Introduction to kidney tests - acid-base metabolism Flashcards

1
Q

Significance of K and PO4 in kidney function tests

A

K and PO4 retained with decreased GFR

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2
Q

Urea and GFR

A
  • Urea is the end product of protein metabolism and is retained with decreased GFR
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3
Q

Creatinine and GFR

A
  • Creatinine is the end product of creatine breakdown and is retained with decreased GFR
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4
Q

Kidney blood flow

A
  • 1500mL/min
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5
Q

GFR

A
  • Most frequent test of kidney function

Based on serum creatinine:

  • Starts to rise - 50% glomeruli lost
  • Marker of progressive kidney damage
  • Poor sensitivity - minor kidney damage
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6
Q

Hierarchy of kidney function tests - inaccurate to accurate

A
  • s-Urea
  • 24h creatinine clearance
  • s-Creatinine
  • eGFR is best index of glomerular function, estimated from s-Creatinine(EPI, MDRD, cockcroft-gault)
  • Direct GFR measurement
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7
Q

What is creatinine dependent on

A
  • Muscle mass
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8
Q

Changes in creatinine levels with age

A

With age muscle mass decreases
- Elderly lower muscle mass than younger

With age, kidney function decreases
With age, glomeruli decrease
- Elderly less glomeruli than younger

Blacks from Africa, USA, West Indies have greater muscle mass - than other ethnic groups

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9
Q

Formula for estimating GFR

A
  • CKD-EPI (based on the largest population of any calculator, best for ‘normal sized’ people)
  • Account for outliers in muscle mass
  • Creatinine clearance = ( Urine Cr * urine volume)/ (plasma Cr* time)
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10
Q

Creatinine origin

A

Muscle mass proportional to creatine proportional to creatinine

  • Creatine + ATP - creatine-P + ADP
  • There is a constant decay of creatine to creatinine
  • CK - creatine kinase is the enzyme that carries out the above reaction
  • Creatine-p - high energy phosphate
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11
Q

Urea origin

A
  • Protein proportional to amino acids proportional to urea
  • Alanine –ALT–> urea + pyruvate

Aspartate –AST–> Urea + oxalo-acetate –> glucose

  • Enhanced by stress: cortisol (glucocorticoid)
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12
Q

Ureamia

A
  • Condition having ‘urea in the blood’
  • Denotes a very high serum urea that is the result of kidney failure
  • Describes the pathological and symptomatic manifestations of severe loss of GFR
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13
Q

AKI

A
  • GFR compromised - low BP, shock

- Decreased blood flow to kidneys

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14
Q

Which waste products accumulate in AKI

A
  • Urea, creatinine, acid, PO4
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15
Q

What should be considered in AKI

A

Review urgently
Consider drugs: ACEI/ARB, NSAID, diuretics (most important drugs of relevance)
- Also obstruction, hydration, infection

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16
Q

Complications of AKI

A
  • Volume overload, raised K+, H+, PO4
  • Initial assessment - volume status(possible dehydration, CHF)
  • s-K, HCO3, PO4, calcium, albumin
  • s-uric acid, magnesium
  • FBC
17
Q

ACEI pathophysiology in AKI

A
  • Reduce systemic vascular resistance
  • Renoprotective - diabetic and renal disease
  • Kidney adverse effects (intrarenal efferent vasodilation, fall in filtration pressure and GFR)
  • Fall in filtration pressure (antiproteinuric and long term renoprotection)
  • GFR dependency on angiotensin II- mediated efferent vascular tone is lost
18
Q

Most common cause of lactic acidosis in hospitalised patients

A
  • Sepsis
  • Usual cause is tissue hypoperfusion
  • Impaired tissue oxygenation, leading to increased anaerobic metabolism
  • Hypovolemia
  • Cardiac failure
  • Sepsis
  • Cardiopulmonary arrest
19
Q

Sepsis 6

A
  1. Deliver O2 to target 94-98% or 88-92% in COPD
  2. Take blood culture
  3. Give IV (intravenous) antibiotics
  4. Start IV resuscitation
  5. Measure serum lactate
  6. Monitor urine output
20
Q

Maintenance of acid base balance

A
  • Lungs remove CO2 (fast)
  • Kidneys reabsorb HCO3- and secrete H+
    H+ + HCO3- –> H2CO3 –> H2O + CO2
  • Lungs - CO2 removal shifts equation to right with loss of H+ and HCO3=
  • Kidneys - PCT - HCO3- reabsorption
  • DCT - H+ secretion, urine acidified
21
Q

What happens in a patient with metabolic acidosis

A
  • The fall in pCO2 will mitigate the fall in pH caused by reduced HCO3
  • In all simple acid-base disorders, the primary abnormality will cause a compensatory response such that the HCO3 concentration and pCO2 will move in the same direction
  • Both will decrease or both will increase
  • These directional changes will act to return the pH toward normal
  • The compensatory responses are mediated by alterations in pH within the respiratory center
  • Respiratory compensation for metabolic acidosis generates a linear relationship between arterial pCO2 and bicarbonate
22
Q

Main cation in extracellular fluid

A

Sodium

23
Q

Main cation in intracellular fluid

A

Potassium

24
Q

How are electrolytes usually measured

A
  • Usually measured with creatinine, urea

- Also chloride, bicarbonate required with acid/base disturbance to determine anion gap

25
Q

What is anion gap due to

A
  • Albumin- phosphate- sulphate-
26
Q

Formula for anion gap

A

Measured cations - measured anions

27
Q

What is the increased AG in acidosis due to

A
  • Ketone- , lactate- ,salicylate- ,ethylene, glycol-
28
Q

DKA - acid added

A
  • Na+ + HCO3- exist in serum
  • Addition of H+
  • Combines with HCO3-
  • Leaving Na+ salt of the acid
  • Na+ ketone-

To maintain pH or H+

  • H+ combines with HCO3- forming H2CO3
  • CO2 blown off
  • Resulting loss HCO3- and H+
  • In serum ketone- exists instead of HCO3-