ELFH: Endocrinology (Thyroid and Adrenal Glands) Flashcards

1
Q

How do hormones work when they arrive at their target?

A

Hormones act by binding to specific receptors either on the target cell surface or on a specific intra-cellular target.

As a result, the affected cell will initiate a series of intra cellular events that result in a response to the bound hormone.

Hormones can bind to many different cells e.g. thyroid hormones or to one specific cell, e.g. adrenal cortex.

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2
Q

How is the Endocrine System Controlled?

A

The hypothalamus is a recipient of sensory information relating to various conditions of the body e.g. appetite, thirst, temperature sleep, fear and sexual arousal.

As a consequence, it releases a series of ‘releasing factors’ (RFs) which reach the pituitary gland via vascular channels known as the portal system. These RFs will stimulate the release of a series of hormones.

The pituitary is divided into an anterior and posterior lobe.

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3
Q

What information does the hypothalamus receive?

A

appetite, thirst, temperature sleep, fear and sexual arousal

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4
Q

what does the hypothalamus send signals to?

A

pituitary gland

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5
Q

what do you call the vascular channels linking the hypothalamus to the pituitary gland called?

A

portal system

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6
Q
A
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7
Q

Hormones released form the anterior pituitary gland?

A

LH & FSH

TSH

GH

prolactin

ACTH

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8
Q

Hormones released by the posterior pituitary gland?

A

ADH

oxytocin

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9
Q

describe the general control of hormones?

A

Hormone release is generally controlled by a feedback mechanism. The release of the hormones from the pituitary will effect a release from the target cell e.g. thyroid hormones.

The target cell release will then negatively feedback on the pituitary to limit the release of the initial stimulating hormones.

This also implies that if the target cell releases less of its product, there will be less negative feedback and the pituitary will release more stimulating hormones!

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10
Q

2 main hormones released by the thyroid gland?

A

T4 and the biologically active form T3

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11
Q

what hormone stimulates the thyroid gland to release T4?

A

TRH

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12
Q

name hormones A, B, C &D

A

Their release is controlled by TSH which they normally negatively feedback.

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13
Q

what does T3 control?

A

They control tissue metabolic rate.

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14
Q

Common causes of hyperthyroidism?

A

Graves disease

toxic multi-nodular goitre

solitary nodule

inflammatory thyroiditis

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15
Q

Graves disease?

A

An autoimmune disease with the production of autoantibodies (IgG) which mimic the action of TSH and stimulate the thyroid to release thyroid hormones regardless of need.

Produces the exophthalmos and is associated with other autoimmune diseases

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16
Q

cause of primary hyperthyroidism?

A

graves disease

Toxic multi-nodular goitre: Nodules may be present for years but run the risk of becoming autonomous hormone releasing adenomas with age

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17
Q

cause of secondary hyperthyroidism?

A

benign tumour of the pituitary gland secretes excessive amounts TSH

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18
Q

Can you describe the clinical features of hyperthyroidism that you may pick up in the dental surgery?

A
  • Palpitations: Increased heart rate such as atrial fibrillation
  • Heart failure: Shortness of breath, orthopnoea, swollen peripheries, reduced exercise tolerance, loss of appetite and tiredness
  • Heat intolerance
  • Exophthalmos: Graves’ disease
  • Tremor: Shown by placing paper across the hands
  • Weakness of limb muscles: Proximal myopathy (where they struggle getting up from sitting position or going up stairs)
  • Goitre: Always look at and feel the neck
    (a swelling in your neck caused by an enlarged thyroid gland)
  • Warm peripheries, warm moist skin, intolerant to heat
  • Weight loss
  • Pretibial myxoedema: Raised purple red lesions on anterior shins
  • Clubbing: Thyroid acropachy
  • History of diarrhoea
  • redness on the palms of your hands.
  • loosening of your nails in their nail beds
  • hives
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19
Q

What blood tests would help you confirm the diagnosis of hyperthyroidism?

A
  • Tyroid Function Tests (TFTs): Raised T3 or T4
  • Thyroid Stimulating Hormone (TSH): Reduced serum TSH (beware rare cases of pituitary TSH adenoma where autonomous increase in release of TSH)
  • Autoantibody screen: Autoantibodies in Graves disease (anti- microsomal and anti-thyroglobulin)
  • Free T4 or T3
  • Thyroid binding globulin
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20
Q

3 main tx options for hyperthyroidism?

A

1) Drugs

  • Anti-thyroid drugs like carbimazole prevent the synthesis of thyroid hormone
  • Beta blockers can diminish some of the effects

2) Radioactive iodine

Iodine131 concentrates in the thyroid to destroy tissue (after the symptoms have been controlled with drugs).

3) Surgery

If medication fails and there are large goitres, then partial removal of the thyroid gland will be required. Full consent for potential damage to the recurrent laryngeal nerve and possible parathyroid function disturbance is required.

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21
Q

what is thyroid crisis?

A

A thyroid crisis is a catastrophic release of thyroid hormones leading to hyperpyrexia, tachycardia, severe restlessness and reduced levels of consciousness, coma and even death.

It can be precipitated by stress, infection, surgery and even radioactive iodine treatment.

A thyroid crisis is treated with carbimazole, propanolol, iodone and high doses of steroids.

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22
Q

What to do as a dentist if pt clearly hyperthyroid?

A

withhold tx as at risk of thyroid crisis

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23
Q

things to be aware of as a dentist and pt has hyperthyroidism?

A
  • Premature eruption of teeth in younger patients
  • A predilection to weakening of the oro-facial skeleton
  • Accelerated periodontal disease
  • Theoretical sensitivity to adrenaline in local anaesthetics
  • Those on drug treatment may demonstrate reduced wound healing and a predisposition to infection
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24
Q

common causes of hypothyroidism? (general)

A

Autoimmune (atrophic)

Hashimoto’s thyroiditis

Iatrogenic

Iodine deficiency

genetic

hypopituitarism

tumours

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25
Q

Autoimmune (atrophic) causes hypothyroidism?

A

Most common cause, lymphoid infiltration and anti-microsomal antibodies, leading to fibrosis and gland atrophy.

This is associated with other autoimmune diseases and is far more common in females.

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26
Q

Hashimoto’s thyroiditis causes hypothyroidism?

A

Autoimmune destruction with anti-microsomal antibodies which try to regenerate leading to nodule and goitre formation.

This is common in females who may be toxic before becoming hypothyroid.

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27
Q

iatrogenic cause of hypothyroidism?

A

Radioactive iodine or surgery will leave 45% of patients hypothyroid at some point

28
Q

iodine deficiency causes hypothyroidm?

A

Thyroid hormone synthesis demands supply of iodine to the gland and in certain areas such as South America, Alps and other mountainous regions.

29
Q

genetic causes of hypothyroidism?

A

Congenital absence of enzymes used in the synthesis of T3 and T4.

30
Q

Hypopituitarism causes hypothyroidism?

A

Rare but lesions here may reduce the release of TSH and other pituitary hormones.

31
Q

tumours cause hypothyroidism?

A

Extrinsic and intrinsic thyroid tumours may invade the substance of the gland and decrease function. Tumours may rarely also secrete hormones

32
Q

Can you describe the clinical features of hypothyroidism you may pick up in the dental surgery?

A

Mental slowness
Macroglossia
Dry, thin hair
Cannot stand the cold
Slow movements and thoughts
Depression
Deafness
Loss of outer eyebrows
Peri-orbital puffiness
Constipation
Deep voice (goitre)
Anaemia (macrocytic)
Cold peripheries
Slow reflexes
Bradycardia
Heart failure
Carpal tunnel syndrome
fatigue

33
Q

what will blood test revel for a pt with hypothyroidism?

A

Low serum-free T3 and T4
High TSH
Positive thyroid antibodies (autoimmune)

associated finding include:
- Macrocytic anaemia
- High cholesterol
- Hyponatraemia (fluid retention)

34
Q

Tx for hypothyroidism?

A

replacement of thyroid hormone with thyroxine supplements, with TSH and free T3 and T4 levels checked to ensure a steady state has been achieved.

35
Q

who may you be cautious giving thyroxine supplements to?

A

history of ischaemic heart disease as the increased heart response may put significant strain on the cardiac tissues.

36
Q

The dental practitioner should be aware of the following in patients with hypothyroidism…?

A
  • Children born with, or who develop the condition, are at risk of significant delayed eruption of teeth. There is also an increased risk of caries and periodontal disease
  • Macroglossia (Fig 1) should alert suspicions and associated taste abnormalities
  • Wound healing will be delayed after surgical events
  • Sedation may precipitate a coma in the poorly treated patient and must be avoided, as should the prescription of narcotic-type drugs such as codeine
  • Surgery and infections may also predispose to a coma onset
37
Q

what is shown here?

A

adrenal glands sit above the kidneys

38
Q

what is released from the adrenal external cortex?

39
Q

The adrenal external cortex is responsible for the release of three main steroids…?

A

Androgens (secondary sex hormones)

Mineralocorticoids, aldosterone (control the sodium and potassium levels)

Glucocorticoids, cortisol (affect glucose, sodium and potassium and immune function)

40
Q

androgens?

A

secondary sex hormones

41
Q

Mineralocorticoids?

A

aldosterone (control the sodium and potassium levels)

42
Q

Glucocorticoids?

A

cortisol (affect glucose, sodium and potassium and immune function)

43
Q

The adrenal internal medulla releases what?

A

Catecholamines (adrenaline and nor adrenaline)

44
Q

Why is there such an overlap in the function of some of the adrenal cortex products?

A

All three of the hormones are derived from cholesterol and the glucocorticoids share some features with the mineralocorticoids and the sex hormones, which can explain the side-effects of excess of these agents.

45
Q

the general role of the adrenal gland?

A

Metabolism (how your body transforms and manages energy from the food you eat)
Immune system
Blood pressure
Response to stress
Development of sexual characteristics

46
Q

The adrenal cortex is under control of individual influences, what are these?

A

aldosterone

ACTH

47
Q

What is the role of aldosterone?

A

Aldosterone is controlled by the renin-angiotenisn axis which is activated when afferent renal blood flow is determined to be low of pressure or volume (juxta glomerular apparatus).

The resultant angiotenisn II will stimulate the zona glomerulosa to release aldosterone which will encourage the re-absorption of sodium and hence water in the distal convoluted tubules.

Potassium is secreted in exchange to maintain electrochemical neutrality. Hence the urine will be more concentrated and more fluid is retained counteracting the initiating hypotension.

48
Q

what controls the release of cortisol?

A

ACTH released by the pituitary gland

In turn, this is controlled by CRF from the hypothalamus.

49
Q

role of ACTH in stimulating the adrenal cortex?

A

ATCH will stimulate the adrenal cortex to release cortisol in response to stress, surgery and infection. The cortisol will inhibit the ACTH release in a negative feedback fashion.

Cortisol will increase the release of glucose from stores and breakdown protein. This helps to deal with the events which have put the patient under threat. These are its glucocorticoid effects. But because of its structural similarity to the mineralocorticoids, it will also promote sodium and fluid retention

50
Q

primary Addison’s is associated with what endocrine disease?

A

adrenal insufficiency

51
Q

what disease causes primary adrenal insufficiency?

A

Addison’s disease

52
Q

what is primary Addison’s disease?

A

arises 80% of the time due to autoimmune destruction of the adrenal cortex. Rare causes are surgery, TB and haemorrhage.

It is associated with other autoimmune diseases such as Graves’, Hashimoto’s and pernicious anaemia.

53
Q

secondary Addison’s disease?

A

Secondary Addison’s is due to failure of the pituitary gland to secrete ACTH.

54
Q

Clinical features of Addison’s include what?

A
  • Weight loss, lethargy and depression
  • Postural hypotension (low sodium retention and thus hypovolaemia)
  • Dehydration
  • Pigmentation of mucosal surfaces (Back to Fig 1), scars and creases. ACTH levels are accompanied by increased MSH secretion
  • Loss of body hair in women due to loss of androgens
  • Addisonian crisis
55
Q

what will blood tests revel in primary Addison’s disease?

A
  • ACTH raised
  • Hyponatraemia
  • Hyperkalaemia
  • Adrenal autoantibodies
  • Confirmed by short synacten test (synthetic ACTH administered and the cortisol levels fail to rise). If the levels rise then the cause is likely to be secondary
56
Q

what will blood tests show in secondary Addison’s disease?

A
  • ACTH raised
  • Hyponatraemia
  • Hyperkalaemia
  • Adrenal autoantibodies
  • Confirmed by short synacten test (synthetic ACTH administered and the cortisol levels fail to rise). If the levels rise then the cause is likely to be secondary
  • As above, but ACTH levels reduced thus no pigmentation changes
  • Look for pituitary problems or patients taking long term steroids inhibiting their own ACTH release
57
Q

tx for Addison’s disease?

A

If the diagnosis is made then patients will require lifelong glucocorticoid (hydrocortisone) and mineralocorticoid (fludrocortisone) replacement.

58
Q

pt with Addison’s disease (adrenal insufficiency), what is the challenge for the dental practitioner?

A

taking long term steroids, e.g. transplant patients, inflammatory bowel disease and rheumatoid arthritis patients.

Their ACTH levels will be reduced and theoretically when they are stressed by surgery, infection etc. they are unable to respond accordingly.

59
Q

disease shown?

A

Pigmentation present in Addison’s disease

60
Q

pt with Addison’s disease, does dental tx carry risk of promoting adrenal crisis?

A

no risk and thus no extra precautions should be taken

61
Q

syndrome associated with overactive adrenal gland?

A

cushing’s syndrome

62
Q

what is cushing’ syndrome?

A

Cushing’s syndrome (Fig 1) arises due to overproduction of cortisol, either by the adrenal cortex or due to exogenous drug taking.

Cushing’s disease is due to increased ACTH release from the anterior pituitary due usually to an adenoma or hyperplasia.

63
Q

What clinical features would be expected in patients suffering with Cushing’s?

A
  • Weight gain
  • Insomnia, depression occasional psychosis
  • Striae, easy bruising
  • Diabetes
  • Muscle weakness, proximal myopathy
  • Hypertension (sodium retention and hypervolaemia)
  • Acne and greasy skin, hirsutism (androgen like activity)
  • Moon face, buffalo hump and central obesity
  • Plethoric complexion
  • Diabetes
  • Poor wound healing and skin infections
  • Osteoporosis
64
Q

The diagnosis is made after clinical features have been recognised. It is confirmed by:

(cushing’s syndrome)

A
  • Raised cortisol levels
  • Dexamethasone suppression test (normal individuals will reduce the serum cortisol levels)
  • Low ACTH indicates adrenal is the site of the problem or exogenous steroid usage
  • High ACTH implies pituitary is the site of the problem (very rarely ectopic ACTH is the cause, e.g. lung cancer)
  • CT or MRI may show adenomas either in adrenal or the pituitary (Fig 1). Ectopic sources demand chest x-rays or body CT scanning
65
Q

tx for cushing’s syndrome?

A
  • Surgery
  • Inhibit cortisol synthesis, e.g. metyrapone or ketaconazole
  • Radiation to the pituitary if surgery is contraindicated
  • Reduce steroid dosage if due to exogenous drug treatment, in exchange for steroid sparing drugs
66
Q

how does cushing’s syndrome affect the dental practitioner?

A
  • Opportunistic infections
  • Diabetic changes
  • Poor wound healing after oral surgery
  • Beware high blood pressure and congestive cardiac issues.