Basic Science Review - Thyroid (Final)

8/13/2019 Basic Science Review - Thyroid (Final)

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BASIC SCIENCE REVIEW

THYROID GLAND

GROUP B1


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APPLIED ANATOMY OF THYROID GLAND

Location

Situated anteriorly in the lowermidline of neck and sides of the neck

Parts

Consists of 2 elongated lateral lobes

(right & left) that are joined by medianisthmus with 2 poles (superior & inferior

poles)

Extent

Gland: Lies against vertebrae C5,

C6, C7 and TI, embracing upper part of

the trachea

Lobe: from middle of the thyroid

cartilage to 4th/5thtracheal ring

Isthmus: overlying from 2ndto the 4th

tracheal rings


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DIMENSIONS AND WEIGHT

SHAPE: varies from H to U shape, has a "butterfly"shape, with two laterallobes connected by isthmus

LOBE: 5cm 2.5cm 2.5cm

ISTHMUS: 1.2cm 1.2 cm

Average WEIGHT: 25g

Superior poles diverging laterally to the level of the oblique lines on thelaminae of the thyroid cartilage

The lower poles diverge laterally at the level of the fifth tracheal cartilage

Larger in females than in males, and enlarged during menstruation andpregnancy


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Capsules

True Capsule formed by peripheral condensation of connective tissue ofgland

It gives off septa which pass to the interior & divide it intolobes & lobules

False Capsule derived from the splitting of pretracheal layer of deepcervical fascia which encloses the gland

Thin along posterior border of the lobes, thickens on innersurface of the gland as suspensory ligament of Berry

This ligament connects the lobe to the cricoid & thyroidcartilages. So thyroid moves with the movement of larynxin respiration & deglutition.


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RELATIONS OF THE LOBES Each lobe has an apex, a base, 3 surfaces: anterolateral, medial &

posterolateral, 2 borders: anterior & posterior

Apex: limited superiorly by attachment to sternothyroid to the oblique lineof the thyroid cartilage

Base: on level of the 4th/5thtracheal ring

Surface

Anterolateral: covered by sternothyroid, sternohyoid, superior belly ofomohyoid, ant.border of sternocleidomastoid, skin & fascia

Medial: trachea & esophagus, inferior constrictor & cricothyroid, externallaryngeal and recurrent laryngeal nerves

Posterolateral: carotid sheath with the common carotid artery, internaljugular vein & vagus nerve

Border

Anterior : related to ant.branch of superior thyroid artery

Posterior: inferior thyroid artery, anastomosis btw superior & inferiorthyroid arteries, parathyroid glands, thoracic duct only on the left side


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RELATIONS OF THE ISTHMUS

Isthmus connects the lower parts of 2 lobes

2 surfaces: anterior & posteriorAnterior: covered by right & left sternothyroid &sternohyoid muscles, anterior jugular veins, fascia and

skin Posterior: 2ndto 4thtracheal rings, higher / lower level

2 borders: superior and inferior

Superior: anastomosis btw right & left superior thyroid

arteries Inferior: inferior thyroid veins leave the gland at this

border


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Blood Supply of Thyroid


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Arterial Supply

superior thyroid artery- branch of external carotid artery

- related to external laryngeal nerve

inferior thyroid artery

- branch of thyrocervical trunk

- related to recurrent laryngeal nerve

lowest thyroid artery (thyroidea ima)

- arises from brachiocephalic trunk/directly from

arch of aorta

accessory thyroid arteries


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Venous drainage

Superior thyroid vein

- drains into internal jugular or common facial

vein

Middle thyroid vein- drains into internal jugular vein

Inferior thyroid vein

- drains into left brachiocephalic vein

Fourth thyroid vein (of Kocher)

- drains into internal jugular vein


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Nerve supply

Middle cervical sympathetic ganglion - mainly

Superior and inferior cervical sympathetic

ganglion - partly


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Lymphatic drainage

Upper deep cervical nodes

- directly or through prelaryngeal nodes

Lower deep cervical nodes

- directly or through pretracheal and

paratracheal nodes.


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Physiology of Thyroid

Gland


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Synthesis, secretion and metabolism

of thyroid hormones

Principal hormones are:

1.T4(thyroxine)

2.T3(Triiodothyronine) 3.RT3(reverse triiodothyronine)

4.calcitonine

T3,T4,RT3: secreted from thyroid follicles RT3: secreted from parafollicular cells


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Steps of thyroid hormones synthesis

1. iodide trapping

2. conversion of iodide into iodine

3. thyroglobulin synthesis 4. the coupling reaction

5. proteolysis of thyroglobulin

6. secretion of thyroid hormones


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Iodide trapping

Uptake of iodide by active mechanisms

The active transport of iodide from circulationinto the colloid of the thyroid follicles is known as

iodide trapping. Iodide trapping is stimulated by TSH.

Conversion of iodide into iodine: By oxidation. It is also known as organification and facilitated

by thyroid peroxidase.


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Thyroglobulin synthesis

It is synthesized in the endoplasmic reticulum of thyroidcells, packed in Golgi body and then secreted into thecolloid by exocytosis

Binding of iodine to thyroglobulin: Reactive iodine binds immediately with tyrosine molecule,

which attached to thyroglobulin molecule at 3 position

Coupling reaction:

Formation of MIT and DIT. 2 DIT molecules undergooxidative condensation to form thyroxine (t4).this known ascoupling reaction.


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Secretion of thyroid hormones

Thyroid cells ingest colloid by endocytosis

The lysosomal enzymes digest the peptide bonds betweeniodinated residues and thyroglobulin : known as proteolysisof thyroglobulin molecule.

Result in formation of free T4,T3,DIT and MIT in cytoplasm. The iodinated tyrosines are deiodinated by the microsomal

enzyme iodotyrosine deiodinase.

T3,T4released from thyroid cells into circulation.

The iodine released by deiodination of MIT and DIT

reutilized by the gland for further synthesis of thyroidhormone

MIT and DIT are not secreted by thyroid gland.


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3 important function of thyroid cells

Actively accumulate iodide from blood for

synthesis of thyroid hormones

Synthesize thyroglobulin molecules and

secrete them into colloid

Digest the colloid and free thyroid hormones

from thyroglobulin molecules to secrete them

into the circulation


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Metabolism of thyroid hormones

Protein binding.

-Thyroid hormones bind with 3 types of plasma

proteins.

1 Thyroxine binding globulin (TBG)

2.Thyroxine binding prealbumin (transthyretin)

(TBPA)

3.Albumin-NormallyT4 binds with TBG and TBPA, T3 binds

with albumin and TBG


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Important of protein binding

1. serve as reservoir of these hormones

2.protects the hormones against metabolic

degradation.

3. provides feedback effect on regulation of

hormone secretion.


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Peripheral conversion

Major product of thyroid gland: T4.

35% of secreted T4is converted to T3incirculation by 5 deiodinase

T3act on target cells : physiologicallyconsidered as the most active hormone

45% T4converted to RT3: RT3is

physiologically inert 20% in conjugated with sulphates and

glucuronides


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Peripheral degradation

Thyroids hormones metabolised by enzyme

deiodinases

5 deiodinase :DI,D2,D3

D1,D2: convert T4to T3and maintain

intracellular T3in target tissues.

D3promotes conversion of T4to RT3

D2in brain maintains the supply of T3to the

neurons.


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T3is degraded to diiodothyronines in liver and

kidney In liver, T4,T3metabolized by conjugation with

sulphates and glucoronic acid.

The conjugated forms are secreted in the bileinto the intestine to reenter the enterohepatic

circulation.

Iodine lost in stool is minimum about 4%


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Feedback regulation of TSH secretion


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Physiologic effects of Thyroid

Hormone


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Target Tissue Effect Mechanism

Heart Chronotropic

Inotropic

no of b-adrenergic-R

Enhance response to

circulating cathecolamine

Adipose tissue Catabolic Stimulate lipolysis

Muscle Catabolic protein breakdown

Bone Developmental Promote normal growthand skeletal development


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Target Tissue Effect Mechanism

Nervous System Developmental Promote normal brain

development

Gut Metabolic rate of carbohydrate

absorption

Lipoprotein Metabolic Stimulate formation of LDL-

receptor

Other Calorigenic Stimulate O2 consumtion bymetabolic active tissue

(except: testes,uterus,

lymph node, spleen, ant

pituitary)

metabolic rate


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Hyperthyroidism


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HYPERTHYROIDISM

A hyper metabolic, biochemical state

It is a multi system disease with elevated levelsof FT4or FT3or both

Prevalence : Women > Men


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Causes of Hyperthyroidism

1. Graves DiseaseDiffuse Toxic Goiter2. Plummers Disease Toxic MNG

3. Toxic phase of Sub Acute Thyroiditis

4. Toxic Single Adenoma

5. Pituitary Tumoursexcess TSH6. Molar pregnancy & Choriocarcinoma (

HCG)

7. Metastatic thyroid cancers (functioning)


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Graves Disease

The most common cause of thyrotoxicosis (50-60%).

Organ specific auto-immune disease

The most important autoantibody is

Thyroid Stimulating Immunoglobulin (TSI) or TSA

TSI acts as proxy to TSH and stimulates T4and T3 Anti thyro peroxidase (anti-TPO) antibodies

Anti thyro globulin (anti-TG) Anti Microsomal andother


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Clinical Symptoms


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Skin

-Warm

-May be erythematous (due to increased blood flow)

-Sweaty and heat intolerance-Hyperpigmentation

-Pruritis


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Eyes- Proptosis

- Lid lag

- Exophthalmos (Graves disease)

- Impaired eye muscle function (Diplopia)

- Periorbital and conjunctival edema

- Gritty feeling or pain in the eyes

- Corneal ulceration due to lid lag and proptosis

- Optic neuritis and even blindness


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Cardiovascular System

- Increased cardiac output

- Tachycardia

- Atrial fibrillation

- Mitral valve problems

- LVH and cardiomyopathy


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Respiratory System

- Dyspnea on rest and with exertion

- tachypnea and hypercapnea

- Respiratory muscle weakness- Decreased exercise capacity

- Tracheal obstruction

- May exacerbate asthma


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GI System

- Weight loss due to increased calorigenesis

- Diarrhoea

- Malabsorption

- Dysphagia

- Increase appetite


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GU System

- Urinary frequency and nocturia

- Enuresis is common in children

- WomenOligomenorrhea or amenorrhea

- Mengynaecomastia, erectile dysfunction


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Neuromuscular System

- Tremors-outstretched hand and tongue

- Hyperactive tendon reflexes


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Psychiatric

- Hyperactivity

- Emotional lability

- Anxiety- Decreased concentration

- Insomnia


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Musculoskeletal system

- Proximal muscle weakness

- Decreased muscle mass and strength

- Hypokelemic periodic paralysis especially in Asian men

- Myesthenia Gravis, especially in Graves disease.


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Treatment

Anti-thyroid drugs

Radioactive iodine

Surgery

Beta-blocker and iodides are adjuncts to above treatment


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Beta Blockers

Prompt relief of adrenergic symptoms Propranolol widely used

Iodides Iodide blocks peripheral conversion of T4 to T3 and

inhibits hormone release.

Before emergency non-thyroid surgery

Decrease vascularity before surgery for Graves disease


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Anti-thyroid Drugs

They interfere with organification of iodinesuppress thyroid

hormone levels

Two agents:

-Tapazole (methimazole)

-PTU (propylthiauracil)


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Anti-thyroid Drugs

Methimazole

Drug of choice for non-pregnant patients because of :

Low cost

Long half life Lower incidence of side effects

Can be given in conjunction with beta-blocker


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Anti-thyroid Drugs

Propylthiouracil

Prefered for pregnant patients

Methimazole is associated with rare genetic abnormalities


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Radioactive Iodine

Treatment of choice for Graves disease and toxic nodulargoiter

Inexpensive

Highly effective

Easy to administer

Safe

Dose depends on estimated weight of gland


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Surgery

Radioactive iodine has replaced surgery for Tx of

hyperthyroidism

Subtotal thyroidectomy is most common

This limits incidence of hypothyroidism to 25%

Total thyroidectomy in large goiter or severe disease


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Hypothyroidism


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Hypothyroidism in adults

Causes :

1. Autoimmune

2. Iatrogenic

3. Transient thyroiditis

4. Iodine deficiency - Endemic

5. Congenital - Dyshormogenesis

6. Infiltrative

7. Secondary hypothyroidism


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Symptoms :

1. Tiredness2. Mental lethargy,poor memory

3. Cold intolerence

4. Weight gain5. Constipation

6. Menstrual disturbances

7. Carpal Tunnel Syndrome


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Signs :

1. Bradycardia

2. Cold extremities,facial pallor

3. Dry,coarse and sparse hair

4. Dry and lemon-yellowish skin (carotenemia)

5. Low-pitched,hoarse voice

6. Myxoedema,periorbital puffiness

7. Bradykinesis ( Slow movements )

8. Delayed reflex of Archilles tendon


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Fetal Hypothyroidism(Cretinism)

Causes:

1. Maternal iodine deficiency

2. Fetal thyroid dysgenesis

3. Inborn errors

4. Maternal antithyroid antibodies

5. Fetal hypopituitary hypothyroidism


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Clinical features

1. Mentally retarded

2. Pot bellies

3. Dwarfsgrowth retardation

4. Macroglossialarge,protruded tongue

5. Deafness

6. Hoarse cry7. Umbilical hernia


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Investigation

1. Thyroid function test

2. ECGSinus bradycardia,low voltage

complexes,ST segment and T wave

abnormalities

Treatment

1. Thyroxine replacement

2. Weight reduction

3. Measure thyroid function every 1-2 year once


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THANK YOU

Basic Science Review - Thyroid (Final)

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