Biochemical tests Flashcards

1
Q

what are the plasma components usually measured?

A

– Sodium
– Potassium
– Chloride
– Bicarbonate
– Urea
– Creatinine

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2
Q

why is water so important?

A

fundamental to all blood test as patients hydration is important

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3
Q

where is sodium present?

A

it is an extracellular cation- outside

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4
Q

what is the main function of sodium

A

maintain osmolality

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5
Q

what are the major route of sodium excretion?

A

kidneys

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6
Q

what hormones help the kidneys excrete/ maintain sodium balance?

A

– Antidiuretic hormone
– Aldosterone
– Thirst

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7
Q

what are changes in serum sodium concentration usually due to?

A

– Diet (rich or low in sodium)
– The amount of water in the blood
– Kidney function

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8
Q

define hypernatraemia

A

Defined as a plasma sodium concentration of:
– > 145 mmol/L

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9
Q

what causes hypernatraemia?

A

– Water depletion
* Loss of water in excess of sodium
* Decreased fluid intake
– Increased sodium intake or retention in excess of
water
* Mineralocorticoid excess
* Medication
* Renal failure

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10
Q

what are some of the signs and symptoms of hypernatraemia?

A

– Dry skin
– Postural hypotension
– Oliguria
– Thirst
– Confusion
– Drowsiness, lethargy
– Extreme cases – coma (>155 mmol/L)

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11
Q

what are the drugs associated with an increased sodium- hypernatraemia?

A

– Corticosteroids
– NSAIDs
– Laxatives
– Lithium

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12
Q

why must you consider the make up of injectable drugs and soluble preps?

A

as sodium content could be high

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13
Q

how do you manage hypernatraemia?

A
  • Identify and treat underlying cause
  • Replace body water
    – Orally
    – Intravenously
  • Dextrose 5% w/v
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14
Q

define hyponatraemia

A

Low sodium is defined as a serum sodium
concentration below 135mmol/L

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15
Q

generally what does low sodium indicate?

A

– Over hydration in the body
– Too little sodium in the body
– Or a mixture of both

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16
Q

what may result from hyponatraemia?

A

May also include cardiac failure, anorexia and oedema.

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17
Q

what are the potential causes of hyponatraemia?

A

– Medication
– Mineralocorticoid deficiency
– Water/fluid excess
* SIADH
* Certain disease states
– Abnormal losses of sodium
* Diarrhoea, DKA
– Alcohol excess
– Severe burns
– Malnutrition
– Dilution of blood sample by IV fluids

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18
Q

how do you manage hyponatraemia?

A

– Identify and correct the underlying cause
– Depending on cause:
* Increased salt intake
* Fluid restriction
– If needed:
* Mild – moderate:
– Slow – sodium, 4 – 8 tablets (2.4 – 4.8g)
– Demeclocycline 900 – 1200mg daily in divided doses
* Severe:
– I/V NaCl

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19
Q

why do you not increase levels of sodium quick?

A

Remember, do not increase levels too
quickly due to the risk of osmotic
demyelination

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20
Q

where is potassium located in the body?

A

in the cell- intracellular cation

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21
Q

how is k+ regulated?

A
  • Regulated by aldosterone, cortisol, insulin and
    glucose
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22
Q

what do changes in k+ have an effect on?

A
  • Changes in potassium levels have a profound
    effect on the nervous and cardiovascular system
  • → fatal in extreme cases
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23
Q

where is k+ absorbed/ eliminated?

A

– Mainly absorbed in the small intestine
– Eliminated via the kidneys

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24
Q

where is k+ in peoples cells when they are hydrated/dehydrated?

A

– Potassium is lost from cells when people are
dehydrated and returns when hydrated

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25
Q

how are k+ levels influenced?

A

– Acid-base disturbances
* Acidosis (K moves out of cells in exchange for H)
* Alkalosis (K moves into cells in exchange for H)
– Catabolic states
– Anabolic states
– Insulin secretion

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26
Q

where is the main route of k+ loss?

A

via kidneys- small amoung in faeces and skin

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27
Q

what are some of the causes of hyperkalaemia?

A
  • Medication
  • Renal
  • AKI
  • CKD
  • Rhabdomyolysis
  • Hypoaldosteronism
  • Advanced CCF
  • Acidosis
  • DKA
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28
Q

how do you exclude pseudohyperkalaemia from hyperkalaemia

A

Delay in sample reaching the lab
* Contamination
* Haemolysis of sample
* Drip arm

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29
Q

what are signs and symptoms of hyperkalaemia?

A
  • Fatigue
  • Muscle weakness
  • Abnormal cardiac conduction
  • Chest pain and palpitations
  • ECG changes
  • Cardiac arrest (severe cases)
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30
Q

how do you manage hyperkalaemia?

A

– Assess patient: ABCDE
– Identify cause/stop potentially offending drugs
immediately
– Rule out a pseudohyperkalaemia
– Ensure adequate hydration
– Consider the severity
* Severe/ECG changes: MEDICAL EMERGENCY

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31
Q

when do you refer someone with hyperkalaemia to hospital?

A

– >6.5mmol/L
– Acute ECG changes and >5.5 mmol/L
– Rapid rise

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32
Q

what do you do if there is mild hyperkalaemia?

A

– Correct underlying cause, repeat blood test
– Medication review and dietary changes are often adequate

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33
Q

what do you do for moderate hyperkalaemia?

A

– Carry out an ECG
* Assess course of action based on this
* No high-risk factors, review patient

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34
Q

what is the 5 step hospital approach for the management of hyperkalaemia?

A
  • Step 1: Protect the heart
  • Step 2: Shift potassium into cells
  • Step 3: Remove potassium from the body
  • Step 4: Monitoring
  • Step 5: Prevention
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35
Q

how do you protect the heart in hyperkalaemia?

A
  • If there are ECG changes
    – 30ml of 10% calcium gluconate IV OR
    – 10ml of 10% calcium chloride IV
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36
Q

how do you shift potassium into cells?

A
  • Insulin-glucose infusion
    – 10 units of soluble insulin in 250ml dextrose 10%
  • 10 – 20mg salbutamol nebuliser
    – IHD
  • Shifts into the cells temporarily, this is a holding measure
    only
    – Does not reduce total body potassium
  • Will start to leak back into extracellular space (2 –
    6 hours)
37
Q

how do you remove potassium?

A
  • Potassium exchange polymers
  • Anion exchange resin
    – Calcium resonium: 15g TDS
  • Potassium binders
    – Patiromer calcium
    – Lokelma (sodium zirconium cyclosilicate)
    dialysis
38
Q

when do you have to do continuous monitoring with hyperkalemia patients?

A

where ECG features are present
k+ every 2-4 hours
* Blood glucose levels
* Baseline, 15, 30, 60, 90, 120 minutes and
up to 6 hours post dose

39
Q

how do you prevent hyperkalemia recurring?

A

Stop nephrotoxic medications and drugs
known to contribute to hyperkalaemia.

40
Q

what are the causes of hypokalaemia?

A
  • Medication
  • Decreased intake
  • Abnormal losses
  • D&V
  • Ileostomy
  • Acid-base
    disturbances
41
Q

what are the signs and symptoms of hypokalaemia?

A
  • Hypotonia
  • Cardiac arrhythmias
  • Muscle weakness
  • Fatigue
  • Confusion
  • Paralytic ileus
42
Q

what are some of the drugs causing hypokalaemia?

A

Salbutamol (especially in high doses)
Thiazide diuretics
Loop diuretics
Insulin
Steroids
Chronic laxative abuse

43
Q

how do you manage hypokalaemia?

A

– Depend on the severity
– Correct underlying cause or disease process
– Use potassium sparing drugs
– Oral treatment
– Intravenous treatment

44
Q

how do you manage mild and moderate hypokalaemia?

A

– Oral replacement
* Sando K®: 1 – 2 tablets TDS
* Kay-Cee-L: 10ml – 20ml TDS
* Slow K: avoid where possible

45
Q

how do you manage severe hypokalemia?

A

– IV replacement (with continuous cardiac monitoring – depending on
potassium concentration)
– Doses vary across guidelines
– Doses and rates may vary in critical care or fluid restricted patients

46
Q

where is there increased risk of digoxin toxicity and why?

A

– There is an INCREASED risk of digoxin
toxicity in the presence of hypokalaemia
– Digoxin competes with potassium ions at
binding sites, therefore, a low potassium
predisposes to toxicity.

47
Q

what is the usual range for chloride?

A

Usual range is 95 – 105mmol/L

48
Q

what does chloride usually follow?

A
  • Movement follows that of sodium
49
Q

what causes and increase in CL-?

A

excess ingestion
dehydration

50
Q

what causes a decrease in cl?

A

vomiting
diarrhoea
diuresis
dehydration

51
Q

what does bicarbonate reflect?

A
  • Reflects renal, metabolic and respiratory functions
52
Q

what would be the signs and symptoms of inc/dec bicarbonate?

A

inc- vomiting
dec- headache, drowsiness, coma

53
Q

what are the causes of increased bicarbonate?

A

excess antacids
thiazide and loop diuretcis
metabolic alkalosis
hypokalaemia
vomiting

54
Q

what are the causes of decreased bicarbonate?

A

diarrhoea
renal failure
diabetes
metabolic acidosis
respiratory alkalosis

55
Q

what is the end product of protein metabolism?

A

urea

56
Q

what causes raised urea?

A

renal failure
sepsis
uti
CCF
dehydrayion
GI bleed

57
Q

what causes decreased urea?

A

pregnancy
low protein
cld
over hydration
starvation

58
Q

what is the end product of metabolism

A

creatine

59
Q

what is the end product of metabolism

A

creatine

60
Q

what happens if kidney filtration is impaired?

A

serum creatine will rise

61
Q

what are reduced levels of calcium associated with?

A

– Renal failure
– Raised phosphate levels (as phosphate binds to
calcium readily)
– Hypoparathyroidism
– Low magnesium levels
– Deficiency/malabsorption

62
Q

what are reduced levels of calcium associated with?

A
  • Raised levels (>2.65mmol/l):– NB. Can be a medical emergency, if >3.75, at risk of M.I
    – 90% of cases are due to malignancy or
    hyperparathyroidism
    – Hyperthyroidism
    – Dehydration
63
Q

how do you manage raised levels of calcium?

A

Manage with fluids initially, if no response
IV bisphosphonates

64
Q

how is magnesium eliminated?

A

via the kidney

65
Q

when is magnesium levels reduced?

A

– Diuretics
– Liver disease
– Diarrhoea

66
Q

when are magnesium levels raised?

A

– Renal impairment

67
Q

what can low levels of mg be assoicated with and why?

A

low levels of CA and K- as magnesium helps transport calcium and k+ ions in and out of cells

68
Q

what are some factors affecting test results?

A
  • How specimens are collected, transported, stored
    and processed
  • When the sample was taken
  • Patient age
  • Gender
  • Nutrition
  • Sitting/standing
69
Q

what are the two examples of potassium binders?

A
  • Patiromer calcium and Lokelma (SZC)
70
Q

when are potassium binders appropiate?

A

– Had an acute episode of hyperkalaemia
between 6.0- 6.4 mmol/L
– There is a clinical case to restart withheld
RAASi therapy at a lower dose once resolved
– Potassium on repeat testing is between 5.5 –
6.4 mmol/L

71
Q

what do you have to monitor with potassium binders?

A

– Following initiation/dose changes check
potassium 1 – 2 weeks after:
* If <4mmol/L: reduce dose of binder
* If 4 – 5.3mmol/L: continue
* If >5.3mmol/L: increase dose of binder

72
Q

what is HCT?

A

– Indicates the proportion of RBC that make up the
blood pool

73
Q

what is MCV?

A

– Average size of the RBC

74
Q

what is MCH?

A

– Average amount of Hb in a RBC

75
Q

what is MCHC?

A

– Average concentration of Hb inside an
average sized cell

76
Q

what do we consider for microcytic anaemia?

A

A low RBC (red blood count), Haemoglobin (Hb),
Haematocrit (HCT) and Mean Cell Volume
(MCV) are suggestive of a microcytic anaemia.

77
Q

what are the causes of iron-deficiency anaemia?

A

– Inadequate diet
– Deficient absorption
– Blood loss
* Menorrhagia
* GI bleeding

78
Q

what is the management of microcytic anaemia?

A

Oral: Iron supplement e.g., ferrous sulphate
200mg OD (65mg elemental iron)
* Continue until normal levels are reached and the
for 3 months thereafter (NICE)
– Parenteral: in presence of malabsorption
e.g., Ferinject®, Cosmofer®

79
Q

what would indicate macrocytic anaemia in blood results?

A

In a macrocytic anaemia the mean cell volume is raised
* A raised MCV with a low haemoglobin suggests vitamin B12 or folate deficiency, these should therefore be tested

80
Q

what is the cause of macrocytic anaemia?

A

This disease affects all the cells of the body and is due to malabsorption of B12 resulting from atrophic gastritis and lack of intrinsic factor secretion

81
Q

what are the causes of macrocytic anaemia?

A

Common features are tiredness and weakness, dyspnoea, sore red tongue, diarrhoea and mild jaundice

82
Q

how would you treat 1- folate deficiency
2- b12 deficiency?

A
  • Folate deficiency: oral folic acid 5mg daily
  • B12 deficiency: replenish stores with hydroxocobalamin (B12):
    – 1mg IM alternate days for 2 weeks.
    – Maintenance 1mg IM every 3 months FOR LIFE
83
Q

what is the function of neutrophils?

A

– Ingest and kill bacteria, fungi and damaged
cells

84
Q

why would neutrophils rise?

A

(Neutrophilia) occurs in bacterial
infections

85
Q

why would neurophils be low?

A

(Neutropenia) occur in viral
infections, acute leukaemia

86
Q

what is CRP and what does it indicate?

A
  • Protein produced in the acute phase
    response
  • Synthesised exclusively in the liver
  • Rises within 6 hours of an acute event
87
Q

when do platelets rise?

A
  • Rise: (Thrombocytosis)
    – Malignant disease
    – Autoimmune disease
    – Inflammation
88
Q

when are platelets low?

A
  • Low: (Thrombocytopenia)
    – Drugs
    – Leukaemia
89
Q

what is ESR?

A

Erythrocyte Sedimentation Rate
(ESR)
* Measure of acute phase response