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phase 2 endo > Thyroid > Flashcards

Thyroid Flashcards

1
Q

what are the causes for physiological thyroid lump/goitre

A

pregnancy and puberty

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2
Q

What is the most important thing to establish in paitient with goitre and how can this be done?

A

hyper, hypo OR euthyroid i.e. TFTs.

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3
Q

what are the common causes of goitre

A
  • Iodin deficiency
  • Secondary due to substance ↓ iodin uptake
  • Congenital
  • Acute throiditis (De Quervain’s)
  • Physiological →pregnancy, puberty
  • Autoimmune: Grave’s/Hashimoto’s
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4
Q

Name 3 types of goitre

A

Multinodular goitre
fibrotic goitre
solitary thyroid nodule

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5
Q

What should be established in MNG

A

Most common and toxic (↑thyrod) or non-toxic i.e. Euthyroid

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6
Q

what is Reidel’s thyroditis

A

fibrotic goitre

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7
Q

what are the types of solitary thyroid nodules

A
  • Cyst
  • Adenoma
  • Discrete nodule in MNG: single toxic adenoma or Aka Plummer’s disease
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8
Q

what is the previlence of malignancy amongst goitre/nodule presentations

A

5%

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9
Q

Name some benign causes for lumps

A

Thyroid adenoma
Thyroiditis
Thyroid cyst
Hyperplastic nodule

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10
Q

What are the risk factors for the lump

A
  • ↓iodin consumption: risk from 5%→40% m.
  • ↑age
  • Exposure to radiation
  • Previous thyroid disease
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11
Q

What are the red flags for a thyroid lump (7)

A
  • FHx of thyroid cancer
  • Hx of previous irradiation/ ↑radiation (env)
  • Child with a thyroid nodule
  • Unexplained hoarseness or stridor + goitre
  • Painless thyroid mass enlarging rapidly over a few weeks
  • Palpable cervical lymphadenopathy
  • Insidious or persistent pain lasting for several weeks
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12
Q

What are the signs associated with thyroid lumps

A
  • Asymptomatic →presence highlighted by someone else
  • Pain
  • RARE: features of compression
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13
Q

What are the steps in examination of thyroid gland

A
  • Thyroid movement on swallowing fluid → ask patient to drink some water
  • ? enlargement OR asymmetry
  • Stand behind the patient →use 2nd and 3rd finger to examine whilst patient swallows
  • Note lumps, asymmetry, size and tenderness
  • Check for regional lymphadenopathy
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14
Q

name 6 investigations used for thyroid lump

A

TFTs, autoantibodies, CXR+ thoracic inlet, USS, Rbonucleotide scan, fine needle aspiration

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15
Q

What do hot, cold and worm areas on the ribonucleotide scan refer to

A

hot/hyperfunctioning i.e. adenoma
worm: normal
cold/hypofunctioning i.e. malignancy

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16
Q

What sort of informations can be generated from USS

A

characterise the nodule i.e. solid, cyst, part or group of lumps

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17
Q

What are the different types of thyroid cancer and what proportion of thyroid cancers are they

A
  • Papillary 60%
  • Follicular ≤25%
  • Medullary 5%
  • Lymphoma 5%
  • Anaplastic: rare
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18
Q

What are the characteristics of papillary thyroid cancer

A
  • Young patients but usually good prognosis

* Spread lymph nodes→ lung via jugulodigastric nodes

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19
Q

What are the characteristics of Follicular thyroid cancer

A
  • Middle–age population

* Spread via blood i.e. bones, lungs

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20
Q

What is the treatment for papillary and follicular thyroid cancer

A
  • Mx: total thyroidectomy ± radioiodine to ablate residual cells
  • Thyroxin →supress TSH
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21
Q

What are the indications for thyroid surgery

A
  • Pressure symptoms
  • Relapse hyperthyroidism after >1 failed course of drug treatment
  • Carcinoma
  • Cosmetic reasons
  • Symptomatic patients planning pregnancy
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22
Q

What is the preparation for thyroid surgery

A
  • Stop thyroid suppressing drugs 10 days prior to surgery as these increase vascularity
  • Check vocal cords by indirect laryngoscopy pre- and post-op
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23
Q

What are the early complications of thyroid surgery

A
  • Recurrent laryngeal nerve palsy
  • Haemorrhage: If compressing airway, instantly remove sutures for evacuation of clot
  • Hypoparathyroidism (check plasma Ca2+ daily; common transient ↓ in serum [])
  • Thyroid storm
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24
Q

what are the later complications of thyroid surgery

A
  • Hypothyroidism

* Recurrent hyperthyroidism

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25
Q

what are the normal levels of TSH T3 and T4

A

TSH 0.4-4.5 mU/L
fT4 9-25 pmol/L
fT3 3.5-7.8 pmol/L

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26
Q

Describe the anatomy of thyroid gland

A

two lobes connected by isthmus, and connected to thyroid cartilage and trachea to permit movement on swallowing

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27
Q

what is the embryological descent of thyroid gland and what is its significance

A

develops in the base of the tongue and moves downwards. It can leave thyroid tissue on the way or at the tongue i.e. lingual thyroid

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28
Q

what is the micro structure of the thyroid gland

A
  • Micro: follicles with cubital cells and colloid

* Parafollicular cells →calcitonin

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29
Q

What are the hormones that regulate the release of T3 and T4 and what controls those hormones

A

TRH and TSH upregulate release they are inhibited by increased T3 and T4

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30
Q

how does formation of thyroglobulin leads to formation of T3 and T4

A

follicular cells →colloid →iodised→ cleaved to T3 and T4 (colloid)→ vesicles transported into the cell →exocytosis of T3 and T4

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31
Q

what are the physiological effect of thyroid hormones on CVS

A

↑HR and ↑CO

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32
Q

what are the physiological effect of thyroid hormones on bones

A

↑turnover and resorption

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33
Q

what are the physiological effect of thyroid hormones on Resp

A

Maintenance of hypoxic and hypercapnic drive

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34
Q

what are the physiological effect of thyroid hormones on GI

A

↑ gut motility

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35
Q

what are the physiological effect of thyroid hormones on neuromuscular

A

↑ speed of muscle contraction/relaxation; ↑protein turnover

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36
Q

what are the physiological effect of thyroid hormones on carbohydrates

A

↑ hepatic gluconeogenesis/glycolysis and GI absorption

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37
Q

what are the physiological effect of thyroid hormones on lipids

A

↑lipolysis, cholesterol synthesis + degradation

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38
Q

what are the physiological effect of thyroid hormones on sympathetic

A

↑catecholamine sensitivity + β receptors in the heart, skeletal muscles, Adipost tissue and lymphocytes & ↓α heart receptors

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39
Q

what are the physiological effect of thyroid hormones on blood

A

↑RBC 2,3-BPG, ↑O2 release in tissues

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40
Q

what are the physiological effect of thyroid hormones

A

CVS ↑HR and ↑CO
Bone ↑turnover and resorption
Respiratory Maintenance of hypoxic and hypercapnic drive
GI ↑ gut motility
Blood ↑RBC 2,3-BPG, ↑O2 release in tissues
Neuromuscular ↑ speed of muscle contraction/relaxation; ↑protein turnover
Carbohydrates ↑ hepatic gluconeogenesis/glycolysis and GI absorption
Lipids ↑lipolysis, cholesterol synthesis + degradation
Sympathetic ↑catecholamine sensitivity + β receptors in the heart, skeletal muscles, Adipost tissue and lymphocytes & ↓α heart receptors

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41
Q

what is the physiology of thyroid hormones in the blood stream?

A
  • 99% of T3 and T4 bound to thyroxin binding globin (TBG)
  • T4→T3 in liver, kidney and muscle
  • Act via nuclear receptor
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42
Q

what is the full name of T3 and T4

A

Triiodothyronine (T3) + L-thyroxin (T4)

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43
Q

Define hyperthyrodsm

A

Excessive secretion of thyroid hormone by thyroid gland

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44
Q

What is the epidemiology of thyrotoxicosis

A
  • 1/2000
  • 75% due to Grave’s disease
  • Peak onset 20-50
  • F:M → 9:1
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45
Q

what are the risk factors for hyprthyrodism

A
  • Family history
  • High iodine intake
  • Smoking – particularly ophthalmopathy
  • Trauma/surgery to the thyroid gland
  • Childbirth
  • HAART
  • Genetic susceptibility – HLA-B8
  • Toxic multinodular goitre
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46
Q

what is the main cause of hyperthyroidism

A

Grave’s disease .e. 75%

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47
Q

name 8 causes for hyperthyrodism

A
  • Grave’s disease i.e. 75%
  • Toxic multinodular goitre
  • Toxic adenoma: single nodule secreting T3 and T4 and highlighted on radioisotope scan
  • Ectopic thyroid: Metastatic follicular thyroid cancer or ovarian teratoma
  • De Quervain’s thyroiditis: transient due to infection; with neck pain, treated with NSAIDs
  • Self-medication: e.g. OTC iodine supplements, ‘energy boosting’
  • Drugs: e.g. amiodarone, lithium, exogenous iodine
  • Post-partum
  • TB
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48
Q

Name 10 symptoms of hyperthyrodism

A
  • Weight loss/Weight gain
  • ↑ or ↓appetite
  • Irritability
  • Weakness and fatigue
  • Diarrhoea ± steatorrhoea
  • Sweating, Tremor
  • Mental illness range: anxiety to psychosis
  • Heat intolerance
  • Loss of libido
  • Oligomenorrhoea or amenorrhoea
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49
Q

what are the signs of hyperthyrodism 11

A 
•	Palmar erythema, Sweaty and warm palms
•	Fine tremor
•	Tachycardia – AF or HF
•	Hair thinning or diffuse alopecia
•	Urticaria, pruritus
•	Brisk reflexes
•	Goitre
•	Proximal myopathy (muscle weakness ± wasting)
•	Gynaecomastia
•	Eyes 
o	Van Graefe’s sign: lid lag
o	Darlymple signs: retracted eye lid
•	Neurological: chorea, periodic paralysis
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50
Q

what is the key differential for hyperthyrodism

A

pheochromocytoma

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51
Q

which investigations help with diagnoses of hyperthyrodism

A 
•	TFTs: TSH and T4 (sometimes T3)
•	ESR and CRP (? inflammation)
•	LFTs
•	Autoantibodies:
o	Antimicrosomal antibodies 
o	Antithyroglobulin antibodies
o	TSH-receptor antibodies 
•	Thyroid USS
•	Thyroid isotope uptake scan
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52
Q

what do following levels tell you about the cause TSH low, T4 high

A

primary hyperthyroidism

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53
Q

what do following levels tell you about the cause TSH high T4 hgh

A

secondary hyperthyroidism

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54
Q

what do following levels tell you about the cause TSH low T4 normal

A

subliminal hyperthyroidism

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55
Q

What is the symptom controlling management of hyperthyroidism

A

• β-blockers: propranolol 40mg (rapid control)

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56
Q

what are the two options for treatment of hyperthyroidism

A 
•	Block and replace
o	Carbmiazole + levothyroxine 
o	↓ risk of iatrogenic hypothyroidism 
•	Dose titration 
o	Carbimazole 20-40mg/ 24 hours PO 4/52 
o	↓ every 1-2 months depending on TFTs
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57
Q

What advice should be given to a patient on carbimazole

A

FBCs+ stop medication if sore throat, mouth ulcers, pyrexia

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58
Q

What are the ADRs of Carbimazole

A
  • Crosses placenta → foetal hypothyroidism
  • Disruption of oestrogen production in pregnancy

neutropenia

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59
Q

What is the prognosis of graves disease

A

stop treatment 18/12 months post start but 50% relapse

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60
Q

what are the non-medical treatments for grave’s disease

A

radio-iodin or surgery

61
Q

what are the complications/ADRs of use of radio-iodine

A

hypothyrodism: 40-80%
takes 3-4 months to take an effect
may worsen eye disease (especially in smokers

62
Q

what are the indications for use of radio-iodine

A

adenomas, multi-nodular goitre, unresponsive

63
Q

what advice should be given to patients undertaking radio-iodine treatment

A

sleep alone, ↓ contact with pregnant and children

64
Q

what is the cure rate for thyroid surgery

A

98%

65
Q

What are the indications for thyroid surgery

A

suboptimal response to other treatment

66
Q

what are the complications of surgery

A

o Hypoparathyroidism
o Vocal cord paralysis
o Hypothyroidism

67
Q

what is the most severe ADR of carbimazole

A

agranlocytosis i.e. neutropinia stop medication if sore throat, mouth ulcers, pyrexia

68
Q

What is the aetiology of grave’s disease

A

• Antibodies bind to GPC thyrotropin receptors →Smooth thyroid enlargement +↑production

69
Q

how can grave’s case eye disease

A

autoantibodies binding to orbital antigene

70
Q

what are the tigers for grave’s disease

A

stress infection childbirth

71
Q

what are the possible prognosis for grave’s disease

A

hyper, eu or hypothyroidism

72
Q

what are the complications of hyperthyroidism

A
  • HF (thyrotoxic cardiomyopathy, ↑ in elderly)
  • Angina
  • AF (seen in 10–25%: control hyperthyroidism and warfarinize if no CI)
  • Osteoporosis
  • Ophthalmopathy
  • Gynaecomastia
73
Q

what are the risk factors for toxic mltinodular goitre

A

elderly iodine deficiency

74
Q

what is the problem with toxic multinodular goitre

A

overproduction of thyroid hormone

75
Q

when is surgery used in treatment of toxic multinodular goitre

A

compression symptoms

76
Q

What are the features of graves’s disease

A

eye disease
• Pretibial myxoedema – oedematis swelling above lateral malleolus
o ↑ glycosaminoglycans →non-pitting pink/purple plaques
o Common dermatopathy i.e. 40% of Grave’s patients
• Thyroid acropachy Dermopathy affecting hands, Causes clubbing with painful swelling of digits
• Moderate gland enlargement →firm
• Thyroid bruit
• Lymphoid hyperplasia i.e. splenomegaly

77
Q

what s the epidemiology of thyroid eye disease

A

25-50% of people with grave’s

78
Q

what are the risk factors for grave’s

A
  • Smoking , HLA-DR3
  • Radioiodine therapy, Grave’s disease
  • Female
79
Q

what are the pathological features of thyroid eye disease

A

Swelling in the orbit due to retro-orbital inflammation and lymphocyte infiltration

80
Q

how do eye damage occur in thyroid eye disease

A
  • TSH-autoantibody stimulates
  • T cell activation →IL-1 and TNF etc
  • Hyperosmotic shift → oedema of the orbital fat and muscles due to infiltration→ fibrosis
  • Forcing the eyeball forward and leading to exophthalmos
81
Q

how does thyroid eye disease progress

A

Deterioration over few months →peak →spontaneous improvement →chronic changes i.e. fibrosis

82
Q

how does thyroid eye disease presents (symptoms)

A 
•	Hyperthyroidism →before/after/hypo/norm.
Symptoms 
•	Eye discomfort/ocular irritation 
•	Grittiness 
•	Tear production↑
•	Photophobia
•	Diplopia: ↓ ocular motility
•	Acuity↓, 
•	Afferent pupillary defect → optic nerve compression: emergency →specialist 
•	↑nerve damage ↓exophthalmus
83
Q

how does thyroid eye disease presents (signs)

A
  • Exophthalmos: protruded eyes
  • Proptosis eyes protruding beyond orbit
  • Conjunctival oedema
  • Corneal ulcers
  • Papilloedema
  • Loss of colour vision
  • Ophthalmoplegia especially upward
84
Q

how can thyroid eye disease be investigated

A
  • CT/MRI orbit→ enlarged eye muscles

* Thyroid antibody, TSH and T4

85
Q

What are the differentials for thyroid eye disease

A

Myoischaemia gravis, Cushion’s, Orbital myositis

86
Q

what is the medical treatment for thyroid eye disease and when is it possible

A

ocular lubricants, treat thyroid disfuntion only possible early on

87
Q

what are the lifestyle advices for people with thyroid eye disease

A

stop smoking, sleep propped up avoid dusty conditions

88
Q

what is the more specialist management of thyroid eye disease

A
  • High-dose steroids (IV methylprednisolone is better than prednisolone 100mg/day PO)
  • Surgical decompression →in sever vision threatening cases/cosmetic when improved
  • Other options: Anti-TNFα antibodies (eg infliximab).
89
Q

How common is thyroid storm

A

0.2/100,000 general populaton and 1-2% hyperthyroidism

90
Q

what is the presentation of thyroid storm

A
  • Variable to recognise
  • Pyrexia (over 41°C) and dehydration
  • Agitation, Confusion, Coma, delirium
  • Tachycardia (↑140bpm), AF, Heart failure
  • Cardiovascular collapse
  • D&V
  • Goitre, Thyroid bruit
  • Acute abdomen (exclude surgical causes)
91
Q

what are the precipotating factors of thyroid storm

A

Recent thyroid surgery or radioiodine; infection; MI; trauma.

92
Q

what are the key steps in management of thyroid storm

A
  • Ask an endocrinologist!
  • IV fluids for dehydration; NG for vomiting
  • Bloods including TSH, T3 and T4 + cultures
  • Sedate if necessary → chlorpromazine 50mg PO/IM
  • Propranolol if not contraindicated (asthma ↓CO) IV
  • High-dose digoxin
  • Carbimazole 15-25mg/6h/PO
  • Lugol’ s solution → iodine oral solution for 7-10/7
  • Hydrocortisone 100mg/6h/IV →prevents peripheral conversion of T4
  • Treat cause and adjust fluids
93
Q

define hypothyroidism

A

OR underactive thyroid; Common endocrine disorder in which the thyroid gland does not produce enough thyroid hormone

94
Q

Define cretinism

A

underactive thyroid in children leading to other range of symptoms

95
Q

what are the two principle cause of hypothyroidism

A

iodine deficiency world wide and Hashimoto’s else where

96
Q

How common is hypothyroidism and what is the sex distribution

A

4/1000 6:1 F:M

97
Q

What are the symptoms of hypothyroidism

A 
Fatigue 
Poor memory and concentration 
Constipation 
Shortness of breath 
Hoarse voice
Heavy periods (and later oligomenorrhoea or amenorrhoea)
Abnormal sensation 
Poor hearing – due to fluid in the middle ear
Reduced libido 
Cold intolerance
98
Q

What are the signs of hypothyroidism

A

Dry, coarse skin
Myoxoedema (mucopolysaccharide deposits in the skin)
Hair loss
Swelling of the limbs
Delayed relaxation of tendon reflexes i.e. ankle jurk
Carpal tunnel syndrome
Pleural effusion, ascites, pericardial effusion

99
Q

What are the uncommon presentations of hypothyroidism

A
  • Acute renal failure
  • Female sexual dysfunction
  • Hypercholesterolaemia
  • Also myxoedema and myxoedema coma
100
Q

What does BRADYCARDIA stand for as mnemonic

A
  • Bradycardic
  • R-reflexes relax slowly
  • A-ataxia (cerebellar)
  • D-dry thin hair and skin
  • Y-yawning, drowsy, coma, tired, sleepy, lethargic
  • C-cold hands, cold dislike
  • A-ascites, pitting oedema (lids, hands and feet), pericardial or pleural effusion
  • R-round puffy face, double chin, obese, increase in weight
  • D-defeated demeanour
  • I-immobile+/- ileus, myalgia, cramps, weakness
  • C-CCF, constipation, carpal tunnel syndrome
101
Q

What are the problems with hypothyroidism in women of child bearing age

A

• Risk of miscarriage and impaired fertility → even in subclinical

102
Q

how common is hypothyroidism during pregnancy

A

0.3-0.5%

103
Q

what are the risks associated with hypothyroidism in pregnancy

A 
o	Low birth weight 
o	Anaemia 
o	Pre-eclampsia
o	Offspring with lower intelligence
o	The risk of infant death around the time of birth
104
Q

what are the characteristics of newborns with hypothyroidism

A

normal birth weight BUT large head and open posterior fontanelle

105
Q

what is the presentation of newborns with hypothyroidism

A

• Signs → similar to adults + developmental
o Drowsiness, hypotonia, hoarseness on crying
o Feeding difficult, constipated, dry skin, cold
o Umbilical hernia, enlarged tongue, jaundice
o Goitre →rare may develop in children
• Developmental problems → if untreated
o Intellectual impairment →IQ↓6-15
o Dysfunctional large and fine motor skills + reduced attention span

106
Q

What is the presnetation of adolexcents with hypothyroidism

A 
•	Symptoms → same as adult +
o	Delayed growth 
o	Overweight 
o	Delayed puberty 
•	Signs → similar to adult
o	Bradycardia, goitre, pallor, ↑hair
107
Q

What are the 3 major types of hypothyroidism

A

primary secondary and transient

108
Q

Name 4 causes of primary hypothyroidism

A

iodine deficiency, Hashioto’s, iatrogenic and congenital

109
Q

Name 3 iatrogenic causes of primary hypothyroidism and prognosis

A

o Radioactive iodin ablation therapy → 80-90% treated develop hypothyroidism within 2-3/12
o Pot-thyroidectomy→ 60-80% post subtotal thyroidectomy will become hypo in 12/12
o Overdose of antithyroid medication

110
Q

what is the aetiology of Hashioto’s

A

o Infiltration of thyroid with T-lymphocytes and autoantibodies against thyroid antigens e.g. thyroid peroxidase, thyroglobulin, TSH receptor

111
Q

define thyroid agenesis

A

Underdevelopment of thyroid gland in T1 due to teratogenic exposure i.e. due to radioactive iodine

112
Q

Define thyroid dysgenesis

A

impaired biosynthesis, storage, secretion, delivery etc of TH

113
Q

What are the 4 main causes of secondary hypothyroid

A

• Hypopituitarism
Sheehan syndrome
pituitary tumour i.e. non-functional adenoma; isolated TSH deficiency (rare)

114
Q

what are the causes of Hypopituitarism

A

traumatic brain injury, radiation therapy of head and neck i.e. malignancy

115
Q

What syndrome causes hypothyroidism in relation to post-partum haemorrhage and how

A

Sheehan due to drop in BP and pituitary ischaemia

116
Q

What are the symptoms of Sheehen

A

amenorrhoea, weakness, lack of lactation, poor wound healing hypothyroid symptoms

117
Q

What are the 3 main causes of transient hypothyroidism

A

• Subacute thyroiditis/ de Quervain’s thyroiditis/ granulomatis
silent thyroid
post-partum thyroditis

118
Q

what is the aetiology and presentation of subacute thyroditis

A

o Post infection →release of lymphocytes against thyroid
o Pain, fever, tenderness
o Hypothyroid lasting weeks-months; sometimes permanent

119
Q

what is silent thyroditis

A

o Silent invasion by immune system , may be permanent

120
Q

how common is potpartum thyroditis and what is the prognosis

A

o In 5% and occurs up to 9/12 postpartum
o ↑thyroid followed by hypothyroidism lasting for ~1 year
o 20-40% remain hypothyroid

121
Q

Name three drug types that may lead to hypothyroidism

A

Amiodarone, lithium, anti-thyroid drugs

122
Q

What is Euthyroid sick syndrome and what causes it

A

• Normal TSH and T4 BUT ↓T3
• Long-standing illness
o Altered uptake or increased protein binding
• Cortisol mediated inhibition of conversion of T4→T3
o Stress related to illness stimulates ↑ cortisol

123
Q

what are the risk factors for hypothroidism

A

• Postpartum ~ 7%
• Advanced age
o ↓iodine uptake and ↑in the half-life of T4 due to anatomical and physiological changes
• Family history of autoimmune thyroid disorders
• Autoimmune endocrine conditions e.g. DM type 1
• Primary pulmonary hypertension
o Defined as a sustained pulmonary arterial pressure >25 mm Hg
o ~30% develop hypothyroidism
• Down syndrome
o ~ 30% develop hypothyroidism
o Found to have high levels of antithyroid peroxidase antibodies – suggests an autoimmune aetiology
o Thyroid dysgenesis may also be a reason
• Turner syndrome
o Hypothyroidism is more prevalent (~50%) among F
o 36% of patients with Turner syndrome have elevated antithyroid peroxidase antibody levels

124
Q

What are the two congenital conditions that increase risk of hypothyroidism and how

A

down’s and Turner’s often via antithyroid peroxidase antibody

125
Q

what bloods are important and why, when diagnosing hypothyroidisem

A

o FBC: May show macrocytosis or normochromic anaemia (less commonly)
o U+Es: Check renal function before radioisotope scan
o LFTs and CK
 Mildly elevated
 Due to myopathy and liver dysfunction
 Returns to normal when hypothyroidism has been treated
o TSH
 One immediately and another several weeks after for confirmation
 Levels may be abnormal due to illness
 Testing is discouraged in hospitalised patients unless thyroid dysfunction strongly suspected
o T4
o Lipid levels
 Cholesterol, LDL and lipoprotein (a) can be elevated

126
Q

what do different levels of TSH and T4 indicate

A

TSH T4 Interpretation
Normal Normal Normal thyroid function
Elevated Low Primary hypothyroidism
Normal/low Low Central/ secondary hypothyroidism
Elevated Normal Subclinical hypothyroidism

127
Q

In what condition/situation abnormal TSH and T4 levels can be accepted

A

After surgery and radiotherapy, TSH and T4 levels may give the impression of hypothyroidism, but this is usually just compensatory, and levels will return to normal after a while.

128
Q

what is a management regiment for hypothyroidism in healthy and young person

A

o Levothyroxine (T4) 50 – 100micrograms /24hours PO
 Review at 12 weeks
 Adjust 6 weekly to normalise TSH
monitor yearly

129
Q

what is a management regiment for hypothyroidism in elderly person or someone with IHD

A

o Start at 25micrograms / 24 hours – increase by 25micrograms/4weeks depending on TSH levels

130
Q

How long does levothyroxine take to alter TSH levels

A

~4 weeks

131
Q

What are the ADRs of levothyroxine

A 
o	Palpitations
o	Abdominal pain, nausea, weight loss, increased appetite
o	Anxiousness, agitation, insomnia
o	Osteoporosis 
(mimic hyperthyroidisme)
132
Q

how does the levothyroxine overdose present

how can it be managed

A

increased sympathetic activity causing hypoglycaemia, heart failure, coma and adrenal insufficiency
beta blockers

133
Q

What is the role of amiodarone in hypothyroidism

A

structurally like T4 so may decrease its release

134
Q

how can hypothyroidism due to amiodarone be controlled

A

thyrodectomy if drug required to be continued; long half life i.e. 80d so withdrawal has little effect

135
Q

what is maxoedema coma

A

• Rare, life-threatening state of extreme hypothyroidism

136
Q

what are the causes of maxoedema coma

A

illness with hypothyroidisem or first presentation

137
Q

what is a presentation of maxoedema coma

A
  • Low temperature without shivering
  • Confusion, ↓HR, hyporeflexia, coma
  • ↓ breathing effort, hypoglycaemia
  • Signs of hypothyroidism, cyanosis, HF
138
Q

What are the finings of investigations in maxoedema coma

A

• Low sodium levels
• Elevated ADH
• Worsening kidney functions – reduced eGFR
also chcek FBCs, cultures, glucose TFTs

139
Q

What is the management of maxoedema coma

A

Investigate and treat cause: MI, infection, GI bleed, CF
• 200-500micrograms IV levothyroxine followed by 100-300mcrograms the following day OR
• T3 (liothyronine) 5–20μg/12h IV slowly
• High flow O2 +ABG
• Blankets for hypothermia
• Crystalloids for hypotension
• IV glucose for hypoglycaemia
• hydrocortisone 100mg/8h IV pituitary hypothyroidism

140
Q

What are the changes in sub-clinical hyperthyroidism

A

Occurs when TSH↓, with normal T4 and T3

141
Q

why is subclinical hyperthyroidism a problem

A

• 41% ↑ all cause mortality i.e. AF

142
Q

what are non-sthyroid causes of subclinical hyperthyroidism

A

o Illness
o Pregnancy
o Pituitary or hypothalamic insufficiency
o TSH supressing medication i.e. thyroxin, steroids

143
Q

what is the management of subclinical hyperthyroidism

A

treat and recheck in 6 months

144
Q

what is subclinical hypothyroidism

A

TSH >4mU/L with normal T4 and T3 + symptoms

145
Q

how common is subclinical hypothyroidism

A

10% in >55s

146
Q

what is the prognosis subclinical hypothyroidism

A

2% frank hypothyroidism + ↑TSH/ 2x risk if thyroid peroxidase antibodies OR male

147
Q

what is the management of subclinical hypothyroidism

A
  • Confirm TSH raise 2-4/12 OR monitor
  • Recheck the history for symptoms → low threshold for treatment as ↑↑ cardiac death
  • Treat if: TSH ≥10mu/L; +ve thyroid autoantibodies, Graves’, autoimmunity
  • TSH 4-10 →6 months treatment + ?if helps with symptoms
148
Q

what are the complications of myxoedema coma

A
  • Hypoglycaemia
  • Pancreatitis
  • Arrhythmias
149
Q

what are the triggers for myxoedema coma

A

thyroidectomy, radioiodine

phase 2 endo (4 decks)

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