1. THYROTOXICOSIS. DIFFUSE TOXIC GOITER
HYPO VS HYPERTHYROIDISM

2. HYPO VS HYPERTHYROIDISM
FINDINGS HYPOTHYROIDISM HYPERTHYROIDISM
METABOLIC Weight gain and cold intolerance,
hyponatremia, decreased sweating
Weight loss and heat intolerence, increased
sweating
SKIN/HAIR Dry, cool skin, coarse and brittle hair Warm, mois skin, dine hair
OCULAR Periorbital edema Ophthalmopathy in Graves disease
GI Constipation and decreased appetite Hyperdefecation/diarrhea, increased
appetite
MSK Hypothyroid myopathy, carpal tunner
syndrome, myoedema
Thyrotoxic myopathy
REPRODUCTIVE Abnormal uterine bleeding, decreased
libido, infertility
Abnromal uterine bleeding, gynecomastia,
decreased linido, infertility
NEURO-PSYCH Hypoactivity, lethargy, depressed mood,
decreased reflexes
Hyperactivity, restlessness, anxiety,
insomina, fine tremors
CARDIOVASCULAR Bradycardia, dyspnea on exertion Tachycardia, palpitations, dyspnea, systolic
HRN
LABS ↑ TSH (if primary)
↓ free T3 and T4
Hypercholesterolemia
↓TSH (if primary)
↑ free T3 and T4
↓ LDL, HDL, and total cholesterol

3. HYPERTHYROIDISM
 Basic Principles
Increased levels of circulating thyroid hormone increases basal metabolic rate (due to increased synthesis of Na•-K• ATPase)
Increases sympathetic nervous system activity (due to increased expression of β1- adrenergic receptors)
 Clinical features include
1. Weight loss despite increased appetite
2. Heat intolerance and sweating
3. Tachycardia with increased cardiac output
4. Arrhythmia (e.g., atrial fibrillation), especially in the elderly
5. Tremor, anxiety, insomnia, and heightened emotions
6. Staring gaze with lid lag
7. Diarrhea with malabsorption
8. Oligomenorrhea
9. Bone resorption with hypercalcemia (risk for osteoporosis)
10. Decreased muscle mass with weakness
II. Hypocholesterolemia
12. Hyperglycemia (due to gluconeogenesis and glycogenolysis)

4. GRAVES DISEASE (1)
Autoantibody (IgG) that stimulates TSH receptor (type II hypersensitivity)
 Leads to increased synthesis and release of thyroid hormone
 Most common cause of hyperthyroidism
 Classically occurs in women of childbearing age (20-40 years)

5. GRAVES DISEASE (2)
Clinical Features
 Hyperthyroidism
 Diffuse goiter-Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy
 Exophthalmos and pretibial myxedema
 Irregular follicles with scalloped colloid and chronic inflammation are seen on histology
 Lab Findings
1. ↑Total and free T4 ; ↑TSH
2. Hypocholesterolemia
3. Increased serum glucose

6. GRAVES DISEASE (3)
Treatment involves β-blockers, thioamide, and radioiodine ablation.
 Thyroid storm is a potentially fatal complication.
 Due to elevated catecholamines and massive hormone excess, usually in response to stress (e.g., surgery or
childbirth)
 Presents as arrhythmia, hyperthermia, and vomiting with hypovolemic shock
 Treatment is propylthiouracil (PTU), and steroids.
PTU inhibits peroxidase-mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral
conversion ofT4 to T3.

7. DIFFUSE TOXIC GOITER (1)
 Diffuse toxic goiter is an autoimmune condition characterized by a diffusely
hyperplastic thyroid gland with excessive overproduction of thyroid hormone. Graves
disease, the most common cause of hyperthyroidism, is characterized by the
stigmata of diffuse toxic goiter, oculopathy, and pretibial myxedema/acropachy.
Diffuse toxic goiter is also present in other autoimmune thyroid conditions that cause
hypothyroidism, most commonly Hashimoto thyroiditis.
 Etiology
 Female sex
 Pregnancy
 Mental stress
 Smoking and alcohol
 Infectious diseases
 Iodine administration
 Drugs such as lithium and iodine-containing agents, as well as agents, including amiodarone, interferons and
interleukins, and antiretroviral agents

8. DIFFUSE TOXIC GOITER (2)
 Diffuse toxic goiter findings on physical examination include a mildly enlarged
thyroid gland (but may be normal in size, many times normal in size, or
difficult to palpate) with a smooth, rubbery firm texture. It is nontender or
mildly tender. Sometimes, a thyroid bruit can be heard by using the bell of the
stethoscope. Toxic multinodular goiters generally occur when the thyroid
gland is enlarged to at least two to three times the normal size. The gland is
often soft, but individual nodules occasionally can be palpated. If the thyroid
is enlarged and painful, the likely diagnosis is subacute painful or
granulomatous thyroiditis. However, also consider degeneration or
hemorrhage into a nodule and suppurative thyroiditis

9. DIFFUS TOXIC GOITER (3)
 Pathophysiology
In diffuse toxic goiter, the thyroid gland is usually enlarged to a variable degree and is vascular
and diffusely affected. This results in a smooth, rubbery-firm consistency, and often a bruit is
heard on auscultation. Microscopically, the thyroid follicular cells are hypertrophic and
hyperplastic, and they contain little colloid (stored hormone) and show evidence of
hypersecretion. Lymphocytes and plasma cells infiltrate into the thyroid gland and may
aggregate into lymphoid follicles.
This condition is an autoimmune disorder whereby the thyroid gland is overstimulated by
antibodies directed to the thyroid-stimulating hormone (TSH) receptor on the thyroid follicular
cells. This antibody stimulates iodine uptake, thyroid hormonogenesis and release, and thyroid
gland growth. Although mainly produced within the thyroid gland, these antibodies reach the
circulation and can be measured by various assays.

10. MULTINODULAR GOITER (1)
Enlarged thyroid gland with multiple nodules
 Due to relative iodine deficiency
 Usually nontoxic (euthyroid)
 Rarely, regions become TSH-independent
leading to T4 release and hyperthyroidism
('toxic goiter').

11. THYROTOXICOSIS (1)
 Thyrotoxicosis is the clinical manifestation of excess
thyroid hormone action at the tissue level due to
inappropriately high circulating thyroid hormone
concentrations

12. THYROTOXICOSIS (2)
 Thyrotoxicosis results from inappropriate activation at any level of the
hypothalamic-pituitary-thyroid axis with increased thyroid hormone
production from thyroid follicles or from release or ingestion of preformed
thyroid hormone

13. THYROTOXICOSIS (3)
Thyrotoxicosis with hyperthyroidism (increased thyroid hormone synthesis)
 THYROID ORIGIN
 Grave’s disease
 Toxic multinodular goiter
 TSH-secreting pituitary adenoma
 Neonatal Graves disease
 Choriocarcinoma
 Hyperemesis gravidarum etc.

14. THYROTOXICOSIS (4)
 Extrathyroidal origin
 Struma ovarii (thyroid hormone production by dermoid tumor of the ovary)
 Metastatic Follicular hyperthyroidism

15. THYROTOXICOSIS (5)
Thyrotoxicosis without hyperthyroidism (increased availability of preformed
thyroid hormone)
 Thyroid origin
 Silent and pospartum thyroiditis
 Subacute thyroiditis
 Drug-induced (amiodarone)
 Radiation thyroiditis
 Extrathyroidal origin
 Exogenous thyroid hormone (ingestion)

16. THANK YOU FOR YOUR ATTENTION
Sources:
Pathoma
First Aid
Medscape
Etc.