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Y2 Clinical Pathology > Core clinical biochemistry > Flashcards

Core clinical biochemistry Flashcards

1
Q

What do endocrine glands do

A

Secrete hormones directly in to the blood stream and act systemically

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2
Q

What does the paracrine system do

A

Secrete hormones that act locally

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3
Q

What do the autocrine secretions do

A

Affect the cell secreting the protein

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4
Q

What is the pituitary gland

A

Situated in the sella turica
Weighs ~ 1g
Consists of two parts: Anterior and posterior
75% anterior lobe adenohypophysis formed by outpouching of the oral cavity (Rathke’s pouch)
25% posterior lobe neurohypophysis- down growth of the hypothalamus

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5
Q

What does the Aden-hypophysis produce

A 
Prolactin
Adenocorticotropic
growth hormone
Thyroid stimulating hormone
Follicle stimulating hormone
Luteinsing
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6
Q

What does the neurohypophysis produce

A

Oxytocin

Antidiuretic peptide

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7
Q

What are the causes of hypo function in the anterior pituitary

A 
Vascular - infarction
Inflammation - granulomatous
Trauma
Autoimmune - Pituitary autoimmune disease
Metabolic
Infection
Neoplasia - non-secretory adenoma, metastatic carcinoma
D3 - doctors
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8
Q

What are the types of anterior pituitary adenomas and how do they present

A

Prolactinoma (galactorrhoea, menstrual disturbance)
Growth hormone secreting (gigantism in children, acromegaly in adults)
ACTH secreting (Cushing’s syndrome)

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9
Q

What is the anatomy of the thyroid gland

A

Bilobed organ joined by an isthmus encased in thin fibrous capsule
~18g in male, ~15g in female
Located at the level of 5th - 7th vertebra
Leans on the thyroid cartilage
Recurrent laryngeal nerve located in the tracheo-oesophageal groove

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10
Q

How does Hashimoto’s present

A 
Autoimmune chronic inflammatory disorder 
Chronic lymphocytic thyroiditis
F>M
Peak age is 59 years
Hypothyroid
Diffusely enlarged non-tender gland
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11
Q

What is Grave’s disease

A 
An autoimmune process
Diffuse hyperplasia of the follicular epithelium
Causes 80% of hyperthyroidism 
F>M
Peak in third and fourth decades
Symptoms: Pretibial myxoedema, hair loss, wide-eyed stare or proptosis, tachycardia, hyperactive reflexes
Enlarged thyroid
T3 and T4 elevated, TSH suppressed
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12
Q

What are hormones

A

Messenger molecules secreted by endocrine glands
They circulate and influence other tissues
Produce long and short term changes in various cells
Can only influence cells that have specific target receptors for that particular hormone

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13
Q

What are three types of hormone and some examples of each type

A 
Peptide hormones (PTH, ACTH, TSH)
Steroid hormones (testosterone, oestradiol, cortisol)
Tyrosine-based hormones (thyroxine T4, Triiodothyronine T3)
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14
Q

What are the three ways that a steroid hormone can interact with a cell

A

The classical model
Receptor-mediated endocytosis
Signalling through cell-surface receptors

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15
Q

What is the classical model of steroid hormone interaction

A

The steroid hormone dissociates from its plasma carrier protein and diffuses across the cell membrane
After gaining entry to the cell, the free hormone binds to an intracellular receptor and alters gene transcription

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16
Q

What is receptor mediated endocytosis type of steroid hormone interaction

A

The steroid hormone, bound to its plasma carrier protein, is Brough into the cell via a cell surface receptor. The complex is broken down inside lysosome and free steroid hormone diffuses into the cell where it subsequently exerts its action at the genomic level or undergoes metabolism

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17
Q

What is signalling through cell-surface receptors type of steroid hormone interaction

A

The free steroid hormone alters intracellular signalling by binding to cell-surface receptors. The steroid hormone could exert these effects directly or could alter signalling by blocking the actions of peptide hormones

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18
Q

What effect does thyroxine-binding globulin have on thyroid function test interpretation

A

Only the free inbound forms are physiologically active. If the level of TBG changes this results in a change in the level of the free hormones. Therefore, measurement of total hormone levels can be misleading

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19
Q

What are causes of abnormal TBG conc

A

Increased:

  • Genetic causes
  • Pregnancy
  • Oestrogens

Decreased:

  • Genetic causes
  • Protein losing states
  • Malnutrition
  • Malabsorption
  • Acromegaly
  • Cushing’s disease
  • High dose corticosteroids
  • Sever illness
  • Androgens
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20
Q

How often should TFTs be repeated

A

Healthy: 3 years

Hyperthyroid:

  • 1-2 months after radioactive iodine, if patient remains thyrotoxic then biochemical monitoring to continue at 4-6 week intervals
  • Following thyroidectomy for Graves’ disease and commencement of levothroxine, serum TSH to be measured 6-8 weeks post-op

Hypothyroidism -monitoring treatment

  • The minimum period to achieve stable conc after a change of dose of thyroxine is 2 months and TFTs should not normally be assessed before this period has elapsed
  • Patients stabilised on longterm thyroxine therapy should have serum TSH checked annually
  • An annual fT4 should be performed in all patients with secondary hypothyroidism
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21
Q

What are the two main types of immunoassay used in clinical chemistry

A

Immunometric assays

Competitive immunoassays

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22
Q

What are the 2 types of adrenal medullary tumours

A

Phaeochromocytoma (adults)

Neuroblastoma (children)

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23
Q

What is a phaeochromocytoma

A

Tumour of neuroendocrine chromaffin cells, the majority in the adrenal medulla

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24
Q

What are the clinical features of phaeochromocytoma

A

Excessive and often episodic release of catecholamines may result in paroxysmal features:

  • Hypertension
  • sweating
  • panic attacks
  • headaches
  • abdominal pain
  • Sometimes nothing!
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25
Q

What follow up tests are done on those with suspected phaeochromocytoma

A 
Clonidine suppression test
Plasma chromogranin A
MRI or CT of adrenals
MIBG scan, especially to detect extra-adrenal phaeochromocytomas or metastases
Genetic counselling or screening
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26
Q

What are the clinical features of Cushing’s

A 
Obesity: moon face, central deposits, lump between shoulder blades
Skin: thin, purple striae, easy bruising
Hypertension
Glucose intolerance
Menstrual disturbances
Thin limbs/muscle weakness
Back pain due to osteoporosis 
Psychiatric disturbances (depression, psychosis)
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27
Q

What is ectopic ACTH secretion most commonly associated with

A 
Benign carcinoid tumours of the lungs 
Small cell tumours of the lungs
Islet cell tumours of the pancreas
Medullary carcinoma of the thyroid
Tumours of the thymus gland
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28
Q

What is diabetes

A

Group of disorder characterised by hyperglycaemia (high blood glucose)
Caused by lack of insulin or reduced action of insulin

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29
Q

Which islet cells produce which substance

A

Alpha cells: glucagon
Beta cells: insulin
Delta cells: somatostatin
F cell: pancreatic polypeptide

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30
Q

What is insulin

A

Soluble protein made of an alpha chain and a beta chain

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31
Q

What are the diagnostic readings for diabetes

A

Fasting glucose: >7mmol/l
Random glucose: >11.1mmol/l
Two hours reading post OGTT> 11.1mmol/l
HbA1c >48mmol/mol

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32
Q

What is HbA1c

A

Reflects average plasma glucose over the previous 8-12 weeks
Diabetes: >48mmol/mol
Pre-diabetes:>41 and <48 mol/mol

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33
Q

What are the types of diabetes

A 
Type 1
Type 2
Gestational
Specific types due to:
-Genetics
-Endocrinopathies
-Disease of the exocrine pancreas
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34
Q

What is type 1 diabetes

A

Autoimmune destruction of insulin producing beta cells in the islet of langerhans
Can occur at any age but peaks around puberty

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35
Q

What are the risk factors for type 1 diabetes

A

Family history
Perinatal factors - low birth weight
Viral infections
Diet - cows milk

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36
Q

How does type 1 diabetes present

A 
Rapid onset (often few weeks)
Weight loss and osmotic symptoms and low energy
Abdominal pain
Often slim
Presents as diabetic ketoacidosis
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37
Q

How is type 1 diabetes managed

A

Insulin injections

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38
Q

How does type 2 diabetes present

A 
Often overweight
Symptoms present over a few months
Minimal weight loss
Complications:
-vision loss
-foot ulcers
-fungal infection
In state of hyperosmolar hyperglycaemia state
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39
Q

How is type 2 diabetes managed

A

Lifestyle:

  • exercise
  • diet and weight loss

Oral therapy:

  • metformin (first line)
  • DDp4 inhibitor, SGLT-2 inhibitor, GLP-1 agonist, sulphonylureas
  • Up to three agents

Insulin:

  • Once daily
  • multiple injections
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40
Q

What is gestational diabetes

A

Diabetes in pregnancy
New and not present prior to pregnancy
Hyperglycaemia first detected in pregnancy
Fasting glucose>5.6mmol/l or 2 hours plasma glucose level of 7.8mmol/l

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41
Q

How is gestational diabetes diagnosed

A

Oral glucose tolerance test

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42
Q

When is gestational diabetes checked in pregnancy

A

12 weeks

If normal repeat at 24 to 28 weeks

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43
Q

What are the risk factors for gestational diabetes

A 
BMI>30
Previous macrosomic baby
Previous gestational diabetes
FH of diabetes
Ethnic minority
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44
Q

Why is gestational diabetes important

A 
Short term:
Macrosomia
Pre-eclampsia
Stillbirth
Neonatal morbidity

Long term:
Obesity (child)
Development of Type 2 diabetes (mother)

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45
Q

How is gestational diabetes managed

A

Diet (if mild)
Limited oral option (metformin or glibenclamide)
Majority require insulin (only during pregnancy)

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46
Q

What is MODY

A

Maturity onset diabetes of the young
Clinically heterogenous disorder characterised by noninsulin-dependent diabetes diagnosed <25 years with autosomal dominant transmission and lack of autoantibodies

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47
Q

What are the causes of secondary diabetes

A

Essentially any condition that damages pancreatic organ:

  • Pancreatitis (gallstones, alcohol)
  • Pancreatectomy (for cancer, trauma
  • Cystic fibrosis
  • Haemochromotosis
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48
Q

What causes drug induced diabetes

A

High dose and prolonged steroid use
Atypical anti-psychotics
Immunotherapy (nivolumab used in melanoma treatment)
Protease inhibitor (used in HIV treatment)

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49
Q

Which endocrinopathies can cause diabetes

A

Cushings syndromes
Acromegaly
Somatostatin secreting tumours (somatostatinoma)
Glucagon secreting tumours (glucagonoma)

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50
Q

What are counter regulatory hormones

A 
Hormones which usually oppose action of insulin
Secreted as a result of stress response
-Glucagon
-Epinephrine/norepinephrine
-Glucocorticoid
-Growth hormone
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51
Q

What stimulates insulin release

A 
Glucose
Fatty acid and ketones
Vagal nerve stimulation
Gut hormones
Drugs (diabetes medication
Prostaglandins
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52
Q

What stimulates inhibition of insulin release

A 
Sympathetic stimulation
Alpha adrenergic agents (adrenaline)
Beta blockers
Dopamine
Serotonin
Somatostatin
53
Q

What is glucagon

A

Polypeptide of 29 amino acids that is rapidly degraded in the tissues (especially in the liver and kidney)

54
Q

What stimulates glucagon release

A 
Amino acids
Beta adrenergic stimulation
Fasting, hypoglycaemia 
Exercise
Cortisol
55
Q

What stimulates inhibition of glucagon release

A 
Glucose
Somatostatin
Free fatty acids
Ketones
Insulin
56
Q

What are the actions of glucagon

A
  • Increase secretion of insulin and growth hormone
  • Reduces intestinal motility and gastric acid secretion
  • Increase glucose levels through:
  • -glycogenolysis
  • -gluconeogenesis
  • -lipolysis
57
Q

What is a multinodular goitre

A

Enlargement of thyroid ± modularity
Most are euthyroid
Large dominant nodules may be mistaken clinically for thyroid carcinoma
Compressive symptoms

58
Q

What is a follicular adenoma

A

Benign encapsulated tumour with evidence of follicular cell differentiation
Females>males
Wide age range, usually fifth to sixth decade
Pailess, chronic
Solitary
Cold nodule on radioactive iodine imaging

59
Q

What is the commonest type of thyroid carcinoma

A

Papillary carcinoma

60
Q

What is papillary carcinoma

A 
Familial autosomal dominant non-medullary thyroid carcinoma
FAP
Cowden's syndrome
Therapeutic irradiation
Radiation exposure
61
Q

How does papillary carcinoma appear macroscopically

A

Ill defined, infiltrative
Some encapsulated
May be cystic
Granular

62
Q

What are types of follicular neoplasms

A

Follicular adenoma
Follicular carcinoma
Hurthle cell neoplasms
Ras mutations

63
Q

What are the clinical behaviours of Hurthle cell carcinoma

A 
Significant incidence of cervical lymph node metastases
Common haematogenous sites:
-bone
-liver
-lung
64
Q

What is primary hyperparathyroidism

A

Excessive secretion of parathyroid hormone form one of more glands

65
Q

What is secondary hyperparathyroidism

A

Hyperplasia of glads with elevated PTH in response to hypocalcaemia:
-renal insufficiency, malabsorption, vitamin D deficiency

66
Q

What is tertiary hyperparathyroidism

A

In association with longstanding secondary hyperparathyroidism

67
Q

What are the hyperparathyroidism signs

A 
Painful bones (classically osteitis fibres cystica)
Renal stones (kidney stones -> renal failure)
Abdominal groans (GI symptoms of nausea, vomiting, constipation, indigestion
Psychiatric moans (lethargy, fatigue, memory loss, psychosis, depression)
68
Q

What is parathyroid adenoma

A

An encapsulated benign neoplasm of parathyroid cells
Symptoms of hypercalcaemia
Association with MEN1 and MEN2 syndrome and hyperparathyroidism and jaw tumour syndrome
Single enlarged parathyroid gland with remaining glans suppressed and small

69
Q

What are the features of secondary and tertiary hyperparathyroidism

A

Non-neoplastic increase in parathyroid parenchymal cell mass within all parathyroid tissue with a known stimulus
Common in patients with renal failure and on dialysis
Identical pathologic features to primary hyperplasia and may be associated with massive gland enlargement

70
Q

What is parathyroid carcinoma and how is it treated and what is the prognosis

A

Malignant tumour derived from parathyroid parenchymal cells
Treated with surgery
50% 10 year survival

71
Q

What are the causes of Cushing’s syndrome

A

Exogenous: excessive glucocorticoid medication

Endogenous causes: adrenal cortical tumours, adrenal cortical hyperplasia and ACTH secreting pituitary adenoma

72
Q

What are the signs and symptoms of Cushing’s syndorme

A 
Hypertension
Moon face
Central obesity 
Buffalo hump
Weak muscles
Osteoporosis
Insomnia 
Excess sweating
Mood swings 
Headaches 
Chronic fatigue
Women may have increase hard growth (hirsutism) and irregular menstruation
73
Q

What is Conn’s syndrome

A

Hyperaldosteronism
Excess production of the hormone aldosterone leading to low renin levels
Primary: adrenal cortical hyperplasia, adenoma and familial hyperaldosteronism
Secondary: low circulating volume or poor renal circulation

74
Q

What are the symptoms of Conn’s syndrome

A 
High BP
Headache
Muscular weakness
Muscle spasms
Cardiac arrhythmia
Excessive urination
75
Q

What is Addison’s disease

A

Adrenal cortical insufficiency
Primary: adrenal dysgenesis, adrenal destruction, autoimmune adrenalitis, TB
Secondary: failure ACTH secretion
High mortality if not diagnosed

76
Q

What makes up the Addison’s disease triad

A

Hyperpigmentation
Postural hypotension
Hyponatraemia

77
Q

How is Addison’s disease treated

A

Long term steroid replacement

78
Q

What is adrenal cortical nodule and who is at greatest risk

A

Benign non-functional nodules of adrenal cortex

Elderly, hypotensive and diabetic patients

79
Q

What are the symptoms of adrenal cortical adenoma

A

Benign neoplastic proliferation of adrenal cortical tissue
Symptoms related to endocrine hyperfucntion:
-Aldosterone-producing tumours cause Conn’s syndrome
-Cortisol producing tumours cause Cushing’s syndrome
-Rare tumours cause virilisation

80
Q

What is adrenal cortical carcinoma

A 
Malignant counterpart adrenal cortical adenoma
Symptoms related to hormone excess
Abdominal mass
5 year survival about 70%
-prognosis is age and stage dependent
81
Q

What is phaeochromocytoma

A

Catecholamine-secreting tumour arising from adrenal medulla

82
Q

What is the phaeochromocytoma rule of 10s

A 
10% bilateral
10% extra-adrenal
10% malignant 
10% familial
10% in children
83
Q

What are the symptoms of phaeochromocytoma

A

Symptoms of hypertension, palpitations, headaches, anxiety

Elevated urine catecholamines, adrenaline, noradrenaline

84
Q

What are the two layers of bone

A

Cortical bone: hard outer layer

Trabecular bone: spongy inner layer

85
Q

How is bone composed

A

Cells:

  • bone forming cells
  • bone resorbing cells
  • bone co-ordinating cells

Extracellular:

  • Organic matrix (30%)
    • mainly collagen (osteoid)
    • ground substance
  • Inorganic components (70%)
    • hydroxyapatite (calcium and phosphate)
    • Minerals (magnesium, sodium, potassium)
86
Q

What is the role of osteoblasts

A

Creates and repairs new bone

87
Q

What is the role of osteoclasts

A

Breakdown old bone

88
Q

What is remodelling of normal bone

A

In a constant state of turnover caused by resorption by osteoclasts and formation osteoblasts
Adult skeleton is replaced every 10 years

89
Q

How is bone disease investigated

A 
Gross structure: Xray, MRI, CT
Bone mass (calcium): DEXA
Cellular function/turnover: biochemistry
Microstructure/ cellular function: biopsy, qCT
90
Q

What is bone alkaline phosphatase

A 
Phosphatase involved in mineralisation
Released by osteoblasts
Release is stimulated by increased bone remodelling:
-Childhood/ pubertal growth spurt
-Fractures
-Hyperparathyroidism
--primary 
--secondary
-Pagets disease of the bone
91
Q

What is P1NP

A

Procollagen type 1N propeptied

  • Synthesised by osteoblasts
    • precursor molecule of type 1 collagen
  • Has low diurnal and intra-individual variation
  • Serum conc not affects by food intake
  • Increased with increased osteoblast activity
  • Decreased by reduced osteoblast activity
92
Q

What are collagen cross-links

A 
NTX, CTX
Cross-linking molecules which are released with bone resorption, correlate highly with bone resorption
Increased in periods of high bone turnover:
-hyperthyroidism
-adolescents
-menopause
Have diurnal variation
Do not predict bone mineral density
Decrease with anti-resorptive therapy
93
Q

What are bone markers

A

Collagen-related markers are based primarily on type 1 collagen, which is widely distributed in several tissues

Changed in bone markers are not disease specific but reflect alterations in skeletal metabolism

Some markers are characterised by significant intra-individual variability

94
Q

What are the uses of new bone markers

A

Evaluation of bone turnover and bone loss
Evaluation of treatment effect (CTX used to monitor response to anti-resorptive therapy)
Evaluation of adherence with medication (P1NP used to monitor compliance with teriparatide; CTX used to monitor compliance/ response to anti-resorptive therapy)

95
Q

What do the T-scores mean

A

-1 and above: normal bone density
Between -1 and -2.5: osteopenia (low bone mass)
-2.5 and below: osteoporosis

96
Q

What are the bone disorders

A 
Metastatic disease
Hyperparathyroidism
Osteomalacia/ Rickets
Osteoporosis 
Paget's disease
97
Q

What is osteoporosis

A

Decreased bone mass and deranged bone micro architecture resulting in failure of structural integrity

A systemic skeletal disease characterised by low bone mass and micro architectural deterioration of bone tissue, with consequence increase in bone fragility and susceptibility to fracture

98
Q

What are the common risk factors for osteoporosis

A
  • ageing

- gluccorticoids

99
Q

How is osteoporosis detected and managed

A

No abnormalities seen in routine biochemical tests
Diagnosis relies on DEXA/ Xray
Increasing use of bone markers in management

100
Q

What is a fragility fracture

A

A fracture caused by injury that would insufficient to fracture a normal bone

A fracture that occurs as a result of minimal trauma such as a fall from a standing height or less, or no identifiable trauma

101
Q

What are common sites of fragility fracture

A

Spine
Neck of femur
Wrist

102
Q

What are the risk factors for fracture

A 
Age
Sex
Recent fragility fracture
Vertebral fractures (number and severity)
Smoking 
Alcohol 
Falls
Drugs
Inflammatory conditions
Malabsorption
T1 DM
Family history 
BMI
103
Q

What is the mechanism of action of bisphosphonates

A

Mimic pyrophosphate structure
Taken up by skeleton
Ingested by osteoclasts
Inhibit osteoclast formation, migration and osteolytic activity, promote apoptosis

104
Q

What are bone metastases and the types

A

Common in several malignancies

Lytic:

  • destruction of normal bone (osteoclasts)
  • breast/ lung
  • kidney/ thyroid

Sclerotic/ osteoblastic

  • deposition of new bone
  • prostate
  • lymphoma
  • breast/ lung

Usual sites of spread:

  • Spine, pelvis femur
  • Humerus, skull
105
Q

What are the presenting symptoms of bone metastases

A

Pain:

  • often worse at night and gets better with movement initially
  • usually becomes constant

Broken bones:

  • pathological fractures
  • commonly femur, humerus, vertebral

Numbness, paralysis, trouble urinating:
-spinal cord compression from bone metastases

Loss of appetite, nausea, thirst, confusion, fatigue:
-symptoms of hypercalcaemia

Anaemia:
-disruption of bone marrow

106
Q

What are the symptoms of hypercalcaemia

A

Mild:

  • polyuria, polydipsia
  • Mood disturbance
  • Anorexia
  • Nausea
  • Fatigue
  • Constipation

Sever:

  • abdominal pain
  • vomiting
  • coma
  • pancreatitis
  • dehydration
  • cardiac arrhythmias
107
Q

What are the causes of hypercalacaemia

A 
Malignancy
Primary hyperparathyroidism
Medications
Vit D excess
Hyperthyroidism
Bone disease/ immobilisation
108
Q

What is PTH

A

Parathyroid hormone
Secreted by chief cells of parathyroid gland
Polypeptide containing 84 amino acids

109
Q

How do the types of hyperparathyroidism present

A

Primary:

  • Calcium usually high
  • PTH inappropriately high
  • Low phosphate and high alk phos common
  • Causes are sporadic or familial

Secondary:

  • Calcium normal or low
  • PTH appropriately high
  • Phosphate high if due to chronic kidney disease
  • Causes are mainly CKD or vit D deficiency

Tertiary:

  • Calcium usually high
  • PTH inappropriately high
  • Phosphate can be high or low
  • Causes: after prolonged secondary HPT, usually in CKD
110
Q

What is Paget’s disease of bone

A 
Rapid bone turnover and formation
Leading to abnormal bone remodelling
Mainly over 50yo
>male
Genetic and environmental triggers
FH in 10-15% of cases
Polyostotic or monostotic
Elevated alkaline phosphatase reflecting increased bone turnover
111
Q

What are the clinical features of Paget’s disease

A

Bone pain
Bone deformity
Fractures
Arthritis
Cranial nerve defects if skull affected (hearing and vision loss)
Risk of osteosarcoma
Most commonly affects pelvis, femur and lower lumbar vertebrae

112
Q

What is osetomalacia

A

Lack of mineralisation of bone
Adult form: widened osteoid seams with lack of mineralisation
Classic childhood rickets: widened epiphyses and poor skeletal growth

113
Q

What are the causes of osteomalacia

A

Insufficient calcium absorption from intestine:
-due to lack of dietary calcium or vitamin D deficiency/ resistance

Excessive renal phosphate excretion:
-Rare genetic forms (hereditary hypophosphataemic rickets)

114
Q

What are the clinical features of osteomalacia

A

Diffuse bone pains (usually symmetrical)
Muscle weakness
Bone weakness
High alk phos, low vit D, possibly low calcium and high PTH (secondary hyperparathyroidism)

115
Q

Who’s is at greatest risk of osteomalacia

A

Adult population at risk:

  • nursing home residents/ elderly
  • asian population (hijab/ burka wearing)
  • malabsorption
116
Q

Why is calcium physiologically important and structurally important

A 
Physiologically:
Blood clotting
Muscle contraction
Neuronal excitation
Enzyme activity (Na/K ATPase, hexokinase etc)
Structurally:
Hydroxyapatite Ca10(PO4)6(OH)2 is the predominant mineral in bone
117
Q

How is adjusted Ca calculated

A

Adjusted Ca = Total Ca + [(40 - Alb) x 0.025]
Reference range for adjusted calcium 2.2-2.6 mmol/L
Equation is not valid if albumin <20g/L

118
Q

Why is phosphate physiologically important

A

The P in ATP - our fuel!
Intracellular signalling
Cellular metabolic processes eg glycolysis

119
Q

Why is phosphate structurally important

A

Backbone of DNA
Component of hydroxyapatite (Ca10(PO4)6(OH)2)
Membrane phospholipids

120
Q

What results from deficiency of phosphate

A

Sever deficiency can be fatal

121
Q

How is homeostasis of calcium regulated

A

Two key controlling factors:

  • Parathyroid hormone (PTH)
  • Vit D and matabolites

Balance of:

  • GI uptake
  • Bone storage
  • Renal clearance
122
Q

What factors affect vit D level

A 
Season
Latitude
Climate
Clothing
Use of sunscreen
Time spent indoors and outdoors
Skin tone
Age
Diet
Body fat and BMI
Malabsorption
123
Q

what are the regulators of calcium and phosphate homeostasis

A 
PTH
Vit D
FGF23
Calcitonin
Oestrogen
124
Q

What are the signs and symptoms of hypocalcaemia

A 
Tetany
Paraesthesia in the extremities
Cramps
Convulsions
Psychosis
125
Q

Why is magnesium physiologically and structurally important

A

Physiological:

  • Cofactor for ATP
  • Neuromuscular excitability
  • Enzymatic function
  • Regulates ion channels

Structural:
-comprises 0.5-1% of bone matrix

126
Q

How is the homeostasis of magnesium controlled

A

Predominantly by the kidneys

127
Q

What are the causes of magnesium depletion

A

Inadequate intake
Renal loss
GI loss
Redistribution into cells

128
Q

What are the signs and symptoms of magnesium depletion

A

Neuromuscular hyperexcitability (tremor, tetany, convulsions), muscle weakness
CNS- depression, psychosis
Cardio- ECG changes, reduced contractility, arrhythmia
GI- nausea and anorexia
Biochemical consequences: hypokalaemia, hypocalcaemia, with associated signs and symptoms

Y2 Clinical Pathology (11 decks)

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