5 - Chemical Pathology > Kidney > Flashcards

Kidney Flashcards

(43 cards)

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1
Q

What are the indications for starting dialysis? (4)

A
  • Hyperkalaemia
  • Uraemia
  • Metabolic acidosis
  • Pulmonary oedema
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2
Q

When do you start dialysis in an anuric patient?

A

Only when they have indications

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3
Q

What complications can uraemia cause? (2)

A
  • Encephalopathy
  • Pericarditis
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4
Q

What is the pathophysiology of rhabdomyolysis?

A

Breakdown of muscle → release of CK

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5
Q

What is the key investigation in rhabdomyolysis?

A

CK

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6
Q

What is unique about the dipstick result in rhabdomyolysis?

A

+ve for blood but when observed under microscope there will be no RBCs - myoglobin

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7
Q

Why is rhabdomyolysis dangerous for the kidneys?

A

Risk of ARF as myoglobin is nephrotoxic

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8
Q

What is the management of rhabdomyolysis?

A

0.9% saline

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9
Q

What is the best measure of kidney function and what’s the normal value?

A

GFR = best measure of kidney (normal = 120ml/min)

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10
Q

How do we estimate GFR?

A

Using clearance - volume of plasma cleared of a marker substance per unit time

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11
Q

What is the formula for clearance?

A

Clearance = (urinary concentration of marker x volume) / plasma concentration of the marker

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12
Q

What are the 3 criteria for using a marker to estimate GFR? (3)

A
  • Freely filtered
  • Not bound to plasma proteins
  • Not reabsorbed / secreted by tubules
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13
Q

What is the gold-standard marker of GFR and why isn’t it used clinically?

A
  • Inulin is the gold-standard marker
  • Not used in clinical practice - requires an IV steady-state infusion
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14
Q

What are the characteristics of blood urea as a marker? (4)

A
  • Endogenous marker (by-product of protein metabolism)
  • Freely-filtered by variable reabsorption by tubular cells
  • Dependent on nutrition, GI bleeding, hepatic function
  • Not used as a marker of GFR but of dehydration
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15
Q

What are the key points about serum creatinine? (3)

A
  • Derived from muscle cells
  • Freely filtered, active secretion into tubules
  • CKD-EPI equation uses creatinine clearance to calculate eGFR - this is what we use in clinical practice
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16
Q

What are the characteristics of Cystatin C? (3)

A
  • Alternative endogenous marker to creatinine - generated by nucleated cells
  • Freely filtered, but almost completely reabsorbed
  • Not really used clinically
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17
Q

What is the gold standard for measuring proteinuria?

A

spot urine protein:creatinine ratio

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18
Q

Is 24-hour urine collection commonly used for measuring proteinuria?

19
Q

What is the gold standard imaging for kidney stones?

Study These Flashcards
A

CTKUB (CT Kidneys, Ureters, Bladder)

20
Q

What is the basic definition of AKI?

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A

Reduction in GFR over 1 week - reversible

21
Q

What are the three main categories of AKI? (3)

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A
  • Pre-renal
  • Renal
  • Post-renal
22
Q

What is the main mechanism of pre-renal AKI?

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A

Reduced renal perfusion

23
Q

What are the causes of pre-renal AKI? (7)

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A
  • Shock
  • Renal artery stenosis
  • Haemorrhage
  • Hypotension
  • Calcineurin inhibitors
  • NSAIDs/ACIs/ARBs
  • Diuretics
24
Q

What are the two key adaptive mechanisms that maintain renal perfusion? (2)

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A
  • Myogenic stretch - afferent arteriole if stretched constricts to reduce high pressure to the bowman’s capsule
  • Tubuloglomerular feedback - high Cl- in the distal tubule → constriction of afferent arteriole
25
What are the key characteristics of pre-renal AKI? (3)
* NO structural renal damage * Responds immediately to restoration of circulating volume * Often precipitated by starting an ACEi
26
What is pre-renal AKI often precipitated by?
ACEi
27
What is the key characteristic of renal AKI?
Structural renal damage is present
28
What are the causes of renal AKI? (8) (MAGIC VAD)
* M - Multiple Myeloma & Myoglobin * A - Amyloidosis & ATN * G - Glomerulonephritis * I - Interstitial disease * C - Contrast * V - Vasculitis * A - Aminoglycosides, Amphotericin, Aciclovir * D - Drugs (other nephrotoxic)
29
What is the most common cause of ATN?
Most commonly caused by prolonged pre-renal AKI → ischaemic injury
30
What are the obstructive causes of post-renal AKI? (4)
- Renal stone * BPH * Transitional cell carcinoma * Extrinsic mass pressing on ureter
31
What happens if post-renal AKI is managed quickly vs slowly? (2)
* If managed quickly - restore GFR with no structural damage * If managed slowly - glomerular ischaemia & tubular damage
32
What are the causes of CKD? (6)
* DM (most common) * Hypertension * Atherosclerosis * Chronic glomerulonephritis * Prostate disease * PCKD
33
Most common cause of CKD?
Diabetes
34
What are the metabolic consequences of CKD? (4)
* Metabolic acidosis * Hyperkalaemia * Normochromic anaemia * Secondary/tertiary hyperparathyroidism
35
What are the major complications of CKD? (4)
* Uraemia (leading to cardiomyopathy, encephalopathy) * Renal osteodystrophy * CVD (most likely to kill them, highly calcified plaques) * Bone disease
36
What are the three types of bone disease in CKD? (3)
* Osteitis fibrosa cystica → bone cysts, Brown's tumours * Adynamic bone disease - resistance to PTH in bones → low bone turnover * Osteomalacia - inadequate mineralisation of bone
37
What are the 6 key aspects that need management in CKD? (6) Remember "AH HMVP" (Ah, Help My Vitamin P!)
* A - Anaemia * H - Hyperkalaemia * H -Hyperparathyroidism * M - Metabolic acidosis * V - Vitamin D deficiency * P - Phosphate (Hyperphosphataemia)
38
How is metabolic acidosis managed in CKD?
Oral sodium bicarbonate
39
What is the management for hyperkalaemia in CKD?
Dietary management
40
How is anaemia managed in CKD?
Artificial EPO (Erythropoietin)
41
What are the two approaches to managing hyperphosphataemia in CKD? (2)
- Dietary management * Phosphate binders
42
How is Vitamin D deficiency managed in CKD?
1-alpha calcidol
43
How is hyperparathyroidism managed in CKD?
Cinacalcet - increases sensitivity of calcium sensing receptors → decreased PTH
5 - Chemical Pathology
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