top of page


An increase in the circulating thyroid hormones (T3 & T4) due to an increase in its synthesis with a decrease in TSH levels.



  • Primary (caused by conditions related to the thyroid gland).

  • Secondary (caused by extra-thyroidal conditions like pituitary gland). 


  1. Primary causes: (MOST COMMON)

    • Graves disease:

      • Most common cause of hyperthyroidism.

      • Autoimmunity.

      • Caused by thyroid stimulating immunoglobulin (IgG Autoantibody), which binds to the thyroid stimulating hormone receptor (TSH) and induces thyroid hormone synthesis and secretion.

    • Nodular goiter:

      • Typically in patients over 40 years.

      • Enlarged glands with mono or multi nodules.

      • If “autonomous” hyperactivity of follicular cells is present → toxic goiter (rare). 

      • Two types:

        • Multinodular (Plummer disease).

        • Solitary nodule:

          • Thyroiditis

          • Viral

          • Lymphatic

          • Postpartum

    • Iodine-induced:​​​​ ​ excess iodine ingestion from diet, radiographic contrast or medication.

  2. Secondary causes:

    • Pituitary tumor.

  3. Others:

    • Factitious hyperthyroidism:

      • Excessive thyroid hormone ingestion (e.g. levothyroxine). 

      • Seen in patients who attempt suicide or want to lose weight.

    • Ovarian tumor (struma ovarii) produce thyroid hormone. 

    • Metastatic thyroid cancer


All symptoms are mainly caused due to increased basal metabolic rate. 

  • Nervousness, insomnia, irritability

  • Hand tremor, hyperactivity

  • Sweating

  • Heat intolerance

  • Increase in appetite, weight loss

  • Palpitation

  • Diarrhea

  • Proximal muscle weakness

  • Menorrhagia # hypothyroidism (oligomenorrhea)


  • Brisk reflex

  • Tremor

  • Increase in BP

  • Goiter (diffused, non tender → graves | tender → thyroiditis| irregular,
    asymmetrical → multinodular| single nodule w\ atrophic thyroid → toxic adenoma)

  • Tachycardia, arrhythmia (PVC, Atrial fibrillation)

  • Specific signs seen in Graves:

  • Proptosis (hallmark of graves), lid lag and retraction

  • Pretibial edema

  • Carotid bruit

Only Graves’s disease of the hyperthyroidism types has eye and skin abnormalities. 

Study guide:


Exopthalmos & Dermopathy

Diffused Goitter 


  • Best initial/most useful screening test is measuring serum TSH level. 


  • Antithyroid drugs (ATD):

    • Methimazole.

    • Propylothiouracel (PTU): can be used in pregnancy.  

    • Indications:

      • Mostly in graves → with pregnant women, children, and those who refuse RAI.

    • Side effects: 

      • Polyarthritis

      • Agranulocytosis.

      • Immunological hepatitis (with PTU).

Methimazole is preferred more than PTU in general except in pregnancy. 


patients on anti- thyroid drug should be told to stoptheintakein case of fever or sore throat.

  • Radioactive iodine (RAI):

    • Indications:

      • Treatment of choice in grave’s disease. 

      • ATD relapses or if the patient develops agranoulocytosis.

      • Elderly.

      • Multinodular and solitary nodule.  

      • Cardiac problems: treatment with methimazole first is recommended. 
        Methimazole should be stopped before starting RAI by 4 days.

    • Side effect:

      • Hypothyroidism (major complication).

      • Could exacerbate proptosis.

      • Could cause thyroiditis.

    • Contraindication: 

      • Pregnancy or breastfeeding, if taken avoid pregnancy for 4-8 months. 

  • Surgery (total removal is preferred):

    • Indications:

      • Patient < 40 Y/O with toxic nodules.

      • Pregnant women and children who cannot tolerate ATD.

    • Side effect:

      • Hypothyroidism

      • Risk of recurrent laryngeal nerve injury.

      • Watch for hypocalcaemia → risk of parathyroid gland removal.

  • Symptomatic treatment:

    • In palpitation: Beta blocker is used with ATD

    • Graves ophthalmopathy:

      • Steroids are the best initial therapy. 

Follow up:

  • ATD:

    • Patient on ATD should be monitored every 4-12 weeks until reaching euthyroid. (4-week check-upàcheck T4 b/c TSH ‘short half-life’ will not respond until 6 weeks). 

    • If euthyroid is accomplished → check every 3-4 months for 12-18 months.

    • If medication is ceased → every 3-4 months to look for relapses. 

  • RAI:

    • Every 4-6 weeks for 3 months.  

    • Then annual visits to check for hypothyroidism. 


  • Agabegi S, Agabegi E, Ring A. Step-up to medicine. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2013.

  • Thyroid and Parathyroid Disorders - American Family Physician [Internet]. 2015 [cited 23 December 2015]. Available from: 

  • Lipsky M, King M. Blueprints family medicine. Baltimore, MD: Lippincott Williams & Wilkins; 2011.

  • Sattar H. Fundamentals of pathology. Chicago:; 2011.

  • Kaplan. Kaplan lecture notes, Medicine, 2014.

Written by:      Rawan Al-Tuwaijri

Revised by:      Jumana AlJohani
                       Bassam Alghamdi

​Format Editor:  Adel Yasky

Web publisher:  Bayan Alzomaili

bottom of page