Penile cancer risk factors

A 
Age: 5-6 th decade
Pre-malignant conditions in 40% cases
Phimosis (unable to retract foreskin): Chronic inflammation
Geography: Asia, Africa, South America
Human Papilloma virus: Types 16 and 18 
Smoking
Immunocompromised patients
129
Q

Squamous carcinoma in situ Mx

A

Circumcision: if prepuce alone (foreskin)

Topical 5 fluorouracil

130
Q

Invasive Squamous carcinoma Mx

A

Prepucial lesions: Circumcision

Glans lesions

  • Superficial: Glans resurfacing
  • Deep: Glansectomy

More advanced disease:

  • Total penile amputation with formation of perineal urethrostomy
  • Inguinal lymphadenectomy
  • If involved lymph nodes. Also in high risk penile cancer cases even when not involved.
131
Q

Upper Urinary Obstructive Uropathy

A

Loin to groin/flank pain on affected side (stretching/irritation of ureter and kidney)
pain on affected side (stretching/irritation of ureter and kidney)

Reduced / no urine output

Non-specific symptoms (e.g. vomiting)

Reduced renal function on bloods

132
Q

Lower Urinary Tract Obstruction (i.e. bladder / urethra)

A

Acute urinary retention (unable to pass urine and increasingly full bladder)

Lower urinary tract symptoms (e.g. poor flow, difficulty initiating urination, terminal dribbling)

Reduced renal function on bloods

133
Q

Benign Prostatic Hyperplasia

A

hyperplasia of the stromal and epithelial cells of the prostate

134
Q

BPH key questions

A

Storage

  • Urgency: If you are watching your favourite TV Programme, and get the feeling of wanting to pass urine, can you delay until the programme is finished?
  • Frequency: How often do you pass urine from the time you wake up in the morning until the time you go to sleep at night?
  • Nocturia: How many times, on average are you woken from sleep because you need to pass urine?

Voiding

  • Hesitancy
  • Poor flow
  • Intermittency
  • Straining to void
  • Terminal dribbling
  • Incomplete emptying
135
Q

Red flags in urinary tract obstruction

A
  • haematuria
  • bedwetting (high pressure chronic retention)
  • suprapubic pain
  • recurrent urinary tract infections
  • back pain and neurological symptoms
136
Q

BPH Ix

A 
Urine dipstick 
PSA 
Rectal exam 
IPSSS
Serum creatinine
Frequency - volume chart 
USS
Cystoscopy
137
Q

BPH Mx

A
  • Alpha blockers (relax smooth muscle; e.g. tamsulosin 400 mcg once daily)
  • 5-alpha reductase inhibitors (block testosterone and reduce the size of the prostate; e.g. finasteride)
  • Anticholinergic (Inhibits bladder smooth muscle contraction)
  • Beta agonist (Inhibits bladder smooth muscle contraction)

Surgery
- Transurethral resection of the prostate (TURP)

138
Q

Acute Urinary Retention

A

complication of BPH, prostate cancer and urethral stricture (women: pelvic prolapse, mass or post surgery for stress incontinence)

  • spontaneous vs precipitated
  • painful (acute) vs painless (chronic)
139
Q

Acute Urinary Retention Ix

A

FBC, renal functions (usually normal in acute urinary retention)
urine dipstick

DRE: Prostate and pelvic mass: anal tone & perianal sensation (S2-3): Cauda equina

140
Q

Acute Urinary Retention Mx

A

catheter and record residual volume

treat cause

141
Q

Chronic retention signs/symptoms

A

Painless and may not feel any difficulty: renal impairment in high pressure chronic retention

Nocturnal enuresis

Sometimes smell slightly like urine due to leakage

Tense, palpable bladder, hypertension, and progressive renal impairment associated with bilateral hydronephrosis and hydroureter commonly leading to uraemia and death

142
Q

Chronic retention Mx

A

Admit cathertise , monitor post obstruction diuresis (>200ml/hr for 2 consecutive hours or >3L/24h)

Definitive: LTC/ISC/Surgery (after at least 6 weeks)

143
Q

Renal stones signs/symptoms

A

asymptomatic and never cause an issue
Renal colic
Excruciating loin to groin pain
Colicky (fluctuating in severity) as the stone moves and settles
May have haematuria, nausea, vomiting and oliguria
May have symptoms of sepsis if infection present (i.e. fever)

144
Q

Renal stones diagnosis

A

Urine dipstick: haematuria and infection
Bloods: FBC, U&Es, CRP, urate and calcium
CT KUB

145
Q

Renal stones Mx

A 
NSAIDs 
e.g. PR diclofenac+/- anti-opiate  
Antiemetic 
Fluids
Antibiotics if infection
  • No pain, no sepsis or AKI = manage conservatively (watchful waiting and Tamsulosin to aid passage)
  • Surgical Interventions
    if stone has not passed in one month and AKI/sepsis/refractory pain: aim to decompress kidney in immediate management

Indications to treat urgently: Pain unrelieved, Pyrexia, Persistent nausea/vomiting and High-grade obstruction

  • Extracorporeal Shock Wave Lithotripsy
  • Ureteroscopy and Laser Lithotripsy
  • Percutaneous Nephrolithotomy (under GA in theatre)
  • Open Surgery
146
Q

Testicular torsion signs/symptoms

A

Acute/sudden onset of unilateral testicular pain

  • nausea/vomiting
  • May be referral of pain to lower abdomen
  • Acutely tender testicle (often difficult to examine due to extent of tenderness)
  • Firm testicle
  • Absent cremasteric reflex
  • Abnormal lie and Horizontal lie
  • Rotated so that epididymis is not in normal posterior position
  • Elevated (retracted) testicle
  • Acute hydrocoele + oedema may obliterate landmarks
147
Q

Testicular torsion Mx

A

Immediate surgical scrotal exploration

- orchiplexy and possible orchiectomy if delayed surgery

148
Q

Torsion of appendage

A

twisting of a vestigial appendage that is located along the testicle. This appendage has no function, yet more than half of all boys are born with one

149
Q

Torsion of appendage

A

very similar to torsion
seen early, may have localised tenderness at superior pole and “blue dot” sign
Testis should be mobile and cremasteric reflex present

150
Q

Paraphimosis

A

Painful swelling of the foreskin distal to a phimotic ring

151
Q

Paraphimosis Mx

A

Iced glove, granulated sugar for 1-2hrs (facilitates manual reduction – osmotic gradient), multiple punctures in oedematous skin

Manual compression of glans with distal traction on oedematous foreskin

Dorsal slit (relieve strangulation of the glans)

152
Q

Priapism

A

• Prolonged erection (> 4hrs), often painful and not associated with sexual arousal

153
Q

Priapism classification

A

Ischaemic (Vascular stasis in penis and decreased venous outflow)

Non-ischaemic (arterial or high-flow)

154
Q

Priapism Mx

A

Ischaemic

  • Aspiration +/- irrigation with saline
  • Injection of alpha-agonist, e.g. phenylephrine 100-200ug every 5-10 mins up to max 1000ug after aspiration: reduce blood flow to penis
  • Surgical shunt

Non-ischaemic

  • Observe, may resolve spontaneously
  • Selective arterial embolization with non-permanent materials
155
Q

Fournier’s gangrene

A

necrotizing fasciitis occurring about the male genitalia

156
Q

Emphysematous pyelonephritis

A

acute necrotizing parenchymal and perirenal infection caused by gas-forming uropathogens, usually E coli

157
Q

Bladder injury

A

Commonly associated with pelvic fracture

  • Suprapubic/abdominal pain + inability to void
  • Suprapubic tenderness, lower abdominal bruising, guarding/rigidity, diminished bowel sounds
158
Q

Bladder injury Mx

A

Large-bore catheter

Antibiotics

159
Q

Urethral injury

A

Posterior urethral injury often associated with fracture of pubic rami

Post. urethra fixed at urogenital diaphragm and puboprostatic ligaments, so bulbomembranous junction most vulnerable

160
Q

Penile fracture

A

Typically happens during intercourse – buckling injury when penis slips out of vagina and strikes pubis

161
Q

Complicated UTI

A
  • systemic symptoms (infection goes into the bloodstream) or

- urinary structural abnormality /stones

162
Q

Common organisms of UTI

A

Escherichia coli is the most common cause
Klebsiella
Proteus: struvite stones – calculi: Produces urease which breaks down urea to form ammonia, which increases urinary pH - precipitation of salts (swarming cultures)
Enterococcus: hospital acquired infections
Pseudomonas: associated with catheters and instrumentation – needs ciprofloxacin

163
Q

UTI diagnosis

A

> 105 - probale UTI
<103 - not significant UTI
104 - contamianed? infection? repeat?

164
Q

Empirical antibiotic treatment for UTI Female

A

Nitrofurantoin or trimethoprim orally (3 days)

165
Q

Empirical antibiotic treatment for UTI Uncatheterised male UTI

A

nitrofurantoin or trimethoprim orally (7 days)

166
Q

Complicated UTI or pyelonephritis (GP) Mx

A

com-amox or co-trimoxazole (14 days)

167
Q

Complicated UTI or pyelonephritis (Hospital)

A

Amoxicillin (enterococci) and gentamicin (coliforms) IV for 3 days

  • (co-trimoxazole and gentamicin if penicillin allergy), stepdown as guided by antibiotic sensitivities
168
Q

Abacterial cystitis/Urethral syndrome + Mx

A

• Pus cells present in urine, but no significant growth on culture

  • alkalinising urine and stop the thing causing it
169
Q

Asymptomatic bacteriuria

A

Patient is asymptomatic, therefore condition is detected incidentally

Significant bacteriuria (>105 orgs/mL)
No pus cells in urine
170
Q

Asymptomatic bacteriuria Mx

A

treat in pregnancy

171
Q

UTI in catheterised patients

A

Catheterised patients with >105 orgs/mL should ONLY be given antibiotics if there is supporting evidence of UTI (fever, symptoms etc.)
Unnecessary antibiotics result in the catheter becoming colonised with increasingly resistant organisms

172
Q

Pyelonephritis

A

Infection in the renal pelvis (join between kidney and ureter) and parenchyma (tissue)

173
Q

Pyelonephritis Ix

A
  • Specimen collection – mid stream as first stream most likely to be contaminated
  • Blood cultures
  • Urine dipstick
  • CT scan
  • USS
  • DMSA scans
174
Q

Pyelonephritis Mx

A

Broad spectrum: IV amoxicillin + Gentamicin (IV Co-trimoxazole + Gentamicin)

adimt, iV fluids, analgesia and antipyretics

Medical Diseases (18 decks)

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