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Physiology for Anaesthetists > Endocrine - Thyroid, parathyroid and adrenal > Flashcards

Endocrine - Thyroid, parathyroid and adrenal Flashcards

1
Q

What are the proportions of T3 and T4 secreted by the thyroid gland

A

T3 - 10%

T4 - 90%

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2
Q

Compare the half lives of T3 and T4

A

T3 - 24 hours

T4 - 7 days

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3
Q

Compare the protein binding of T3 and T4 in blood. What is the purpose of this protein binding

A

T3 - Albumin (99.7% bound)
T4 - thyroglobulin

Provide a large reservoir of thyroid hormone which delays onset of symptoms of hypothyroidism

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4
Q

How much T4 is converted to T3 and what is the rest of T4 converted into

A

50% T4 converted to T3

50% T4 converted to rT3 (reverse T3) –> inactive hormone

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5
Q

How does tri-iodothyronine (T3) exerts its effect

A

Diffuses across cell membranes to reach the cell nucleus where it regulates gene transcription

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6
Q

Which tissues are not affected by triiodothyronine

A

Thyroid

spleen

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7
Q

What are the effects on metabolism of hypo and hyperthyroidism

A

Hyperthyroidism

  • -> Increased BMR
  • -> Increased Lipolysis
  • -> increased gluconeogenesis
  • -> increased avaiability of ffas and glucose

Opposite in hypothyroidism

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8
Q

How does T3 affect growth

A

Hypothyroidism in childhood causes growth retardation

It stimulates neuronal myelination and nerve axon growth (CNS)

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9
Q

How does hyperthyroidism affect the respiratory system

A

Increased O2 consumption and CO2 production –> increased Ve

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10
Q

How does hyperthyroidism affect the CVS

A

Increased T3 –> increased number of B-adrenergic receptors in the heart –> increased HR and contractility and therefor CO

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11
Q

How does hypo and hyperthyroidism influence the CNS

A

Hypothyroidism –> depressed mood and psychosis

Hyperthyroidism –>Anxiety

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12
Q

How does hyperthyroidism affect the muscles

A

T3 induces protein catabolism of proximal muscles leading proximal myopathy

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13
Q

Describe the microanatomy of the thyroud

A

Multiple follicles interspersed with parafollicular C cells and endothelial cells.

A follicle contains follicular cells arranged in a sphere surrounding a core of thyroglobulin or ‘colloid’

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14
Q

Draw a diagram and describe the mechanism of thyroid hormone synthesis

A

Page 393 Chambers

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15
Q

How is Iodide transported from the capillary into the follicular lumen

A

I- is transported via the Na+/I- cotransporter into the follicular cell after which it diffuses into the follicular lumen

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16
Q

What happens to Iodide once it is in the follicular lumen

A

TSH stimulates thyroid peroxidase using H2O2 to oxidise it into more reactive Iodine (I2).

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17
Q

What happens to I2 (Iodine) in the follicular lumen>

A

I2 bings to tyrosine residues on the thyroglobulin molecule forming mono-iodotyrosine MIT (One iodine binds) and Di-iodotyrosine DIT (Two iodines bind)

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18
Q

How are T3 and T4 formed and released into circulation

A

Oxidative coupling promoted by TSH in the follicular lumen creates T3 (MIT + DIT) and T4 (DIT + DIT) which are endocytosed linked to throglobulin by follicular cells (TSH). The T3 and T4 are then removed from thyroglobulin and released into circulation.

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19
Q

How long can the thyroid glands store of T3 and T4 meet the bodies requirements

A

1 - 3 months

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20
Q

Descirbe the hypothalmo-pituitary-thyroid axis

A

TRH –> + TSH –> (T4) + T3 –> - TRH –> - TSH

Only unbound T3 can inhibit hypothalamus

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21
Q

What is the most common cause of hypothyroidism. Describe the pathophysiology

A

Hashimotos thyroidisits –> autoimmune attache of thyroid peroxidase (I- –> I2) or thyroglobulin –> Reduced T3 and T4 secretion –> increased TRH and TSH

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22
Q

What is the most common cause of hyperthyroidism. Describe the pathophysiology

A

Graves disease: autoimmune antibodies that bind to and active the TSH (or thyrotropin) receptor on the thyroid leading to autonomous production of T3 and T4 –> decreased TRH and hence TSH

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23
Q

Describe and classify the clinical effects of Grave’s disease

A 
EFFECTS DUE TO HYPERTHYROIDISM
Symptoms
- palpitations
- heat intolerance
- weight loss
- fine tremor
- diarrhoea
- Excessive sweating

Signs

  • Tachycardia
  • Atrial Fibrillation
  • Lit lag
  • Goitre

EFFECTS DUE TO AUTOANTIBODIES

  1. Exophthmalmos
  2. Proptosis
  3. Conjunctivitis
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24
Q

Describe the three treatment options in hyperthyroidism

A
  1. Treat hyperadrenergism (beta blockade)
    - Atenalol 25 - 50 mg daily up to 200 mg daily to get HR < 90 if BP allows
  2. Thionamides (inhibit thyroid peroxidase and conversion Iodide to Iodine) –> prevent T3/T4 synthesis: both oxidation of I- and oxidative coupling (thyroid peroxidase)
    - Methimazole
    - Propylthiouracil
    - Carbimazole
  3. Radioiondine
    - -> I- is concentrated by the thyroid gland
    - -> likewise 131 I is concentrated (radioactive)
    - -> Beta - radiation emtted causes damage and necrosis of thyroid tissue
  4. Surgery
    - -> total thyroidectomy
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25
Q

What is the mechanism of action of thionamides

A

Methimazole
Propylthiouracil
Carbimazole

MOA:

  1. Inhibit thyroid peroxidase
    - -> Inhibit conversion of iodide to iodine (I2) –> No MIT/DIt formation
    - -> reduced oxidative coupling of MIT and DIT –> reduced T3/T4 synthesis

Propylthiouracil only:
2. Inhibit peripheral conversion of T4 to T3

NB these drugs:

  1. Do not inactivate T3 and T4 stores in the peripheral blood and thyroid
  2. Do not interfere with replacement (exogenous) thyroid hormones
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26
Q

Do the thionamides inactivate peripheral and thyroid stores of T4 and T3

A

No

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27
Q

Do the thionamides interfere with replacement (exogenous) thyroid hormones

A

No

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28
Q

What are the risks associated with total thyroidectomy

A

Recurrent laryngeal nerve palsy
Parathyroid gland damage
Postoperative hematoma –> airway obstruction

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29
Q

How is orbitopathy of Graves disease treated

A
  1. Corticosteroids

2. Surgical debulking

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30
Q

Why should a CT scan be ordered prior to thyroid surgery

A

To identify compression of surrounding structures

  1. Trachea - stridor
  2. SVC obstruction - Syncope
  3. Sympathetic chain (Horner’s - Ptosis/Miosis/Anhidrosis
  4. Recurrent laryngeal nerve (Hoarse voice)
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31
Q

What are the options for airway management in a severely compressed trachea

A
  1. Gas induction
  2. Awake flexible scope endotracheal intubation
  3. Tracheostomy under local anaesthesia
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32
Q

If recurrent laryngeal nerve monitoring is used –> what are the implications and why is this done

A

To determine bilateral RLN injury and requirement of tracheostomy prior to extibation. Its on some specialized ETT tubes the electrodes of which is carefully placed between the cords during endotracheal intubation

Muscle Relaxants can’t be used. So Reminfentanyl infusion is commonly used

33
Q

List the postoperative complications of Thyroid surgery

A
  1. Haemorrhage –> rapid airway obstruction (remove clips compress and back to theatre)
  2. Recurrent Laryngeal nerve palsy (if bilateral –> complete vocal cord paralysis –> tracheostomy)
  3. Severe hypocalcaemia –> damaged parathyroid glands –> severe hypocalcaemia may cause laryngospasm.
  4. Tracheomalacia
    - -> Flaccid tracheal cartilage which collapses on inspiration especially in patients with long standing goitres. (Deflate ETT cuff prior to extubation to check for air leak.
34
Q

Explain the mechanism for Trousseau’s and Chvostek’s sign

A

Hypocalcaemia

Calcium is integral to the normal function of the cell membrane Na+ channels. Hypocalcaemia BRINGS THE THRESHOLD POTENTIAL NEARE TO RMP resulting in more likely spontaneous depolarization of neurons –> tetany and paraesthesias.

35
Q

List the physiological functions of calcium

A
  1. Structure - bones
  2. Haemostasis (Essential cofactor)
  3. RMP (Threshold)
  4. Neurotransmitter release (exocytosis)
  5. Excitation-contraction coupling (actin-myosin)
  6. Cell signalling (2nd messenger)
36
Q

Describe the distribution (%) of calcium in the body

A

Bone –> 99%
Teeth and soft tissue –> 1%
ECF –> 0.1 % ( 1/3 of this in the plasma)

37
Q

What percentage of plasma calcium is free in the active ionized form

A

45% (1.1 - 1.4 mmol/L)

total plasma calcium range: 2.2 - 2.6 mmol/L

38
Q

How is ionized calcium affected by changes in albumin

A

Its unchanged

39
Q

What is the formula for corrected calcium

A

Corrected Ca = Measure Ca + 0.02(40 - serum ALB)

Ca (mmol/L)
ALB (g/L)

Each 1 g/L decrease in serum ALB leads to a decrease in plasma Ca by 0.02 mmol/L

40
Q

Logically, how can plasma Calcium levels be altered

A
  1. Increased/Decrease GIT absorption
  2. Increase/Decrease Renal excretion
  3. Movement of Ca between body compartments
41
Q

Name the hormones involved in Calcium homeostasis

A
  1. Parathyroid hormone –> increase Ca
  2. Vitamin D –> increase Ca
  3. Calcitonin –> Decrease Ca
42
Q

Where are the parathyroid glands located

A

There are four of them located on the posterior surface of the thyroid gland

43
Q

What stimulates the secretion of PTH from the parathyroid glands?

A

Fall in plasma Calcium concentration

44
Q

Describe the action of parathyroid hormone

A
  1. GIT (indirect effect)
    - upregulates renal enzyme 1 alpha-hydroxylase –> increased activatoin of Vitamin D –> increased GIT absorption of Ca and PO4
  2. Kidneys
    - Increase Ca absorption
    - Decrease PO4 absorption
  3. Bone
    - Stimulate osteoclasts to resorb bone –> released stored Ca
45
Q

Describe the synthesis of vitamin D. What is the rate limiting step and what controls this rate limiting step?

A

Vitamin D is a steroid hormone

SKIN
7- dehydrocholesterol –> UV light –> cholecalciferol

DIET
Absorption of cholecalciferol (Vitamin D3)

LIVER
Cholecalciferol –> 25 hydroxylase –> Calcidiol (25 hydroxycholecalciferol)

KIDNEY
Calcidiol –> 1 alpha hydroxylase –> Calcitriol (1,25 hydroxycholecalciferol) This is the biologically active form of Vitamin D.

The rate limiting step is the action of 1 alpha hydroxylase (kidney). PTH controls the activity of 1 alpha hydroxylase and therefore PTH controls the plasma concentration of active vitamin D

46
Q

Describe the actions of 1,25 hydroxycholecalciferol = Calcitriol = Active vitamin D

A
  1. GIT
    - Increased absorption of Ca and PO4
  2. Kidney
    - Increased absorption of Ca and PO4
47
Q

Describe the secretion of calcitonin

A

Secreted by the parafollicular C cells of the thyroid gland. Secreted when total plasma calcium is above 2.4 mmol/L

48
Q

Describe calcitonin’s role in Calcium homeostasis

A

Minor role.
Only secreted when Total Plasma Calcium > 2.4 mmol/L.

DECREASES plasma calcium by

  1. GIT
    - decreases absorption of Ca and PO4
  2. Kidneys
    - decrease reabsorption of Ca and PO4
    - decreases activity 1 - alpha - hydroxylase (decrease active Vit D)
  3. Bone
    - decrease osteoclast activity –> decreased bone resoprtion
49
Q

What unexpected effect does PTH have with regards to phosphate homeostasis and explain the effect of this on plasma calcium concentration.

A

Unlike, 1,25 hydroxycholicalciferol (active vit D), PTH causes reduced PO4 reabsorption in the proximal convoluted tubule in the kidney.

Reduced plasma phosphate –> reduced formation with calcium with insoluble salts –> increased free ionized calcium.

50
Q

What hormones apart from PTH, Vit D and calcitonin have an impact on calcium homeostasis

A

Gonadal steroids –> increase bone density
Corticosteroids –> decrease bone density
GH –> increase bone density

and hence all affect calcium homeostasis

51
Q

Summarise the endocrine response to hypocalcaemia

A

Low calcium sensed by parathyroid glands. PTH release. PTH –> increased GIT absorption Calcium and increased renal reabsorption calcium. PTH also increase the rate of activation of Vitamin D. Vitamin D also has the same effect as PTH on Ca absorption in the kidneys and GIT. PTH leads to bone resorption and Vit D leads to bone calcification so the effect on bone is negligible.

52
Q

Summarise the endocrine response to hypercalcaemia

A

High calcium sensed by PTH glands. Reduced PTH reduced Ca absorption kidneys and GIT. Reduced rate of activation vitamin D. Reduced Ca absorption kidneys and GIT.

Also calcitonin is released from parafollicular C cells

Overall effect is reduced Vit D absorption GIT, reabsorption kidney.

53
Q

Where does 25 hydroxylation of vitamin D occur

A

The liver

54
Q

Where does 1 alpha hydroxylation of Vitamin D occur

A

The kidneys

55
Q

Explain the mechanism of renal osteodystrophy and how is it treated

A

CKD –> reduced 1 alpha hydroxylation of Vitamin D –> Reduced activated Vitamin D and hypocalcaemia results. PTH secretion increases which results in extensive demineralization of bone as Calcium is redistributed to the ECF.

Rx: Supplemental activated vit D = Calcitriol (1,25 hydroxycholecalciferol)

56
Q

Explain the mechanism of bone disease in cirrhosis (chronic liver disease)

A

More complex than in CKD

  1. Alcoholism is associated with dietary Ca deficiency
  2. Haemochromatosis is complicated by gonadal failure –> osteoporosis
  3. Severe liver dysfunction –> impaired 25 hydroxylation of vit d therefore –> deficient active vit D
57
Q

What vertebral level are the adrenals

A

T12

58
Q

Describe the anatomy of the adrenals

A 
ADRENAL CORTEX
(mnemonic is GFR)
Zona glomerulosa (mineralocorticoid)
Zona fasciculata (glucocorticoid)
Zona reticularis (androgens)

ADRENAL MEDULLA
Modified sympathetic ganglion innervated by T5-T9 pre-ganglionic sympathetic neurons.
–> SNS + –> chromaffin cells release granules containing
1. Adrenalin (80%)
2. Noradrenalin (20%)

59
Q

What is the name of the cells in the adrenal medulla that release adrenalin

A

chromaffin cells

60
Q

What are the names of the weak andorgens secreted by the Zone Reticularis of the adrenal cortex and what is the fate of these hormones

A

Androstenedione
dehydroepiandrosterone

Converted to testosterone by peripheral tissues

61
Q

What % of mineralocorticoid activity is contributed by aldosterone. What contributes the remainder

A

Aldosterone 95%

Cortisol 5%

62
Q

What are the four triggers for aldosterone secretion

A
  1. Angiotensin II (RAAS)
  2. Hyperkalaemia –> directly triggers renal cortex to release aldosterone
  3. Acidaemia –> directly triggers renal cortex to release aldosterone
  4. ACTH (main role is for the release of cortisol)
63
Q

Summarise the functions of cortisol

A

METABOLIC

  • -> increase plasma [glucose]
    1. Gluconeogenesis stimulated
    2. Amino acids mobilized from skeletal muscle
    3. Accelerated lipolysis –> glycerol used in gluconeo
    4. Reduced peripheral glucose utilization

CARDIOVASCULAR

  1. Increased vasculature sensitivity catecholamines
  2. Increased plasma volume (mineralocorticoid)
64
Q

What additional effects does cortisol have in chronic excess (e.g. Cushings)

A
  1. Osteoporosis
  2. Anti-inflammatory and immunosuppressive
  3. CNS –> euphoria, psychosis and memory loss
  4. Peptic ulceration
65
Q

Summarise the regulation of cortisol release

A

Diurnal pattern of CRH release by hypothalamus or increased release during times of physiological stress.

Hypothalamus –> CRH –> Anterior Pituitary –> ACTH –> Zona fasciculata (adrenal cortex) –> cortisol

Cortisol 90% bound by cortisol binding protein and albumin

Cortisol 10% unbound –> biologically active –> unbound cortisol inhibits hypothalamus from secreting CRH.

66
Q

What is the final step in the biosynthesis of cortisol and how does etomidate affect this

A

Final step: hydroxylation of 11-deoxycortiisol by the enzyme 11 - beta - hydroxylase.

This enzyme is reversibly inhibited by etomidate.

67
Q

Describe the structure of catecholamines

A

BENZENE RING with 2 OH- groups

AMINE side chain

68
Q

What are catecholamines derived from. What are the two possible sources for this molecule

A

Tyrosine

Sources

  1. diet
  2. hydroxylation of phenylalanine in the liver
69
Q

Where are catecholamines synthesized

A

In chromaffin cells in the adrenal medulla

70
Q

What is the rate limiting step of catecholamine synthesis

A

Conversion of tyrosine to L-DOPA

71
Q

Draw a diagram which describes synthesis and metabolism of catecholamines

A

See page 399 Chambers

72
Q

Why can’t adrenalin be synthesized at sympathetic nerve terminals

A

PNMT (Phenylethanolamine N-methyl Transferase) which converts adrenalin to Noradrenalin is only present in the Adrenal Medulla

73
Q

Is catecholamine controlled by a negative feedback loop?

How is secretion controlled>

A

No.
Stimuli (Exercise/trauma/pain/hypovolaemia/hypothermia/anxiety)

–> Hypothalamus increase SNS output –>AP’s in pre-ganglionic SNS nerves that terminate on chromaffin cells in the adrenal medulla. Acetylcholine is released at the terminal synapse.

–> Ach –> activates nicotinic receptors on chromaffin cell membrane –> increased membrane Na and K permeability –> net depolarization –> open voltage gated Ca channels –> influx Ca leads to exocytosis of the catecholamine containing granules –> exoctyosis of granules

74
Q

What are the physiological effects of adrenalin

A

METABOLIC

  • Adrenalin stimulates glycogenolysis
  • Adrenalin also increase release of ffa’s and aa’s from adipose tissue

HEART
- B1 receptors: inotropy and chronotropy

VASCULATURE

  • a1 vasoconstriction (peripheral tissues)
  • B2 vasodilation (skeletal muscle)

LUNGS
- B2 bronchodilatation

75
Q

What are the physiological effects of noradrenalin

A

METABOLIC

  • promotes gluconeogenesis
  • promotes lipolysis

VASCULATURE
- alpha 1 vasoconstriction with reflex bradycardia

CNS
- normal functioning

76
Q

What are the half lives of adrenalin and noradrenalin

A

both: 2 minutes

77
Q

How are adrenalin and noradrenalin metabolized

A

Both: sequentially metabolized by COMT and MAO

Catechol-O-methyltransferase = COMT

Monoamine Oxidase = MAO

Metanephrine and normetanephrine are intermediates of metabolism

Vanillylmandelic acid (VMA) is produced

78
Q

How is phaeochromocytoma often diagnosed with regard to catecholamine metabolism

A

Urinary metanephrine/ Vanillylmandelic acid levels

Physiology for Anaesthetists (61 decks)

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