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Fabulous Five - Pathology > Chem Path > Flashcards

Chem Path Flashcards

1
Q

What is the most common electrolyte abnormality in hospital patients? How common is it?

A

Hyponatraemia. It is found in 1 in 4 patients.

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2
Q

What is the underlying pathology of hyponatraemia?

A

It is due to an excess of ADH, causing an excess of water in the body.

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3
Q

What is the normal range for plasma sodium?

A

135-145mmol/L

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4
Q

What is the first step is assessing a patient with hyponatraemia?

A

Assessing the hydration status

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5
Q

What is the best way to assess the hydration status of a patient?

A

Clinical picture, and the urine sodium

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6
Q

What are the symptoms of hyponatraemia, in order of earliest to latest?

A
  • Nausea and vomiting
  • Confusion
  • Seizures
  • Coma and death
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7
Q

What is involved in the clinical assessment of a patient’s hydration status?

A
  • Heart rate and blood pressure
  • Skin turgor
  • Mucosal surfaces
  • Urine output
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8
Q

What would you find on clinical assessment of a hypovolaemic patient?

A
  • Dry mucosal surfaces
  • Reduced skin turgor
  • Reduced urine output
  • Reduced blood pressure
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9
Q

What would you find on clinical assessment of a hypervolaemic patient?

A
  • Raised JVP

- Peripheral and pulmonary oedema

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10
Q

In hypervolaemic hyponatraemia, what are the main causes? How do these cause a low sodium?

A

‘The Three Failures’

  • Heart failure (reduced BP, increased ADH)
  • Liver failure (increased NO, reduced BP, increased ADH)
  • Renal failure (not excreting the water)
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11
Q

In hypovolaemic hyponatraemia, what are the main causes?

A

GI:
- Diarrhoea and vomiting

Renal:

  • Diuretics
  • Salt losing nephropathy
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12
Q

What are the two main stimuli to ADH secretion?

A
  • Reduced blood pressure

- Increased serum osmolality

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13
Q

How should you treat hypervolaemic hyponatraemia?

A
  • Fluid restriction

- Correct the cause

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14
Q

In euvolaemic hyponatraemia, what are the main causes? How do these cause a hyponatraemia?

A
  • Hypothyroidism (reduced BP, increased ADH)
  • Adrenal insufficiency (reduced cortisol, reduced water loss)
  • SIADH (too much ADH)
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15
Q

How should you treat hypovolaemic hyponatraemia?

A
  • Restore fluid with 5% dextrose
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16
Q

How should you treat euvolaemic hyponatraemia?

A
  • Investigate causes with TFTs, synACTHen test and urine/plasma osmolality
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17
Q

In a patient with SIADH, what osmolalities would you fin din the serum/urine?

A
  • Reduced serum osmolality

- Raised urine osmolality

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18
Q

In fluid restricting a patient, how much total fluid should be taken in?

A

750ml a day (less than 1L)

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19
Q

When is the use of hypertonic saline (2.7%) indicated?

A

When the hyponatraemia is causing either:

  • A reduced GCS
  • Seizures

Seek expert help before administering

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20
Q

When correcting hyponatraemia, what rate should the sodium be corrected at? What is at risk at higher rates?

A

No more than 8-10mmol/L per hour. At higher rates, you risk a central demyelination.

If it has been corrected too quickly, bring the sodium bac down again.

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21
Q

How can SIADH be diagnosed?

A

As a diagnosis of exclusion, endocrine tests must be performed, and the serum and urine osmolalities must be low and high respectively.

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22
Q

What are the causes of SIADH?

A
  • Any cerebral pathology (malignancy, infection)
  • Any pulmonary pathology (malignancy, infection)
  • Drugs (opiates, SSRIs)
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23
Q

How should you treat SIADH?

A
  • Fluid restrict
  • Treat the cause

There are some medial therapies with demeclocycline and tolvaptan, but these are rarely used.

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24
Q

In hypovolaemic hypernatraemia, what are the most common causes?

A

GI:
- Diarrhoea and vomiting

Skin:
- Excessive sweating, burns

Renal:
- Loop diuretics

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25
Q

In hypervolaemic hypernatraemia, what are the most common causes?

A
  • Mineralocorticoid excess (Conn’s syndrome)

- Use of hypertonic saline

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26
Q

In diabetes insipidus, what are the initial investigations you should perform and why?

A
  • Blood glucose (exclude mellitus)
  • Blood potassium and calcium (exclude other electrolyte imbalances
  • Assess urine to plasma osmolality
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27
Q

Once diabetes insipidus is suspected, what investigation will determine the type and, therefore, treatment? How does this work?

A

The water deprivation test. After 8 hours of no fluid, assess the change in urine concentration:

  • Normal: >600 change
  • Primary polydipsia: less than this
  • Central: will increase with desmopressin
  • Nephrogenic: will not change with desmopressin
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28
Q

How do you treat diabetes insipidus?

A
  • Treat the hypovolaemia and hypernatraemia with 5% dextrose
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29
Q

What is the normal range of potassium?

A

3.5 - 5.5 mmol/L

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30
Q

What two hormones control potassium levels?

A
  • Angiotensin II

- Aldosterone

31
Q

What are the main causes of hyperkalaemia?

A
  • Renal failure
  • Drugs (ACEi, ARB, spironolactone)
  • Low aldosterone
  • Increased release (rhabdomyolysis, acidosis)
32
Q

How do you treat hyperkalaemia?

A
  • 10mls of 10% calcium gluconate (to stabilise the myocardium)
  • 100mls of 20% dextrose
  • 10mls of insulin (K+ absorption into cells)
  • Nebulised salbutamol
  • Treat the underlying cause
33
Q

In a patient with high sodium and low potassium, what does this suggest?

A

Conn’s syndrome (hyperactive adrenals)

34
Q

In a patient with low sodium and high potassium, what does this suggest?

A

Addison’s disease (inactive adrenals)

35
Q

How does acidosis cause hyperkalaemia?

A

The intake of H+ ions to correct the pH, will push K+ ions out of the cell.

36
Q

What are the main causes of hypokalaemia?

A
  • GI loss (diarrhoea and vomiting)
  • Renal loss (hyperaldosterism, excess cortisol, diuretics, Bartter)
  • Redistribution into the cells (alkalosis)
37
Q

What is Bartter’s syndrome?

A

A disease which causes malformed Na+/K+/Cl channels, raising distal nephron Na+ levels.

38
Q

Describe each type of renal tubular necrosis

A

Type I:
- Distal failure of H+ excretion, causing acidosis and hypokalaemia

Type II:
- Proximal failure to reabsorb bicarbonate, causing acidosis and hypokalaemia

Type III:
- Rare and rarely relevant

Type IV:
- Aldosterone deficiency or resistance, causing acidosis and hyperkalaemia

39
Q

How do you manage a patient with hypokalaemia?

A

If potassium is >3.0:

  • Oral SandoK tablets
  • Monitor serum potassium levels

If potassium <3.0

  • IV potassium chloride
  • Maximum rate of 10mmol/L per hour (can cause arrhythmias if higher)

For any potassium imbalance, treat the underlying cause.

40
Q

What is the normal range for blood pH?

A

Between 7.35 and 7.46

41
Q

What is the normal CO2 level in the blood?

A

4.7 - 6 kPa

42
Q

What is the normal bicarbonate level in the blood?

A

22 - 30 mmol/L

43
Q

What is the normal O2 level in the blood?

A

10 - 13 kPa

44
Q

In metabolic acidosis what will you expect the parameters of a blood gas to be? What can cause this?

A
  • pH: reduced
  • CO2: normal or reduced (depends on compensation)
  • Bicarbonate: reduced

This can be caused by excess lactate in DKA, or renal tubular acidosis (decreased H+ excretion) or an intestinal fistula (bicarbonate loss).

45
Q

In respiratory acidosis what will you expect the parameters of a blood gas to be? What can cause this?

A
  • pH: reduced
  • CO2: reduced
  • Bicarbonate: normal or increased (depends on compensation)

This can be caused by lung injury (pneumonia, COPD) or decreased ventilation (morphine overdose)

46
Q

In metabolic alkalosis what will you expect the parameters of a blood gas to be? What can cause this?

A
  • pH: increased
  • CO2: normal or increased (depends on compensation)
  • Bicarbonate: increased

This can be caused by pyloric stenosis, hypokalaemia or an ingestion of bicarbonate.

47
Q

In respiratory alkalosis what will you expect the parameters of a blood gas to be? What can cause this?

A
  • pH: increased
  • CO2: reduced
  • Bicarbonate: normal or reduced (depends on compensation)

This can be caused by mechanical ventilation or an anxiety/panic attack

48
Q

What is the anion gap? What is it usually contributed to by, and what is the usual range?

A

It is the gap between the total cation and anion charge. It is usually accounted for by albumin, with a normal range of 14 - 18 mmol/L.

49
Q

What can cause an elevated anion gap?

A

KULP:

  • Ketoacidosis (DKA, alcoholism, starvation)
  • Uraemia (renal failure)
  • Lactic acidosis
  • Toxins (ethylene glycol, methanol, paraldehyde, salicylate)
50
Q

What is the osmolar gap? What is the normal range?

A

The difference between the measures osmolality and the calculated osmolarity. It is normally less than 10.

51
Q

What can cause an elevated osmolar gap?

A

This is indirect evidence of an abnormal solute in the blood. It can be used to differentiate causes of an elevated anion gap.

52
Q

What is involved in the normal function of the liver?

A
  • Intermediary metabolism
  • Xenobiotic metabolism
  • Protein synthesis
  • Bile synthesis
  • Reticulo-endothelial function (immune modulating)
53
Q

What is intermediary metabolism?

A

It is an enzyme controlled process that extracts energy and uses it to construct cellular components.

54
Q

In liver failure, why can a patient become encephalopathic?

A

There is increased ammonia, which is encephalotoxic

55
Q

What enzyme is involved in many of the xenobiotic functions of the liver?

A

P450

56
Q

What is the function of bile?

A
  • Excretion
  • Micelle formation
  • Digestion
57
Q

In a liver function test, what is measured?

A

Liver cell damage:

  • AST and ALT
  • AlkPhos
  • GGT
  • Bilirubin
  • AFP

Liver function:

  • Clotting factors
  • Albumin
  • Glucose
58
Q

What is the function of the aminotransferases?

A

They are involved in amino acid metabolism

59
Q

Where can they be found? What is the normal level? When can they be raised?

A

They are predominately found in hepatocytes, but can be found in the muscle, brain and kidneys.

The normal level is less than 40iu/L.

They can be raised in hepatocellular death.

60
Q

How can the relative levels of the aminotransferases specify the cause of hepatocellular death?

A

If AST:ALT is >2 this is likely alcoholic.
If it above this with no alcohol history, it is likely cirrhosis.

If AST:ALT is <1.1, it is likely viral damage.

61
Q

What is the function of alkaline phosphatase?

A

This is largely unknown.

62
Q

What is the normal level of ALP? When can it be raised?

A

It is normally between 30 and 150 iu/L.

It can be raised in cholestasis and bone disease. It is also raised in pregnancy and malignancy.

63
Q

What is gamma-glutamyl transferase involved in?

A

It is involved in amino acid metabolism.

64
Q

What is the normal level of GGT? When can it be raised?

A

It is normally between 30 and 150 iu/L.

It is raised in chornic alcohol use. It can also be raised in bile duct disease and metastasis.

65
Q

What is the role of albumin?

A

It is primarily involved in controlling the oncotic pressure of blood.

66
Q

When can albumin levels be low?

A
  • Low production (liver disease)
  • Loss of albumin (renal or GI loss)
  • Sepsis (capillary leakage)
67
Q

Why can clotting factors be a better marker than albumin for acute disease?

A

The half life of clotting factors is much shorter (albumin is 20 days, clotting factors are mere hours) so any change can be detected far closer to a change in pathology.

68
Q

What is the role of alfa fetoprotein?

A

It is primarily involved in foetal immune modulation. In adults, its purpose in unclear.

69
Q

When can alfa fetoprotein be raised?

A

It is raised in hepatocellular carcinoma, and is a good cancer marker for testicular cancer as well. It is also raised in pregnancy.

70
Q

In raised bilirubin, what is the best way to consider the pathology involved?

A

Consider the rest of the liver function test:

Normal hepatic enzymes:

  • Haemolysis
  • Gilbert’s syndrome

Raised ALP:

  • Obstructive jaundice (gall stones, pregnancy)
  • Non-obstructive jaundice (PBC, PSC)

Raised AST/ALT:
- Acute or chronic hepatocellular damage

71
Q

What is the significance of pale stools and dark urine when considering a raised bilirubin?

A

This shows the jaundice is obstructive, giving this clinical picture.

72
Q

What is the ‘liver panel’?

A

This are further tests that can be made when the liver function test is unclear. It involved:

  • Hepatitis screen
  • CK, TFTs
  • Alpha-1-antitrypsin
  • Immunoglobulins
73
Q

In a patient with a raised ALT, what must be considered when discussing management?

A

You must look at the other markers in the LFTs.

If isolated raised ALT:
- Discuss lifestyle changes

If symptomatic/unisolated raised ALT:

  • Conduct liver function tests and liver screen to determine cause
  • Treat the cause

Fabulous Five - Pathology (3 decks)

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