Thyroid Diseases

PETER S. AZNAR, MD, FPSP, MHPE

Definition of Terms:

Primary hyperthyroidism is the term used

when the pathology is within the thyroid gland.

Secondary hyperthyroidism is the term used

when the
thyroid gland is stimulated by excessive thyroid-
stimulating hormone (TSH) in the circulation.
• Thyrotoxicosis:
– Is defined as the state of thyroid
hormone excess

• Hyperthyroidism
– Is the result of excessive thyroid
gland function
• Hyperthyroidism
– Thyrotoxicosis (most common cause)
a) increase T3 and T4

Other Causes:
• Diffuse hyperplasia
• Graves disease (85% of cases)
• Hyperfunctional multinodular goiter
• Multifunctional adenoma of thyroid
• Clinical
– Hypermetabolic state
• Skin – warm, soft and flushed
• Heat intolerant
• Sweating
• Weight loss (despite increase appetite)
• Cardiac - earliest S/S – increase HR (A fib
in older patients)
• Neuromuscular
• Thyrotoxicosis effects:

– Increase in metabolic rate

– Flushing of face and hands
– Onycholysis – painless separation of the nail
from the nail bed
– Increase skin pigmentation (Pretibial Myxedema)
 Graves disease

• Most common cause of endogenous

hyperthyroidism
• Characteristics:
– Hyperthyroidism
– Infiltrative ophthalmopathy
– Localized infiltrative dermopathy
• Ocular
– Wide, staring gaze and lid lag
Hypothyroidism
• Hashimoto’s Thyroiditis
– Mean Annual incidence:
• Women 4:1000 men 1:1000
• 10:1 female predominance
• 45-65 years old
• Risk factors; TPO antibodies (90%) Japanese,
previous history, high I intake
• Average age: 60
• Frequently associated to other autoimmune
disorders such as: SLE, Sjogrens disease
• Present in patients with Turner syndrome
• Progressive depletion of thyroid epithelial
cells replaced with mononuclear cells and
fibrosis
• Maybe associated with goiter
• No cancer risk
• Subacute (granulomatous) thyroiditis (De
Quervain thyroiditis)

– 5:1 female preponderance

– 30-50 years old
– Cause by viral infection
– History of URTI prior to onset of thyroiditis
• Riedel thyroiditis

– Fibrosis of thyroid and neighboring

structures

– Presents as hard and fixed thyroid which

clinically is similar to CA
• Congenital Hypothyroidism (Cretinism)

• Prevalence: 1 in 3000 to 4000 newborns

– Cause: Dysgenesis 85%

– Dx: Blood screening
Thyroid Neoplasms
• Adenomas

– Discrete solitary masses

– Derived from follicular epithelium
– Not predecessors of malignancy
– Mostly nonfunctional
Pathogenesis:
– Toxic adenoma
• TSH receptor pathway is important
signaling for hormone production
• Hot nodules – increase iodine uptake
• Usually present as unilateral painless mass
• Take up less radioactive iodine compared to
normal thyroid parenchymal cells
• Cold nodules
• 10% of cold nodules – malignant
• Hot nodules rarely malignant
 Thyroid Carcinomas

• Most appear in adults

• Female predominance (early and middle adult)
• Most CA are well differentiated:
– Papillary CA (80% of cases)
– Follicular CA (15% of cases)
– Medullary CA (5% of cases)
– Anaplastic CA (<5% of cases)
• Most common inherited thyroid CA
– Familial medullary CA

• History of exposure to ionizing radiation

during first 2 decades of life is one of the
most important factors predisposing one to
thyroid cancer
• Pre existing thyroid disease have increase
predisposition to develop follicular carcinoma
• Papillary Carcinoma
– Most common of thyroid carcinoma
– Any age
– Vast majority of carcinoma associated with
ionizing radiation exposure
– Solitary or multi-focal nodules
– Are non-functional tumors
• Painless masses
• metastasis to cervical lymph nodes
 Follicular Carcinoma
• Second most common form of thyroid carcinoma
• Decrease incidence in areas of dietary iodine
deficiency
• Do not arise from pre-existing adenomas
• Present most often as solitary nodules with no
iodine uptake (cold nodules)
• Metastasize via blood to lungs, bone and liver
• Unlike papillary carcinoma, regional nodal
involvement is uncommon
 Medullary Carcinoma
• Secrete calcitonin from “C” cells
• May arise as solitary nodule or multiple
lesions
• “C” cell hyperplasia
 Anaplastic Carcinoma

• Most aggressive thyroid neoplasms

• Predominantly in elderly patients
– Areas with endemic goiter
• Death in <1 year (compromise of neck)
• Distant metastasis is common
Thyroid Function Tests
Definition of Terms:

Primary hyperthyroidism is the term used

when the pathology is within the thyroid gland.

Secondary hyperthyroidism is the term used

when the thyroid gland is stimulated by
excessive thyroid-stimulating hormone (TSH) in
the circulation.
Sources:

Thyroid Releasing Hormone – Hypothalamus

Thyroid Stimulating Hormone – Anterior Pituitary Gland

Thyroid Hormone – Thyroid Gland

 Thyroid Stimulating Hormone (TSH)

– Gold standard test for all thyroid conditions

Thyroxine (T4)
– 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”
– Most T4 is bound to Thyroxine-Binding
globulin
– Free thyroxine affects tissue function in
the body, but bound thyroxine does not
• Free thyroxine (FTI or FT4)

– Tells how much free T4 is present compared

to bound T4
– The FTI can help tell if abnormal amounts of
T4 are present because of abnormal
amounts of thyroxine-binding globulin
• Triiodothyronine (T3)
– 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 which
stimulates the metabolism of almost every
tissue in the body
 Normal Hyperthyroidism Hypothyroidism Hypothyroidism
primary secondary
TSH Normal Low High Low
T4 Normal High Low Low
Diseases of the Parathyroid Gland
Responsible for Calcium
and
Phosphorous metabolism
Types of Hyperparathyroidism:

Primary hyperparathyroidism
an autonomous overproduction of parathyroid
hormone (PTH), usually resulting from an
adenoma or hyperplasia of parathyroid tissue.

Secondary hyperparathyroidism
compensatory hypersecretion of PTH in response
to prolonged hypocalcemia,most commonly from
chronic renal failure
Types of Hyperparathyroidism:

Tertiary hyperparathyroidism
persistent hypersecretion of PTH even after the
cause of prolonged hypocalcemia is corrected, for
example after renal transplant.
Primary Hyperparathyroidism
– Adenoma (85% to 95%)
– Primary hyperplasia: 5% to 10%
– Parathyroid carcinoma: <1%

– Women > Men 4:1

– Cyclin D1 gene inversions leading to overexpression of cyclin D1
– Involve in MEN1 mutations
Hypoparathyroidism
Etiology:
• Surgically induced hypoparathyroidism
• Autoimmune hypoparathyroidism
• Autosomal-dominant hypoparathyroidism
• Familial isolated hypoparathyroidism (FIH)
• Congenital absence of PT gland
Features:
• Tetany
(+) Chvostek sign
(+) Trousseau sign
• Mental status changes
• Intracranial manifestations
• Ocular disease
• Cardiovascular manifestations
• Dental abnormalities
Pseudohypoparathyroidism:
occurs because of end-organ resistance to
PTH
THANK
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