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Endocrine I > Thyroid Gland Lecture (Dr. Lopez) > Flashcards

Thyroid Gland Lecture (Dr. Lopez) Flashcards

1
Q

Thyroid Gland

A
  • Produces the Prohormone RETRAIODOTHYRONIN (T4) and Active Hormone TRIIODOTHYRONINE (T3)
  • The Thyroid Follicle is the Functional Unit of the Gland
    a) Surrounded by a single-layer of Epithelial Cells

b) Follicular Lumen itself is filled with Colloid
c) Size of the Epithelial Cells and Amount of Colloid change with activity

  • Also contained C Cells:
    a) Parafollicular Cells
    b) Secrete CALCITONIN
  • Receives RICH Blood Supply
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2
Q

Thyroid Hormone are Synthesized by the Follicular Epithelial Cells

A
  • Colloid is composed of Newly Synthesized Thyroid Hormones attached to THYROGLOBULIN
  • Epithelium sits on a Basal Lamina (Outermost part of the Follicle)
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3
Q

The Secretory products of the Thyroid Gland are Iodothyronines

A
  • Thyroid Hormones contain LARGE Amount of IODINE
  • Synthesis of the Hormones occurs part INTRACELLULARLY and part in the EXTRACELLULAR Compartment
  • T4 is the MAJOR Secretory Product (T4: T3 ratio is as HIGH as 20:1)

**T4 is produced very rapidly and there is 10x more T4 than T3 produced!!!!!

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4
Q

Peripheral Conversion of T4 and T3

A
  • PERIPHERAL Conversion occurs through the Action of DEIODINASE
    a) 10 to 20% of Circulating T3 comes from Direct Secretion from Thyroid Gland

b) 80 to 90% is produced by PERIPHERAL CONVERSION
- Provides circulating T3 for UPTAKE by other tissues in which T3 Supply is TOO LOW

  • There are some Clinical States associated with a Reduction in the Conversion of T4 to T3:
    a) Fasting
    b) Medical and Surgical Stress
    c) Catabolic Diseases
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5
Q

Factors affecting the Conversion of T4 and T3

A

INCREASE Conversion:

  • Obesity
  • Cold Exposure
  • Hyperthyroid

DECREASE Conversion:

  • Pregnancy
  • Fasting
  • Beta Blockers
  • Hepatic and Renal Failure
  • Aging
  • Hypothyroid
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6
Q

Synthesis of Thyroid Hormones is Complex

A

1) Synthesis of TG; Extrusion into Collicular Lumen
- Site: ROUGH ER, Golgi Apparatus

2) Na+, I- Cotransport
- Site: BASAL MEMBRANE
- Inhibited by PERCHOLARATE, THIOCYANATE

3) Oxidation of I- —> I2
- Site: APICAL (Luminal) MEMBRANE
- Enzyme: PEROXIDASE
- Inhibitor: PTU

4) Organification of I2 into MIT and DIT
- Site: APICAL MEMBRANE
- Enzyme: PEROXIDASE
- Inhibitor: PTU

5) Coupling Reaction of MIT and DIT into T3 and T4
- Site: APICAL MEMBRANE
- Enzyme: PEROXIDASE
- Inhibitor: PTU

6) Endocytosis of Tg
- Site: APICAL MEMBRANE

7) Hydrolysis of T4 and T3; T4 and T3 Enter Circulation
- Site: LYSOSMES
- Enzyme: PROTEASES

8) Deiodination of residual MIT and DIT recycling of I- and Tyrosine
- Site: INTRACELLULAR
- Enzyme: DEIODINASE

*****When the availability of IODIDE is Restricted, the formation of T3 is favored!!!!

**PTU is an Effective TREATMENT for HYPERTHYROIDISM

****High levels of I- INHIBIT Organification and Synthesis of Thyroid Hormones: WOLFF-CHAIKOFF EFFECT!!!!!!!!!!!!

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7
Q

Levels of Iodine/ Iodide in the Thyroid Gland

A
  • Iodine is STORED and IODINATED as TYORSINES of Thyroglobulin (8,000 Microgram toal, of which 600 microgram is T3 and T4)
  • Enough Hormone is stored as IODINATED TG in the Follicular Colloid to last the body for 2 to 3 Months!!!
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8
Q

Activity of Thyroid Gland

A
  • The activity of the Thyroid Gland can be assessed by RADIOACTIVE IODINE Uptake
    1) Hyperthyroidism

2) Extreme Stimulation of Thyroid Gland (High Turnover0
- Ex: Graves’ Disease, associated with Thrytoxicosis

3) Normal
- Perchlorate can inhibit

4) Hypothyroidism

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9
Q

Transport of Thyroid Hormones

A
  • Circulate in the Bloodstream either bound to Plasma Proteins (99%) or free (1%)
  • There is an Equilibrium between Bound and Free circulating T3 and T4 in the bloodstream

Main Binding Proteins:

1) THYROXINE- BINDING PROTEIN (TBG) (70%)
- Synthesized in the Liver
- Binds 1 molecule of T3 or T4
- Has HIGHER Affinity for T4 than T3

2) TRANSTHYRETIN (TTR) (10 to 15%)
3) ALBUMIN (15 to 20%)

  • ***Most circulating Thyroid Hormone is T4!!!
  • T4 Half Life: 6 days
  • T3 Half Life: 1 day
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10
Q

Changes in the Blood Levels of TGB alter then fraction of Free Thyroid Hormone

A

1) HEPATIC FAILURE (Decrease Blood Levels of TBG)
- Transient INCREASE in the Level of FREE T3 and T4

  • Followed by INHIBITION of Synthesis of T3 and T4 (Negative Feedback)

2) PREGNANCY (Increase TBG Levels)
- INCREASE Bound T3 and T4 = DECREASE Free T3 and T4

  • The Transient DECREASE in Free T3 and T4 causes and INCREASE in Synthesis and Secretion of T3 and T4
  • INCREASE Total levels of T3 and T4 but levels of Free, Physiologically Active, Thyroid Hormones are normal (Person say to be Clinically EUTHYROID)
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11
Q

Major Controls of the Synthesis and Secretion of Thyroid Hormones via the HPT Axis

A

1) Role of TSH is t Regulate:
- The Growth of the Thyroid Gland (Trophic Effect)

  • The Secretion of Thyroid Hormones

2) TSH is Regulated by:
- Thyrotropin-Releasing Hormone (TRH)

  • Free T3
    3) TSH Secreiton, in Contrast to the Secretion of GH, occurs at a Steady Rate
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12
Q

Actions of TSH on the Thyroid Gland

A
  • cAMP is the Second Messenger for TSH
  • TWH has two Types of actions on the Thyroid Gland:
    1) INCREASES the Synthesis and Secretion of Thyroid Hormones

2) TROPHIC Effect on Thyroid Gland

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13
Q

Thyroid Stimulating Immunoglobulins stimulate TSH Receptor without TSH Hormone

A
  • TSH levels are LOWER than NORMAL because the High Circulating Levels of Thyroid Hormones INHIBITS TSH Secretion!!!
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14
Q

Summary of Factors affecting Thyroid Hormone Secretion

A

STIMULATORY FACTORS:

  • TSH
  • Thyroid Stimulating Immunoglobulins
  • Increased TBG Levels (Ex: Pregnancy)

INHIBITORY FACTORS:

  • Iodide Deficiency
  • Deiodinase Deficiency
  • Excessive Iodide Intake (WOLFF-CHAIKOSS EFFECT)
  • Perchlorate, Thiocyanate
  • Propylthiouracil (PTU)
  • Decreased TBG levels (Ex: Liver Disease)
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15
Q

New Proteins are Synthesized under the Direction of Thyroid Hormones

A

1) Vast array of New Proteins:
- Na+/ K+ ATPase
- Transport Proteins
- B1-Adrenergic Receptors
- Lysosomal Enzymes
- Proteolytic Proteins
- Structural Proteins

2) In Most Tissues, Synthesis of Na/ K_ ATPase is stimulated by THYROID HORMONES

3) In Cardiac Muscle Cells:
- Myosin
- B1 Adrenergic Receptors
- Ca2+ ATPase

4) In the Liver and Adipose Tissue, Thyroid Hormones include the Synthesis of Key Metabolic Enzymes

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16
Q

Thyroid Hormones has a wide range of Actions in the Human Body

A

GRWOTH:

  • Growth formation
  • Bone Maturation

CNS:
- Maturation of CNS

BMR:

  • Incr Na+/ K+ ATPase
  • Ince O2 Condumption
  • Incr Heat Production
  • Incr BMR

METABOLISM:

  • Incr Glucose Absorption
  • Incr Glycogenolysis
  • Incr Gluconeogenesis
  • Incr Lipolysis
  • Incr Protien Synthesis and Degradation (Net Catabolic)

CARDIOVASCULAR:
- Incr Cardiac Output

17
Q

Thyroid hormones Increase Basal metabolic Rate (BMR)

A
  • The Increased activity of the Na+/ K+ ATPase accounts for MOST of the Increase in the Metabolic Rate
  • *** This leads to an INCREASE in O2 Consumption and Heat Production
  • The Increase in BMR produced by a single dose of Thyroxine (T4) occurs after Several Hours but is Long Lasting (> 6 hrs)

***HYPERTHYROIDISM leads to a HIGH BMR, while HYPOTHYROIDISM causes a LOW BMR

18
Q

Thyroid Hormones on Glucose Absorption

A
  • Thyroid Hormones INCREASE Glucose Absorption and potentiates the effects of other Hormones on GLUCONEOGENSIS, LIPOLYSIS, and PROTEOLYSIS
19
Q

Actions of Thyroid Hormones on Metabolism

A

1) LIPID METABOLISM:
A) Stimulate FAT Mobilization –> Increased Concentration of FA in Plasma

B) Enhance OXIDATION of FA

C) Plasma Concentration of Cholesterol and Triglycerides are INVERSELY Correlated with Thyroid Hormones
- INCREASED Blood Cholesterol concentration in Hypothyroidism

D) Required for conversion of CAROTENE to VITAMIN A
- Hypothyroid Patients can suffer from Blindness and yellowing of Skin

2) CARBOHYDRATE METABOLSIM
- Increased Gluconeogenesi and Glycogenolysis to generate Free Glucose

  • Enhancement of Insulin-Dependent Entry of Glucose into Cells
20
Q

Cardiovascular Effects of Thyroid Hormones

A

INDIRECT:
- Incr Heat Production and CO2 in Tissues

  • DECR Peripheral Vascular Resistance
  • DECR Diastolic Blood Pressure
  • Reflex INCR Adrenergic Stimulation

DIRECT:
- INCR Cardiac Muscle

  • Myosin Heavy Chain Alpha/ Beta ratio
  • Na+/ K+ ATPase
  • Sarcoplasma Ca-ATPase
  • Beta Adrenergic Signaling
  • G Protein Stimulator/ Inhibitor Ratio
  • INCR Ventricular Contractility and Function
  • DECR Peripheral Vascular Resistance
  • *****All of these lead to INCREASED CARDIAC RATE AND OUTPUT!!!!!!!!!
  • Increased Blood Volume
21
Q

Thyroid Hormones stimulates the Synthesis of Cardiac B1 Adrenergic Receptors

A
  • When Thyroid Hormone levels are High, the Myocardium has an Increased number of B1 Receptors and it more Sensitive to Stimulation by SYMPATHETIC Nervous System

Sympathetic: NE = Beta 1
- Positive Effect on HR and Muscle Contraction

Parasympathetic: ACh = M2
- Negative Effect on HR and Muscle Contraction

22
Q

Additional Effects of Thyroid Hormones

A

1) GROWTH:
- Thyroid Hormones act SYNERGISTICALLY with GH and SOMATOMEDIN to promote Bone Formation

2) CNS
- Thyroid Hormones are important for CNS Maturation

  • Deficiency fo Thyroid Hormones during the PERINATAL period leads to:
    A) Abnormal Development of Synapses
    B) Decreased Dendritic Branching and Myelination
  • Neural Changes induced by Thyroid Hormone Deficiency during the Perinatal period are IRREVERSIBLE and lead to CRETINISM unless Replacement Therapy is started soon after birth
23
Q

Thyroid Pathophysiology

A 
1) METABOLISM:
A) Excess:
- Heat Intolerance
- Weight Loss
- INCR BMR

B) Deficiency:

  • Cold Intolerance
  • Weight Gain
  • Decr BMR

2) BONE:
A) Excess:
- Osteoporosis

B) Deficiency:
- Stunted Growth

3) CNS:
A) Excess:
- Agitation
- Anxiety
- Difficult Concentrating
- Hyperreflexia

B) Deficiency:

  • Cretinism (Congenital)
  • In Adults: Listlessness, Slowed Movement, Somnolence, Impaired Memory, Decr Mental Capacity

4) SKIN
A) Excess:
- Sweating

B) Deficiency:
- Myxedema

5) CV SYSTEM
A) Excess:
- Tachycardia
- Atrial Fibrillation
- Palpitations
- High output Heart Failure

B) Deficiceny:

  • Bradycardia
  • Decr Contractility
  • Decr Cardiac Output
  • Heart Failure

6) INTESTINE
A) Excess:
- Diarrhea

B) Deficiency:
- Constipation

24
Q

Causes of Hypotheyroidism

A

PRIMARY:
- Agenesis

  • GLAND DESTRUCTION (Ex: Surgical Removal, Irradiation, Autoimmune Disease, Idiopathic Atrophy)
  • ** HASHIMOTO’S THYROIDITS
  • Inhibition of Thyroid Hormones Synthesis and Release (Ex: Iodine Deficiency, Inherited Enzyme Defects, Drugs that Interfere with Thyroid Homeostasis)
  • Transient (Ex: After surgery or Therapeutic Raidoiodine, Postpartum, Thyroiditis)

SECONDARY:

  • Hypothalamic Disease
  • Pituitary Disease (Ex: SHEEN’S Syndrome)
  • Resistance to Thyroid Hormoens
25
Q

General Symptoms of Hypothyroidism

A
  • DECR BMR
  • DECR Heat production
  • Cold Sensitivity
  • Weight Gain
  • Positive Nitrogen Balance
  • Positive Nitrogen Balance
  • DECR Cardiac Output
  • Hypoventilation
  • Lethargy
  • Dropping Eyelids
  • Myxedema
  • Growth Retardation
  • Mental Retardait (Perinatal Period)
  • Goiter
  • Menstrual Dysfunction
26
Q

Treatment of Hypothyroidism

A

REPLACEMENT DOSES of T4:
- Because Metabolism of T4 DECREASES and the Plasma Half-Life INCREASES with Age, Higher Doses are required in younger Patients

  • In Women beyond, Menopause, Overprescribing T4 can contribute to the development of OSTEOPOROSIS
27
Q

Hashimoto’s Thyroiditis

A
  • Thyroid Hormone Synthesis is impaired by THYROGLOBULIN or TPO Antibodies, which leads to a DECREASE i T3 and T4 Secretion
  • TSH Levels are HIGH!!!
    (Have Trophic Effect aka GOITER)
28
Q

Cretinism

A

CAUSES:

  • Impaired development of Thyroid Gland
  • Maternal Intake of Anti-thyroid Medication or Excess Iodine
  • Inherent Deficient in the Synthesis of Thyroid Hormones

SYMPTOMS:

  • Feeding Problems
  • Respiratory Difficulty
  • Protruding Tongue
  • Curse Facial Features
  • Growth Retardation
  • Mental Retardation
  • Jaundice
  • Dry Skin
  • Hypotonia

**UNTREATED POSTNATAL HYPOTHYROIDISM results in CRETINISM!!!!!!!!

29
Q

Hypothyroidism due to Iodine Deficiency

A
  • Leads to tangent DECREASE in the Synthesis of Thyroid hormone
  • TSH Levels are Elevated

GOITER:
- If the Gland Maintains normal Blood Levels of Thyroid hormones, patient is EUTHYROID and Asymptomatic

  • If Gland cannot maintain Normal Blood Levels of Thyroid Hormones, patient exhibits Hypothyroid
30
Q

Hyperthyroidism

A
  • Due to the Thyroid Hormone OVERPRODUCTION (Thyrotoxicosis = Hyperthyroidism)

1) PRIMARY HYPERTHYROIDISM:
A) Graves Disease (Most Common cause of Thyrotoxicosis)
**MAJOR CLINICAL SIGNS: Exophthalmos (Abnormal Protrusion of the Eyeball) and Periorbital Edema (Due to Recognition by the Anti-TSH Receptor Antibodies of a Similar EPITOPE within the Orbital Cells)

  • *DIAGNOSED BY: Elevated Serum FREE, Total T4 or T3 levels, and Clinical Sings of GOITER and OPHTHALMOPHATY
  • *TSH levels are LOW (Due to Negative Feedback by HIGH Levels of Thyroid Hormones)
* *Presence of Circulating TSI (Thyroid- Stimulating Immunoglobulins)
    - These help distinguish GRAVES Disease from Adenoma of Pituitary Thyroptrophs (A SECONDARY ENDOCRINE DISEASE)

2) Other Causes:
- TSH Secreting Pituitary Adenoma (SECONDARY HYPERTHYROIDISM)

3) TSH Levels:
- Decrease due to NEGATIVE FEEDBACK of T3 on the Anterior Lobe of the Pituitary Gland

  • If defect is in the Anterior Pituitary TSH levels are INCREASED
31
Q

Circulating levels of TBG can be Indirectly assessed using T3 Resin UPTAKE TEST

A
  • A Resin with Anti T3 Antibodies on it ABSORBS T3

- TBG also binds to T4 and T3

32
Q

Changes in the Blood Levels o TBG and Free Thyroid Hormones in Clinical Scenarios

A

1) HYPERTHYROIDISM
- Incr T4
- Incr T3 Resin Uptake

2) HYPOTHYROIDISM
- Decr T4
- Decr T3 Resin Uptake

3) HIGH TBG
- INCR T4
- DECR T3 Resin Uptake

4) LOW TBG
- DECR T4
- INCR T3 Resin Uptake

5) HEPATIC FAILURE
- DECR TBG
- INCR T3 Resin Uptake

6) PREGNANCY
- INCR TBG
- DECR T3 Resin Uptake

33
Q

In General about Thyroid

A
  • HYPERHTYROIDISM (Too much Thyroid Hormone in the Bloodstream): INCREASES the speed of Bodily Functions and Leads to Weight Loss, Sweating, Rapid Heart Rate, and High Blood Pressure, among other Symptoms
  • HYPOTHYROIDISM (Not enough Thyroid Hormone of the Body’s Needs): Without enough Thyroid Hormone, Many of the Body’s Functions SLOW DOWN; People may have symptoms such as fatigue, Weight Gain, and Cold INTOLERANCE
34
Q

Goiter

A
  • Goiter can develop in response to MULTIPLE Imbalances and Disease within the HPT Axis, Coexisting with Hypothyroidism, Euthyroidism (Normal), and Hyperthyroidism

These Imbalances Include:

1) HYPERTHYROIDISM:
- Excessive Stimulation of the TSH Receptor by an AUTOANTIBODY (Graves Disease)

  • Excessive Secretion of TSH from a TSH-Producing TUMOR (Ex Secondary Hyperthyroidism)
  • Thyroid Hormone- Producing (TOXIC) Adenoma (NODULAR) or Toxic Multinodular Goiter

2) PRIMARY HYPOTHYROIDISM
- Lack of adequate IODINE in the Diet (Nontoxic Goiter, Edemic Goiter)

  • Sporadic Hypothyroidism of unknown Etiology (Nontoxic Goiter)
  • Chronic Thyroiditis (Hashimoto Disease; Autoimmune Induced Deficiency in Thyroid Function)
35
Q

The TSH Test is Used for Diagnosing BOTH Hyperthyroidism and Hypothyroidism

A 
HYPERTHYROIDISM:
1) Gaves Disease
A) TSH: Decrease
B) T3/T4: Increase
C) TSI: POSITIVE
D) Radioactive Iodine Uptake Test: INCREASE
2) Thyroiditis (With Hyperthyroidism)
A) TSH: Decrease
B) T3/T4: Increase
C) TSI: Negative
D) Radioactive Iodine Uptake Test: DECREASE
3) Thyroid Nodules (Hot, or Toxic)
A) TSH: Decrease
B) T3/T4: Increase 
C) TSI: Negative
D) Radioactive Iodine Uptake Test: INCREASE or NORMAL
HYPOTHYROIDISM:
1) Hashimoto's Disease (Thyroiditis, EARLY Stage)
A) TSH: Increase
B) T3/T4: DECREASE or NORMAL
C) Antithyroid Antibody: POSITIVE

2) Hashimoto’s Disease (Thyroiditis, LATER Stage)
A) TSH: Increase
B) T3/T4: DECREASE
C) Antithyroid Antibody: POSITIVE

3) Pituitary Abnormality
A) TSH: DECREASE
B) T3/T4: DECREASE
C) Antithyroid Antibody: NEGATIVE

Endocrine I (13 decks)

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