Lecture 3 - Renal Flashcards

1
Q

What is a consequence of renal failure when hypoalbuminaemia results?

A

Oedema

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2
Q

What haematological abnormality does chronic renal failure cause?

A

Moderately severe, normocytic, normochromic, non-regenerative anaemia = EPO deficiency AND Urinary loss of AT - consequence of protein-losing nephropathy = hyper-coagulable (prothrombotic) state

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3
Q

How can urea and creatinine be used to differentiate between AKI/ARF and CKD/CRF?

A

Abrupt increase = AKI/ARF Progressive and slow increase = CKD/CRF

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4
Q

What is hyperphosphatemia a feature of all forms of azotemia?

A

Feature of all forms of azotemia (pre-renal, renal and post renal) - 85-90% is reabsorbed as PO4 in proximal tubule via Na-PO4 co-transporter

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5
Q

Where does PTH act to promote calcium re-absorption?

A

Ascending limb of the loop of Henle, distal tubule and the collecting tubule

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6
Q

Where does Vitamin D act to promote Ca2+ reabsorption?

A

In the distal nephron

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7
Q

What are the steps involved in renal secondary hyperparathyroidism?

A
  1. Renal disease (causes a loss of nephrons) meaning reduced GFR and less PO4 filitered out meaning mild hyperphosphatemia develops
  2. Damaged tubular cells or inhibition of a-hydroxylase by increased PO4 means less conversion of Vitamin D
  3. Less Vitamin D means decreased intestinal absorption and bone reabsorption
  4. Reduced vitamin D reduces Vitamin D inhibition of PTH synthesis
  5. Decreased Ca2+ causes increased PTH production and increased a-hydroxylase activity
  6. Increased PTH can compensate up to point, after that increased phosphate occurs
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8
Q

Name the condition below and state how kidney failure can cause it:

A

Fibrous osteodystrophy

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9
Q

What is increase amylase and lipase seen in cases of renal failure?

A

These are excreted by the kidney. Decreased GFR induce serum accumulation of amylase and lipase

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10
Q

Why is increase potassium seen in renal failure?

A

Hyperkalemia = feature of advanced post-renal azotemic and oliguric or anuric acute renal failure.

K+ movement from cell to lumen occurs through K+ channels opened by aldosterone. Enhanced when urinary flow rate through the tubule is high. High flow rate means K+ is washed away quickly and thus the concentration gradient is maintained.

Movement is reduced when urinary flow rate is lower as K+ stays in the tubule and thus concentration gradient is diminished

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11
Q

Is metabolic acidosis typically worse in CKD or acute renal failure?

A

Metabolic acidosis is typically much worse in cases of acute renal failure as the kidneys have had insufficient time to adapt

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12
Q

What does the finding of isothenuria suggest?

A

suggestive of renal failure means that the kidneys are unable to concentrate urine

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13
Q

What does the finding of proteinuria suggest?

A

Varies in severity but more likely to occur in chronic kidney disease than in acute kindey insufficiency

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14
Q

What finding would be indicative of glomerular damage?

A

Findings that are suggestive of glomerular damage:

  1. Proteinuria (large size protein)
  2. Hypoalmbuminaemia (severe proteinuria)
  3. Hypercholesterolaemia (urinary loss of lipase - NEPHROTIC SYNDROME)
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15
Q

What is renal tubular acidosis and what are the two main types that can occurs:

A

Proximal RTA (Type 2) = decreased HCO3- reabsorption in the proximal tubule

Distal RTA (Type 1) = defective acid excretion (impaired H+ secretion) in the collecting ducts

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16
Q

What is fanconi syndrome?

A

Fanconi Syndrome - combination of proximal tubular defects - acquired or heriditary:

  • Proximal RTA
  • Glycosuria
  • Phosphaturia
  • Proteinuria/aminoaciduria
17
Q

What is fractional excretion?

A

Fractional amount of plasma that is filtered by the glomerulus - then excreted into the urine

18
Q

When is GGT released into the urine?

A

Acute tubular damage

19
Q
A
20
Q

Comment on the usefulness of using GGT as a marker of glomerular damage:

A

GGT = enzyme present on membrane of epithelial tubular cells

  • Not filtered by glomerulus = not influenced by serum [GGT]
  • Increased during acute tubular damage - quikcly released by membrane = early marker
  • Affected by USG = urinary GGT: creatinine ratio
  • Inactivated by acidic urine (pH 5) - Lack of RI = high individual variability