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Y2 Endocrine Block > PBL 3: Thyroid Gland > Flashcards

PBL 3: Thyroid Gland Flashcards

1
Q

where is the thyroid gland located

A

located in anterior neck, between C5-T1

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2
Q

Thyroid gland is an _______ gland. It has two lobes, connected with a middle part called the _______

A

endocrine

isthmus

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3
Q

The thyroid gland sits behind the strap muscles. what are they called

A

sternohyoid

sternothyroid

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4
Q

where are the parathyroid glands found and how many do we have

A

found on the posterior aspect of the two lobes of the thyroid gland
4

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5
Q

the compartment is bound by the __________ fascia

A

pretracheal

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6
Q

what does the Parathyroid gland produce

A

PTH

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7
Q

what are the cell types in the parathyroid gland

A

chief cells
oxyphil cells
water clear

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8
Q

what are the hormones of thyroid gland stored in

A

stored in cavities, surrounded by secretory cells (follicular cells)

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9
Q

what is a thyroid follicle

A

Small spherical grouping of follicular cells
The outer spherical layer - follicular cells
The inner cavity- colloid core (glycoprotein)

see pics

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10
Q

What does the colloid core consist of?

A

Thyroglobulin- Thyroid hormone precursor proteins

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11
Q

where are the parafollicular/C cells found

A

in between the follicular cells

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12
Q

what do parafollicular/C cells secrete?

A

Calcitonin- Ca lowering hormone

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13
Q

what epithelium are follicular cells normally?

A

Simple cuboidal epithelium

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14
Q

What happens to thyroid follicle structure when stimulated to release T4/T3

A

Follicular Cells become columnar and lumen is depleted of colloid

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15
Q

What happens to thyroid follicle structure when suppressed

A

Follicular Cells appear flattened and colloid accumulates in the lumen

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16
Q

what is the arterial supply of the thyroid gland

A

Superior thyroid arteries- supplies anterior and superior portion
Inferior Thyroid arteries- supplies posterior and inferior portion

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17
Q

what is the venous drainage of the thyroid gland

A

venous plexus formed by superior, middle and inferior thyroid vein
Superior + middle- drains into internal jugular vein
Inferior- drains into brachiocephalic vein

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18
Q

what regulates thyroid hormone action

A

hypothalamic- pituitary-thyroid axis

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19
Q

what does the hypothalamus secrete and what effect does that hormone have on the anterior pituitary gland

A 
Secretes TRH (thyroid releasing hormone)
TRH acts on thyrotrophs cells in anterior pituitary gland to release TSH (thyroid stimulating hormone)
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20
Q

what effect does TSH have on the thyroid gland

A

TSH acts on the thyroid gland to cause synthesis and secretion of T3/T4

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21
Q

what sub-units does TSH have

A

alpha- same as FSH, LH and HCG

beta- unique

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22
Q

how does negative feedback work in TSH secretion?

A

if T3 and T4 levels high:

T3 and T4 negative feedbacks to hypothalamus and pituitary gland to inhibit TSH production

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23
Q

what happens in primary hypothyroidism and give example

primary- problem with main organ

A
  • Underproduction of T3/T4 due to abnormal thyroid gland
  • High TSH but low T3/T4
  • Hashimoto’s Thyroiditis
24
Q

what happens in secondary hypothyroidism

A
  • Underproduction of T3/T4 due to abnormal anterior pituitary gland
  • Low TSH and T3/4
  • Sheehan’s syndrome
25
Q

what happens in tertiary hypothyroidism

A
  • Underproduction of T3/T4 due to abnormal hypothalamus
  • Low T3/T4, variable TSH, Low TRH
  • RARE
26
Q

what molecule is neccesary for thyroid hormone synthesis

A

Iodine

27
Q

where is iodine found

how much iodine do our bodies need

A

seawater, fruit and vegetables

150-300 ug/day

28
Q

where is iodine deficiency prominent and what does it lead to

A

high altitudes

leads to endemic goitre (enlarged thyroid)

29
Q

Iodine is reduced to ______ and then absorbed in the _____

A

Iodide

GI tract

30
Q

Describe the first step in thyroid hormone biosynthesis

Iodine transport

A
  • Iodide transported into the follicular cells by Na/I active transporter against the chemical gradient from the basolateral membrane (energy required)
  • iodide then diffuses to apex of cells and is transported by the protein- PRENDERIN into vesicles fused with the apical cell membrane
31
Q

Describe the second step in thyroid hormone biosynthesis

organification

A
  • Oxidation of iodide to iodine occurs in the vesicles and it binds to tyrosine residues on Thyroglobulin- in the colloid (this process is called organification and catalysed by the enzyme thyroid peroxidase)
  • Iodine combines with tyrosine residues on thyroglobulin to form MIT or DIT
32
Q

Describe the third step in thyroid hormone biosynthesis (T3 and T4 formation)

A
  • Peroxidase then combines MIT+ DIT = T3 and DIT+DIT = T4. This takes place within the thyroglobulin proteins
  • peroxidase is more efficient at combining 2 DIT therefore there is more T4*
  • Endocytosis of thyroglobulin into follicular cells
  • The endocytosed thyroglobulin undergoes proteolysis (lysosyme) to release the T4 and T3.
  • T4 and T3 are transported out of the cell and into the circulation.
33
Q

T_ is more metabolically active than T_

A

3

4

34
Q

T_ released in greater amounts than T_

A

4

3

35
Q

How does T4 become T3

A

T4 in the periphery undergoes 5’deiodination to form T3

36
Q

how much of circulating thyroxine (T4) is free and bound

A

Free- 0.5%

Bound- 99.5%

37
Q

what is the importance of free Thyroxine

A
  • Free component is active and regulated, therefore, only free t4 is measured
  • Bound to thyroid binding globulin, transthyretin and albumin
38
Q

what is the active version of T and what does is bind to

A

T3 is the active version which binds to nuclear receptors

39
Q

what are the thyroid hormone action on skeletal, cardiovascular and metabolic system

A

Skeletal: bone turnover
Cardiovascular: heart rate
Metabolic: lipids and glucose

40
Q

what is the definition of Hyperthyroidism

A

Condition that occurs due to excessive production of thyroid hormone by thyroid gland

41
Q

what are the causes of hyperthyroidism

A

– Auto immune- Graves’ disease
– Toxic adenoma- benign tumour of thyroid gland
– Multinodular goitre- excess production of thyroxine (T4) without requiring stimulation from TSH
– Thyroiditis- inflammation of thyroid gland leading to excess production of thyroxine
– Excessive administration of thyroxine- use of thyroxine to lose weight

42
Q

what are the clinical features of Graves disease

A

1) Dysthyroid eye disease/ Graves’ Ophthalmopathy
- 50% of patients seen with this
- lid retraction and lid lag
- pre-orbital oedema (puffy eyes or swelling under eyes)
- proptosis (abnormal anterior protrusion of eyes)
- diplopia (double vision)
- optic nerve compression is rare

2) Dermopathy- Pretibial myxoedema
3) Thyroid acropachy- characterised by soft tissue swelling and finger clubbing

43
Q

what are the clinical features of Hyperthyroidism

A 
• Weight loss 
- Tachycardia
• Tremor 
- Hypertension
• Heat intolerance 
- Palpitations
• Diarrhoea 
- Sweating
44
Q

what are the treatment for Hyperthyroidism

A

Anti-thyroid drugs
Radioiodine therapy
Surgery

45
Q

what are the anti-thyroid drugs.

describe mechanism of action and adverse effects

A

1) Carbimazole
Inhibits action of thyroid peroxidase enzyme- reduces thyroid hormone production
Adverse effects:
- Aplasia cutis
- Rash
- Bone marrow suppression so causes agranulocytosis

2) Propylthiouracil
Inhibits thyroid peroxidase
Inhibits T4 to T3 conversion
watch LFTs

46
Q

How does radioiodine therapy work in treatment for Hyperthyroidism

A
  • Use if beta emission to destroy thyroid tissues
47
Q

what are the side effects of radioiodine therapy

A

may worsen eye disease - so need steroid cover
radiation risk
defer conception for 4 months
leads to hypothyroidism (main side effect)

48
Q

What is the surgery for Graves disease and what are the complications

A 
Removal of thyroid gland
Complications:
• Haemorrhage
• Rec laryngeal palsy- hoarse voice
• Permanent hypocalcaemia- damage to parathyroid glands
• Hypothyroidism
49
Q

what is the definition of hypothyroidism

A

Condition that occurs due to not enough production of thyroxine by thyroid gland

50
Q

what are the causes of hypothyroidism

A

Primary- pathology of thyroid gland

Severe iodine deficiency

Autoimmune thyroiditis (Hashimotos)

  • Destruction of the thyroid gland (anti TPO antibody)
  • May be positive family history, more common in females

Thyroiditis
- Viral and often painful

Iatrogenic

  • Thyroidectomy
  • Following radio iodine therapy
  • Drug-induced (Amiodarone, lithium, sunitinib)

Secondary- pathology of the pituitary gland
Pituitary disease
– Secondary hypothyroidism

51
Q

what are the clinical features of hypothyroidism

A 
– Depression
– Lethargy
– Weight gain
– Bradycardia
– Dry skin
– Constipation
– Cold intolerance
– Poor concentration
– Hoarseness
– Menorrhagia
– Coarse, thin hair
– Anaemia
– Slow relaxing reflexes
– May have goitre
52
Q

what is the treatment for hypothyroidism and what are the long-term goals

A

Levothyroxine

  • Generally need 1.7-2.0 micrograms / kg /day
  • Best taken on an empty stomach
  • Avoid taking with proton pump inhibitors, ferrous sulphate or calcium

Long term goals:
– Resolve symptoms and normalise TSH
– Full suppression of TSH associated with Atrial
fibrillation and osteoporosis

53
Q

what are the investigations for hypothyroidism

A

Measure
– Free T4
– TSH

• Primary hypothyroidism
– High TSH and low T4
• Secondary hypothyroidism
– Low TSH and low T4

54
Q

Thyroid cancer has good prognosis if cancer is differentiated. give examples of the differentiated cell

A
  • papillary
  • follicular
  • mixed
  • medullary carcinoma of thyroid
55
Q

thyroid cancer has poorer prognosis if cancer is undifferentiated. give examples of the undifferentiated cell

A
  • anaplastic

- small cell

Y2 Endocrine Block (21 decks)

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