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Endocrinology > week 3 > Flashcards

week 3 Flashcards

1
Q

define primary and secondary thyroid disease

A

primary = disease affecting thyroid itself (goitre or non-goitrous)

Secondary - Hypothalamic or pituitary disease (No thyroid gland pathology)

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2
Q

commonest cause of primary thyroid disease?

A

AI thyroid D most commonly

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3
Q

why are diabetes patients with poor glycemic control more prone to infection?

A

they are IC - high BG causes WBC to stop working as effectively

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4
Q

what thyroid hormones in inactive and when?

A

T4, always (free) until converted to T3

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5
Q

what are some thyroid hormones (TH)?

A

TSH - Thyroid stimulating hormone/thyrotropin.

T4 - thyroxine (80% of TH secreted)

T3 - triiodothyronine (remaining 20%)

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6
Q

how are T3/4 found in the body?

A

[>99%] bound to plasma proteins (TBG, albumin and pre-albumin)

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7
Q

what is TBG

A

Thyroxine-binding globulin

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8
Q

what is TSH release by and why?

A

thyrotroph cells in anterior pituitary in response to thyrotropin releasing hormone (TRH)

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9
Q

what does TSH levels reflect?

A

Reflects tissue thyroid hormone action

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10
Q

what is the Hypothalamic-pituitary-thyroid (HPT) axis

A

negative feedback system responsible for the regulation of metabolism..

senses low T3/T4 and releases TRH.

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11
Q

bloods/biochemical PC of primary hypothyroidism

A

Free T3/4 low

TSH high

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12
Q

bloods/biochemical PC of primary hyperthyroidism

A

Free T3/4 high

TSH low

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13
Q

bloods/biochemical PC of secondary hyperthyroidism

A 
Free T3/4 high
TSH high (or ‘normal’)
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14
Q

bloods/biochemical PC of secondary hypothyroidism

A 
Free T3/4 low
TSH low (or ‘normal’)
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15
Q

define hypothyroidism

A

in insufficient secretion of thyroid hormones from the thyroid gland

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16
Q

define Myxoedema

A

severe hypothyroidism and is a medical emergency

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17
Q

what is Pretibial myxoedema? why does it occur?

A

it’s a rare clinical sign of Graves’ disease, an autoimmune thyroid disease which results in hyperthyroidism

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18
Q

what are three risk factors for developing hypothyroidism

A

white ethnicity

female

area of high iodine intake

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19
Q

causes of primary hypothyroidism

A

Goitrous:

Chronic thyroiditis, (Hashimoto’s thyroiditis), Iodine deficiency

[Drug-induced (e.g. amiodarone, lithium), Maternally transmitted (e.g. antithyroid drugs), Hereditary biosynthetic defects]

Non-goitrous:

Atrophic thyroiditis

[Post-ablative therapy (e.g. radioiodine, surgery)
Post-radiotherapy (e.g. for lymphoma treatment)
Congenital developmental defect}

Self-limiting

[Following withdrawal of antithyroid drugs
Subacute thyroiditis with transient hypothyroidism
Post-partum thyroiditis]

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20
Q

what are the three commonest causes of primary hypothyroidism?

A

Chronic thyroiditis (Hashimoto’s thyroiditis)

Iodine deficiency

atrophic thyroiditis

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21
Q

what are the causes of secondary hypothyroidism?

A

Diseases of the hypothalamus and pituitary gland (multiple!):

[Infiltrative
Infectious
Malignant
Traumatic
Congenital
Cranial radiotherapy
Drug-induced…]
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22
Q

Chronic thyroiditis (Hashimoto’s thyroiditis): how common is it and what is it?

A

commonest cause of hypothyroidism in the Western world. (F>M, strong FHx)

Autoimmune destruction of thyroid gland and reduced thyroid hormone production

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23
Q

what is Hashimoto’s thyroiditis characterised by?

A

Antibodies against thyroid peroxidase (TPO)

T-cell infiltrate and inflammation microscopically

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24
Q

clinical features of Hypothyroidism? hair and skin

A

hair and skin = coarse/sparse hair, dull expressionless face, periorbital puffiness, pale skin cool and doughy to touch, vitiligo, hypercarotenaemia.

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25
Q

clinical features of Hypothyroidism? thermogenesis

A

intolerant to cold

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26
Q

clinical features of Hypothyroidism? fluid retention

A

pitting oedema

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27
Q

clinical features of Hypothyroidism? cardiac

A

Reduced heart rate
Cardiac dilatation
Pericardial effusion
Worsening of heart failure

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28
Q

clinical features of Hypothyroidism? metabolic

A

hyperlipidaemia.
decreases appetite
weight gain

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29
Q

clinical features of Hypothyroidism? GI

A

Constipation
(Megacolon and intestinal obstruction)
(Ascites)

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30
Q

clinical features of Hypothyroidism? resp?

A

Deep hoarse voice
Macroglossia (large tongue)
Obstructive sleep apnoea

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31
Q

clinical features of Hypothyroidism: neuro?

A 
Decreased intellectual and motor activities
Depression, psychosis, neuro-psychiatric
Muscle stiffness, cramps
Peripheral neuropathy
Prolongation of the tendon jerks
Carpal tunnel syndrome
(Cerebellar ataxia, encephalopathy)
Decreased visual acuity
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32
Q

clinical features of Hypothyroidism: reproductive?

A

Menorrhagia
Later oligo- or amenorrhoea
Hyperprolactinaemia - ↑TRH causes ↑ PRL secretion

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33
Q

lab investigations of primary hypothyroidism

A

↑TSH and ↓fT4/3 – cardinal abnormalities

Other abnormalities:
Macrocytosis (↑MCV)
↑Creatine kinase (CK)
↑LDL-cholesterol
Hyponatraemia -↓renal tubular water loss
Hyperprolactinaemia -↑TRH leads to ↑PRL (often mild)
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34
Q

diagnosis for AI hypothyroidism

A

anti-TPO antibody (anti-thyroglobulin)

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35
Q

management of hypothyroidism

A

thyroxine (levothyroxine) gradually until normal metabolic rate restored

check TSH 2 months after any dose change

once stabilised TSH should be checked 12-18 months

Secondary hypothyroidism: TSH unreliable (↓TSH production), Titrate dose of levothyroxine to the fT4 level

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36
Q

why must levothyroxine be given gradually?

A

Rapid restoration of metabolic rate may precipitate cardiac arrhythmias, also caution in Hx of IHD (lower dose, gradual).

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37
Q

drugs in management of hypothyroidism

A

levothyroxine mainly.

levothyroxine combination with T3 rarely given (some patients like as onset+ elimination quicker)

[take before breakfast without other medications]

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38
Q

pregnancy and hypothyroidism

A

inc dose 25%-50% of T4 (as there is inc in TBG)

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39
Q

myxoedema coma

A

elderly women with long standing but frequently unrecognised or untreated hypothyroidism

Mortality up to 60%

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40
Q

what findings are seen on myxoedema coma?

A

ECG: bradycardia, low voltage complexes, varying degrees of heart block, T wave inversion, prolongation of the QT interval
Type 2 respiratory failure: hypoxia, hypercarbia, respiratory acidosis
Co-existing adrenal failure is present in 10% of patients

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41
Q

treating myxoedema coma

A

ABCDE,
Passively rewarm: aim for a slow rise in body temperature
Cardiac monitoring for arrhythmias
Close monitoring of urine output, fluid balance, central venous pressure, blood sugars, oxygenation
Broad spectrum antibiotics
Thyroxine cautiously (hydrocortisone - adrenal failure)

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42
Q

define thyrotoxicosis

A

the clinical, physiological and biochemical state arising when the tissues are exposed to excess thyroid hormone

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43
Q

define hyperthyroidism

A

refers specifically to conditions in which overactivity of the thyroid gland leads to thyrotoxicosis

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44
Q

Thyrotoxicosis – symptoms and signs(cardiac)

A 
Palpitation, atrial fibrillation (AF)
Cardiac failure (very rare)
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45
Q

Thyrotoxicosis – symptoms and signs (sympathetic)

A

tremor

sweating

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46
Q

Thyrotoxicosis – symptoms and signs CNS

A

Anxiety, nervousness, irritability, sleep disturbance

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47
Q

Thyrotoxicosis – symptoms and signs GI

A

Frequent, loose bowel movements

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48
Q

Thyrotoxicosis – symptoms and signs -vision

A 
Lid retraction (not specific to Graves’)
Double vision (diplopia)
Proptosis (Graves)
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49
Q

Thyrotoxicosis – symptoms and signs (hair and skin)

A

Hair change – brittle, thin hair

Rapid fingernail growth

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50
Q

Thyrotoxicosis – symptoms and signs -reproductive

A

Menstrual cycle changes, including lighter bleeding and less frequent periods

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51
Q

Thyrotoxicosis – symptoms and signs muscles

A

Muscle weakness, especially in the thighs and upper arms

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52
Q

Thyrotoxicosis – symptoms and signs - metabolism + thermogenesis

A

weight loss and inc appetite

intolerance to heat

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53
Q

causes of thyrotoxicosis associated with hyperthyroidism

A

Excessive thyroid stimulation:
Graves’ disease
Hashitoxicosis
Thyrotropinoma (THSoma, very rare)
Thyroid cancer (only very rarely cause thyrotoxicosis)
Choriocarcinoma (trophoblast tumour secreting hCG)

Thyroid nodules with autonomous function:
Toxic solitary nodule
Toxic multinodular goitre

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54
Q

key causes of thyrotoxicosis associated with hyperthyroidism

A

Graves’ disease
Toxic solitary nodule
Toxic multinodular goitre

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55
Q

key causes of thyrotoxicosis not associated with hyperthyroidism

A

Subacute (de Quervain’s) thyroiditis

Post-partum thyroiditis

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56
Q

causes of thyrotoxicosis not associated with hyperthyroidism

A

Thyroid inflammation (thyroiditis):
Subacute (de Quervain’s) thyroiditis
Post-partum thyroiditis
Drug-induced thyroiditis (e.g. amiodarone)

Exogenous thyroid hormones:
Over-treatment with levothyroxine
Thyrotoxicosis factitia

Ectopic thyroid tissue:
Metastatic thyroid carcinoma
Struma ovarii (teratoma containing thyroid tissue)
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57
Q

Graves’ disease epidemiology

A

female, 20-50years, genetics susceptible (70%) and FHx in women strong. Smoking important.

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58
Q

Graves’ disease lab findings

A

↓TSH and ↑fT4/3 – cardinal abnormalities

Other abnormalities:
Hypercalcaemia and ↑Alkaline phosphatase
Reflective of increased bone turnover
Graves’ associated with osteoporosis
Leucopenia (↓white cell count)
Often mild and related to the disease rather than treatment (ATD-induced agranulocytosis)
TSH receptor antibody (TRAb)
No need to image thyroid gland if raised titre found
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59
Q

Graves’ disease diagnosis

A

TSH receptor antibody

anti-TPO of present (70-80% and 40% anti-thyroglobulin)

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60
Q

clinical sign specific to Graves’ disease

A

pretibial myxoedema
thyroid acropachy
thyroid bruit
graves’ eye-disease

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61
Q

graves’ ophthalmopathy/thyroid eye disease

A

smoking cessation important

TRAb driven pathophysiology

Most disease is mild but can be severe and sight-threatening (unilateral/bilateral. 20% get and 20% have before graves’ diagnosis)

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62
Q

treatment of graves eye disease

A

Mild disease treated with topically (e.g. lubricants)

More severe disease: steroids, radiotherapy (poor evidence base), surgery

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63
Q

nodular thyroid disease epidemology

A 
Older patients
More insidious onset
Thyroid may feel nodular
Asymmetrical goitre 
(smooth in Graves’)
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64
Q

tests for nodular thyroid disease

A

↑fT4/3, ↓TSH
Antibody negative (TRAb)
Scintigraphy: high uptake
Thyroid US

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65
Q

what is thyroid storm? common signs/sympotms? who is it commonly seen in?

A

Medical emergency, Severe hyperthyroidism,

Respiratory and cardiac collapse, Hyperthermia, Exaggerated reflexes, May require mechanical ventilation

Typically seen in hyperthyroid patients with an acute infection/illness or recent thyroid surgery

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66
Q

treatment for thyroid storm

A

Treatment: Lugol’s Iodine, glucocorticoids, PTU, β-blockers, fluids, monitoring

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67
Q

treatment of hyperthyrodism

A

antithyroid drugs (ATDs), BB, radioiodene, thyroidectomy

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68
Q

name two ATDs and their MOA

A

carbimazole - 1st line.
PTU/propylthiouracil - 1st line only in 3rd trimester.

MOA: inhibition of TPO thereby blocking thyroid hormone synthesis

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69
Q

difference between carbimazole and PTU?

A

once vs twice daily dosing. lower rate of side effects with carbimazole. PTU 10x less potent

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70
Q

which ATD carries risk of aplasia in early pregnancy and which drug has risk of liver disease?

A

PTU - liver

carbimazole - aplasia in pregnacy

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71
Q

side effects of ATDs?

A

Generally well tolerated drugs
1-5% will develop allergic type reactions – rash, urticaria, arthralgia
Cholestatic jaundice, ↑liver enzymes, fulminant hepatic failure (PTU)
Agranulocytosis (cannot be used again if have - 6 weeks=highest risk. 0.3% people - )

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72
Q

whitest be done when prescribing ATD’s?

A

tell patient orally and in writing - stop drug and have urgent FBC checked in event of fever, oral ulcer or oropharyngeal infection
(Agranulocytosis)

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73
Q

BB: MOA, BB of choice, side effects in hyperthyrodism

A

Mechanism: β-adrenoceptor blockade, reduced activity of sympathetic nervous system (Useful for immediate symptomatic relief of thyrotoxic symptoms)

Propranolol is the drug of choice - Additional benefit of inhibition of DIO1

Use with caution in those with asthma as Risk bronchospasm - use CCB

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74
Q

radioiodene when is it used? contraindicated?

A

1st choice treatment for relapsed Graves’ disease and nodular thyroid disease. Safe, no increased risk of thyroid cancer

Contraindicated in pregnancy; Relatively contraindicated in active thyroid eye disease (can be used with steroid cover); Contact precautions (stay away from children/pregnant)

[High risk of hypothyroidism when used in Graves’ disease]

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75
Q

thyroidectomy when is it used? problems?

A

Useful when radioiodine is contraindicated,leaves Scar

Surgical/anaesthetic risks:
recurrent laryngeal nerve palsy
Hypothyroidism
Hypoparathyroidism

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76
Q

what is thyroiditis? causes of it?

A

inflammation of the thyroid

Hashimoto’s
De Quervain’s/subacute (viral)
Post-partum
Drug-induced (amiodarone, lithium)
Radiation
Acute suppurative thyroiditis (bacterial)
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77
Q

subacute thyroidits course

A

self-limiting - neck tenderness, fever, or other viral symptoms. (viral trigger)

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78
Q

amiodarone and the thyroid

A

TFTs anormal in half of patients (inhibition of DIO1- ↑fT4, ↓fT3, normal TSH). hypo in 13% (iodene rich areas) and hyper in 2% (iodine deficient areas)

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79
Q

subclinical thyroid disease is what?

A

Abnormal TSH with normal thyroid hormone levels.

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80
Q

subclinical hypothyroidism

A

Risk of progression to overt hypothyroidism
Higher risk if strongly TPO antibody positive
Treatment generally advised if TSH >10
Always treat in pregnancy to maintain normal TSH

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81
Q

Subclinical hyperthyroidism

A

Risk of progression to overt hyperthyroidism
Often seen in multinodular goitre
Association with osteoporosis and atrial fibrillation
Treatment generally advised if TSH <0.1 (or if co-existing osteoporosis/fracture or AF)

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82
Q

non-thyroidal illness/sick euthyroid syndrome

A

Commonly encountered in the unwell, hospitalised patient
Refers to the impact of intercurrent illness (e.g. severe infection) on the HPT axis
TSH typically suppressed initially then rises during recovery
Avoid checking TFTs in unwell patients unless clinical suspicion of thyroid disease

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83
Q 
68 yr old lady 
Tiredness
Weight gain
Slowness
Goitre

TSH 42 mU/L
Free T4 4 pmol/L

A

primary hypothyroidsim

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84
Q

normal ranges of TSH and free t4

A

TSH 0.4-4.0 mU/L

Free T4 9.8-18.8 pmol/L

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85
Q

68 yr old lady
Family history of thyroid disease
Tiredness
Goitre

TSH 12 mU/L
Free T4 11 pmol/L
TPO Antibodies 200 (elevated)

A

Subclinical hypothyroidism

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86
Q 
52 yr old male
Headache
Visual field defect
Dizziness/weakness
Poor libido/loss of erections
TSH 0.20 mU/L
Free T4 6 pmol/L
A

Pituitary tumour causing secondary hypothyroidism

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87
Q 
32 yr old lady 
Weight loss and tremor
Feels tired
Sleep disturbance
TSH <0.01 mU/L
Free T4 54 pmol/L
A

Graves’ disease

do additional antibody tests

88
Q 
70 yr old lady 
Diagnosed with atrial fibrillation
No symptoms
TSH <0.01 mU/L
Free T4  26 pmol/L
A

Toxic multinodular goitre

89
Q 
32 yr old
Sore throat and febrile illness
Tired, weight loss, poor sleep
GP blood tests:
TSH<0.01, T4 36 pmol/L
Seen in clinic 6 weeks later
TSH 12 mU/L, Free T4 9 pmol/L
A

Subacute thyroiditis

90
Q

solitary thyroid lump. how many people have them? how many benign?

A

5% female population has them, 95% benign

91
Q

what can cause a benign Solitary Thyroid Nodule

A

Cyst
Colloid Nodule
Benign Follicular adenoma
Hyperplastic Nodule

92
Q

what can cause a malignant Solitary Thyroid Nodule

A 
PAPILLARY THYROID CARCINOMA – 80%
Follicular Thyroid Carcinoma
Medullary Thyroid Carcinoma
(Lymphoma)
(Poorly Differentiated)
93
Q

how can you tell if a lump in the neck in a solitary thyroid nodule?

A

moves on swallowing? (invested in pre-trchela fascia).

pain is an uncommon feature (usually caused by bleed into a cyst causing pain)

94
Q

Hx, exam, investigation of solitary thyroid nodule

A

neck irradiation, FHx of thyroid Cancer

LN, hoarseness

TSH, USS-FNA

95
Q

treatment for malignant solitary thyroid nodule

A

lobectomy or thyroidectomy (consider radioactive iodine)

96
Q

Follow up of a Differentiated Thyroid Cancer

A

TSH lower level of normal (0.4-4 mU/l)
Thyroglobulin – protein precursor of T4/T3; made by thyroid follicular epithelial cell - Use Tg as a tumour cell marker for follow up of patient

Get TSH/Tg measured every 6 months for first 5 years then annually for next 5 years

97
Q

which thyroid cancer speads by LNs?

A

papillary (commonest 80%)

98
Q

what investigation is good at showing is LN involvement?

A

USS

99
Q

follicular thyroid carcinoma (how common and prognosis)

A

10%, diagnosis depends on invasion of the capsule or vascular invasion (minimally to wide invasive) - surgery usually sufficient

100
Q

how do follicular thyroid carcinomas spread?

A

Haematogenous spread

101
Q

treatment of FTC (follicular)

A

most are minimally invasive and treated with lobectomy - if significant vascular involement then thyroidectomy

102
Q

thyroid lymphoma clinical picture

A

long-standing (AI) hypothyroidism, 70-80 female, rapid growth

103
Q

what is needed to diagnoses thyroid lymphoma

A

core biopsy

104
Q

treatment of thyroid lymphoma

A

steroids if actually unwell, radio/chemotherapy. goodish prognosis

105
Q

medullary thyroid carcinoma arrises from which cell? why is this important?

A

rare tumour of the parafollicular cells which secrete CALCITONIN – can be used as a tumour cell marker

106
Q

how can medullary thyroid carcinoma be diagnosed? what should also be check once diagnosed with MTC?

A

FNA – presence of amyloid or Calcitonin positive stains

Should always Check 24 hour urinary metanephrines and genetics

107
Q

what genes can be associated with medullary thyroid cancer?

A

MEN2a and MEN2b (familial)

[can also be sporadic or non-MEN familial]

108
Q

MEN2a(b) gene gives increased incidence of what conditions? why is it important to identify MEN2a link?

A

Medullary TC, Phaeochromocytoma, Hyperparathyroidism

prophylactic thyroidectomy as child possible

109
Q

what to do if suspect a multi-nodular goitre?

A

Assess Function
Assess Structure – what is being squashed (symptoms of stridor or choking lying flat)?

TSH
CT scan

110
Q

in a multi nodular goitre what are the results of the investigations?

A

TSH – usually normal or slightly suppressed; occasionally needs antithyroid drugs (Radioactive iodine/RAI)

CT scan:
Retrosternal Extension
Tracheal Compression

111
Q

treatment of multi nodular goitre

A

Most can leave alone

RAI if significant hyperthyroidism

Surgery if structural problem (or significant retrosternal extension)

112
Q

who is surgery offered to with retrosternal goitres?

A

Lifestyle interfering symptoms

Possibility of cancer

Significant tracheal compression (?<7 mm)

Tracheal Flow Loops if other respiratory potential causes of orthopnoea/breathing difficulties

? Audible Stridor

113
Q

when is a flow volume loop done concerning goitres??

A

if there is another potential cause for breathlessness.

114
Q

what does the thyroid gland secrete?

A

Thyroxine (T4)
Tri-iodothyronine (T3)
Calcitonin

115
Q

structure of the thyroid gland

A

bow tie (2 lobes with isthmus)

116
Q

blood supply to the thyroid gland

A

highly vascular organ,

sup and inferior thyroid arteries (branch of external carotid +/- thyroidea ima).

Three pairs of veins drain- superior/ middle thyroid vein > internal jugular, inferior thyroid vein> brachiocephalic veins

117
Q

where is the thyroid located?

A

5th cervical- 1st thoracic vertebrae/ 2-4th tracheal rings

118
Q

innervation of the thyroid

A

autonomic nerve supply (Parasympathetic from vagus nerves, and sympathetic fibers from superior, middle, and inferior ganglia of the sympathetic trunk

119
Q

what is the posteromedial aspect of the thyroid gland is attached by

A

berry’s ligament

120
Q

cells of the thyroid

A

follicle made up of follicular cells (Colloid is enclosed by follicular cells, colloid is a tyrosine-containing thyroglobulin)

parafolicular C cells (secrete calcitonin)

121
Q

Release of Thyroid Hormones.

A

Iodine ions travel from blood supply through follicular cell to colloid thyroglobulin with T3 and T4. pinocytosis then occurs in and binds to lysosomes in follicular cell with causes T3 and T4 to be released and then diffuse into bloodstream

122
Q

what the the pyramidal lobe of the thyroid

A

extra lobe

123
Q

Synthesis and Storage of T3 and T4?

A

iodine taken up by follicle cells, then done attached to tyrosine residues on thyroglobulin to form MIT and DIT. coupling of MIT-DIT or DIT x2 occurs to form T3/T4 respectively. They are stored in colloid thyroglobulin until required.

124
Q

what is Inhibited by CARBIMAZOLE & PROPYLTHIOURACIL used to treat hyperthyroidism

A

iodine attached to tyrosine residues on thyroglobulin to form (MIT) & (DIT)

125
Q

thyroid hormones. which is secreted more, which is more potent? where does conversion take place?

A

T4 = 90%, T3 is more potent.

T4 made to T3 in liver and kidney (T3 is major biologically active thyroid hormone)

126
Q

why do T3 and T4 bind to plasma proteins?

A

hydrophobic/ lipophillic

127
Q

which plasma proteins do T3/4 bind to?

A

thyroxine binding globulin (TBG) ~70%

Transthyretin (TTR) (thyroxine binding prealbumin) ~20%

Albumin (~5%)

[unbound in biologically active form]

128
Q

what does T3 do once converted from T4?

A

enters nuclear receptor of target cell → mRNA →proteins → biological resp

129
Q

effects of thyroid hormones on basal metabolic rate

A

Thyroid hormones inc basal metabolic rate

Increase number & size of mitochondria
Increase oxygen use and rates of ATP hydrolysis
Increase synthesis of respiratory chain enzymes

130
Q

effects of thyroid hormones on thermogenesis

A

inc thermogenesis

131
Q

effects of thyroid hormones on metabolism

A

Carbohydrate metabolism:

inc blood glucose – due to stimulation of glycogenolysis and gluconeogenesis.
inc insulin-dependent glucose uptake into cells

Lipid metabolism :
Mobilise fats from adipose tissue
inc fatty acid oxidation in tissues

Protein metabolism
inc protein synthesis

132
Q

Thyroid Hormone Effects-

Growth and Development

A

Growth:
Growth hormone releasing hormone (GHRH) production & secretion requires thyroid hormones
Glucocorticoid-induced GHRH release also dependent on thyroid hormones (permissive action)
GH/somatomedins require presence of thyroid hormone for activity (permissive action).

Development of foetal & neonatal brain
Myelinogenesis & axonal growth require thyroid hormones

Normal central nervous system activity:
Hypothyroidism - slow intellectual functions
Hyperthyroidism – nervousness, hyperkinesis & emotional lability

133
Q

Thyroid Hormones Permissive Sympathomimetic Action

A

increase responsiveness to adrenaline & sympathetic NS neurotransmitter, noradrenaline, by increasing numbers of receptors

cardiovascular responsiveness also increased due to this effect – increased force and rate of contraction of heart

(BB like propranolol used to treat symptoms)

134
Q

how are thyroid hormones regulated?

A

TRH=THYROTROPHIN RELEASING HORMONE

TRH release from hypothalamus stimulates TSH release form anterior pituitary.

135
Q

inc TSH does what to t3/t4 secretion?

A

inc TSH = stimulates T3/4 release

136
Q

t3/4 effect on TRH?

A

negative feeback (inc T3/4 reduce TRH)

137
Q

TSH receptor is found where?

A

thyroid folicular cell

138
Q

what external factors can regulate thyroid hormones conc?

A

low temp (inc TRH/TSH), stress(inhibits TRH/TSH), circadian rhythm (low in morning, highest late at night)

139
Q

what are DeIodinase Enzymes? what do they do?

A

Subfamily of 3 enzymes (type 1, 2 and 3) important in the activation and deactivation of thyroid hormone (tissue regulation)

add/remove an iodine atom.

140
Q

3 types of DeIodinase Enzymes another locations?

A

Type I (D1) is commonly found in the liver and kidney

Type II (D2) is found in the heart and skeletal muscle, CNS, fat, thyroid, and pituitary

Type III (D3) found in fetal tissue and placenta and brain (except pituitary)

141
Q

what is the main determinant of T3?

A

D2 (activates T4->T3 in tissues)

142
Q

what are the four different thyroid hormone recpetors? why is this useful?

A

Thyroid hormone receptor alpha – TRα1, TRα2

Thyroid hormone receptor beta –TRβ1. TRβ2

(different effect/sensitivity per tissue)

143
Q

what occurs if person is Resistant to thyroid hormone alpha (RTHα)

A

delayed bone development
chronic constipation
bradycardia
impaired neurological development

144
Q

what occurs if person is Resistant to thyroid hormone beta (RTHβ)

A 
impaired HPT axis
goitre
affected colour vision
abnormal cochlea 
tachycarida
impaired neurological development
145
Q

deficiency of thyroid hormones cause by what? are the conditions goitrous or not?

A

Primary (gland) failure – may be associated
with enlarged thyroid (goitre)

Secondary to TRH or TSH (no goitre)

Lack of iodine in diet (may be associated with goitre)

146
Q

what are the symptoms of hypothyroidism?

A 
Reduced BMR
Slow pulse rate 
Fatigue, lethargy, slow response times and mental sluggishness
Cold-intolerance
Tendency to put on weight easily
147
Q

what is myxoedema (hypothyroidism in adults) signs

A

puffy face, hands & feet

148
Q

what is cretinism (hypothyroidism in kids) signs

A

dwarfism & limited mental functioning due to deficiency of thyroid hormones present at birth

149
Q

symptoms of hyperthyroidism

A 
Increased  BMR
Very fast pulse rate 
Increased nervousness and excessively emotional.
insomnia
Sweating &amp; heat intolerance
Tendency to lose weight easily
150
Q

condition commonly causing hyperthyroidism? signs?

A

Graves’ disease.

Autoimmune disease – Thyroid stimulating immunoglobulin (TSI) acts like TSH but unchecked by T3 & T4.
Exophthalmos
Goitre – enlarged thyroid gland

151
Q

why does Exophthalmos occur?

A

bulging eyes due to water retaining carbohydrate build up behind eyes.

152
Q

whiter the 5 types of thyroid cancer?

A

papillary, follicular, medullary, anaplastic, other (lymphoma…)

153
Q

what makes up differentiated thyroid cancer/DTC?

A

papillary, follicular.

refers to histology, most cancer cells take up Iodine and secrete Thyroglobulin, DTC are TSH driven - good prognosis (95% after 10 years)

154
Q

what do most DTC present with?

A

palpable nodule (thyroid or LN)

5% with local/disseminated mets

155
Q

who does DTC occur in?

A

white adults with radiation exposure.

156
Q

papillary thyroid cancer. how common, spread and associations

A

commonest, LN, spread to lungs, bone, liver, brain; associated with hashimoto’s thyroiditis

157
Q

follicular thyroid cancer. how common, spread and associations

A

2nd commonest, haematogenously spread. incidence inc in regions of relative iodine deficiency

158
Q

investigation of potential DTC

A

US guided FNA (+excision biopsy of LN).

159
Q

what do to if suspect DTC and vocal cord palsy?

A

pre-operative laryngoscopy

[make sure of no recurrent laryngeal nerve injury]

160
Q

clinical predictors of malignacy in thyroid nodule?

A 
<20 or >50
Nodule increasing in size
> 4cm in diameter
History of head and neck irradiation
Vocal cord palsy
161
Q

treatment for DTC?

A

surgery +/- RAI

162
Q

what are the three types of surgery for DTC and which is preferred?

A

Thyroid lobectomy with isthmusectomy
Sub-total thyroidectomy
Total thyroidectomy

Sub-total thyroidectomy

163
Q

why is a Sub-total thyroidectomy operation of choice for DTC?

A

leave on 5% in situ so chance of recurrence low

leaving decreases chance of complications (vocal cord palsy, parathyroid destruction)

164
Q

what happens post-op to DTC patients?

A

risk assessed by AMES(age, mets, extent and size of primary tumour). - basically low and high risk groups made depending on how advanced cancer was before surgery

165
Q

treatment for low and high risk groups post surgery for DTC?

A

low -TSH-supression via thyroxine

high- RAI

166
Q

when whole body iodine scan done? what preparations are necessary?

A

Usually performed 3-6 months post-op.

use rhTSH is far better as no need to stop T3/T4 - as need high TSH for scan

167
Q

why is a high TSH needed for a whole body iodine scan?

A

as sensitivity is determined by ensuring that TSH is elevated

inc TSH helps cancer cells to recognise iodine and uptake it - making results clearer

168
Q

what is TRA/Thyroid Remnant Ablation?

A

rhTSH and high dose of RAI given - patient kept in lead room for 2/3 days (inpatient)

169
Q

side effects of RAI?

A

few, patients usually well, sore salivary glands/throat possible

170
Q

how is TRA followed up?

A

patient maintained on T4 to suppress TSH. this reduced recurrence rates (suppress long-term = extra protection)

thyroglobulin (Tg) can be used as tumour marker, should be undetectable. (very sensitive test)

171
Q

what is thyroglobulin. why can it be used as a tumour marker? what happens if positive?

A

a protein produced by thyroid cells and (most) thyroid cancers.

with most of thyroid cells and cancer destroyed in successful treatment, level should be nothing and if increases then shows cancer still there.

if + = do whole body iodine scan

172
Q

what do to if patient with PMHx of DTC has positive Tg but negative whole body iodine scan? how to treat?

A

PET scan. positive means cancer has changed an become anaplastic.

use biologics (Sorafenib and Lenvatinib)

173
Q

recurrence of DTC: when? where? rate?

A

<2 years after op.

LN>thyroid

30% rate but if it uptakes iodine then is curable (via TRA)

174
Q

what does TRA increase risk of?

A

AML (acute myeloid leukaemia). highest at 15 years post-treatment [no other cancer risk or is to fertility/offspring.]

175
Q

how does cold exposure cause a release of thyroxine?

A

hypothalamus (TRH), ant pituitary (thyrotropin), thyroid (thyroxine)

176
Q

(paired) hormones from ant pit?

A 
ATCH - cortisol
TSH - thyroxine
Lh/FSH - Testosterone/estradiol
GH - IGF1
Prolactin
177
Q

post pituitary hormones?

A

vasopressin, OXT

178
Q

what is the difference between micro/macroademona?

A

≤ 1cm: Microadenoma

> 1cm: Macroadenoma

179
Q

what are the complications of a non-functioning pit ademona?

A

Compression on optic chiasma (Bitemporal hemianopia)
Compression on other structures eg cranial nerve 3,4,6
Hypoadrenalism
Hypothyroidism
Hypogonadism
(Diabetes Insipidus)
GH deficiency

180
Q

what are the benign causes of a raised prolactin?

A

Physiological - breast feeding - pregnancy - stress - sleep

Drugs - Dopamine antagonists eg metoclopramide - Antipsychotics eg phenothiazines - antidepressants eg TCA, SSRIs - other, estrogens, coccaine

181
Q

what are the pathological causes of a raised prolactin?

A

Hypothyroidism
Stalk lesions: iatrogenic, road accident
Prolactinoma

182
Q

signs and symptoms of raise prolactin in female

A 
EARLY presentation
Galactorrhoea
30-80%
Menstrual irregularity
Ammenorrhoea
Infertility
183
Q

signs and symptoms of raise prolactin in male

A 
LATE Presentation
Impotence
Visual field abnormal
Headache
Ant pit malfunction
184
Q

investigating prolactinoma

A 
prolactin conc,
MRI pituitary (tumour, pit stalk, optic chiasma)
visual fields (bitemproal hemianopia)
pit tests (other Hormones affected?)
185
Q

treatment of prolacitnoma

A

Cabergoline (twice oral per week) - dopamine agonists (work very well)

186
Q

what is acromegaly?

A

GH excess

187
Q

acromegaly sings and symptoms

A 
giant, 
thickened soft tissues					- skin, large jaw, sweaty, large hands
Hypertension (heart), cardiac failure
Headaches (vascular)
Snoring/Sleep apnoea
Diabetes mellitus
Local pituitary effects					- visual fields, hypopituitarism
Early CV Death
Colonic polyps and colon cancer
188
Q

how is acromegaly diagnosed? other tests that are important to consider?

A

IGF1
GTT (GH not suppressed)

Visual field
CT or MRI pituitary scan
Pituitary function tests ie the “other hormones

189
Q

treatment for acromegaly

A

Pituitary surgery
(+/-External radiotherapy to pituitary fossa)
Retest GTT (if too high need drug therapy)

190
Q

what drugs can be used in acromegaly?

A

Dopamine Agonist -Cabergoline

Somatostatin Analogues - octreotide, sandostatin LAR, lanreotide.

GH Antagonist -
Pegvisomant

191
Q

what is cushion’s syndrome caused by??

A

excess cortisol

192
Q

what occurs in cushing’s syndrome due to excess cortisol?

A 
Protein loss
Myopathy; wasting
Osteoporosis; fractures
Thin skin;  striae, bruising
Altered Carbohydrate/Lipid metabolism; Diabetes mellitus, Obesity
Altered psyche; psychosis, depression
193
Q

what occurs in cushing’s syndrome due to excess mineralocorticoid

A

hypertension, oedema

194
Q

what occurs in cushing’s syndrome due to excess androgen

A

Virilism
Hirsutism
Acne
oligo/amenorrhoea

195
Q

what does cushion’s cause to be in excess?

A

cortisol, mineralocorticoid, androgen

196
Q

what is cushion’s characterise (compared to obesity? )

A 
Thin Skin
Proximal myopathy
Frontal balding in women
Conjunctival oedema (chemosis)
Osteoporosis
buffalo hump, moon face
197
Q

what is the diagnostic test for cushing’s?

A

screening = overnight Dexamethasone suppression test

definitiative = 2day Dexamethasone suppression test

198
Q

what is the difference between cushings disease and syndrome?

A

Pituitary (majority) = Cushing’s Disease

ALL others are Cushing’s Syndrome: Adenoma of adrenal (B/M), ectopic (thymus, lung, pancreas), pseudo (steroid meds, alcohol, depression)

199
Q

DD of cushing’s: blood results pituitary cause (disease)

A

abn - low dose dexa test
<300 - ACTH
suppress by 50% - high dose exam suppression

200
Q

DD of cushing’s: blood results ectopic cause

A

abn - low dose dexa test
>300 - ACTH
nil- high dose exam suppression

201
Q

DD of cushing’s: blood results adrenal cause

A

abn - low dose dexa test
<1 - ACTH
nil - high dose exam suppression

202
Q

treatment of pituitary Cushing’s disease

A

hypophysectomy +/-radiotherapy (recurrance); bilateral adrenalectomy

203
Q

treatment of adrenal Cushings syndrome

A

Adrenalectomy

204
Q

treatment of ectopic Cushings syndrome

A

remove source

OR bilateral adrenalectomy

205
Q

drugs used in the treatment of cushings?

A

Metyrapone - if other treatments fail - while waiting for radiotherapy to work
- S/E common

Ketoconazole (hepatotoxic)

Pasireotide: (new somatostatin analogue; receptor 2 and 5 blocked)

206
Q

pan Hypopituitarism causes what?

A 
Anterior Pitutary
Growth Hormone; growth failure
TSH; hypothyroidism
LH/FSH; Hypogonadism
ACTH; hypoadrenal
Prolactin; none known

Posterior Pituitary
Diabetes Insipidus

207
Q

causes of Hypopituitarism (many)

A 
Pituitary Tumours
Secondary metastatic lesions
Local brain tumours
Granulomatous diseases
(TB, sarcoidosis)
Trauma(road accidents, skull fractures)
Hypothalamic diseases
(Syphilis, meningitis)
Iatrogenic; surgery
Autoimmune;Sheenan – post pregnancy infarction
Infection; meningitis
208
Q

Symptoms and signs of anterior hypopituitarism

A 
Menstrual irregularities (F)
Infertility, impotence
Gynaecomastia (M)
Abdominal obesity
Loss of facial hair (M)
Loss of axillary and pubic hair (M&amp;F)
Dry skin and hair
Hypothyroid faces
growth retardation (children)
209
Q

treatment of pan Hypopituitarism

A 
Thyroxine
Hydrocortisone	
ADH			
GH
Sex Steroids: HRT/Oest/prog pill for female	+ Testosterone for males
210
Q

GH in adults

A 
Improves well being and Quality of life
Decreases abdominal fat
Increases muscle mass, strength, exercise capacity and stamina
Improves cardiac function
Decreases cholesterol and increases LDL
Increases bone density
Given by daily SC injection
211
Q

Testosterone Replacement in hypopituitarism

A 
IM injection every 3-4 weeks (sustanon)
Skin gel (testogel, tostran)
Prolonged IM injection 10-14 wks (nebido)
(Oral tablets (restandol))
212
Q

risks of testosterone replacement

A

Prostate Enlargement. Does NOT cause prostate cancer but may make it grow - monitor PR exam and PSA at start
Polycythaemia - monitor FBC
Hepatitis (only for oral tablets) - monitor LFTs

213
Q

causes of cranial D.insipidus

A

familail (DIDMOAD = DI, DM, optic atrpohy, deaf)

acquired (idiopathic and trauma (RTA/sugery/skull #))

Rare (tumour, sarcoid, irradtions, meningitis )

214
Q

how is DI diagnosed?

A

Water Deprivation test

215
Q

why do DI occur?

A

reduced ADH/vasopressin

216
Q

how is DI treated?

A

desmopressin (oral, inhale, injection)

Endocrinology (7 decks)

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