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BDS2 BAMS > Pituitary and Thyroid > Flashcards

Pituitary and Thyroid Flashcards

1
Q

what is an endocrine disease

A

dysfunction of hormone secreting gland

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2
Q

what controls hormone secretion

A

negative feedback regulation

More hormone secretes less hormone is allowed to be secreted
Switches off secretion to keep blood level at same level

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3
Q

what is the spread of hormones

A

widespread
multisystem

(unlike nerve)

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4
Q

where is hormone effect determined

A

where receptors are located

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5
Q

what are the 2 types of endocrine failure

A

gland failure (primary)

control failure (secondary)

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6
Q

what is primary endocrine faillure

A

gland failure

gland can make but not being asked to

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7
Q

what is secondary endocrine failure

A

control failure

gland cannot make

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8
Q

multiple endocrine neoplasia is

A

Tumour or cancers in one gland are prone to getting different endocrine tumour/cancer in other glands

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9
Q

where is the pituitary gland

A

in the sella turcica in the skull

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10
Q

what is the function of the pituitary gland

A

controls many other gland activities

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11
Q

what controls the pituitary gland

A

hypothalamic control - releasing hormones

Triggers other hormones for other body functions – fire to particular areas particular glands, trigger other pathways

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12
Q

4 anterior pituitary hormones

A

TSH - Thyroid Stimulating Hormone

ACTH - Adrenocorticotrophic Hormone
Encourage adrenal gland to make cortisol

GH - Growth Hormone

LH, FSH, Prolactin

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13
Q

2 posterior pituitary hormones

A

ADH - Anti Diuretic Hormone
diabetes insipidus
control of body fluids – concentrate urine

Oxytocin

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14
Q

how is the pituitary gland controlled

A

Controlled by a mixture of endocrine and neurogenic stimuli

Hypothalamus – allows messenger hormones to pass to pituitary to venous plexus to

Tumour in pituitary gland
- cannot grow in size as in bony space
- Squash gland – so cannot make other hormones
Tends to be multi system disease

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15
Q

what type are pituitary tumours

A

adenomas

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16
Q

are pituitary tumours benign or malignant mainly

A

benign

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17
Q

functional adenoma

A

make hormone as well as being tumour

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18
Q

functional adenoma of prolactin/ACTH above 40 yrs causes

A

Amenorrhoea-Galctorrhoea syndrome or Cushing’s disease

Producing excess ACTH

Not switched off by normal feedback as tumour don’t respond to normal trigger

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19
Q

functional adenoma of growth hormone above 40 yrs causes

A

Acromegaly

Growth hormone in excess

Stop growth agree – nose, ears, forehead, fingers, feet

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20
Q

non functional adenoma

A

squash gland but doesn’t make hormones, space occupying

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21
Q

non functional adenoma effect above 60 yrs

A

Mass effects - visual field defects, other hormone deficiencies

Gradually spread out of sella turcica

  • Pushes on brain above – optic chiasm (eye nerves cross – affect vision, particular peripheral end up with tunnel vision)
  • –Take out nasal fields from both eyes so only get lateral field
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22
Q

how to remove a pituitary tumour

A

Transsphenoidal surgery to remove tumour

  • Through nose
  • Remove most of tumour and pressure easily
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23
Q

what happens if a child lacks growth hormone

A

Growth failure in children

reduced height (not dwarf but child like – correct proportions but small)

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24
Q

what happens if an adult lacks growth hormone

A

increased fat
reduced vitality

not really notice to same extent as fully grown,

causes subtle changes, anabolic, build body up – maintain blood sugar, fat levels

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25
Q

what happens is there is excess growth hormone in a child

A

giantism’ in children

Apparent – child very large but correct proportion (giantism)

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26
Q

giantism

A

excess growth hormone in a child
giantism’ in children

child very large but correct proportion (giantism)

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27
Q

what happens if there is excess growth hormone in an adult

A

Acromegaly in Adult

all stopped growth plates cannot change (limbs, spine) but membranous bone can continue to grow (skull thicker, hand and feet bigger, mandible will get bigger (dentures don’t fit, teeth become spaced), and so will soft tissue)

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28
Q

how to assess Growth hormone levels

A

measure IGF-1
(insulin like growth factor 1)

and compare to old photographs

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29
Q

what type of onset does acromegaly have

A

insidious

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30
Q

what is the peak incidence for acromegaly

A

30-50yrs

can take 10-15 yrs till changes obvious enough

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31
Q

what is a possible cause of acromegaly

A

benign pituitary tumour (functional adenoma)

  • MEN-1
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32
Q

what are general presenting features of acromegaly

A

coarse features

enlarged supra-orbital ridges

Broad nose, thickened lips & soft tissues

enlarged hands
- carpal tunnel syndrome - finger numbness,

Type 2 diabetes mellitus

  • insulin resistance from increased GH
  • Raise blood sugar in growth hormone
  • Can get type 2 diabetes
  • Fighting against insulin trying to reduce blood sugar

Cardiovascular disease

  • ischaemic heart disease
  • —Heart will increase in size and become less efficient
  • acromegalic cardiomyopathy
  • —-Acromegalic – heart muscle changed in size and function so inefficient

Change in lipid balance in blood

Enlarged tongue
- Bite and catch on teeth

Interdental spacing

‘shrunk’ dentures

Reverse overbite

  • Becomes class 3
  • Wear facets don’t make sense in occlusion

Visual field defects
- III, IV and VI nerve palsies possible as well

Hyperprolactinaemia
- Prolactin tumour

Hypopituitarism
- not making other hormones to right level (ACH, FSH and LH – upset menstrual cycle)

reduced life span

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33
Q

what is acromegalic cardiomyopathy

A

heart muscle changed in size and function so inefficient

34
Q

excess thyroid

A

hyperthyroidism

35
Q

deficiency in thyroid

A

hypothyroidism (a.k.a. Myxoedema)

36
Q

what is the common cause for hyperthyroidism

A

primary (gland failure)

secondary is rare
thyrotoxicosis without hyperthyroidism is different

37
Q

what is the common cause for hypothyroidism

A

primary (gland failure)

secondary less common

38
Q

myxoedema is

A

hypothyroidism (deficient)

39
Q

Graves disease

A

autoimmune disease that causes 70-80% cases in hyperthyroidism

40
Q

how does graves disease cause hyperthyroidism

A

Auto antibodies stimulating the TSH receptor

  • Immune system making hormone (protein) which fits receptor for TSH on thyroid gland
  • So makes more thyroid hormone

Gets exercised and increase in size gland – Goitre

Control still working fine
- But no chance to take effect as been overridden by TSH receptor activation

41
Q

2 classes of tumours in pituitary gland that can cause excess thyroid

A

Toxic multi-nodular goitre

Toxic adenoma

42
Q

effects of hyperthyroidism

A

Increased metabolism
- Makes metabolism run too fast

hot & excess sweating,

weight loss

diarrhoea

Lower blood sugar quicker

palpitations

  • Tachycardia and atrial fibrillation
  • Lost normal rhythm
  • Increased BP and heart failure
  • Tendency for heart failure - extra oxygen demand will worsen

muscle weakness

irritable/manic/anxious
- brain excitable

Eye retraction and lid lag
- eyelid is further back as muscle more excited can see white layer of sclera above eyelid

43
Q

where is the thyroid gland

A

at the base of the neck

44
Q

characteristic sign of Grave’s disease

A

diffuse goitre

45
Q

what chemical is needed for thyroid hormones

A

Need iodine for thyroid hormones

- Gland increases in size if low iodine so increases blood flow so more chance for blood to be caught

46
Q

organ specific autoimmune diseases

A

run in families
- if have one more likely to have another, genetically coded

vitiligo, PA, Type 1 DM, Coeliac, Myaesthenia gravis, Graves disease

47
Q

non thyroid effects of Graves disease

A

Opthalmopthy (Swelling in soft tissue around eye)

  • Fat cells in orbit
  • Antibody triggers inflammation– get red, hot swollen fat cells in orbit
  • Volume to increases
  • Pushes eyeball out of socket
  • Inflammation around eye
  • Same antibody causing graves’ disease
  • Scleral injection
  • Propotosis
  • Periorbital oedema

Conjunctival oedema
- chemosis

48
Q

how to treat graves disease

A

Block thyroid hormone effect

Will not improve eye – caused by antibody causing high thyroid levels
- Only way to stop is by stopping immune reaction is steroid

49
Q

7 primary causes of hypothyroidism

A

Autoimmune (Hashimoto’s) thyroiditis (90% cases!)

  • Organ specific
  • Gland eaten away by immune cells in inflammatory process

Idiopathic atrophy

Radioiodine treatment/thyroidectomy surgery
- iodine concentrated in gland and causes cell damage when alpha released, goes over active to normal to underactive with age

Iodine deficiency

Drugs
- carbimazole, amiodarone, lithium

congenital

  • gland not going to work
  • tested when born
  • can lead to developmental problems

Take off too much gland if hyperthyroidism excessively treated

50
Q

secondary causes of hypothyroidism

A

hypothalamic/ pituitary disease

- tumours squashing cells making TSH

51
Q

effects of hyperthyroisim

A

Reduced metabolism

  • tired
  • bradycardia, hyperlipidaemia

cold intolerance

weight gain

constipation

hoarse voice

goitre (Hashimoto’s)
- as gland inflamed and attacked by immune system

puffed face & extremities

angina

‘slow’, poor memory,
- psychiatric or confusion

hair loss
- common lateral 1/3 of eyebrow

dry coarse skin

delayed reflexes

52
Q

what is myxoedema

A

Swelling within the tissue caused by hypothyroidism

- Often in leg

53
Q

hashimoto’s thyroiditis effects

A

Middle aged and elderly women
- Presents at later age but start young

Idiopathic atrophy
- Can lead to loss of gland

54
Q

2 presenting features of Hashimoto’s thyroiditis

A

Goitre

Hypothyroid features

55
Q

associations of Hashimoto’s thyroiditis

A

All familial auto immune diseases (few exception) effect women more than men
- Vitiligo, PA, Type 1 DM, Addison’s disease

Down’s syndrome

56
Q

idiopathic atrophy of thyroid gland incidence

A

Increased incidence with age

10x more in females

likely autoimmune cause

  • lymphocyte infiltrate
  • associated with organ specific autoimmune disease
57
Q

effect of idiopathic atrophy of gland

A

loss of gland

58
Q

3 investigations for thyroid disease

A

Blood
- TSH,T3 &T4

Imaging

  • ultrasound scan (cysts)
  • radioisotope scans - gland uptake

Tissue
- fine needle aspirate/biopsy (FNA & FNB)
FNB take some gland cells out via need
- Quick biopsy without surgery

59
Q

TSH

A

thyroid stimulating hormone from anterior pituitary

60
Q

blood investigation for thyroid disease

A

TSH, T3 and T4

61
Q

2 imaging investigations for thyroid disease

A
  • ultrasound scan (cysts)

- radioisotope scans - gland uptake

62
Q

tissue investigation for thyroid disease

A

fine needle aspirate/biopsy (FNA & FNB)

FNB take some gland cells out via need
- Quick biopsy without surgery

63
Q

how to read radioisotope scans

A

To see if gland is working carry out a radioisotope scan
- radioactive concentrated in gland see if taken out of blood and back in

Normal gland makes hormone – brighter colour

Missing part
- Lobe on both sides – left missing part – tumour or cyst not producing hormone
Goitre
- Non functional as no hormone release

So much hormone in small area pituitary switched off TSH production but tumour is still making excess (functional adenoma)
- Hyperthyroid due to one tumour

64
Q

investigation results for hyperthyroid pituitary cause

A

T3 and TSH raised

rare (primary??)

65
Q

investigation results for hyperthyroid graves disease causes

A

Stimulation of gland not from pituitary
- TSH is low

But T3 still high
- as auto antibody signalling

common (Secondary??)

66
Q

investigation results for hypothyroid pituitary cause

A

Not asking to make thyroxin

TSH and T4 are low

rare (Secondary??)

67
Q

investigation results for hypothyroid gland failure causes

A

Negative feedback to make more thyroxin

TSH high
- but gland being destroyed by disease so cannot cause effect

T4 low

common (primary??)

68
Q

5 types of hyperthyroidism treatment

A 
Carbimazole 
- titration 
block & replace - T4 as required 
- Drug blocks effect of hormone 
- Make hormone less effective 
- Take back to normal and be less effected

β-blockers

  • treat effects of hyperthyroidism
  • —anxiety, increased BP

Radioiodine - 131I
- hypothyroid risk with time - review!

Surgery - partial thyroidectomy
- usually follows drug therapy to stabilise

Graves’ ophthalmopathy

  • Graves disease- largest causes
  • —Ophthalmopathy not fixed as caused by antibody not hormone – harder
69
Q

carbimazole drug treatment of hyperthyroidism

A 
- titration 
block & replace - T4 as required 
- Drug blocks effect of hormone 
- Make hormone less effective 
- Take back to normal and be less effected
70
Q

treatment of hypothyroidism

A 
Give hormone (T4 tablets)
- Hormone replacement therapy – return physiology to normal

Increase dose slowly

  • IHD
  • Slowly over 6 month – as heart and metabolic tissues need to adapt
  • –increase metabolic rate – diet pills (get effects hyperthyroidism)

Recheck using TSH as a guide if gland failure
- TSH will reduce to normal level – can use to tell when normal placement

71
Q

how to assess if successful hypothyroidism treatment

A

Recheck using TSH as a guide if gland failure

- TSH will reduce to normal level – can use to tell when normal placement

72
Q

why does hormone replacement therapy for hypothyroidism need to be gradual

A

Increase dose slowly
- IHD

Slowly over 6 month – as heart and metabolic tissues need to adapt
—increase metabolic rate – diet pills (get effects hyperthyroidism)

73
Q

2 causes of thyroid enlargement

A

Goitre

Solitary nodule enlargement

74
Q

solitary nodule enlargement of thyroid

A
  • adenoma, carcinoma, cyst formation possible

- low cancer risk – suspicious/more in children or elderly

75
Q

goitre of thyroid

A

Diffuse enlargement of the thyroid gland – often Iodine deficient
—-mountainous areas of developing countries

diffuse, nodular

Drug related?

76
Q

thyroid cancer

A

Usually with a thyroid swelling

Young or Elderly

  • papillary (80%) or folicular in younger
  • undifferentiated in elderly

‘Cold’ nodules on radioisotope scans

often TSH sensitive - give T4 post surgery

generally a good prognosis in young

  • 5% 10 year mortality in Papillary but
  • 80% 10 year mortality in Folicular

new treatments available

77
Q

hyperthyroid impact on dental care

A

High energy – hard to be seated, state may not be best for making decisions on treatment

pain anxiety and psychiatric problems

caution for treatment until controlled
- Can do emergency treatment whilst waiting to settle

78
Q

hypothyroid impact on dental care

A

avoid the use of sedatives if severe

79
Q

treated thyroid problem or on hormone replacement therapy

A

treat patient as normal

80
Q

what is the dentist’s role in goitre detection

A

Goitre detectable to the dentist

If find goitre in examination refer to GP immediately

BDS2 BAMS (54 decks)

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