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Clinical Pathology > Core Clinical Biochemistry > Flashcards

Core Clinical Biochemistry Flashcards

1
Q

endocrine gland

A

secrete hormones into blood stream and act systemically

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2
Q

paracrine gland

A

hormones act locally

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3
Q

autocrine

A

cell secreting the protein

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4
Q

What are the most common primary pituitary tumours

A

adenomas
clinical effect secondary to hormone produced
local effects to pressure on optic chiasm or adjacent pituitary

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5
Q

what are the types of anterior pituitary adenoma?

A

Prolactinoma
growth hormone secreting
ACTH secreting

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6
Q

Prolactinoma

A

most common

galactorrhoea and menstrual disturbance

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7
Q

growth hormone secreting

A

gigantism in children

acromegaly in adults

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8
Q

ACTH secreting

A

cushing’s syndrome

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9
Q

what is Hashimoto’s?

A

chronic lymphocyte thyroiditis
autoimmune chronic inflammatory disorder
females > males

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10
Q

are the serum antibodies high or low in Hashimoto’s?

A

high

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11
Q

what does Hashimoto’s increase the risk of?

A

thyroid lymphoma

papillary carcinoma

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12
Q

What is graves disease?

A

autoimmune disease

clinical hyperthyroidism

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13
Q

what is the most common cause of hyperthyroidism

A

graves disease

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14
Q

what are the signs of hyperthyroidism?

A

hair loss, proptosis, tachycardia, hyperactive reflexes

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15
Q

What are the thyroid antigens like in Graves disease??

A

T3 and T4 elevated

TSH markedly suppressed

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16
Q

what is a multinodular goitre?

A

enlargement of thyroid with varying degrees of nodularity

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17
Q

Associated features of multinodular goitre

A

tracheal compression or dysphagia may develop with large nodules

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18
Q

what is follicular adenoma?

A

encapsulated tumour with evidence of follicular cell differentiation

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19
Q

who gets follicular adenoma?

A

females > males

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20
Q

how does follicular adenoma present?

A

painless neck mass

solitary nodule - 1 lobe

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21
Q

what is the most common malignant tumour of the thyroid?

A

thyroid carcinoma

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22
Q

which is the most common type of thyroid carcinoma?

A

papillary carcinoma

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23
Q

causes of papillary carcinoma

A 
familial - autosomal dominant non-medullary thyroid carcinoma 
FAP 
Cowden's syndrome
therapeutic irradiation 
radiation exposure
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24
Q

genetic abnormalities in papillary carcinoma?

A

RET or NTRK1
BRAF V600E mutation
RAS mutation

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25
Q

What is follicular carcinoma

A

10-20% all thyroid cancers

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26
Q

How do most follicular carcinomas present?

A

90% present with solitary nodule in thyroid

10% distant mets

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27
Q

what is primary hyperparathryroidism

A

excessive secretion of parathyroid hormone from one or more glands

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28
Q

what is secondary hyperparathyroidism

A

hyperplasia of glands with elevated PTH in response to hypocalcaemia
- renal insufficiency, malabsorption, vit D deficiency

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29
Q

aetiology of primary hyperparathyroidism

A

aging
tumorigenesis in general
ionizing radiation
male

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30
Q

clinical features of PHPT

A 
asymptomatic 
arterial hypertension 
psychiatric 
hypercalcaemia 
decreased renal function 
osteoporosis 
hypercalcaemia
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31
Q

most common cause of PHPT

A

adenoma

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32
Q

causes of SHPT

A

non-neoplastic increase in parathyroid paranchymal cell mass

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33
Q

what patients is SHPT common in

A

renal failure

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34
Q

what is cushing’s syndrome?

A

prolonged cortisol exposure

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35
Q

exogenous causes of cushing’s

A

excessive gluticocorticoids

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36
Q

endogenous causes of Cushing’s

A

adrenal cortical tumours
adrenal cortical hyperplasia
ACTH secreting pituitary adenoma
small cell lung carcinoma

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37
Q

sign’s and symptoms of cushing’s

A 
moon face 
high BP 
central obesity 
weak muscles and bone 
excess sweating 
mood swings 
headaches 
chronic fatigue 
women increased hair growth
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38
Q

what is conn’s syndrome

A

primary hyperaldosteronism

leads to low renin

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39
Q

causes of conn’s syndrome?

A

adrenal cortical hyperplasia
adenoma
familial hyperaldosteronism

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40
Q

sign’s and symptoms of Conn’s syndrome

A

high BP
muscle weakness
muscle spasms
excessive urination

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41
Q

what is Addison’s disease?

A

primary adrenal cortical insufficiency

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42
Q

what causes Addison’s disease?

A

adrenal dysgenesis

adrenal destruction

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43
Q

clinical features of Addison’s disease

A

triad of hyperpigmentation, postural hypertension, hyponatraemia

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44
Q

treatment for Addison’s disease

A

long term steroid replacement

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45
Q

what is phaeochromocytoma

A

catecholamine-secreting tumour arising from adrenal medulla

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46
Q

what are the symptoms of phaeochromocytoma

A

hypertension, palpitations, headaches, anxiety

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47
Q

what is the normal blood glucose level

A

5mmol/L

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48
Q

group of hormones that increase blood glucose

A

glucagon
adrenaline
growth hormone
cortisol

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49
Q

where is glucagon produced

A

alpha cells

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50
Q

what does adrenaline and growth hormone do?

A

stimulate glycogenolysis

stimulate lipolysis

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51
Q

what does cortisol do?

A

stimulate gluconeogenesis
increase glycogen sythesis
stimulate proteolysis
reduce tissue glucose use

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52
Q

what is hypoglycaemia

A

less than 4

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53
Q

what is hyperglycaemia

A

greater than 11mmol/l

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54
Q

symptoms of diabetes

A

thirst, polyuria, weight loss, tiredness

55
Q

signs of diabetes

A

dry mouth, weight loss, glycosuria, hyperglycaemia

56
Q

Diagnosis of diabetes

A 
typical symptoms and 
random plasma glucose >11.1mmol/L 
fasting plasma glucose >7.0mmol/L 
2hr post load plasma glucose >11.1 mmol/L during 75g oral glucose tolerance test 
HbA1c >48 mmol/mol
57
Q

glucose tolerance test

A

oral or IV

58
Q

OGTT

A

fasting plasma glucose
75g oral glucose load
plasma glucose at intervals and at 2 hours post glucose load
interpretation: fasting: normal <6.1mmol/L, diabetic >7mmol/L
2 hour post glucose load: normal <7.8mmol/L, diabetic >11.1 mmol/L

59
Q

what is borderline diabetes?

A

impaired fasting glucose >6.1mmol/L
impaired glucose tolerance: 2 hour post-glucose load plasma glucose >7.8 and <11.1 mmol/L
HbA1c 42-47 mmol/mol

60
Q

Investigations in diabetes

A 
HbA1C 
renal function 
liver function 
lipids 
thyroid function
61
Q

diagnosis of gestational diabetes

A

75g 2 hour OGTT
fasting plasma glucose >5.6mmol/L
2 hour post-glucose load plasma glucose >7.8mmol/L

62
Q

insulin dependent diabetes mellitus

A

autoimmune destruction of beta cells
insulin deficient
usually young but can be any age

63
Q

autoantibody tests for DM1

A

ICA, IA2 GAD

64
Q

Type 2 diabetes

A

insulin resistant/ deficient
often obese/ overweight
usually hypertensive and hyperlipidaemic

65
Q

gestational diabetes

A

arising or diagnosed in pregnancy

resolves after pregnancy

66
Q

secondary DM

A 
chronic or acute pancreatits 
calcific, tropical pancreatitis 
pancrectomy 
pancreatic cancer 
cystic fibrosis 
haemachromotosis
67
Q

what is haemachromotosis

A

hereditary iron overload storage disorder

68
Q

what does calcium do in the body

A 
muscle contraction 
neuronal excitation 
enzyme activity 
blood clotting 
the key mineral in bone
69
Q

what does phosphate do in the body

A 
ATP
intracellular signalling 
metabolic processes e.g. glycolysis 
backbone of DNA 
cembrane phospholipids
70
Q

what does magnesium do in the body

A 
cofactor for ATP 
neuromuscular excitation 
enzymatic funtuin 
regulates ion channels 
bone matrix
71
Q

cause of increase/ decrease

A

intake
storage
excretion/ loss
tissue redistribution

72
Q

controlling factors of calcium

A

parathyroid hormone vitamin D and metabolites

73
Q

normal calcium range

A

2.2-2.6mmol/L

74
Q

total calcium =

A

ionised Ca + bound Ca + complexed Ca

75
Q

what is ionised calcium

A

physiologically active fraction

76
Q

what is bound calcium

A

physiologically inactive

albumin main binding protein

77
Q

what is adjusted calcium

A

corrected for changes in albumin

patient samples adjusted for better diagnostic performance

78
Q

what effect does acidosis have on bound calcium

A

reduces bound Ca

79
Q

what effect does alkalosis have on bound calcium

A

increases bound calcium

80
Q

what does affect of reducing binding protein have on total calcium

A

reduce total calcium

81
Q

parathyroid glands produce which hormone

A

PTH

82
Q

what does PTH do

A

stimulate bone - increase Ca turnover, GI - vit D increases Ca absorption, kidney - decrease Ca clearance to release calcium

83
Q

what does calcium stimulate

A

parathyroid to stop producing PTH

84
Q

what are the symptoms of hypercalcaemia?

A

bones - bone aches and pains
stones - kidney stones
moans - GI conditions
groans - psychological conditions

85
Q

what can phosphate deficiency cause?

A

weakness and dysfunction
haemolysis, thrombocytopenia, poor granulocyte formation
confusion irritability and coma

86
Q

how much calcium do the bones store?

A

25 Mol - 99%

87
Q

which organ helps regulate calcium and phosphate levels?

A

kidney

88
Q

which organs regulate magnesium?

A

gut
bones (60%)
intracellular space in muscles
kidney

89
Q

at what point is Calcium levels a medical emergency?

A

> 3.5mmol/L or <1.6mmol/L

90
Q

what is the composition of bone

A

cortical bone - outer layer
trabecular bone - spongy, inner
cells - bone forming and bone resorbing cells
Extracellular - organic matrix mainly collagen, inorganic components e.g. minerals

91
Q

what do osteoblasts do?

A

make osteoid - type 1 collagen mainly
make hormones - alkaline phosphatase
prerequisite for mineralisation

92
Q

what are osteoblasts that are trapped within the matrix called?

A

osteocytes

93
Q

what are osteoclasts?

A

break down bone
repair and maintenance
produce TRAP and Cathepsin K enzymes which breakdown extracellular matrix

94
Q

how are osteoclasts regulated?

A

PTH, calcitonin, IL-6

95
Q

what do osteocytes do?

A

regulating bone matrix turnover

96
Q

what is the bone cycle

A

resting
resorption
osteoid formation
mineralisation

97
Q

what enzyme mineralises bone

A

hydroxyapatite enzyme

98
Q

how is bone disease investigated

A

X-Ray
Bone Mass - DEXA
cellular function - biochemistry
Microstructure - biopsy, qCT

99
Q

biochemical markers of bone formation

A

alkaline phosphatase
osteocalcin
procollagen type I peptides

100
Q

Biochemical markers of bone resorption

A

hydroxyproline
crosslinked telopeptides of type I collagen
tartrate-resistant acid phosphatase
cathepsin K

101
Q

ALP

A

health:
50% liver
50% bone

102
Q

bone alkaline phosphatase

A

released by osteoblasts
stimulated by increased bone remodelling
e.g. hyperparathyroidism
Pagets

103
Q

what synthesises procollagen type 1N propeptide?

A

osteoblasts

104
Q

when are collagen cross-links increased

A

high bone turnover
diurnal variation
do not predict bone mineral density

105
Q

uses of bone markers

A

evaluation of bone turnover and bone loss
evaluation of treatment
evaluation of compliance with medicine e.g. P1NP monitor compliance with teriparatide

106
Q

what does a T-score of -1 and above mean

A

bone density normal

107
Q

T-score -1 - -2.5

A

osteopenia

108
Q

T-score

A

osteoporosis

109
Q

describe osteoporosis

A

loss of bone with propensity to fractures

no routine abnormalities in routine biochemical tests

110
Q

diagnosis of osteoporosis

A

DEXA/ X-ray

111
Q

common sites of fracture in osteoporosis

A

spine
NOF
wrist

112
Q

investigation for 2nd causes of osteoporosis

A 
calcium and bone profile 
U&amp;Es
TFTs 
FBC
Vit D 
PTH 
plasma viscosity 
coeliac screen
113
Q

treatment options for osteoporosis

A

antiresorptive treatments

anabolic treatments

114
Q

bisphosphonates what do they do?

A

inhibit osteoclast formation - promote apoptosis

115
Q

side effects of bisphosphonates

A

oesophageal upper GI problems
flu-like
osteonecrosis of jaw
atypical femur fractures

116
Q

What are lytic bone mets

A

destruction of normal bone

117
Q

which cancers are lytic bone mets seen in

A

breast/ lung/ kidney/ thyroid

118
Q

what are sclerotic/ osteoblastic mets

A

deposition of new bone

119
Q

where are sclerotic mets seen

A

prostate
lymphoma
breast
lung

120
Q

usual sites of bone mets

A

spine, pelvis, femur, humerus, skull

121
Q

presenting symptoms of bone mets

A 
pain 
broken bones 
numbness, paralysis, trouble urinating 
loss of appetite, nausea, thirst, confusion, fatigue 
anaemia - disruption of bone marrow
122
Q

primary hyperparathyroidism blood results

A

High Ca
PTH: innapropriately high
low phosphate and high alk phos
sporadic or familial

123
Q

secondary hyperparathyroidism blood results

A

normal or low Ca
PTH: appropriately high
phosphate high if CKD
CKD or Vit D deficiency

124
Q

PHPT presentation

A

now much earlier and asyptomatic

used to be hypercalcaemia and renal and skeletal disease

125
Q

PTHT causes

A

adenomas - 85% cases

glandular hyperplasia - 6-10%

126
Q

clinical manifestations of PHPT

A

renal disease - nephrolithiasis, chronic kidney disease
bone disease - osteoporosis
proximal muscle wasting

127
Q

what is Paget’s disease

A

rapid bone turnover and formation leading to abnormal bone remodelling

128
Q

which age group - pagets

A

over 50

129
Q

what elevated bone marker would you see

A

alkaline phosphatase

130
Q

clinical features of Pagets?

A 
bone pain 
bone deformity 
fractures 
arthritis 
cranial nerve defects 
risk of osteosarcoma
131
Q

what is osteomalacia?

A

lack of mineralisation of bone

132
Q

causes of osteomalacia

A

insufficient calcium absorption from gut due to dietary insufficiency or vit D deficiency
excessive renal phosphate excretion

133
Q

alkaline phospatase is increased in all bone disorders except..

A

osteoporosis

Clinical Pathology (8 decks)

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