Renal physiology Flashcards

1
Q

What is the single best assesor of renal function?

A

GFR - normal 120ml/hr however there is an age related decline of 1ml/hr/yr (so 70 may be normal for 70 yr old etc.)

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2
Q

Define clearance, and what s the gold standard for GFR measurement?

A

Clearance = volume of plasma that can be completely cleared of a marker substance per unit time.

marker must be freely filterd by glomerulus, not bound to protein & not secreted/reabsorbed by tubular cells. If so clearance = GFR

Gold standard = inulin (but reserved for research only)

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3
Q

What about creatinine as a marker for GFR?

A
  • Good in that it is freely filtered
  • however it is actively secreted into urine by tubular cells
  • and because it is derived from muscle cells, it is very variable between individuals.
  • So best to monitor trend & look for change over time
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4
Q

Single sample urine examination: used for what? (1), when would you want 24hr urine collection (1)

A
  • Proteinuria quantification - protein: creatinine ratio (PCR)
  • no longer use 24hr urine collection for PCR, however can be used for
    • electrolyte estimation
    • stone forming elements (in pts with renal stones)
  • dipstick testing & microscopy examination can also be done with single sample
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5
Q

Urine dipstick testing: which of the following is ture regarding urine dipstick testing?

  1. If the dipstick is negative for blood it reliably excludes haematuria
  2. haematuria is the only cause of +ve dipstick for blood
  3. you can reliable exclude bacteruria if the urine dipstick is negative for nitrites
  4. the urine dipstick detects Bence Jones proteins (BJ)
  5. Glycosuria detected by the dipstick means the pt has diabetes
A

Correct answer = 1 - very sensitive for blood.

But haematuria not he only cause for +ve: can get with rhabdomyolysis, free Hb, semen

Dipstic not really specific for proteins - cannot detect BJ proteins, sensitive for albumin

Glycosuria - can have normal plasma glucose but tubular defect - so does not mean pt has DM

Leucocyte esterase - released from neutrophils - but not diagnostic as can get sterile pyuria.

Nitrites - Specific but not sensitive.

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6
Q

Urine microscopy - what can it detect (3)

A

Centrifuged and examined for:

  • crystals
  • RBCs - consistently raised sshould be investigated
  • WBCs
  • Casts - contents inside renal tubules solidify & are passed into urine
  • Bacteria - not v. useful
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7
Q

50 yr old known alcoholic, presents unwell + seemingly intoxicated with AKI. Urine microscopy reveals calcium oxalate crystals. What is your most likely dx?

A

ethyline glycol poisoning

  • toxic metabolites which causes metabolic acidosis, and get oxalate precipitation in the kidneys - giving calcium oxalate crystals
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8
Q

You admit a 28 yr old man who you suspect has a renal stone, what is your first choice of imaging?

  1. Plain KUB
  2. CT
  3. US KUB
  4. IVU
  5. MRI
A

correct answer - CT scan (recent change in choice)

CT most sensitive, US is best if looking for obstruction

radionucleotide imaging - better for paediatrics as less radiation

biopsy -

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9
Q

Name a class of drugs that may predispose to pts developing pre-renal AKI

A

NSAIDs - decrease dilation of afferent arteriole

ACEis - constrict efferent arteriole

Diuretics if they result in volume depletion

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10
Q

Regarding hyperkalaemia, which of the following is true?

  1. it can lead to ECG changes e.g. peaked P waves and flattened T waves
  2. In those with CKD, dietary intake is a major cause & high potassium levels are found in foods such as milk
  3. NSAIDs can lower potassium levels
  4. Hyperaldosteronism is a common cause
  5. all of the above
A

Correct answer is 2

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11
Q

Your pt with CKD has been started on an erythopoetin stimulating agent (ESA) but does not respond. what could be the cause?

  1. Fe def
  2. TB
  3. malignancy
  4. B12 folate def
  5. Hyper PTH
  6. any of the above
A

Correfct answer - 6

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12
Q

AKI can be classified into pre-renal, renal and post-renal causes.

What is the hallmark of pre-renal AKI? & why does it occur? Give 4 causes

A

hallmark - reduced renal perfusion . Which could be as part of:

  • general systemic reduced organ perfusion
  • or selective renal ischaemia

But kidney itself is fine. It occurs when normal adaptive mechs fail to maintain renal perfusion (baroreceptors, RAS, SNS). Causes:

  • Hypovolaemia - sepsis
  • Hypotension
  • oedematous state - fluid in wrong compartments
  • Selective renal ischaemia - RTA
  • Drugs affecting glomerular blood flow
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13
Q

How does pre-renal AKI cause ATN?

A
  • Since pre-renal AKI is not assc with renal abnormality, it responds immidiately to restoration of circulating vol
  • Prolonged insult though leads to ischaemic injury > ATN (which does not respond to vol restoration)
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14
Q

Post renal AKI: what is the hallmark? give 3 causes.

Pathophysiology of post renal AKI, Rx (1)

A

Hallmark - physical obstruction to urine flow

  1. ureteric obstruction
  2. Prostatic/urethral obstruction
  3. blocked urinary catheter

Pathophysiology - GFR depends on pressure grad, obstruction increases pressure - no longer grad > reduced GFR.

Rx - immidiate relief of obstruction = full restoration of GFR. (but prolonged obstruction leads to structural damage - scarring etc)

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15
Q

A 68yr old man with previously normal RF is found to have a creatinine of 624umol/l (v. high). Renal US shows the following appearance in both kidneys. What is the likely cause of his AKI?

  1. R. Sided renal stone
  2. Left ureteric transitional cell carcinoma
  3. Membranous GN
  4. BPH
  5. Amyloid
A

correct answer - BPH

post renal - causing bilat hydronephrosis

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16
Q

Renal causes of AKI: abnormality in any part of nephron. (4)

A
  1. vascular disease e.g. vasculitis
  2. glomerular e.g. GN
  3. tubular disease e.g. ATN
  4. interstitial disease e.g. analgesic nephropathy
17
Q

3 mechanisms of Direct tubular injury

A
  • most common = ischaemia
  • endogenous toxins
    • myoglobin - e.g. with rhabdomyolysis
    • Ig e.g. myeloma
  • exogenous toxins
    • contrast, drugs
18
Q

One word answer. Patient has new onset AKI. What is the likely diagnosis?

A

Free myoglobin - due to rhabdomyolysis

19
Q

A 40 year old female presents with a rash and AKI is diagnosed. What is the most likely cause of her renal failure from the following list?

A

HSP

20
Q

CKD stages based on what?

A

Reducing GFR

21
Q

Commonest causes of CKD (4)

A
  • DM
  • GN
  • HTN
  • atheoscleroticc renal disease
  • PKD
  • infective/ obstructive renal disease
22
Q

Functions of kidney

A

Functions:

  • Excretion of water-soluble waste
  • Water balance
  • Electrolyte balance
  • Acid-base homeostasis
  • Endocrine functions: EPO, RAS, Vit D
23
Q

Consequences of CKD: (4)

A
  1. Progressive failure of homeostatic function
    • electrolyte abnormality - hyperkalemia
    • Acidosis
  2. Progressive failure of hormonal function
    • Vit D def & Hyper PTH = renal bone disease
    • anaemia - reduced EPO prod
  3. cardiovascular disease - this is what kills CKD pts
    • vascular calfication
    • uraemic cardiomyopathy
  4. Death
24
Q

Give 2 consequences of renal acidosis

A

Happens due to failure of H+ excretion by kidneys

results in:

  • muscle/protein degradation
  • osteopenia due to bone resorption as a result of acidosis
  • cardiac dysfunction - reduced heart contractility

Treated by oral sodium bicarb

25
Q

Anaemia of CKD

A

Progressive decline in EPO producing cells (usually when GFR<30 & gives normochromic normocytic anaemia)

Need to distinguish from other common causes of anaemia

B12/folate/Fe def

Rx - can now give ESA (EPO stimulating agents) which increase Hb

26
Q

Renal bone disease: they result in reduced bone density, bone pain & fractures. Can be split into:

  1. Disorders of high bone turnover & high PTH (2)
  2. disorders of low bone turnover & low/norm PTH (2)
A

High PTH:

  • osteitis fibrosa cystica
  • mixed osteodystrophy

Low/norm PTH

  • osteomalacia
  • adynamic bone disease
27
Q

Briefly describe why CKD pts get Hyper PTH

A
  • CKD > reduced excretion of phosphate + reduced vit D
  • So low Ca + absorption from gut & reduced Ca in plasma because binds with phosphate CaPO4 to compensate
  • Results in increased PTH from parathyroid glands
  • HyperPTH > stimulate osteoblasts > increase bone turnover > osteitis fibrosa cystica
28
Q

Osteitis fibrosa cystica

A

Pt has - reduced bone strength + increased risk of fractures

Due to Osteoclastic resorption of bone (due to high PTH) & replacement with fibrous tissue

  • Irregularly woven bone, with cyst formation and abnormal osteoid
29
Q

adynamic bone disease - why does it happen? (1)

A

Excessive suppression of PTH (to prevent osteitis fibrosa) - results in low bone turnover & reduced osteoid

30
Q

CKD treatment - 3 aspects

A
  1. phosphate control
    • eat less
    • phophate binders - so absorb less
  2. Vit D receptor activators - so kidneys dont have to (1alpha calcidol)
  3. PTH suppression - to prevent osteitis
31
Q

Why do you get vasuclar calfication in CKD? (1)

A

because CKD cant excrete phosphate > get CaPO4 crystals which deposit and calcify in arteries

32
Q
A