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Endocrine & Diabetes > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

Describe the thyroid

A

-Shaped like bow tie in lower neck
-Just under thyroid cartilage (Adams apple)
-Thyroid disease common: 2-5% of community
-More common in women (autoimmune- antibodies attack thyroid)
-Thyroid problems:
=Overactive
=Underactive
=Goitre (globally enlargement) or nodules (lumps)

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2
Q

Describe the thyroid follicle

A
  • Follicle filled with colloid (T3/T4)
  • Surrounded by thyroid epithelial cells
  • Hormones secreted directly into blood stream (no ducts)
  • C cells= interfollicular/ parafollicular, calcitonin (calcium regulation)
  • Sympathetic nerve endings
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3
Q

What happens in the thyroid epithelium cells?

A
  1. Trapping of iodide from the plasma
  2. Oxidation of iodide by a thyroid peroxidase using H2O2
  3. Incorporation of iodine into tyrosyl residues on thyroglobulin to make mono- and di-iodotyrosine
  4. Coupling of iodotyrosyl residues to make T4, T3 and rT3 on thyroglobulin
  5. Re-absorption of colloid into cell in globules
  6. Thyroglobulin proteolysis by lysosomes
  7. Release of T4, T3, etc. and secreted into bloodstream
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4
Q

What is the difference between T3 and T4?

A

-T4= pro-hormone so inactive, converted to T3 by removal of one iodine via deiodinase enzymes
-T3 active hormone
=Always available substrate in bloodstream

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5
Q

How do thyroid hormones circulate in the blood?

A 
-Bound to proteins
=Thyroxine Binding Globulin (TBG) 70%
=Transthyretin 20%
=Albumin 10%
Therefore, free hormone that is active =0.05%, bound hormone inactive 99.95%
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6
Q

How do we control the conversion of T4 to T3?

A

-TSH receptor in thyroid gland stimulates thyroid to make and secrete hormones
-Predominantly T4 made ratio of 14:1 T3
-Most T3 made by peripheral conversion (removing one iodine molecule)
=80% T3 produced from peripheral conversion of T4 in liver, kidney and muscle
=20% T3 produced from thyroid gland
-Thyroid hormones (T3) act on nuclear receptors so transported into cell via proteins, controls transcription of DNA

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7
Q

Describe the pituitary control of thyroid hormone production

A

-Hypothalamus makes thyrotropin releasing hormone (TRH)
-Acts on anterior pituitary= TSH
-T4 and T3 production in thyroid
-Controlled by negative feedback loops
=Hormone produced inhibits hormone that triggered own release (inhibit release of TSH and TRH)

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8
Q

What are the actions of thyroid hormone?

A

-Growth development= pregnancy
-Basal metabolic rate
regulator of metabolism
-Thermogenesis in brown adipose tissue (create heat)
-Activate mental processes= underactive feel slow down and depressed, agitated and irritable if overactive

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9
Q

What are the causes of primary hyperthyroidism?

A

-Graves disease (75%)
-Toxic Multinodular Goitre (MNG) (15%)
=Or singular toxic nodule
-Thyroiditis

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10
Q

Describe Graves disease

A
  • Autoimmune disease
  • TSH receptor Antibodies attack thyroid to make it overactive
  • Can be associated with eye disease (antibodies attack orbital)
  • Butterfly/ bowtie swelling on neck= smooth goitre
  • Technetium scan- activity of thyroid, whole gland takes up radio active substance
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11
Q

Describe Toxic Multinodular Goitre (MNG)

A
  • Multiple lumps (nodules) on enlarged thyroid (goitre), benign growths
  • Often one or more lumps will be overactive
  • Can get lid lag or lid retraction, but no other features of thyroid eye disease, trigger sympathetic nerve endings
  • Unaffected gland switched off as no TSH

-More common with older age
=Bigger and bulkier= compress trachea and oesophagus

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12
Q

Describe thyroiditis

A
  • Temporary overactivity of thyroid/ gland damage so releases pre-formed hormone
  • Can be followed by period of underactivity
  • Triggered by pregnancy, infection or some drugs (eg amiodarone)
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13
Q

What are the symptoms over primary hyperthyroidism?

A
  • Weight loss despite good appetite (often very hungry) (basal metabolic rate high)
  • Tiredness (nervous exhaustion feeling)
  • Tremor (SNS activation)
  • Hot, sweaty
  • Palpitations
  • Diarrhoea (GI working faster, water not reabsorbed)
  • Light/absent menses
  • Mood: irritable, anxiety
  • Eyes (change in appearance, red, gritty, painful, double vision)
  • Muscle weakness, particularly proximal (thigh)
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14
Q

How can history contribute/ indicate primary hyperthyroidism?

A
  • PHx and Meds: check about asthma and heart disease (relevant to use of propranolol/ beta blocker and risk from tachycardia respectively)
  • FHx: autoimmune disease (Type 1 diabetes, pernicious anaemia, Addison’s disease, coeliac)
  • SHx: smoking (eye disease risk x10), job and family (radio-iodine)
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15
Q

How does examination indicate primary hyperthyroidism?

A

-Agitated, talk fast
-Warm, sweaty
-Tremor
-Increased Heart Rate (HR), may be in Atrial Fibrillation (AF)
-Smooth goitre (Graves) vs MNG vs single nodule vs no goitre (thyroiditis)
-Bruit (whooshing sound) heard over goitre almost diagnostic of Graves
-Eyes:
=Lid retraction and lid lag in any cause of overactive thyroid.
=Any other eye signs indicate Graves disease

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16
Q

Describe how eyes may present in primary hyperthyroidism

A

-Lid retraction
-Lid lag
=Associated with any cause of thyrotoxicosis

-Graves Disease:
=Redness
=Gritty sensation
=Dry or watery eyes
=Pain on eye movement (inflammation of muscles)
=Swelling around the eyes
=Proptosis (pushed forward appearance of eyes)
=Double vision
=Loss of colour vision
17
Q

What tests are diagnostic of primary hyperthyroidism?

A
  • Thyroid function tests prove hyperthyroidism
  • TRAbs (TSH Receptor Antibodies) significantly positive indicates Graves- autoimmune problem
  • TPO (thyroid peroxidase) antibodies less specific, positive also in hypothyroidism
  • If TRAbs are negative, do scintigraphy (often technetium rather than radio-iodine uptake)- no= thyroiditis
18
Q

How is thyroiditis treated?

A
  • Beta blocker

- Thyroxine later (damaged thyroid so underactive)

19
Q

What are the anti thyroid drugs?

A
  • Carbimazole and propylthiouracil (PTU)
  • Decrease production of thyroid hormone (block TPO)
  • Not for thyroiditis (high T4 levels are due to release of hormone stores from damaged gland, but gland is not actually overactive)
  • Rare side effect of agranulocytosis (<1/500)= bone marrow not producing neutrophils
20
Q

What other drugs are used in primary hyperthyroidism?

A

-Propranolol good for tremor and increased HR

=Contraindicated in asthma

21
Q

What treatments (other than drugs) are used in primary hyperthyroidism management?

A

-Radioactive iodine (I131) - capsule, taken up by overactive gland
=Risk of long term hypothyroidism
=Avoid pregnancy for 6 months.
=Restrict contact with children under 12 and pregnant women
=Don’t share bed with partner for 4 days
-Surgery
=Risk of long term hypothyroidism or damage to recurrent laryngeal nerve and parathyroid glands (control calcium)

22
Q

How do we choose management options dependent on cause of primary hyperthyroidism?

A

-Graves often treated with ATDs first time round
=12-18 month course of tablets
=60-70% chance of relapse

-I131 for recurrent Graves
=Once it returns it will keep coming back
-I131 for TMNG or toxic nodule
=No chance of long term remission with a course of tablets
-Risk of hypothyroidism after I131
=lower with TMNG and toxic nodule than Graves
-Risk of thyroid eye disease flaring up after I131
-Tend to save surgery for patients with goitre

23
Q

How does thyroid eye disease develop?

A

-B cells produce TSH receptor antibodies dock with TSH receptors in thyroid gland, stimulated to make T3 and T4 to suppress TSH by negative feedback
-Antibodies bind to receptors in connective tissue behind orbit (eye),
=affects adipocytes leading to adipogenesis= new fat calls increase= push eyes forward
=Affects fibroblasts, increase matrix production, retain fluid swelling of muscles and tissues behind eyes
=Increase in pressure

24
Q

Describe the assessment of graves eye disease

A

-Are there symptoms/ signs of thyroid eye disease
=Proceed to eye-focussed history and examination
=No= no further action (management)

25
Q

What indicates thyroid eye disease in a history?

A
  • Change in appearance of eyes or periorbital tissues
  • Corneal symptoms (grittiness, photophobia, watering)
  • Extra-Ocular Muscle (EOM) restriction (eg diplopia/double vision)
  • Symptoms of EOM inflammation (pain at extreme gaze)
  • Orbital ache unrelated to gaze
  • Symptoms of optic neuropathy* (decreased colour vision, blurred vision)
  • “Popping” of eye; inability to close lids (globe subluxation= need urgent ophthalmology referral)
26
Q

What indicates thyroid eye disease on examination?

A 
-Redness 
=(either eyes themselves or eyelids)
-Eyelids: 
=thickening or oedema, 
=lid retraction
-Chemosis
-Proptosis (eyes pushed forward)
-Test eye movements (“H”)
-Lagophthalmos (inability to close eyelids without forcing)
-Optic nerve 
=Visual Acuity (Snellen chart)
=Fundoscopy or slit lamp to visualise head of optic nerve
27
Q

What are the parts of the eye that are affected by thyroid eye disease?

A
  • Preseptal eyelid
  • Pretarsal eyelid
  • Carcuncle= inner part of eye (corner)
  • Plica= next to carcuncle, folded up conjunctiva, expands as eye looks other way
28
Q

How does activity and severity affect thyroid eye disease management?

A
  • Need to differentiate between active and inactive
  • Only active disease responds to steroids
  • Severe but inactive disease is treated with corrective surgery

-There are scoring systems to help us
=Eg Clinical Activity Score (looks at pain, redness, swelling and change in function)
=Different classifications for severity, none of which are perfect

29
Q

How is Graves eye disease managed?

A

-Unless mild, should manage in joint thyroid eye clinic
-Achieve euthyroidism
=Both hyper and hypothyroidism are bad
=Can have active eye disease without thyroid being overactive
=Thyroid eye disease can even present many months before thyroid disease develops

  • Smoking cessation (smokers have 9x increased risk of developing severe disease and respond less well to treatment)
  • Topical lubricants
  • Selenium 200mcg daily (antioxidant)
  • Steroids (oral or iv if active eye disease)
  • Other immunosuppression (eg cyclosporine)
30
Q

How is Graves disease diagnosed on a CT scan?

A

-50% should be behind red line (across bony prominences)

=Enlarged medial and inferior rectus muscles

31
Q

What occurs if the initial management doesn’t work?

A
  • Consider orbital radiotherapy
  • Consider immunosuppressant treatment (eg cyclosporine) as it is TRAbs that drive the eye disease
  • Surgical decompression if evidence of optic neuropathy and raised intraocular pressure
32
Q

What happens once active eye disease settles?

A

-Elective decompression to resolve residual proptosis
-Squint surgery if EOM restriction
-Eyelid surgery if residual swelling or retraction
(In that order)

33
Q

What is thyrotoxicosis?

A

T4 is high and TSH is low/ suppressed

Endocrine & Diabetes (45 decks)

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