Yr 3 - Skills & Extras > U&Es Interpretation > Flashcards

U&Es Interpretation Flashcards

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1
Q

What is creatinine?

A

creatinine is a waste product from protein and muscle breakdown

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2
Q

How is creatinine produced?

A
  1. Creatine is a substance produced by the liver
  2. Creatine is phosphylated to make creatine phosphate
  3. Creatine phosphate is broken down to ATP an creatinine
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3
Q

How is creatinine excreted?

A

renally

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4
Q

What does one’s baseline creatinine depend on?

A

Muscle mass

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5
Q

How is urea produced?

A

The urea cycle converts ammonia (toxic product of deamination reactions of amino acids) to urea in the liver.

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6
Q

How is ammonia produced?

A

Ammonia is the waste produced by metabolism of nitrogen-containing compounds like proteins and nucleic acids.

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7
Q

How is urea excreted?

A

Renally

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8
Q

Is serum creatinine or urea more specific for renal function?

A

Creatinine (BUT urea increases is increased earlier in renal disease)

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9
Q

What can cause increased urea?

A
  • Dehydration
  • GI bleed (protein meal)
  • Increased protein breakdown e.g. surgery, infection, malignancy
  • High protein intake
  • Drugs
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10
Q

What can cause decreased urea?

A
  • Malnutrition
  • Liver disease
  • Pregnancy
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11
Q

What criteria defines an AKI

A
  • Rise in serum creatinine >50% from baseline OR;
  • Urine output <0.5ml/kg/hr for 6 hours
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12
Q

Potential investigations in AKI?

A
  • Urine dipstick
  • Bloods – FBC, U&Es, CRP, Ca2+, phosphate, PTH
  • VBG – check for metabolic acidosis & low bicarbonate, hyperkalaemia
  • Accurate fluid balance chart – requires catheterisation
  • Stopping of any renal-excreted drugs
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13
Q

Give 2 causes of pre-renal AKI

A
  • Hypovolaemia/sepsis (most common AKI cause)
  • Renovascular disease (e.g. renal artery stenosis)
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14
Q

Describe urea vs creatinine level in pre-renal failure

A

Both increased but increase in urea > increase in creatinine

Since creatinine is not reabsorbed, but is increased only as a result of reduced GFR, plasma urea concentration tends to rise out of proportion to the rise in plasma creatinine concentration in patients with prerenal AKI, and this results in increased BCR/UCR.

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15
Q

Pre-renal failure can cause intra-renal failure. What complication is most commonly seen/

A

Acute tubular necrosis

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16
Q

Management of pre-renal failure?

A

IV fluid resuscitation

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17
Q

What is the most common cause of intrinsic renal failure?

A

Acute tubular necrosis (ischaemic or nephrotoxic)

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18
Q

Give some causes of intrinsic renal failure

A
  • ATN (ischaemic or nephrotoxic)
  • Acute interstitial nephritis
  • Acute glomerulonephritis
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19
Q

What type of renal failure would haematuria and/or proteinuria suggest?

A

Intra-renal failure

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20
Q

In a patient’s history, what may suggest intra-renal failure?

A
  • Causative drugs
  • Renal hypoperfusion
  • Other glomerulonephritis symptoms
  • Haematuria
  • Proteinuria
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21
Q

Give some investigations for intra-renal failure?

A
  • Urine dipstick
  • Urine protein-creatinine ratio
  • Possible further tests:
    • Nephritic screen (if suspect glomerulonephritis): ANA, ANCA, anti-GBM, RhF, hepatitis serology, anti-phospholipid Ab
    • Renal biopsy – unexplained AKI, glomerulonephritis suspected, positive nephritic screen
    • Creatinine kinase – if suspect rhabdomyolysis
    • Serum bicarbonate
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22
Q

Management for glomerulonephritis?

A

Immunosuppressants

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23
Q

Main complication of intra-renal failure?

A

Irreversible renal damage

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24
Q

Cause of post-renal failure?

A

Urinary tract obstruction (prostate, stones, structure, tumour, blood clots etc)

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25
Describe urea vs creatinine level in **post-renal** failure
Increased urea = increased creatinine
26
1st line imaging in post-renal failure?
Renal tract USS
27
Management of post-renal failure?
Relieve obstruction e.g. catheterise (urinary/suprapubic) if urethral or nephrostomy if ureteric
28
Main complication of post-renal failure?
Pyelonephritis (can progress to irreversible renal damage)
29
What criteria defines CKD?
Presence of **marker of kidney damage** (e.g. proteinuria) OR **decreased GFR** for \>3 months.
30
Give 5 common causes of CKD
1. Diabetes (2ary glomerular disease) 2. Chronic HTN 3. Chronic glomerulonephritis diseases (e.g. vasculitis) 4. Polycystic kidney disease 5. Drugs
31
Investigation for glomerulonephritis?
Kidney biopsy
32
Give some complications of CKD
* HTN * Oedema * Anaemia * Renal osteodystrophy * Hyperkalaemia * Hyperlipidaemia
33
What critieria indicates the need for dialysis?
* **A** – Acidosis * **E** – Electrolyte abnormalities (e.g. hyperkalaemia, hyponatraemia, hypercalcaemia) * **I** – Intoxicants (methanol, lithium, salicism) * **O** – Overload (acute pulmonary oedema) * **U** – Uraemia In chronic renal failure, regular dialysis is required when the GFR is **\<15ml/minute**.
34
Is sodium an extracellular or intracellular ion?
Extracellular
35
Effect of aldosterone on Na+ and K+?
increases N+ reabsorption and K+ excretion from DCT
36
Effect of ADH on Na+ and K+?
* Causes reabsorption of H20 (alone) from the collecting duct which **dilutes** the level of sodium in the body (can lead to hyponatraemia) * Increases potassium loss into the urine
37
Give some causes of hyponatraemia in the context of **hypovolaemia** (i.e. Na+ lost and water follows)
From kidneys: * Diuretics * Addison's disease (increased K+) * Kidney injury * Osmotic diuresis From elsewhere: * Diarrhoea/vomiting * Fistula * Burns
38
How does diarrhoea/vomiting affect Na+ level?
Hyponatraemia
39
How do burns affect Na+ level?
Hyponatraemia
40
Give some causes of hyponatraemia in the context of **euvolaemia** (i.e. H20 gained and normal Na+)
From kidneys: * SIADH * Hypothyroidism * Glucocorticoid insufficiency From elsewhere: * H20 intoxication
41
How does SIAD affect sodium levels?
Hyponatraemia (due to increased ADH causing dilution of sodium)
42
How does hypothryoidism affect sodium levels?
Hyponatraemia
43
Give some causes of hyponatraemia in the context of oedema (i.e. H20 gained and normal Na+)
* Congestive cardiac failure * Hypoalbuminaemia (e.g. cirrhosis or nephrotic syndrome)
44
Why does hypoalbuminaemia lead to hyponatraemia?
Hypoalbuminemia causes a shift of fluid from the plasma to the interstitial spaces and a decrease in serum volume, with _release of ADH_ → hyponatraemia
45
What specific test can be used to test for Addison's disease?
Synacthen (synthetic ACTH) test or 9am cortisol screening
46
What specific test can be used to test for SIADH?
Confirmed by combination of **low plasma osmolality** and **high urine osmolality** (i.e. low sodium in blood, high sodium in urine)
47
Management of SIADH?
Fluid restriction
48
Cause of hypernatraemia in the context of normovolaemia
Iatrogenic (e.g. excess IV crystalloids, sodium containing drugs)
49
Cause of hypernatraemia in the context of hypovolaemia
* Producing **small volumes of concentrated urine** (normal response to hypovolaemia) * Fluid loss → diarrhoea, vomiting, burns * Not producing small volumes of concentrated urine (abnormal response to hypovolaemia) * Diabetes insipidus * Osmotic diuresis (e.g. DKA)
50
Is potassium intracellular or extracellular?
90% intracellular
51
Why do H+ and K+ concentrations vary together?
H+ and K+ concentrations vary together because both compete for Na+ symporter in cells and DCT
52
How does insulin affect K+?
**increase cellular K+ uptake** by stimulating cellular Na+(in)/K+(out) pumps
53
How do catecholamines affect K+?
**increase cellular K+ uptake** by stimulating cellular Na+(in)/K+(out) pumps
54
How does aldosterone affect K+?
increases Na+(in)/K+(out) pumps in distal convoluted tubule and therefore **increases K+ excretion**
55
Give some causes of hypokalaemia due to **increased renal excretion**
* Diuretics (except K+ sparing) * Endocrinological – steroids, Cushing’s disease, Conn’s syndrome * Renal tubular acidosis * Hypomagnesaemia
56
How vomiting/diarrhoea affect K+?
Hypokalaemia
57
Give some causes of hypokalaemia due to **increased cellular uptake**
* Salbutamol * Insulin * Alkalosis
58
Management of hypokalaemia?
* Treat cause * Add potassium chloride to IV fluids
59
Give some causes of hyperkalaemia due to **reduced renal excretion**
* Acute/chronic kidney injury * Drugs (K+ sparing diuretics, ACEi, NSAIDs) * Addison’s disease
60
How does hypomagnesaemia affect K+?
Causes hypokalaemia
61
How do NSAIDs affect K+?
Hypokalaemia
62
Give some causes of hyperkalaemia due to excess K+ load
* Iatrogenic * Massive blood transfusion
63
Give some causes of hyperkalaemia due to increased cellular release
* Acidosis * Tissue breakdown e.g. rhabdomyolysis, haemolysis
64
ECG changes seen in hyperkalaemia?
* Low flat P waves * wide bizarre QRS * slurring into ST segment * tall tented T waves
65
Give 4 pharmacological agents that may be used in the management of hyperkalaemia
1. Calcium gluconate 2. Insulin & glucose 3. Salbutamol 4. Calcium resonium
66
How is calcium gluconate effective in managing hyperkalaemia?
* **_Protects myocytes_** (required if ECG changes or K+ \>6.5) * Works in minutes * Lasts 30-60 minutes
67
How is insulin+glucose effective in hyperkalaemia?
* Temporarily shift K+ into cells * Check capillary glucose before & after * Gradually decreases K+ * Lasts 60 mins _Nebulised salbutamol_ may be added for same effect
68
What is the only treatment that actually **_removes_** K+ from body?
Calcium resonium
69
Calcium homeostasis:
70
Give some causes of hypocalcaemia due to **increased renal excretion** (increased phosphate, increased PTH)
* Drugs (loop diuretics) * CKD * Rhabdomyolysis/tumour lysis syndrome
71
Give some PTH-related causes of hypocalcaemia (increased phosphate, decreased PTH)
* Hypoparathyroidism * Hypomagnesaemia * Pseudohypoparathyroidism (resistance to PTH) * Cinacalcet
72
Give some causes of hypocalcaemia due to **increased deposition/reduced uptake** (decreased phosphate, increased PTH)
* Bisphosphonates * Vitamin D deficiency
73
How do bisphosphonates affect calclium?
Hypocalcaemia
74
Management of vitamin D deficiency?
Vitamin D analogues e.g. alfacalcidol
75
Give some causes of hypercalcaemia
* Decreased renal excretion: * **Drugs** (thiazide diuretics) * Increased release from bones: * **Boney metastasis** (increased ALP) * **Myeloma** (normal ALP) * **Sarcoidosis** * **Thyrotoxicosis** * Excess PTH: * **1ary hyperparathyroidism** (increased PTH) or 3ary hyperparathyroidism (massively increased PTH) * **Excess vitamin D intake** * **Dehydration** (raised urea & albumin)
76
How does thyrotoxicosis affect calcium?
Hypercalcaemia
77
How do bony mets affect calcium?
Hypercalcaemia
78
How does myeloma affect calcium?
Hypercalcaemia
79
How does sarcoidosis affect calcium?
Hypercalcaemia
80
What is hypophosphataemia seen in?
* Vitamin D deficiency * Refeeding syndrome * 1ary hyperparathyroidism * Poor nutrition/alcoholism
81
How does PTH affect phosphate?
Hypophosphataemia
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