Thyroid and Parathyroid Histology Lecture (Dr. Cole) Flashcards
Formation of the Thyroid Gland
- The ENDODERMAL MASS of Cells Invaginates into the Underlying MESODERM, creating the THYROID DIVERTICULUM that is positioned BETWEEN the ANTERIOR Two-Thirds and POSTERIOR One-Third of the Developing Tongue
- The Thyroid Diverticulum grows INFERIORLY, often between the Skeletal Elements of the Second and Third PHARYNGEAL Arches
- It then MIGRATES to a position ANTERIOR to the Upper Portion of the Developing Trachea
- The Thyroid Gland response to Thyroid Stimulating Hormone (TSH) at about week 22 in the Fetus. The Congenital absence of the Thyroid gland causes IRREVERSIBLE Neurologic Damage in the Infant (CRETINISM).
Anatomy
- The Thyroid Gland consists of Two Lobes connected by a Narrow Band of Thyroid tissue called the ISTHMUS
- The Thyroid Gland is located between the LARYNX and the Lobes rest on the sides of the TRACHEA
- The Thyroid Gland is surrounded by a DOUBLE CONNECTIVE TISSUE CAPSULE
- Two pais of PARATHYROID Glands are located on the POSTERIOR SURFACE of the Thyroid Gland, Between or Outside the Two Capsules
Thyroid Gland
- Each lobe consists of FOLLICLES (Structural and Functional Unit) filled with COLLOID
Thyroid Follicle
- Single layer of Epithelium (Follicular)
- Varies from CUBOIDAL to COLUMNAR with activity
- Surrounds CENTRAL LUMEN of COLLOID
- THYROGLOBULIN (TGB)
Regulation of Thyroid
- Follicular Epithelium has receptors for Thyroid Stimulating Hormone (TSH) from Anterior Pituitary
- Controls both SYNTHESIS (Exocrine) and Secretion (Endocrine) of Thyroid Hormones
Thyroxine = TETRAIODOTHYRONINE = T4
TIIODOTHYRONINE = T3
Synthesis of Thyroid Hormones PART 1
1) Binding of TSH to its Receptors in the Follicle Cells of the Thyroid Gland causes the Cells to actively transport Amino Acids and Iodide Ions, (I-) across their Cell Membrane, from the Bloodstream into the CYTOSOL
- As a result, the Concentration of IODIDE ions “Trapped” in the Follicular Cells is many times HIGHER than the Concentration in the Bloodstream
Synthesis of Thyroid Hormone PART 2
2) IODIDE ions then move to the LUMEN of the FOLLICLE CELLS that border the COLLOID. There, the ions undergo OXIDIZATION
- The Oxidization of TWO IODIDE Ions (2 I-) results in IONDIDNE (I2), which passes through the Follicle Cell membrane into the Colloid
Synthesis of Thyroid Hormone PART 3
3) Addition of IODINE to TYROSINE residues of TGB by TYROSINE PEROXIDASE, released into the Lumen by Exocytosis
- THYROID PEROXIDASE activity and the IODINATION Process can be Inhibited by PROPYLTHIOURACIL and METHYL MERCAPTIOMIDAZOLE (MMI)!!!!!!!!!!!!!!!
- These ANTITHYROID Drugs are used to INHIBIT the Production of Thyroid Hormone by HYPERACTIVE GLANDS
Storage of Thyroid Hormones
- Thyroid Hormones are stored EXTRACELLULARLY as TGB!!!!!
Secretion (Endocrine)
1) ENDOCYTOSIS and Digestion of COLLOID as a result of TSH Stimulus
2) Colloid Droplets FUSE with Lysosomes
3) Digestive Enzymes BREAKDOWN TGB, releasing T3, T4, and IODINE
4) T3 and T4 diffuse through membrane into CAPILLARY
5) Capillary Transport is facilitated by THYROXINE-BINDING Protein
Circulating T3 and T4
- IN the Bloodstream, >1% of the Circulating T3 and T4 remains UNBOUND
- This free T3 and T4 can cross the LIPID BILAYER of Cell Membranes and be taken up by Cells. The remaining 99% is bound to Specialized THYROXINE-BINDING GLOBULINS (TBGs), to ALBUMIN, or to other Plasma Proteins This “PACKAGING” prevents their FREE Diffusion into Body Cells
- When Blood Levels of T3 and T4 begins to DECLINE, bound T3 and T4 are released from these Plasma Proteins and readily cross the Membrane of Target Cells
- T3 has a SHORTER HALF LIFE (18 Hours), is MORE POTENT, and LESS ABUNDANT than T4. The Half life of T4 is 5 to 7 days and represents about 90% of the Secreted Thyroid Hormones
Functions of Thyroid Hormone
- Stimulates BASIC Metabolic Rate
- Augments Thermogenesis
- Augments Glucose Production
- Required for NORMAL Development of the CNS
Thyroid Disorders: Hyperthyroidism
- Excessive Production of TSH
SYMPTOMS:
- Increased METABOLIC RATE, Weight Loss, Hyperactivity, and Heat Intolerance
COMMON CAUSES:
- Excessive STIMULATE by Adenohypophysis
- Loss of FEEDBACK Control by Thyroid Gland (Graves’ Disease)
- Ingestion of T4 (Used for Weight Loss)
Graves’ Disease
- Cuased by AUTOIMMUNE DISORDER that produces ANTIBODIES to the receptors for TSH on the Follicular Epithelium
- Antibodies bind to the Receptor and Chronically stimulate it
- Inflammatory response with Cytokine Production. which reinforces the Autoimmune Response
- The result is TOO MUCH CIRCULATING THYROID HORMONE
- Enlargement of the Thyroid Gland (GOITER), Bulging of the Eyes (EXOPHTHALMOS), TACHYCARDIA, Warm Skin, and Fine Finger tremors are typically Clinical Features
TREATMENT:
- Surgical Removal, Radioactive Iodine
POST TREATMENT:
- Post treatment regime requires Supplementation of Thyroid Hormones
Hypothyroidism
- Caused by INSUFFICIENT Production of Thyroid Hormone
SYMPTOMS:
- Low Metabolic Rate
- Feeling of being Cold
- Weight Gain (Some patients)
- In the Adult, Hypothyroidism is manifested by COARSE SKIN with PUFFY Appearance due to the accumulation of PROTEOGLYCANS and RETENTION of Fluid in the Dermis of the Skin (MYXEDEMA) and Muscle
CAUSES:
- Decreased Iodine Intake
- Iodine Pituitary Stimulation
- Post Therapeutic or Destruction of the Thyroid by the Immune System
Hashimoto’s Disease
- An Autoimmune Disease associated with HYPOFUNCTION of the Thyroid Gland
- It is caused by AUTOANTIBODIES (Known as Antimicromosomal Antibodies) to Thyroid Perixodase and Thyroglobulin
TREATMENT:
- Oral Thyroid Mediation
Goiter: Enlargement of the Thyroid Gland
- Vary considerably in Size, and Enlargement may be diffuse throughout the Whole Gland or Irregular and affecting Part or all of One Lone
- Many Nodules in the Thyroid is called a MULTINODULAR GOITER
- Goiters are either ENDEMIC or SPORADIC
- ENDEMIC GOITER is caused by IODINE DEFICIENCY
a) Pituitary Releases more TSH but the Gland cannot Respond
b) Can be avoided by adding Iodine to the diet (In 1924, Morton became the first company to produce Iodized salt for the table to help prevent Goiters)
c) One formed, the ONLY TREATMENT is SURGERY!!!
The “Goiter Belt”
- An inland region of the US, encompassing the Great Lakes, Midwest, and Intermountain Regions, where Goiter was once common, as diet was based primarily on foods grown on Iodine-Depleted Soil, which triggered the development of Goiter
Congenital Hypothyroidism
- Condition of SEVERELY Stunted Physical and Mental Growth due to UNTREATED Congenital deficiency of Thyroid Hormones
- FKA CRETINISM
- Can be Endemic, Genetic, or Sporadic
- SPORADIC and GENETIC Forms result from Abnormal development or Function of the Fetal Thyroid Gland. This type of Cetisnism has been almost completely Eliminated in developed countries with early diagnosis by Newborn Screening Programs followed by Lifelong Thyroid Hormone treatment
Congenital Hypothyroidism Cont
- Poor length Growth is apparent as early as the First Year of Life. Adult state without treatment ranges from 1 to 1.6 meters, depending on Severity, Sex and other genetic factors
- Bone Maturation and Puberty are SEVERELY DELAYED
- OVULATION is IMPEDED and INFERTILITY is Common
- Neurological impairment may be Mile, with reduced Muscle Tone and Coordination, or so severe that the person cannot stand or walk
- Cognitive Impairment may also range from Mild to so Severe that the person is NONVERBAL and DEPENDENT on other for Basic Care
Calcitonin
- Acts to DECREASE CALCIUM Concentration by inhibiting Bone Resorption
- Binds to Receptor on OSTEOCLASTS
- HYPERCLACEMIA: High Blood levels of Ca2+ stimulates Calcitonin Secretion
***The Follicular Epithelium also contains about 10% of shattered PARAFOLLICULAR CELLS, also called C CELLS. C Cells, derived from the NERUAL CREST, contain Small Cytoplasmic Granules representing the STORED HORONE CALCITONIN
Formation of Parathyroid Glands
- The Parathyroid Glands originate from the InTERACTION of the ENDODERM of the Third and Fourth Pouch
- The position of the Glands REVERSES during DEVELOPMENT. The pair of Glands which is ultimately INFERIOR develops from the THIRD POUCH and the pair of Glands which is ultimately SUPERIOR develops from the FOURTH POUCH
- Migration of the THYMUS (Also Pouch 3) repositions the Parathyroid 3 Glands to more INFERIOR POSITIONS
Parathyroid Cells
Two Cell populations supplied by SINUSOIDAL Capillaries:
1) The more Numerous CHIEF or PRINCIPAL Cells
2) The OXYPHIL or ACIDOPHILIC Cell
***Cells are arranged in CORDLIKE or FOLLICULAR-like CLUSTERS
***Chief (Principal) Cells: Secrete PARATHYROID HORMONE
*****Oxyphil Cells: Function unknown, ? Transitional Chief Cells
Calcium Sensing in the Parathyroid Gland
- The Ca2+ Sensing Receptor (CaSR) is associated with G Protein in the Plasma Membrane of CHIEF CELLS. Serum Ca2+ binding to the Extracellular Region of the CaSR Triggers the release of INTRACELLULAR Signals SUPPRESSING the Secretion of PARATHYROID HORMONE, with the consequent DECREASE in the Serum Ca2+ Concentration.
- When the serum Ca2+ Concentration DECREASES, the Secretion of Parathyroid Hormone is stimulated, resulting in an INCREASE in Serum Ca2+
