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Year 3 Pathologies > Renal and Urology > Flashcards

Renal and Urology Flashcards

1
Q

What is the definition of an Acute Kidney Injury?

A

Acute decline in renal filtration function characterised by a rise in serum creatinine or a fall in urine output

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2
Q

What are the three types of AKI?

A

Pre-renal

Intrinsic Renal

Post-renal

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3
Q

Causes of Pre-renal AKI

A

Impaired renal perfusion

Hypovolaemia

Heart Failure

Excess afferent vasoconstriction

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4
Q

Causes of Intrinsic Renal AKI

A

Structural Injury (Acute Tubular Necrosis)

Glomerulonephritis

Acute Interstitial Nephritis

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5
Q

Causes of Post-renal AKI

A

Obstruction between renal pelvis and urethra

Ureteric obstruction in lumen, in wall or by compression

Bladder outflow obstruction

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6
Q

What is the KDIGO criteria for AKI?

A
  • Stage 1 : Serum creatinine baseline x1.5 - 1.9 or greater than 26 micromol/L increase OR less than 0.5mL/kg/h for 6-12hrs
  • Stage 2 : Serum creatinine baseline x2 - 2.9 or greater than OR less than 0.5mL/kg/h for 12hrs
  • Stage 3 : Serum creatinine baseline x3 or over or greater than 354 micromol/L increase OR less than 0.3mL/kg/h for 24hrs or anuria
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7
Q

Symptoms of AKI

A
  • N + V
  • Dehydration
  • Confusion
  • Reduced urine output or changes to urine colour
  • High BP
  • Abdominal Pain
  • Slight Backache
  • Oedema
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8
Q

Other Diagnostic Factors of AKI

A
  • Arrhythmias
  • Dizziness and other orthostatic symptoms
  • Uraemia (pericarditis, encephalopathy)
  • Pulmonary and peripheral oedema
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9
Q

Risk Factors of AKI

A
  • Advanced age
  • Underlying kidney disease
  • Diabetes Mellitus
  • Sepsis
  • Iodinated contrast
  • Surgery, trauma, haemorrhage
  • Pancreatitis
  • Malignant Hypertension
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10
Q

Primary Investigation to order for AKI

A

Urinalysis - Perform urine dipstick testing for blood, protein, leukocytes, nitrites and glucoses as soon as AKI suspected

U&Es - urea, creatinine, potassium

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11
Q

What is the diagnostic criteria for AKI?

A
  • Increase in serum Cr by 26 umol/L or more within 48 hours
  • Increase in serum Cr by 50% or more in the last week
  • Fall in urine output to less than 0.5 ml/kg/hr for 6 hours
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12
Q

Management of AKI if patient is hypovolaemic?

A
  • Fluid resuscitation
  • Review medications and stop nephrotoxins
  • Identify and treat underlying cause
  • Consider vasopressor if patient remains severely hypotensive
  • If refractory or complications, consider renal replacement therapy
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13
Q

What are the nephrotoxic medications to stop?

A
  • D - diuretics
  • A - ACEi, ARBs, Antibiotics
  • M - metformin
  • N - NSAIDs
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14
Q

Management of AKI if patient is hypervolaemic?

A
  • Loop diuretic (under specialist supervision) and sodium restriction
  • Identify and treat underlying cause
  • Consider renal replacement therapy
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15
Q

How is hyperkalaemia treated?

A
  • IV calcium gluconate (stabilise cardiac membrane)
  • Combined insulin/dextrose infusion, Nebulised salbutamol (move K+ from extracellular to intracellular compartment)
  • Calcium, loop diuretics, dialysis (remove potassium)
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16
Q

What is Renal Calculi and what are the other names for it?

A
  • Presence of calculi within urinary system
  • AKA urilithiosis, nephrolithiosis
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17
Q

What are the three places renal calculi can cause an obstruction?

A
  • Ureteropelvic junction
  • Pelvic brim
  • Vesicoureteric junction
18
Q

What are the types of stones formed?

A
  • Calcium Oxalate (most common - 80%)
  • Struvite
  • Uric acid (not visible on X-Ray)
  • Hydroxyapatite
19
Q

What are the diagnostic factors for renal calculi?

A
  • May be asymptomatic until obstruction
  • Acute severe loin to groin pain (renal colic)
  • N + V
  • Unable to lie still/writhing in pain
  • Urinary symptoms (urgency, frequency, haematuria)
20
Q

What are the risk factors of renal calculi?

A
  • Dehydration
  • High protein intake
  • High salt intake
  • Structural abnormalities
  • Previous kidney stones
  • FHx of kidney stones
21
Q

What are the investigations of renal calculi?

A
  • Non-contrast CT KUB
  • Urine Dipstick (blood + infection)
  • Blood test (calcium, infection, kidney function)
  • Abdominal X-Ray
  • US KUB for pregnant women and children
22
Q

What is the management for renal calculi?

A
  • NSAIDs (diclofenac)
  • IV Paracetamol
  • Antiemetics for N + V (ondansetron)
  • IV Antibiotics if infection
23
Q

What is the surgical management based on renal stone size?

A
  • Stone less than 10mm : offer SWL and consider URS if there is contradiction for SWL
  • Stone between 10 and 20mm : consider URS or SWL or PCNL if both of those fail
  • Stone larger than 20mm (incl. staghorn) : Offer PCNL or URS if PCNL is not an option
24
Q

What are the surgical options for renal calculi?

A
  • Shockwave lithotripsy SWL
  • Ureteroscopy URS
  • Percutaneous nephrolithotomy PCNL
  • Open Surgery
25
Q

What is surgical management based on ureteric stone size?

A
  • Stone less than 10mm : Offer SWL and consider URS if not possible
  • Stone between 10 to 20mm : Offer URS, consider SWL or PCNL if not possible
26
Q

Prevention of renal calculi

A
  • Increase fluid intake
  • Low animal protein
  • Low salt diet
  • Thiazide diuretics + Potassium Citrate
  • No carbonated drinks

For Oxalate Stones:
- reduce oxalate rich food e.g. spinach, beetroot, nuts
- cholestyramine and pyridoxine reduces urinary oxalate secretion

For Uric Acid Stones:
-reduce foods e.g. anchovies, spinach, tuna
- allopurinol
-urinary alkalinization e.g. oral bicarbonate

27
Q

What is Nephrotic Syndrome?

A

Condition characterised by loss of protein in the urine due to increased glomerular permeability
Results in low serum albumin and oedema

Presence of an AKI, hypertension and an active urinary sediment

28
Q

What are causes of Nephrotic Syndrome?

A
  • Common causes : primary glomerular diseases such as minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy
  • Secondary causes include systemic diseases such as DM, lupus and amyloidosis
  • Complications of nephrotic syndrome include infection, thrombosis and malnutrition
29
Q

History and Examination of Nephrotic Syndrome

A
  • Proteinuria, hypoalbuminuria and peripheral oedema
  • Oedema, particularly around eyes, legs, hands and feet
  • Fatigue, anorexia and decreased urine output
  • Very important to obtain MHx of infection and medication + FHx for history of renal disease
30
Q

Investigations of Nephrotic Syndrome

A
  • First line is Urine Dipstick test to show increased levels of proteinuria
  • 24 hour urine collection (protein excretion of greater than 3.5g/day = nephrotic syndrome)
  • Blood tests will show hypoalbuminuria, hyperlipidemia and elevated serum creatinine
31
Q

Management of Nephrotic Syndrome

A
  • First line treatment involves corticosteroids such as prednisolone for a period of 4-6 weeks
  • In cases of steroid resistance or dependence, additional immunosuppressive agents such as cyclophosphamide or mycophenolate mofetil may be used
  • Diuretics can help manage oedema and anticoagulants may be required to prevent thrombosis
  • Regular monitoring of BP, serum electrolytes and renal function
32
Q

What is Diabetic Nephropathy?

A

Deterioration of kidney function due to diabetes, it is a common cause of CKD

33
Q

History and Examination of Diabetic Nephropathy

A
  • Oedema
  • Diabetic Symptoms
  • Lethargy
  • Hypertension

Due to protein in urine:
- Oedema (especially eyes, hands, legs, feet)
- Frothy urine
- Confusion
- N+V
- Loss of apetite

34
Q

What are the investigations of Diabetic Nephropathy?

A
  • Urinalysis : ACR > 2.5mg/mol = microalbuminuria and ACR > 3mg/mol = proteinuria (screen annually)
  • Renal Biopsy for Kimmelstiel-Wilson Nodules
35
Q

What is the management of Diabetic Nephropathy?

A
  • Give ACEi/ARBs if ACR > 3mg/mol (even if normotensive)
  • Improve glycemic control (SGLT-2 Inhibitors)
  • Smoking cessation
  • Target BP 130/80
36
Q

Pathophysiology of Diabetic Nephropathy

A
  • Diabetes = Increased BGC and BP
  • This leads to glomerular hypertension
  • If this state is sustained it leads to microalbuminuria and then proteinuria
  • This then leads to Glomerular and Interstitial Fibrosis
  • This decreases GFR and leads to renal failure if not managed
37
Q

What is CKD?

A

Chronic kidney disease, also called chronic kidney failure, involves a gradual loss of kidney function.

38
Q

What are the common causes of CKD?

A
  • Diabetic nephropathy
  • Chronic glomerulonephritis
  • Chronic pyelonephritis
  • Hypertension
  • Adult polycystic kidney disease
39
Q

H&E of CKD

A

Usually asymptomatic
Possible late stage features
- Oedema e.g. ankle swelling, weight gain
- Polyuria
- Lethargy
- Pruritis (secondary to uraemia)
- Anorexia, which may result in weight loss
- Insomnia
- N + V
- Hypertension

40
Q

What are the investigations for CKD?

A
  • RFTs

Stage 1 - GFR>90ml/min with some sign of kidney damage on other tests

Stage 2 - 60-90ml/min with some sign of kidney damage

Stage 3a - 45-59ml/min, a moderate reduction in kidney function

Stage 3b - 30-44ml/min, a moderate reduction in kidney function

Stage 4 - 15-29ml/min, a severe reduction in kidney function

Stage 5 - <15ml/min, establish kidney failure - dialysis or a kidney transplant may be needed

41
Q

Management of CKD

A

Hypertension:
- ACEi
- Prescribe if ACR > 70mg/mmol
- Rise in creatinine expected
- Furosemide, especially is stage 3 onwards

Anaemia:
- Oral iron, switch to IV if 10-12g/dl not reached in 3 months
- IV iron if on ESA or haemodialysis (correct deficiencies first)
- ESAs if QoL can be improved

Bone disease:
- Reduce phosphate intake
- Phosphate binders
- Vitamin D supplements

Tolvaptan shown to reduce rate of CKD progression in ADPKD, given to patients who have CKD stage 2 or 3 and is rapidly progressive.

42
Q
A

Year 3 Pathologies (12 decks)

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