CLINICAL ASPECTS OF
THYROID DISORDERS
Alaa Wafa MDAssociate Professor of Internal Medicine
PGDIP DM Cardiff University UKDiabetes & Endocrine Unit.
Mansoura University( Sem 5 ) 2015
Janet ,,Case 5 Scenario
A 30-year-old woman Nervousness, irritability, palpitations
and heat intolerance. Lost 9.1 kg despite a good appetite. Her eyes bulge. Diffuse enlargement thyroid gland. Carbimazole and propranolol are
prescribed.
Where to look for Thyroid Gland?
Clinical Anatomy of Thyroid
Where to look for Thyroid ?
Clinical Exam. of Thyroid• Have patient seated on a chair• Inspect neck before & after
swallowing• Examine with neck in relaxed
position• Palpate from behind the patient• Remember the rule of finger tips• Use the tips of fingers for
palpation• Palpate firmly down to trachea
Clinical Exam of Thyroid
Goiter
• A swollen thyroid gland
• Assessment;– how big, how
quickly has it developed, is it smooth or nodular, is it painful, any associated lymph nodes, any sudden changes, is it big enough to cause local symptoms (e.g. breathing problems)
Thyromegaly
The Neck Lateral view of enlarged thyroid.
The Neck Carcinoma thyroid.
Goiter.
Aspects That Will Be Addressed
• Hyperthyroidism• Hypothyroidism• Thyroiditis
Hyperthyroidism
Hyperthyroidism Symptoms Hyperactivity/ irritability Heat intolerance and sweating Palpitations Fatigue and weakness Weight loss with increase of appetite Diarrhoea Polyuria Oligomenorrhoea, loss of libido
Hyperthyroidism Signs Tachycardia (AF) Tremor Goiter Warm moist skin Proximal muscle
weakness Lid retraction or
lag Gynecomastia
Causes of HyperthyroidismMost common
causes Graves disease Toxic multinodular
goiter Autonomously
functioning nodule
Rarer causes Thyroiditis or other
causes of destruction Thyrotoxicosis factitia Iodine excess (Jod-
Basedow phenomenon) Secondary causes (TSH
or ßHCG)
Graves Disease Autoimmune disorder Abs directed against TSH receptor
with intrinsic activity. Thyroid and fibroblasts
Responsible for 60-80% of Thyrotoxicosis
More common in women
Graves Disease Eye Signs(Ophthamopathy)
N - no signs or symptomsO – only signs (lid retraction
or lag) no symptomsS – soft tissue involvement
(peri-orbital oedema)P – proptosis (>22 mm)
(Hertl’s test)E – extra ocular muscle
involvement (diplopia)C – corneal involvement
(keratitis)S – sight loss (compression
of the optic nerve)
Ophthalmopathy Signs of Graves’s ophthalmopathy are
divided into two components: 1) Spastic: Stare, lid lag and lid retraction
which account for the “frightened” facies. 2) Mechanical: Proptosis of varying
degrees,ophthalmoplegia,and congestive occulopathy characterized by chemosis,conjunctivitis,periorbital swelling and the potential complications of corneal ulceration,optic neiritis and optic atrophy.
Hyperthyroid Eye Disease Hyperthyroidism (any cause)
Lid lag, lid retraction and stare Due to increased adrenergic
tone stimulating the levator palpebral muscles.
True Graves’ Ophthalmopathy Proptosis Diplopia Inflammatory changes
• Conjunctival injection• Periorbital edema• Chemosis
Due to thyroid autoAb’s that cross-react w/ Ag’s in fibroblasts, adipo-cytes, + myocytes behind the eyes.
Neonatal hyperthyroidism born to mother with Graves’ disease
A Color Atlas of Endocrinology p51
“Exophthalmos”
Proptosis
Lid lag
Thyroid Ophthalmopathy
Ophthalmopathy in Graves
Periorbital edema and chemosis
Ophthalmopathy in Graves
Occular muscle palsy
Severe Exophthalmia
Dermopathy• Usually occurs over the dorsum of the legs or feet
and is termed localized or pretibial myxedema.• It is usually a late phenomenon• The affected area is usually demarcated from the
normal skin by being raised and thickened and having a peau d’ orange appearance;it may be pruritic and hyperpigmented.
• The most common presentation is non pitting oedema,but lesions maybe plaque like,nodular or polypoid.
• Clubbing of the fingers and toes accompanies and is termed thyroid acropachy
Thyroid Dermopathy
Pink and skin coloured papules, plaques on the shin
Thyroid Acropachy
Thyroid acropachy. This is most marked in the index fingers and thumbs
Graves with Acropathy
Graves Goiter Acropathy
Clubbing andOsteoarthropathy
Thyroid Acropathy
Onycholysis
Investigations Thyroid function test: TSH- Undetectable T4 - Raised T3 - Raised
TSH-receptor antibodies(TRAb)-elevated in Graves’s disease
Isotope scanning- Increased uptake
Nucleotide Scintigraphy
Graves Disease
Graves Disease
I 123 or TC 99m Normal v/s Graves
Toxic Multinodular Goiter (TMG)
Thyrotoxicosis- TreatmentThree modalities:
Radioactive iodine
antithyroid drugs
surgery
Hyperthyroidism (Treatment)
1) β-blockers (symptom control) Propranolol (Inderal ®)
2) 131-RAIA (70% thyroidologists prefer) Dosing
• Graves: 10-15 mCi• Toxic MNG/Adenoma: 20-30 mCi
Absolute contraindications• Pregnancy and lactation (excreted in breast milk)!
Pregnancy should be deferred for at least 6 months following therapy with radio-active 131
It is advisable to avoid 131-Rdio-active iodine therapy in patients with active moderate severe Graves’ ophthalmopathy.
Hyperthyroidism (Treatment)3) Antithyroid Drugs (30% thyroidologists prefer)
Propylthiouracil (PTU) • 100 mg bid-tid to start
Methimazole• 10X more potent the PTU • 10 mg bid-tid to start
Complications of ATD’s • Agranulocytosis (1/200-500)
• usually presents w/ acute pharyngitis/ tonsilitis or pneumonia.
• Rash • Hepatic necrosis, Cholestatic jaundice • Arthralgia
Hyperthyroidism (Treatment)
4) Surgery (sub-total thyroidectomy)
Indications• Patient preference• Large or symptomatic goiters• When there is question of malignancy
Need to be euthyroid prior to surgery • To ↓ the risk of arrhythmias during induction of anesthesia• To ↓ the risk of thyroid storm post operatively• ATD’s + β-blockers
Risks• Permanent hypoparathyroidism• Recurrent laryngeal nerve problems• Permanent hypothyroidism
Hypothyroidism
Hypothyroidism Symptoms Tiredness and
weakness Dry skin Feeling cold Hair loss Difficulty in
concentrating and poor memory
Constipation
Weight gain with poor appetite
Hoarse voice Menorrhagia, later
oligo and amenorrhoea
Paresthesias Impaired hearing
Hypothyroidism Signs Dry skin, cool extremities Puffy face, hands and feet Delayed tendon reflex
relaxation Carpal tunnel syndrome Bradycardia Diffuse alopecia Serous cavity effusions
infant cretin
Causes of Hypothyroidism Autoimmune
hypothyroidism (Hashimoto’s, atrophic thyroiditis)
Iatrogenic (I123treatment, thyroidectomy, external irradiation of the neck)
Drugs: iodine excess, lithium, antithyroid drugs, etc
Iodine deficiency Infiltrative disorders
of the thyroid: amyloidosis, sarcoidosis, haemochromatosis, scleroderma
Lab Investigations of Hypothyroidism
TSH , free T4 Ultrasound of thyroid – little value Thyroid scintigraphy – little value Anti thyroid antibodies – anti-TPO S-CK , s-Chol , s-Trigliseride Normochromic or macrocytic anemia ECG: Bradycardia with small QRS
complexes
Treatment of Hypothyroidism Levothyroxine
If no residual thyroid function 1.5 μg/kg/day Patients under age 60, without cardiac disease
can be started on 50 – 100 μg/day. Dose adjusted according to TSH levels
In elderly especially those with CAD the starting dose should be much less (12.5 – 25 μg/day)
Thyroiditis
Thyroiditis Acute: rare and due to suppurative
infection of the thyroid Sub acute: also termed de
Quervains thyroiditis/ granulomatous thyroiditis – mostly viral origin
Chronic thyroiditis: mostly autoimmune (Hashimoto’s)
Thyroiditis The most common form of thyroiditis
is Hashimoto thyroiditis, this is also the most common cause of long term hypothyroidism
The outcome of all other types of thyroiditis is good with eventual return to normal thyroid function
Thank you
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