• GENERAL ASPECTS OF THYROID GLAND
– Anatomy: weight range from 12 to 30g
– Located in the neck, anterior to the trachea
– Produces: T4 & T3 (active hormone)
• Thyroid hormones:
– T4: (Thyroxine) is made exclusively in thyroid gland
• Ratio of T4 to T3 ; 5::1
• Potency of T4 to T3; 1::10
• T4 is the most important source of T3 by peripheral tissue deiodination “ T4 to T3 “
– T3: (Triiodothyronine) main source is peripheral deiodination:
• Ratio of T3 to T4 ; 1::5
• Potency of T3 to T4; 10::1
• T3 is the most important because more than 90% of the thyroid hormones physiological effects are due to the binding of T3 to Thyroid receptors in peripheral tissues.
• PHYSIOLOGY EFFECTS OF THYROID HORMONES
• THEY ARE NOT ESSENTIAL FOR LIFE, BUT ARE EXTREMELY HELPFUL
THYROID GLAND DISORDERS
– Affects every single cell in the body
• Modulates:
– Oxygen consumption
– Growth rate
– Maturation and cell differentiation
– Turnover of Vitamins, Hormones, Proteins, Fat, CHO
• MECHANISMS OF THYROID HORMONE ACTION
– Act by binding to Nuclear receptors, termed Thyroid Hormone Receptors (TRs), Increasing synthesis of proteins
– At mitochondrial level increases number and activity to increasing ATP production
– At Cell membrane increases ions and substrates transmembrane flux
• THYROID HORMONE EFFECTS
– CALORIGENESIS
– GROWTH & MATURATION RATE
– C.N.S. DEVELOPMENT & FUNCTION
– CHO, FAT & PROTEIN METABOLISM
– MUSCLE METABOLISM
– ELECTROLYTE BALANCE
– VITAMIN METABOLISM
– CARDIOVASCULAR SYSTEM
– HEMATOPOIETIC SYSTEM
– GASTROINTESTINAL SYSTEM
– ENDOCRINE SYSTEM
– PREGNANCY
– CALORIGENESIS
• Controls the Basal Metabolic Rate (BMR)
– CHO METABOLISM
• Increases:
– Glucose absorption of the GI tract
– Glucose consumption by peripheral tissues
– Glucose uptake by the cells
– Glycolysis
– Gluconeogenesis
– Insulin secretion
– GROWTH & MATURATION RATE
– C.N.S. DEVELOPMENT & FUNTION
• “ESSENTIAL” in the newborn to prevent development of “CRETINISMS” & to a normal “IQ”
• Modulation of brain cerebration
• Mood modulation
- FAT & PROTEIN METABOLISM
• Increase lipolysis and lipid mobilization with:
– Cholesterol
– Triglicerides
– Free fatty acids
– MUSCLE METABOLISM
• Modulates;
– Strength & velocity of contraction
– ELECTROLYTE BALANCE
• Low Thyroid hormones could induce hyponatremia
– VITAMIN METABOLISM
• Modulates vitamin consumption
– HEMATOPOIETIC SYSTEM
• Could induce anemia
– CARDIOVASCULAR SYSTEM
• Hyperthyroidism, increases:
– Heart rate & myocardial strenght
– Cardiac output
– Peripheral resistances (Vasodilatation)
– Oxygen consumption
– Arterial pressure
• Hypothyroidism, reduces:
– Heart rate & myocardial strenght
– Cardiac output
– Peripheral resistances (Vasodilatation)
– Oxygen consumption
– Arterial pressure
• Modulate bowel movements and absorption
– ENDOCRINE SYSTEM
• Modulates pituitary axis, affecting GH, ACTH, FSH, LH, so-on
– PREGNANCY
• Modulates growth rate and affects lactation
THYROID GLAND DISORDERS
• DIVIDED INTO:
– THYROTOXICOSIS (Hyperthyroidism)
• Overproduction of thyroid hormones
– HYPOTHYROIDISM (Gland destruction)
• Underproduction of thyroid hormones
– NEOPLASTIC PROCESSES
• Beningn
• Malignant
• LABORATORY EVALUATION
TSH normal, practically excludes abnormality
– If TSH is abnormal, next step: Total & Free T4 & T3
- TSI (Thyroid Stimulating Ig)
- TPO (Thyroid Peroxidase Ab)
- Antimitochondrial Ab
- Serum Tg (Thyroglobulin)
- Radioiodine uptake & Thyroid scaning
- FNA, Fine-needle aspiration
- Thyroid ultrasound
• TSH High usually means Hypothyroidism
– Rare causes:
• TSH-secreting pituitary tumor
• Thyroid hormone resistance
• Assay artifact
• TSH low usually indicates Thyrotoxicosis
– Other causes
• First trimester of pregnancy
• After treatment of hyperthyroidism
• Some medications (Esteroids-dopamine)
• THYROTOXICOSIS:
– is defined as the state of thyroid hormone excesss
• HYPERTHYROIDISM:
– is the result of excessive thyroid gland function
• Abnormalities of Thyroid Hormones
– Thyrotoxicosis
• Primary
• Secondary
• Without Hyperthyroidism
• Exogenous or factitious
– Hypothyroidism
• Primary
• Secondary
• Peripheral
• Causes of Thyrotoxicosis:
– Primary Hyperthyroidism
• Grave´s disease
• Toxic Multinodular Goiter
• Toxic adenoma
• Functioning thyroid carcinoma metastases
• Activating mutation of TSH receptor
• Struma ovary
• Drugs: Iodine excess
– Thyrotoxicosis without hyperthyroidism
• Subacute thyroiditis
• Silent thyroiditis
• Other causes of thyroid destruction:
– Amiodarone, radiation, infarction of an adenoma
• Exogenous/Factitia
– Secondary Hyperthyroidism
• TSH-secreting pituitary adenoma
• Thyroid hormone resistance syndrome
• Chorionic Gonadotropin-secreting tumor
• Gestational thyrotoxicosis
• Symptoms:
– Hyperactivity
– Irritability
– Dysphoria
– Heat intolerance & sweating
– Palpitations
– Fatigue & weakness
– Weight loss with increased appetite
– Diarrhea
– Polyuria
– Sexual dysfunction
• Signs:
– Tachycardia
– Atrial fibrillation
– Tremor
– Goiter
– Warm, moist skin
– Muscle weakness, myopathy
– Lid retraction or lag
– Gynecomastia
– * Exophtalmus
– * Pretibial myxedema
• Differential diagnosis:
– Panic attacks
– Psychosis
– Mania
– Pheochromocytoma
– Hypoglycemia
– Occult malignancy
• Treatment:
– Reducing thyroid hormone synthesis:
• Antithyroid drugs (Methimazole, Propylthyouracil)
• Radioiodine (131I)
• Subtotal thyroidectomy
– Reducing Thyroid hormone effects:
• Propranolol
• Glucocorticoids
• Benzodiazepines
– Reducing peripheral conversion of T4 to T3
• Propylthyouracil
• Glucocorticoids
• Iodide (Large oral or IV dosage) (Wolf-Chaikoff effect)
• Treatment: Special considerations:
– Thyrotoxic crisis or Thyroid storm:
• It´s a life-threatening exacervation of thyrotoxicosis, acompanied by fever, delirium, seizures, coma, vomiting, diarrhea, jaundice.
• Mortality rate reachs 30% even with treatment
• It´s usually precipitated by acute illness, such as:
– Stroke, infection,trauma, diabeic ketoacidosis, surgery, radioiodine treatment
• Propylthyouracil IV or Nasogastric tube
• Radioiodine (131I)
• Propranolol
• Glucocorticoids
• Benzodiazepines
• Iodide (Large oral or IV dosage) (Wolf-Chaikoff effect)
• HYPOTHYROIDISM
– Primary
• Autoimmune (Hashimoto´s)
• Iatrogenic Surgery or 131I
• Drugs: amiodarone, lithium
• Congenital (1 in 3000 to 4000)
• Iodine defficiency
• Infiltrative disorders
• Hashimoto´s Thyroiditis or Goitrous thyroiditis
•
– Mean anual incidence:
• Women 4:1000 Men 1:1000
• Risk factors; TPO antibodies (90%) Japanese, previous history, high I intake
• Average age: 60
• Frequently associated to other autoimmune disorders such as: AR, SLE, Sjogren´s so-on.
• Treatment: Levothyroxine
• CONGENITAL HYPOTHYROIDISM
• Prevalence: 1 in 3000 to 4000 newborns
– Cause: Dysgenesis 85%
– Dx: Blood screning (TSH &/or T4)
• Treatment:
– Supplemental Tx. With Levothyroxine is “essential” for a normal C.N.S. Development and prevention of mental retardation
HYPOTHYROIDISM
– Secondary
• Pituitary gland destruction
• Isolated TSH deficiency
• Bexarotene treatment
• Hypothalamic disorders
– Peripheral:
• Rare, familial tendency
• Symptoms:
– Tiredness
– Weakness
– Dry skin Sexual dysfunction
– Dry skin
– Hair loss
– Difficulty concentrating
• Signs:
– Bradycardia
– Dry coarse skin
– Puffy face, hands and feet
– Diffuse alopecia
– Peripheral edema
– Delayed tendon reflex relaxation
– Carpal tunel syndrome
– Serous cavity effusions.
• SPECIAL TREATMENT CONSIDERATIONS
• Myxedema coma
– Reduced level of consciousness, seizures
– Hypotension/shock
– Hypothermia
– Hyponatremia
• Usually in elderly hypothyroid pts.
• Usually precipitated by intercurrent illnesses that impairs ventilation
• It´s an Emergency with a high mortality rate
• Treatment: Lyotironine(T3) or T4, Hydrocortisone, external warming, IV fluids
• Elderly patients
• Coronary Artery Disease
• Poor adrenal gland reserve
• Childrens
• Pregnancy
• Emergency surgery (Non thyroid related)
