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Endocrine I > Thyroid and Parathyroid Histology Lecture (Dr. Cole) > Flashcards

Thyroid and Parathyroid Histology Lecture (Dr. Cole) Flashcards

1
Q

Formation of the Thyroid Gland

A
  • 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).
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2
Q

Anatomy

A
  • 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
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3
Q

Thyroid Gland

A
  • Each lobe consists of FOLLICLES (Structural and Functional Unit) filled with COLLOID
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4
Q

Thyroid Follicle

A
  • Single layer of Epithelium (Follicular)
  • Varies from CUBOIDAL to COLUMNAR with activity
  • Surrounds CENTRAL LUMEN of COLLOID
  • THYROGLOBULIN (TGB)
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5
Q

Regulation of Thyroid

A
  • 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

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6
Q

Synthesis of Thyroid Hormones PART 1

A

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

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7
Q

Synthesis of Thyroid Hormone PART 2

A

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

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8
Q

Synthesis of Thyroid Hormone PART 3

A

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

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9
Q

Storage of Thyroid Hormones

A
  • Thyroid Hormones are stored EXTRACELLULARLY as TGB!!!!!
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10
Q

Secretion (Endocrine)

A

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

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11
Q

Circulating T3 and T4

A
  • 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
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12
Q

Functions of Thyroid Hormone

A
  • Stimulates BASIC Metabolic Rate
  • Augments Thermogenesis
  • Augments Glucose Production
  • Required for NORMAL Development of the CNS
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13
Q

Thyroid Disorders: Hyperthyroidism

A
  • 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)
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14
Q

Graves’ Disease

A
  • 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

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15
Q

Hypothyroidism

A
  • 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
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16
Q

Hashimoto’s Disease

A
  • 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

17
Q

Goiter: Enlargement of the Thyroid Gland

A
  • 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!!!

18
Q

The “Goiter Belt”

A
  • 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
19
Q

Congenital Hypothyroidism

A
  • 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
20
Q

Congenital Hypothyroidism Cont

A
  • 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
21
Q

Calcitonin

A
  • 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

22
Q

Formation of Parathyroid Glands

A
  • 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
23
Q

Parathyroid Cells

A

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

24
Q

Calcium Sensing in the Parathyroid Gland

A
  • 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+
25
Q

Parathyroid Hormone

A
  • PTH acts on OSTEOBLASTS to promote OSTEOCLASTS ACTIVITY—–> INCREASE in Circulating Calcium Levels
  • Acts on RENAL TUBULES to stimulate RESORPTION of Calcium
  • Controls rate of Ca2+ UPTAKE in GI Tract by regulating production of Vitamin D (Kidneys)
  • Vitamin D Stimulates Cells of Intestinal Mucosa to ABSORB Ca2+ and Synthesizing CALBINDIN (Carrier Protein)
26
Q

Metabolism of Vitamin D and Calcium Absorption

A

1) IN the DUODENUM, CALCITRIOL Binds to Cytosol and nuclear receptors in Enterocytes and induces the Synthesis of Calcium-Binding Protien CALBINDIN by Increasing the Expression of a specific mRNA.
2) CALBINDIN transprots Ca2+ across the Enterocyte and, through a Ca2+ INSENSITIVE ATPASE DEPENDENT CHANNEL, into the Bloodstream (ACTIVE TRANSPORT)
3) The JEJUNUM and ILEUM, Ca2+ is transported across the Intracellular space into the blood (PASSIVE TRANSPORT)
4) LOW Ca2+ in SERUM stimulates 1 ALPHA HYDROXYLASE to produce 1,25 Hydrocycholecalciferol (biologically active Calcitiol)
5) HIGH Ca2+ is Serum stimulates 24- Hydroxylase to produce BIOLOGICALLY INACTIVE 24, 25 Hydroxycholecalciferol

27
Q

Hypoparathyroidism

A
  • Deficiency in SECRETION of PTH
  • Blood Calcium is LOW but Bone Calcium is NOT Released
  • Ca2+ deficiency results in Spontaneous Depolarization of Neurons and Muscle Fibers resulting in TETANY
28
Q

Hyperparathyroidism

A
  • HIGH Blood Calcium Levels (Hypercalcemia)
  • Results in BONE LOSS: Can result in Osteomalacia and Osteitis Fibrosa Cystic
  • Causes Abnormal Calcium Deposition in Arteries and Kidneys
29
Q

Rickets and Osteomalacia

A
  • In Children, a DEFICIENCY of Vitamin D Causes Rickets, In Adults, the corresponding clinical condition is Osteomalacia. The Calcification of the Bone Matrix Osteoid is deficient in BOTH Conditions
  • In Rickets, Boen Remodeling is DEFECTIVE. The ends of the Bone BULGE (Rachitic Rosary at the Costochondral Junctions), and poor Calcification of the LONG BONE Causes BEINGIDN (Bowlegs or Knock-Knees)
30
Q

Rickets and Osteomalacia Cont

A
  • In Osteomalacia, pain, partial Bone Fractures, and Muscular Weaknesses are typical in the Adult
  • Chronic Renal Failure or a Congenital Disorder, resulting in the LACK of 1 ALPHA HYDROXYLASE, can also cause RICKETS or OSTEOMALACIA
31
Q

PTH and Calcitonin

A

1) Blood Calcium Concentration Drops

2) Release of PTH
- CHIEF Cells of the Parathyroid Gland release Parathyroid Hormone (PTH)

3a) Effects of PTH on BONE:
- Inhibits OSTEOBLASTS
- Stimulates OSTEOCLASTS
- Bone is BROKEN DOWN, releasing Calcium ions into Bloodstream

3b) Effects of PTH on KIDNEYS:
- PTH Stimulates KIDNEY TUBULE Cells to recover Waste Calcium from the Urine
- PTH Stimulates KINDEY TUBULE CELLS to Release CALCITRIOL

3c) Effects of CALCITRIOL on INTESTINE:
- Stimulates Intestine to Absorb CALCIUM from Digesting Food

4) Blood Calcium Levels INCREASE

5) CALCITONIN Release:
- High Concentration of Calcium stimulates PARAFOLLICULAR Cells in the Thyroid to RELEASE CALCITONIN

6) Effects of Calcitonin on BONE:
- Stimulates OSTEOBLASTS
- Inhibits OSTEOCLASTS
- Calcium is REMOVED from tBlood and used to BUILD BONE

32
Q

Activation of Mature Osteoclasts

A

1) A MONOCYTE, derived from Bone Marrow, reaches an area of Bone Formation and Remodeling. A RECEPTOR for M-CSF is expressed on its Surface
2) The monocyte becomes a MACROPHAGE. M-CSF LIGAND BINDS THE M-CSF RECEPTOR and induces the expression of RANK (Transmembrane Receptor for activation of Nuclear Factor Kappa B) for its LIGAND (RANKL) expressed on the surface of Osteoblasts
3) The Osteoblast-expressed Transmembrane Protein Ligand RANKL BINDS TO THE OSTEOCLAST RANK (RECEPTOR) and COMMITS THE CELL TO OSTEOCLASTOGENESIS. The Mononucleated Monocyte becomes a Multinucleate OSTEOCLAST PRECURSOR, which still cannot reabsorb Bone.
4) RANKL-stimulated Osteoclastogenesis is Inhibited by the Osteoblast-derived RANKL Decoy protein OSTEOPROTEGERIN. Osteoprotegerin blocks RANKL binding to its receptor RANK. By this mechanism, the Osteoblast (more specifically, Osteoprotegerin) regulates the population of Functional Osteoclasts. Note that Osteoblasts control Osteoclast differentiation, not function

5) RESTING OSTEOCLAST
- A Resting (Nonfunctional) Osteoclast uncouples from the Osteoblast

6) FUNCTIONAL OSTEOCLAST
- The maturation of Osteoclasts is completed when the SEALING ZONE and RUFFLED BORDER appear. The formation of the sealing zone requires ALPHA, GAMMA, BETA 3 INTEGRIN!!!!!

Endocrine I (13 decks)

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