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Year 3 Lecture Content > Renal Disease > Flashcards

Renal Disease Flashcards

1
Q

What is the function of the kidney?

Which type of function is usually disturbed early in aki and disturbed in CKD?

A
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2
Q

What is the definition of AKI for

Stage 1

Stage 2

Stage 3

A
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3
Q

What are prerenal causes of AKI?

A

In sepsis -> vasodilation causes oedema to go into the other compartments which means less bloods goes to the kidney

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4
Q

Intrinsic renal causes of AKI

A
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5
Q

Post renal causes of AKI

A
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6
Q

How does AKI develop?

How do you differentiate between pre-renal uraemia and intrinsic renal AKI with blood tests?

What are the commonest cause of unrecognised AKI?

A

Commonest cause of unrecognised AKI is hypovolaemia(dehydration) and sepsis.

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7
Q

Should fluid be given in pre renal uraemia or intrinsic renal damage?

A
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8
Q

What are the bichemical changes that occur in intrinsic AKi and why do they occur?

ph less than what is life threatning?

K+ above what level is life threatning

Retaining nitrogenous waste material causes what clinical features?

Retaining salts and waters cause what problems?

Do you see endocrine problems in AKI?

A

Retain acidic waste products of metabolism

– 100 mmol/day from metabolism

– Life threatening once plasma pH < 7.0

life threatning once [K+} >8 mmol/L

  • Retain nitrogenous waste products – Nausea; malaise; confusion (late features)
  • Retain salt & water – Reduced GFR – Usually hyponatraemic (sodium loss +/- water retention)

You do NOT see endocrine problems in AKI

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9
Q

What does this person have?

A

Acute kidney injury

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10
Q

How is AKI managed?

A
  • Distinguish between pre-renal, intrinsic renal and post-renal causes
  • ASK FOR SENIOR REVIEW +/- REFERRAL TO AKI TEAM
  • Identify underlying cause if possible - THINK bleeding, sepsis, drugs
  • Stop / avoid ACEi /ARBs, NSAIDS and other potentially nephrotoxic medication •Correct life-threatening fluid, electrolyte and acid/base abnormalities
  • Restore renal perfusion if pre-renal (except heart failure)
  • Support renal function in life-threatening intrinsic AKI (haemofiltration, dialysis)
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11
Q
A

she has intrinsic kidney injury because her sodium is low and potassium is ranged.

Her urea and creatinine both raised.

Sodium urine >40

Treatment: she needs dialysis as she has life threatning complication

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12
Q
A

He has pre-renal injury because he has low blood pressure.

Urea is not as raised as creatinine. (urea went up more than creatinine)

sodium is very low.

Management: give fluid (getting blood takes longer)

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13
Q

what is chronic kidney disease?

A
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14
Q

How is CKD monitored?

A

Cockcroft is no longer used it is replaced by egfr

GFR 24 hour is used in children as they do nt have a lot of muscle so it helps measure their creatinine

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15
Q

When is eGFR used compared to creatinine in CKD?

A
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16
Q

What is used to give the prognosis of CKD?

A
17
Q

What is the consequences that is seen with people with CKD stage 3a,3b,4 and 5.

What eGFR is stage 5?

A
18
Q

What biochemical changes are seen in CKD stage 3-4?

A

Elevated creatinine, reduced eGFR

  • Elevated ACR(albumin creatinine ratio)
  • Endocrine changes – Reduced 1 alpha hydroxylation of Vitamin D
  • Causes hypocalcaemia and secondary hyperparathyroidism

– Reduced Erythropoietin, causing anaemia

  • Lipids – Elevated Cholesterol & Triglyceride partly accounts for increased risk of CHD
  • Impaired immune function
19
Q

What biochemical changes are seen in CKD stage 4-5?

A
  • Elevated creatinine and urea (uraemic symptoms develop)
  • High phosphate
  • Acidosis
  • Hyperkalaemia - offset by increased gut losses until late stage
20
Q

what are examples of the following types of CKD

Glomerular damage

Healthy nephron in diseased kidney
Tubular damage

What problems do they cause

A
21
Q

What disease or problems in the bone can occur due to the following problems?

Decrease in plasma calcium

Increase in PTH

Increase in calcium and phosphate product due to increase in plasma phosphate

Dissolved bone buffers after metabolic acidosis

A
22
Q

Management of CKD - Stages 2-3a

A

Monitor at risk patients

– eGFR and ACR – cardiovascular risk factors (BP, lipids) – Stage 3a – bone profile, PTH

  • Treat cause if possible (diabetes, hypertension, recurrent UTI)
  • Avoid precipitants of AKI (see AKI slides)
  • Slow progression – block RAA system (ACEi / ARB) if ACR raised, antihypertensives +/- statins
23
Q

Specialist management of CKD stages 3b to 5+

A

Refer to nephrology at CKD Stage 3b-4 and / or endocrine abnormalities present – Endocrine / metabolic abnormalities corrected

  • Alfacalcidol (1,25 –OH vitamin D) – corrects calcium and prevents tertiary hyperparathyroidism • Erythropoietin – prevents anaemia
  • Phosphate binders – reduces risk of metastatic calcification
  • Modified diet – low potassium
  • Fluids

– Correction of acid-base disturbance (bicarbonate)

– Renal replacement therapy (haemodialysis, peritoneal dialysis or transplant) if life-threatening acidosis, hyperkalaemia, severe uraemia, fluid overload

24
Q

What are the differences between AKi and CKD?

A
25
Q

Comparison of major metabolic disturbances between AKI and CKD

A
26
Q

Renal tubular disorders

What problem occurs due to glucose transporter defect?

What problems occur due to amino acid transporter defect?

What problem occurs due to phosphate transport defect

What is a global tubular defect?

A

Specific transport defects

– Glucose

• Renal Glycosuria

– Amino acids

  • Selective – e.g. Cystinuria
  • Generalized (eg Fanconi syndrome)

– Phosphate

  • Hypophosphataemic ricketts
  • Global tubular defect – Fanconi Syndrome (glycosuria, amino aciduria, phosphaturia, proximal RTA)
27
Q

What are the different types of renal tubular acidosis?

Type 1, 2, and 4

A
28
Q

Other non-renal causes of abnormal urea and creatinine

Think about when urea is high or low

When creatinne is high or low what could it be due to?(think about where creatinine is made)

A

Year 3 Lecture Content (33 decks)

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