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

dralaawafa@hotmail.com