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Pathology > Chemical Pathology- Part 1 (p72-85- Fluid balance, electrolytes, acid-base, LFTs, porphyrias, pituitary + thyroid) > Flashcards

Chemical Pathology- Part 1 (p72-85- Fluid balance, electrolytes, acid-base, LFTs, porphyrias, pituitary + thyroid) Flashcards

1
Q

What % of body is water?

A

60

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2
Q

What is ratio of intracellular:extracellular fluid?

A

2:1

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3
Q

What does extracellular fluid include (three different things)?

A

Intravascular
Interstitial (between cells- largest component)
Transcellular- epithelial lined spaces e.g. CSF, joint fluid etc

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4
Q

Define osmolality

A

Total number of particles in solution- measured with an osmometer (units- mmol/kg)

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5
Q

Define osmolarity

A

The concentration of a solution- calculated (units mmol/l)

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6
Q

What physiological determinants of osmolality and osmolarity are there in serum/plasma?

A 
Na+
K+
Cl-
HCO3-
Urea
Glucose
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7
Q

What pathological determinants of osmolality and osmolarity are there in serum/plasma?

A

Endogenous (e.g. glucose) or exogenous (e.g. ethanol)

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8
Q

Osmolarity calculation?

A

2(Na+ + K+) + urea + glucose

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9
Q

What is the osmolar gap?

A

The difference between osmolality and osmolarity

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10
Q

Why is the osmolar gap useful in metabolic acidosis?

A

If osmolarity is lower than osmolality we can assume there are extra unmeasured solutes that are dissolved

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11
Q

Normal range for serum osmolality?

A

275-295 mmol/kg

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12
Q

Normal range for Na+?

A

135-145mmol/l

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13
Q

What maintains Na+ as mainly an extracellular cation?

A

Na+/K+ ATPase

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14
Q

What would you see in symptomatic hyponatraemia?

A

N+V (<136mmol/l)
Confusion (<131mmol/l)
Seizures, pulmonary oedema (<125mmol/l)
Coma (<117mmol/l)

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15
Q

How do you determine whether it is a true hyponatraemia?

A

Using serum osmolality:
High-
Glucose/mannitol infusion

Normal-
Spurious
Drip arm sample
Pseudohyponatraemia

Low-
True hyponatraemia

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16
Q

What causes of pseudohyponatraemia are there?

A

Hyperlipidaemia

Paraproteinaemia

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17
Q

What would you be considering aetiology and treatment wise in a hypervolaemic hyponatraemic patient?

A

Three failures- heart, renal and liver

Treatment:
Fluid restrict and treat cause

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18
Q

What would you be considering aetiology and investigation wise in a euvolaemic hyponatraemic patient?

A

Hypothyroidism
Glucocorticoid insufficiency
SIADH

investigations:
TFTs
Short synacthen test
Paired urine and serum osmolality

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19
Q

What would you be considering diagnosis and treatment wise in a hypovolaemic hyponatraemic patient?

A

Diarrhoea
Vomiting
Diuretics
Salt losing nephropathy

Treatment
Fluid restoration with 5% dextrose

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20
Q

How does liver failure cause hyponatraemia?

A

There is poor breakdown of vasodilators like nitric oxide, these cause a low BP and subsequent ADH release causes water retention, which dilutes down sodium

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21
Q

What is the risk when treating hyponatraemia?

A

Rapid correction can lead to central pontine myelinolysis (locked in syndrome) therefore increase Na+ by 1mmol/l/hr

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22
Q

Why is hyponatraemia post surgery common?

A

Over hydration with hypotonic IV fluids

Transient increase in ADH due to stress of surgery

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23
Q

What is the lab criteria for SIADH?

A

True hyponatraemia
Clinically euvolaemic
Inappropriate high urine osmolality and increased renal sodium excretion (>20mmol/l)
Normal 9am cortisol and TFTs (diagnosis of exclusion)

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24
Q

Causes of SIADH?

A

Malignancy- small cell lung cancer (most common), pancreas, prostate, lymphoma)
CNS disorders- meningoencephalitis, haemorrhage, abscess
Chest- TB, pneumonia, abscess
Drugs- opiates, SSRIs, carbamazepine, PPIs

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25
Q

Treatment of SIADH?

A

Fluid restriction and treat cause, demeclocycline and tolvaptan induce a state of diabetes insipidus that may help

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26
Q

Symptoms of hypernatraemia?

A

Thirst -> confusion -> seizures + ataxia -> coma

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27
Q

What causes are there of hypovolaemic hypernatraemia?

A

GI loss- vomiting, diarrhoea
Skin loss- excessive sweating, burns
Renal loss- loop or osmotic

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28
Q

What causes are there of euvolaemic hypernatraemia?

A

Respiratory (tachypnoea)
Skin (sweating + fever)
Renal (DI)

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29
Q

What causes are there of hypervolaemic hypernatraemia?

A 
Mineralocorticoid excess (Conn's syndrome)
Hypertonic saline
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30
Q

What can rapid correction of hypernatraemia lead to?

A

Cerebral oedema

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31
Q

Clinical features of DI?

A

Hypernatraemia (lethargy, thirst, irritable, confusion, coma, fits)
Clinically euvolaemic
Polyuria and polydipsia
Urine:plasma osmolality <2

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32
Q

What is the difference between cranial and nephrogenic DI?

A

Cranial- lack of ADH

Nephrogenic- receptor defect (insensitivity)

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33
Q

Causes of cranial DI?

A

Surgery, trauma or tumours

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34
Q

Causes of nephrogenic DI?

A

Inherited channelopathies
Lithium, democlocycline
Hypercalcaemia

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35
Q

How is DI diagnosed?

A

8h fluid deprivation test:
Normal- urine conc >600mOsmol/kg
Primary polydipsia- urine conc 400-600
Cranial DI- urine only concentrates after desmopression
Nephrogenic- low concentration after desmopressin

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36
Q

Normal range of potassium?

A

3.5-5.5mmol/l

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37
Q

Causes of hypokalaemia?

A

Either depletion or shift into cells- rarely decreased intake

GI loss
Renal loss- hyperaldosteronism, excess cortisol, diuretics, osmotic diuresis
Redistribution into cells
Rare tubular acidosis or hypomagnesaemia

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38
Q

What are the 3 types of renal tubular acidosis and how are they different?

A

Type 1- most severe, distal failure of H+ excretion and subsequent acidosis and hypokalaemia (failed hydrogen potassium pumping)
Type 2- Milder, proximal failure to reabsorb bicarbonate, leads to acidosis and hyperkalaemia
Type 4- aldosterone deficiency or resistance (acidosis and hyperkalaemia)

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39
Q

Treatment of hypokalaemia?

A

Oral SandoK and monitoring potassium levels or if lower than 3.0 consider intravenous potassium chloride

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40
Q

Causes of hyperkalaemia?

A

Excessive intake-
oral, parenteral or stored blood transfusion

Transcellular movement (ICF>ECF)- 
acidosis, insulin shortage (DKA) and tissue damage/catabolic state
Decreased excretion- 
Acute renal failure (oliguric phase)
CRF
K-sparing diuretics (spironolactone)
Mineralocorticoid deficiency (Addison's)
NSAIDs, ACEi, ARBs
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41
Q

Treatment of hyperkalaemia?

A

10ml 10% calcium gluconate, 100mls 20% dextrose and 10 units insulin. Salbutamol useful as well

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42
Q

Normal blood pH range?

A

7.35-7.45

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43
Q

Normal blood CO2 range?

A

4.7-6kPa

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44
Q

Normal blood bicarbonate range?

A

22-30mmol/l

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45
Q

Normal blood O2 range?

A

10-13kPa

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46
Q

What are the steps in checking for an acidosis/alkalosis?

A

Check pH
CO2- does it fit with pH
Bicarbonate- does it fit with pH
Compensation- Any? Partial? Complete?

47
Q

What would you see in a metabolic acidosis?

A

pH low, bicarb low, CO2 normal or low if compensated

48
Q

Causes of metabolic acidosis?

A

Lactate build up in DKA
Renal tubular acidosis
Intestinal fistula

49
Q

What would you see in a metabolic alkalosis?

A

Raised pH and bicarb, CO2 normal or raised if compensated

50
Q

Causes of metabolic alkalosis?

A

Pyloric stenosis
Hypokalaemia
Ingestion of bicarb

51
Q

What would you see in a respiratory acidosis?

A

Low pH, bicarb normal or raised if compensated, high CO2

52
Q

Causes of resp acidosis?

A

Lung injury- pneumonia
COPD
Decreased ventilation- Morphine OD

53
Q

What would you see in a resp alkalosis?

A

Raised pH, bicarb normal or low if compensated, low CO2

54
Q

Causes of resp alkalosis?

A

Mechanical ventilation

Anxiety/panic attack

55
Q

What is the anion gap?

A

Difference between total concentration of principal cations and anions - i.e. Concentration of unmeasured anions in plasma

56
Q

Normal range for anion gap?

A

14-18mmol/l

57
Q

Causes of elevated anion gap metabolic acidosis?

A

KULT
Ketoacidosis- diabetic, alcoholic, starvation
Uraemia- renal failure
Lactic acidosis
Toxins- ethylene glycol, methanol, paraldehyde, salicylate

58
Q

Which LFTs are markers of liver cell damage?

A 
ALT
AST
Alk Phos
GGT
Bilirubin
59
Q

Which LFTs are markers of synthetic function?

A

Clotting (INR)
Albumin
Glucose

60
Q

When are the aminotransferases (AST/ALT) raised?

A

When hepatocytes die

61
Q

What would you see in terms of LFTs in alcoholic liver disease?

A

AST:ALT = 2:1

62
Q

What would you see in terms of LFTs in viral liver disease?

A

AST:ALT = <1:1

63
Q

When is ALP raised?

A

Cholestasis (intrahepatic or extrahepatic) and bone disease, very high in pregnancy

64
Q

When is gamma GT (GGT) raised?

A

In chronic alcohol use
Bile duct disease
Metastases
Also used to confirm hepatic source of raised ALP

65
Q

What are porphyrias?

A

Disorders caused by deficiency in enzymes, involved in haem biosynthesis, leading to build up of toxic haem precursors

66
Q

What is the inheritance pattern of acute intermittent porphyria (AIP)?

A

Autosomal dominant

67
Q

What causes AIP?

A

HMB (hydroxmethylbilane) synthase deficiency

68
Q

Symptoms of AIP?

A

Neurovisceral- Abdo pain, seizures, psych, N+V, tachycardia, HTN, sensory loss, muscle weakness, constipation, incontinence, NO cutaneous manifestations

69
Q

How is AIP diagnosed?

A

ALA + PBG in urine (‘Port wine urine’)

70
Q

How do you treat AIP?

A

Avoid precipitating factors, analgesia, IV carbohydrate/haem arginate

71
Q

What are the two types of acute poryphrias with skin lesions?

A 
Hereditary coproporphyria (HCP) + Varegiate poryphria (VP)
Same neurovisceral lesions with skin lesions
72
Q

How do non-acute porphyrias present and what are the three types?

A 
Skin lesions ONLY
e.g. 
Congenital Erythopoietic porphyria (CEP)
Erythropoietic protoporphyria (EPP) 
Porphyria Cutanea Tarda (PCT)
73
Q

What is a typical feature of erythropoietic protoporphyria (EPP)?

A

Photosensitivity
Burning
Itching oedema following sun exposure

74
Q

What causes PCT?

A

Uroporphyrinogen decarboxylase deficiency

75
Q

Symptoms of PCT?

A

Cutaneous- vesicles (crusting, pigmented, superficial scarring) on sun exposed sites

76
Q

How is PCT diagnosed?

A

Increased urinary uroporphyrins + coproporphyrins + ferritin

77
Q

How is PCT treated?

A

Avoid precipitants (alcohol, hepatic compromise), phlebotomy

78
Q

Name 5 hormones released by the hypothalamus?

A 
GHRH
GnRH
TRH
Dopamine
CRH
79
Q

What action does GHRH have on pituitary hormones?

A

Stimulates GH

80
Q

What action does GnRH have on pituitary hormones?

A

Stimulates LH/FSH

81
Q

What action does TRH have on pituitary hormones?

A

Stimulates TSH and prolactin

82
Q

What action does dopamine have on pituitary hormones?

A

Inhibits prolactin

83
Q

What action does CRH have on pituitary hormones?

A

Stimulates ACTH

84
Q

What does a combined pituitary function test (CPFT) involve?

A

Administration of LHRH, TRH and insulin then measurement at 0, 30, 60, 90 and 120 minute levels of pituitary hormones

85
Q

When is a CPFT indicated?

A

Assessment of all components of anterior pituitary function used particularly in pituitary tumours or following tumour treatment

86
Q

When is a CPFT contraindicated?

A

IHD
Epilepsy
Untreated hypothyroidism

87
Q

What is an easy way to assess whether a pituitary adenoma is likely to be benign or aggressive?

A

Size
Microadenoma <10mm usually benign
Macroadenoma >10mm usually aggressive

88
Q

What can a pituitary adenoma compress and subsequently lead to?

A

Optic chiasm -> bitemporal hemianopia

89
Q

Which hormones are released from the neurohypophysis (posterior pituitary gland)?

A

ADH

Oxytocin

90
Q

What are the causes of excess ADH?

A

Lung paraneoplasia- SCC, pneumonia
Brain- traumatic injury, meningitis, primary or secondary tumours
Iatrogenic- SSRIs, amitryptilline, carbamazepine, PPIs

91
Q

What is diabetes insipidus?

A

Increased diuresis due to either failure of production (neurogenic) or insensitivity (nephrogenic) to ADH, leading to decreased urine osmolality and increased serum osmolality

92
Q

What would you suspect if TFTs showed a raised TSH and low T4?

A

Hypothyroidism

93
Q

What would you suspect if TFTs showed a raised TSH and normal T4?

A

Treated hypothyroidism or sub-clinical

94
Q

What would you suspect if TFTs showed a raised TSH and T4?

A

TSH secreting tumour or thyroid hormone resistance

95
Q

What would you suspect if TFTs showed a low TSH and high T3 and T4?

A

Hyperthyroidism

96
Q

What would you suspect if TFTs showed a low TSH and normal T3 and T4?

A

Subclinical hyperthyroidism

97
Q

What would you suspect if TFTs showed a low TSH and low T4?

A

Central hypothyroidism (hypothalamic/pituitary disorder)

98
Q

What would you suspect if TFTs showed a raised (then later decreased) TSH and low T3 and T4?

A

Sick euthyroidism. Body tries to shut down metabolism as thyroid gland has reduced output

99
Q

What causes of high uptake hyperthyroidism are there?

A

Graves disease
Toxic multinodular goitre
Toxic adenoma (hot nodule on isotope scan)

100
Q

What is F:M ratio of Graves?

A

9:1

101
Q

What causes of low uptake hyperthyroidism are there?

A

Subacute De Quervains thyroiditis (self-limiting post-viral painful goitre)- initially hyper then hypo
Postpartum thyroiditis

102
Q

What autoimmune causes of hypothyroidism are there?

A

Primary atrophic hypoT

Hashimotos

103
Q

What non immune causes are there of hypothyroidism?

A

Iodine deficiency (mr. Worldwide)
Post-thyroidectomy/radioiodine
Drug-induced- antithyroid drugs, lithium, amiodarone

104
Q

How does primary atrophic hypothyroidism differ from Hashimotos?

A

Primary atrophic- diffuse lymphocyte infiltration + atrophy. No goitre so small thyroid. No known antibodies

Hashimotos- Plasma cell infiltration + goitre, elderly females, initial hashitoxicosis, auto-antibody titres raised

105
Q

Treatment of hyperthyroidism?

A

Depends on aetiology.
Low uptake- symptomatic with beta blockers, NSAIDs for De Quervains
High uptake- BB + antithyroid therapy (carbimazole/propylthiouracil)
Can also use radioiodine or surgery

106
Q

Why is propylthiouracil rarely used nowadays?

A

Risk of aplastic anaemia

107
Q

Treatment of hypothyroidism?

A

Thyroid replacement therapy

108
Q

Most common type of thyroid neoplasia?

A

Papillary

109
Q

5 subtypes of thyroid neoplasia?

A 
Papillary- >60%
Follicular- 25%
Medullary- 5%
Lymphoma- 5%
Anaplastic- Rare
110
Q

Treatment of papillary thyroid neoplasia?

A

Surgery +/- radioiodine and thyroxine to decrease TSH

111
Q

What might you see on histology of papillary thyroid neoplasia?

A

Psammoma bodies

112
Q

What is medullary thyroid neoplasia linked to?

A

MEN2 (they also produce calcitonin)

113
Q

What are the three different types of multiple endocrine neoplasia?

A

MEN1 (3Ps)- Pituitary, pancreas (insuloma), parathyroid
MEN2a (2Ps1M)- Parathyroid, phaeochromocytoma, medullary (thyroid)
MEN2b (1P, 2Ms)- Phaeochromocytoma, medullary thyroid, mucocutaneous neuromas (+ marfanoid)

Pathology (13 decks)

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