CALCIUM HOMEOSTASIS-III-HYPERCALCEMIA

HIGHER BLOOD CALCIUM LEVELS-TREATMENTS

When the blood calcium levels rises above the normal range the condition is known by medical terms as Hypercalcemia.If left untreated it may result into serious unwanted consequences.

Symptoms

Although the patient is asymptomatic but he may demonstrate the following consequences:-

1.Weariness

2.Renal stones

3.Constipation

4.Stomach pain

5.Weakness

6.Confusion

7Delirium 

Causative Diseases

These causes can easily be remembered by the ananym CHIMPANZEES

Calcium suplementations used in excess

Hyperparathyroidsm

Iatrogenic (Urinary retension of calcium by overuse of thiazide diuretics)

Malignancy/Milk alkali syndrom caused by excessive intake of calcium and alkali through milk.

Paget's disease(Abnormal bone destruction and reformation) 

Addison's Disease

Neoplasm

Zollinger-Ellison's syndrom

Excess vitamin-D

Excess vitami-A

Sarcoid a disease in which there are abnormal collections of inflammatory cells to form granuloma 
TREATMENT OPTIONS
1.Rehydration with saline and diuresis with loop diuretics like furosamide
2.Bisphosphonates
3.Calcitonin
4.Gallium nitrae
5.Plicamycin
6.Glucocorticoids
1.Bisphosphonates
a)Etidronate
b)Pamidronate
Mechanism Bisphosphonates are working by inhibiting osteoclastic activity that means they reduce both bone resorption and bone formation of hydroxyapatite crystals.  
Routes of admn:- Etidronate by oral and i.v.
                              Pamidronate by i.v. only
Uses 1.Malignancy associated hypercalcemia
         2.Paget's disease
         3.Bone osteoporosis.
2.Calcitonin
A 32 member aminoacid peptide synthesized and secreted by the parafollicular C cells of the thyroid gland
Mechanism 
It decreases osteoclastic bone resorption as well as kidney calcium and phosphorus reabsorption.
Uses
1.Paget's disease
2.Hypercalcemia
3.Osteoporosis
Salmon fish calcitonin is more potent than humen calcitonin and have longer half life.
Side effects
1.Allergic reactions
2.Gastri Intestinal distress
3.Flushing,redness and tingling of the face.
3.Gallium nitrate
Gallium nitrate is working by bone resorption and thereby it decreases blood calcium levels.
Use Malignant hypercalcemia
Toxicity Nephrotoxic
4.Plicamycin
This is a cell destructing antibiotic reduces blood calcium levels
Mechanism
It inhibit the action of PTH on osteoclasts and also inhibiting the action of vit.D
Use Malignant hypercalcemia and Paget's disease
Toxicity 1.Thrombocytopenia and hemorrhage
               2.Liver and Kidney toxicity
               3.Nausea and vomiting and loss of appetite.
5.Glucocorticoids
(e,g) Prednisone
Mechanism These medicines work by decreasing calcium absorption by the intestines and increasing the calcium excretion by kidneys.
Uses Hypercalcemia due to lymphoma and sarcoid.

CALCIUM HOMEOSTASIS-PART-II

CALCIUM METABOLIC DEFECTS-TREATMENTS

HYPOCALCEMIA

 Symptoms 1.Muscular excitability

                    2.Parasthesiasis

                    3.Laryngospasm

                    4.Seizures

                    5.Tetany

                    Chvostek's and Troussean's sign

The facial muscle spasm that occurs when the facial nerve is streatched towards the anterior to the ear.This condition is known as Chvostek's syndrom

Carpal or carpopedal spasms in the hands during or after tied a tight cuff for a blood pressure measurement due to the occlution of the blood in that area.This condition is known as Troussean's syndrom

Common causes of Hypocalcemia

1.Chronic renal failure or End Stage Renal Failure

2.Parathyroid deficiency

3.Vitamin D deficiency

4.Malabsorption due to some diseases

5.Malnutritions.

Treatment options for Hypocalcemia

1.Calcium salts

a)Calcium chloride

b)Calcium gluceptate

c) Calcium gluconate

d)Calcium carbonate

Side effects

1.Peripheral vasodilation

2.Transienttigling

3.Rapid infusions may cause arrhyhmias

2.Vitamin D preparations 

a)Calcitrol a metabolite of vitamin D can cause quick raising of calcium levels

b)Ergocalciferol (Vit.D-2)

c)Cholecalciferol(Vit.D-3)

Mechanism Vitamin d is helping and facilitating calcium absorption at the intestine and decreasing its excretion by the kidneys.

Clinical Indications

1.Osteoporosis

2.End Stage Kidrey Failure

3.Rickets due to inadequate intake vit D

4.Rickets due to tissue resistance to vit- D

5.Osteomalacia

6.Hypoparathyroidism

Side effects

1.Vascular calcifications

2.Kidney calcium stones

3.Soft tissue calcium deposits.

 

CALCIUM HOMEOSTASIS-PART-I

CALCIUM METABOLISM

Calcium is an important mineral that our body needs for various functions.Unlike iodine which is almost available in our body mostly in the form of thyroid hormone,  plasma protein bound  and as a free iodine  ion or elemental iodine.Iodine may not stay in our body as a free ion unless for elimination.But in the case of calcium our body needed it in all the forms mostly ionic form for the contractions of various smooth muscles like heart,liver,kidney,pancreas,lungs and stomach etc.etc..About 80% of calcium is stored in bone as phosphates.

Calcium is distributed in our body almost in compartments including bones,plasma,intra-cellular (ICF) and extra-cellular(ECF) fluids.

Our bone contains most of the calcium content of our body  approximately 80% as phosphate salts.Approximately our body's total content of calcium is 1 kg.Bone serves as healthy and safety storage for calcium and phosphorus.10% of calcium is exchanged between bone and ECF in almost every day. 

Thus ECF serves as the next storage compartment,followed by blood plasma {2.3 mmol per liter(9.5 mg/dl) out of which the ionized calcium is 1.4mmol per liter(5.5 mg/dl) and ICF (>0.0002 mmol per liter)}

Calcium helps blood clotting factors by activating them at times of need.

The nerve cells are very sensitive to calcium concentration of in plasma as a small decrease in calcium level below the normal range (Hypocalcemia)may cause the opening of the voltage gated sodium channel and sodium is leaked into the cells of nerve axons and causes nerve hyper excitability which results in muscular spasms a disease known as tetany and paraesthesia (a pricking skin sensation around the mouth and extermities)

Conversely if the plasma calcium level rises above the normal range (Hypercalcemia) the sodium exchange is restriced from out side to inside of the nerve and muscular cells and the nerves are hyper polarised,and lost their normal sense of excitability,and become weak and tired leads to smooth muscle weakness which causes,lethergy,anorexia,constipation and emotions.

Calcium gives the structure,shape and strength for bones by forming as phosphate salts (calcium hydroxyapatite)

Pharmacokinetics

A normal daily diet contains 30 mmol calcium out of which 6 mmol is absorbed by our intestine daily.

Calcium absorption is almost regulated by vitamin D-3 a cholesterol derivative prepared by our skin. 

95% of the calcium from the glomerular filterate is reabsorbed by the kidneys leaving a small fraction to be excreted.If this level is disturbed by some pathological defects such as defects in calcium metabolism or bone desorption then there are possibilities of kidney stone formations occurs.

 

  In general calcium is metabolized  by our body in three ways as follows

1.By a hormone secreted by parathyroid gland (PTH)

2.By calcitonin an hormone secreted by paraglobular cells of thyroid glands

3.By viamin D-3.
1.Parathyroid glands are two pairs in number and each pair is positioned at either lobe of the thyroid glands.As these glands are situated at the back of the thyroid glands these glands are not visible during an exhamination of neck.The usual weight of parathyroid glands are  30 gms in men and 35 gms in women.
The major function of this gland is to maintain calcium and phosphate levels in a very narrow ranges in order to regulate the neuro muscular functions properly.Thus the PTH takes active part in the homeostasis of calcium. 
To keep up the plasma calcium ion within almost in a stable range thyroid and parathyroid glands working in an opposite direction to each other.Thus when the plasma concentrations of calcium ion rises above the narrowly fixed set level (Hypercalcemia) the thyroid secretion of calcitonin act on it and bring it down to normal range.
Conversely if the plasma calcium level go down below the normal set level(Hypocalcemia) then Para Thyroid Hormone (PTH) secreted by parathyroid gland act on it to raise its level to normal range.
Pathology
Hypocalcemia
Hypercalcemia 
 

THYROID DISEASES-IV-HYPER THYROIDSM

THYROTOXICOSIS-TREATMENTS

This is the over whelming secretions of thyroid hormone above the body's need.Unlike in hypothyroidsm in this condition the main cause of defect is on the gland only and not originated from the pituitary or hypothalamus.

Graves's Disease

This is having a synonym as Diffuse Toxic Goiter .This is most probably attacking young children but rarely target adult.

In this condition the gland is stimulated on TSH receptors not by TSH from the pituitary but by the autoimmune antibodies in the blood.Hence when pituitary is normal,and hypothalamus is normal but the gland is overstimulated by the body's own defence system. 

These antibodies are having prolonged gland stimulating effects and since they are only mimiking the action of pituitary and testing for TSH in the blood may not give positive results.

The required results will be yielded only by the titration of these antibodies in the blood.

Symptoms 

1.Diffusely enlarged nontender goiter

2.Nervousness,weakness,and insomnia. 

3.Heat intolerance and heavy sweating.

4.Weight loss inspite of elevated appetite

5.Tremour,muscle weakness

6.Palpitation and tachky arrythmias

7.Incomplete and slow eye lid closing (Exophthalmos)

8.Loose motion

9.Periorbital edema.

Plummer's Disease

This a highly toxic form of nodular goiter.This is more common in adults over 50 years and mostly females.The actual cause is unknown but preferably arise from untreated long standing non toxic goiter. 

In this disease one or more adenomatous nodules of the thyroid gland autonomously secreting excess hormone without being stimulated by pituitary hormone.Enlargedv nodules are formed within the goiter.

Basically deficiency in dietary iodine may cause not only hypothyroidsm but some times cause hyperthyroidsm too as follows by counter activity.

a)Availability of less dietary iodine leads to less T-4 production.

b)Less T-4 production may induce more mutations and introductions of TSH cells.

c)TSH cells on pseudostimulation by body's auto immune antibodies will induce more nodular autonomous T-4 producing cells which secretes automatically without getting any pituitary stimulation excess T-4 hormone result in Hyperthyroidsm.

Symptoms

Many of the symptoms are similar to Graves disease except the goiter shows enlarged nodules inside and usually in this disease slow eye lid movement is absent.

Heart abnormalities are more impressive and predominant in this disease.

Jodebasedow Phenomenon

It is a kind of Hyperthyroidsm in which there is a over production of thyroid hormone due to sudden large intake of iodine.either by food,by drugs (e.g.Antiarrhythmic drugs like amiodarone) or by contrast media like radio iodine.

Factitious Hyperthyroidsm

This hyperthyroidsm occurs mostly by misguided weightloss treatments which involves excessive intake of thyroid replacement agents.

Many of the symptoms of hyperthyroidsm like exophtalmia,glandular swelling.and auto immune activity are all absent in the diagnosis of this disease.

TREATMENTS

1.Beta-adrenergic blockers-Propranolol

Propranolol can reduce some of the peripheral symptoms of hyperthyroidsm such as

Palpitations

Tremour

Tachycardia(Increased heart beats)

Sweatting

Nervousness

In addition to the above symptomatic releives propranolol also inhibit the conversion of T-4 to T-3 in the circulation.

2.Propylthiouracil and Methimazole

Chemically these are sulphur containing thiamides.

They suppress the production of T-3 and T-4 by inhibiting the coupling of thyroglobulin molecule.

Can be taken orally

Side effects 1.Agranulocytosis (Rare but very serious)

2.Rash(Most common)

3.Edema

3.Iodine salts

The mechanism is not clear.Usually thyroid gland cannot take iodide as it is unless it should be converted into nonpolar inorganic iodine molecule.Hence ingesting large quantity of polar iodide ion may well result in decreased conversion into polar form and decreased iodine uptake and eventually leads to decreased productions of the T-4,decreased vascularity and decreased gland size.

Iodides are nowadays not used as a sole thrapy but in conjunction with thioamide and propranolol in thyroid cresis.Iodides also can be used prior to surgery.

Preparations 1.A mixture of iodine and potassium iodide (Lugol's solution)

2.Potassium iodide.

Side effects

1.Anaphylactic reactions such as Angioedema and swelling of the larynx

2.Iodism charectorised by burning taste,and mouth

3.soreness of teeth and mouth

4.swelling of eyelids

5.Cold like  senses

6.Breathing problem

7.Enlargement of the salivary glands

4.Ionic inhibitors

These are perchlorates and thiocyanates.

They competitively inhibit the iodide transport mechanism.

Nowadays their use is limited in favour of other advanced therapies

5.Radio Iodine

The mechanism is thyroid gland can readily absorb iodine in radioform which can ablate the gland and decrease the hormone production.

It can be used very coveniently to adults ove 21 years.

This is very useful in treating Profuse Grave's Disease which is not responding properly to drugs and surgery.

One common advantage with iodine is that there is no any upto date proof  Iodine can cause cancer

Side effects 

Delayed hypothyroidsm has been observed.

Contraindications

Radio iodine is highly contraindicated in pregnancy and milk feeding. 

THYROID STROM 

It is a dangerous emergency situation caused by extreme effects of hyperthyroidsm.

This condition is elevated by sickness,trauma,stress and surgery of the patient who is already thyrotoxic.

Treatments include the treatments of hyperthyroidsm especially and preferably with the beta blockers like propranolol,and glucocorticoids to inhibit the plasma conversions of T-3 to T-4.

Other options are a)Propyl thiouracil and methimazole, 

b)I.V sodium iodide injections

 

 

THYROID DISEASE-III -THYROID DEFICIENCY TREATMENTS

HYPOTHYROIDSM-THYROID UNDER ACTIVITY

This is the inability of the thyroid to secrete sufficient quantity of hormone needed by the body.This is ranges from mild and clinically unimportant to moderate to severe.When the condition go to extreme it may result in life threatening myxedema coma.

Classifications

Primary  1.This is due to tissue damages or malfunctions of the gland by diseases,or destructive therapies such as over or toxic radiations by radio therapies,and mistaken surgeries.

2.Under development and under maturity of the gland by incompetence or congenial.e.g cretinism

Secondary This is a passive inactivity of the gland by not get enough or nil stimulation by TSH secretion from the pituitary gland.In this the gland is healthy but there may be some problem at the anterior pituitary- gland axis and thereby no secretion of the TSH from the pituitary gland.This may be due to some disease in pituitary gland.

Tertiary In this even if both thyroid and pituitary glands are healthy there may be some problem or defects at the hypothalamus pituitary axis so that there is no hypothalamus secretion of Thyrotropin Releasing Hormone (TRH), to stimulate anterior pituitary to release TSH to stimulate thyroid.

Causes

Hashimoto's thyroditis This is an autoimmune condition in which gland is ineffective as its hormones are inactivated by circulating lymphocyts.This condition is chronic and the gland is damaged by lymphocytes,a kind of WBCs as our body's own immunity.

Toxic treatments of Hyperthyroidsm This may be due to careless and toxic radio iodine treatment of hyperthyroidsm,partial removal of the gland,and over administrations of anti thyroid agents.

Surgical damages

Goiter 1)Endemic goiter this condition develops due to the insufficient or zero intake of dietary iodine supplements.This is common in the region where there are soils devoid of iodine contents.

2)Sporadic goiter This is due to the high intake of foods drugs especially herbal medicines containing a chemical known as Progoitrin which is inactive but will be hydrolysed and converted by our body to the active Goitrin.

Goitrin prevent the oxidation of iodine to iodide and blocking the uptake of iodide by the colloidal thyroglobulin to synthesize the hormone.

Vegetables like cabbage,cauliflower,mustard,spinach,brussels,sprouts,peanuts,horse radish and kale are found to be containing more progoitrin.

Drugs such as Propyl thiouracil,iodide,phenylbutazone,cobalt and lithium are said to be goitrogenic

3.Acute thyroiditis,nodules,nodular goiter and thyroid cancer are also said to contribute hypothyroidsm but to a lesser extend.

Symptoms 1)A the start,signs of lethergy,followed by fatigue,forgetfulness,cold like feelings,weight gain without any proper cause,and difficult tight motion.

2)If not properly attended at the beginning the disease will progress further leads to signs of myxedema will surface such as dry flaky inelastic skin,coarse hair,slowed speech and thought,hoarseness,puffy face,hands and feet.Eyelid loop,hearing loss,menorrhagia,impotence,decreased libido, finally losses all reflexes ends in coma.

TREATMENTS

Treatments are mainly based on replacement therapy by drugs

Desiccated thyroid preparations-Variant ratio preparations

In olden days the desiccated thyroid preparation were considered as drug of choice but slowly they lost its favour as more favourable synthetic safe and fast therapeutic agents such as synthetic levothyroxin preparations are available.

Eventhough the desicated thyroid preparation met the USP creteria they are not bioequivalent as their T-3 and T-4 contents are varying.The contents are variying according to their source of preparations.Porcine gland preparations were having higher T-3 to T-4 variations when compared with the preparations from ovine and bovine sources.
Fixed ratio preparations
These are synthetic preparations in order to minimize the variations of the ratio of T-4/T-3.and they almost mimic the glandular functions.In these preparations T-3 component are almost unnecessary because of its disadvantages like tremor,headache,palpitations and diarrhea.Hence preparations like Levothyroxin (Levothroid,Synthroid,and Levoxyl) contains only T-4 and hence the disadvantages of T-3 are nill.Eventhough these contains only T-4 after consumption the body would convert it to T-3 and get the glandular benefits with minimum side effects.Hence these preparations are the drugs of choice.
The average adult maintenance dose is 75 to 150 mic.gm/day for Levothroid and Synthroid.
The dose range is shown to be 1.5 to 1.7 or an average of 1.6 mic/kg/day.for otherwice healthy patients.
Elderly or longtime ill patients require 50 to 100 mic.gm/day as an average dose.
Thyroxin levels become normal within a few weeks and full recovery may be seen after 3 to 6 months.
Precautions and monitoring effects to the patients
1.Adult patient with a history of heart problems should begin with a low dosage like 25 mic.gm/day and gradually increase the dose after 3 to 4 weeks to 100 mic/gm/day. 
2.Patient should be watched for cardiac arrhythmias,palpitations,and anginal pain on initiating the therapy. 
3.Serum T-4,RT-3U,and TSH levels should be monitored.FTI should also to be monitored.
4.Sensitive TSH test should be observed 2 to 6 months after the last dosage is recommended .However the test continue to change for 1 year. Testing early may result into over treatment.
5.Long time Levothyroxine may precipitate hyperthyroidsm;even at the recommended constant dosage T-4 level may increase to induce thyrotoxicosis and hence monitor carefully.
6.Patients receiving replacement therapy with low TSH values may have lower bone mineral density since the excess hormone accumulation may have the effect on the bone resorption to the boneformation equillibrium to result in bone fracture.
7.Cholestyramine a bile acid cholesterol reducing drug may lower the bioavailability of thyroxine on co-administration.
Mixedema coma The most serious emergency situation of hypothyroidism claims high mortality rate.
Common in elderly patients and in patients with under estimated diagnoses.
Precipitating factors are alcohol,sedatives and narcotic uses;over use of anti thyroid agents;
Abrupt discontinuation of thyroid hormone therapy.
Infections;
Exposure to extreme cold temperatures;
Toxic radiations;
Thyroid surgery.
Symptoms
The patient will fall from lethargy to coma.
Hypothermia,and a fall in respiration follows.
Decrease in metabolic rate leads to fluid retension 
Decrease in sodium level.
Decrease in heart rate.
Treatments include rapid restoration of T-3 and T-4 levels to normal
Desiccated thyroid preparations can be tried with risk.More preferably the synthetic Liothyronine (Cytomel)is reseved for the treatments of Myxedema coma.
A loding dose of 400 to 500 mic.gm is given as an I.V. bolus.followed by a maitenance dose of 25 mic.gm is given orally every 6 hrs.
Treatment should be continued until improvement is noted.Then Levothyronine is discontinued followed by the Levothyroxine with the maitenance dose of 100 mic.gm/day.

THYROID DISEASES-II -FTI TESTS

FREE THYROID INDEX TEST-FTI

This is an estimation of free thyroid hormone most importantly T-4 which is the major contributor of the thyroid secretion but minor contributor of the effects of thyroid.

Usually the secretion of T-4 is more in hyperthyroidism and less in hypothyroidism as there may not be much change in the secretions of T-3.

Hence T-4 estimation which is freely circulating in the blood is very important index of assessing the patient's condition.Even though the effects of thyroid is mostly contributed by T-3 it is not important to asses it as a factor because most of the T-3 conversions from T-4 happens only in circulation and not within the thyroid gland

Also this not a separate test rather an estimation of T-4 level which is freely circulating in the blood by mathematical relationship between Resin Triiodothyronine Uptake(RT3U) and serum T-4 levels as follows

FTI = TT-4 x RT-3U/mean serum RT-3U

TT-4 = Total serum T-4;

FTI is higher in hyperthyroidism in which TBG the thyroxin binding globulin is less and vice versa
Alternatively thyroid functions can be assessed by TSH test.TSH the thyroid stimulating hormone is secreted by the pituitary gland according to the thyroid functions.
If pituitary secretes high TSH secretions which elevates the serum TSH level above the normal that means the thyroid gland is underacting which is known as Hypothyroidism.
But if the pituitary secretions of TSH is less which is reflected by the depression of serum TSH level then it means the thyroid gland is over acting which is known as Hyperthyroidism
The normal range of serum TSH level is 3.9 to 4.6 milliunits/Liter.(American Thyroid Association)

THYROID DISEASES-I

THYROID-A VIEW

The thyroid gland which is looking like a butter fly with  spreaded wings is situated in the anterior(front side)of the neck or throat just below the laryngeal prominence (Adam's Apple).It contains two lobes on either side spreaded like the wings of a butterfly.

Thyroid gland is one of the largest ductless gland (endocrine) in our body and it controls many important body functions such as rate of use of energy sources.protein synthesis and controls the body's responses to other hormones.

The thyroid gland synthesizes,stores and secretes hormones which are controlling and participating the processes like growth and protein anabolism.These hormones are as follows:-

1.Tetraiodo thyronine or thyroxine (T-4)-Less active-More stable-and Major secretion of the gland

2.Triiodo thyronine (T-3)-More active-Less stable-Minor secretion of the gland.

A portion of the thyroid gland is secreting a hormone known as calcitonin which is controlling calcium metabolism.

The sequences of thyroid secretion of hormones are as follows,

In our brain system there is a gland like a peanut known as thalamus.Below the thalamus a minute part of the brain is known as hypothalamus which is controlling all our endocrine systems including thyroid.

Hypothalamus secrets a hormone known as Thyrotropin Releasing Hormone(TRH) which inturn stimulates anterior pitutary gland to release Thyrotropic Hormone or Thyroid Stimulating Hormone(TSH) which inturn stimulate thyroid gland to secrete its hormones T-4 and T-3 which on free circulation will send the negative feed back signals to the anterior pitutary to stop to secret the TH.The process will continue like a cycle.Thus the amount of the free circulating hormones are maintained in a constant level.

Synthesis Thyroid hormones are synthesised by thyroid gland by combining tyrosine with the available iodine.

Iodine containg foods like sea foods are essential for the synthesis of thyroid hormones.The food release in the plasma iodide in an inorganic form.

Before synthesis starts a process of manipulating the iodide ion by a process known as the organification which involves the iodide oxidised by peroxidase and bound to tyrosyl residues within the thyroglobulin molecule as follows

1.The inorganic iodide from the plasma is trapped by the gland and the process is known as iodide pump

2.The inorganic iodide has to undergo the organification after thatTyrosine combines with iodide to form Mono Iodo Tyrosine(MIT)

3.MIT binds with another iodide ion to form Di Iodo Tyrosine(DIT)

4.Two DIT couples to form the stable T-4,the Thyroxin

5.One MIT and one DIT couples to form the unstable T-3 which is highly active

Hormone Transport
1.After the gland get stimulated by TSH (Thyrotropic Hormone or Thyroid Stimulating Hormone) from the anterior pituitary gland the T-3 and T-4 are cleaved from the thyroglobulin and released into the blood circulation.
2.In the blood the hormones are bound up with plasma proteins like thyroxine binding globulin (TBG),Prealbumin and Albumin in order to protect them from inactivation by early metabolic processes.These protein carriers help the hormones to reach the site of action very easily.
Metabolism Mostly occur at pituitary,liver,and kidney by conversion of 80% of T-4 into T-3.
The active T-3 is responsible for 99% of the thyroid activity in our body and its abnormal elevation and fall are the complete representations of thyroid dysfunctions.
T-3 is further degraded step by step by a process of deiodization finally converted to thyronine and excreted in feces and urine.
Functions of thyroid hormones
1.Growth
2.Delelopment of our body
3.Energy production by increasing the rae of basal metabolism.
4.Tissue sensitivity to hormones like adrenalin and there by affecting cardio vascular system like increasing heart rate,blood flow,cardiac out put,metabolic rates
5.Increasing the activity of nervous system.
6.Causing tremour.
7.Thyroid over activity may cause sleepiness and tired
8.Thyroid underactivity may cause somnambulance.
9.Affecting lipid meabolism.
Thyroid tests-A.Serum Total T-4 Test.
1.Radio immuno assays these tests more sensitive and rapid to assay total thyroxine T-4.which will indicate the total availability of hormone to the tissues.
Unless otherwice not affected by other factors like pregnancy kidney failure,or liver damage an elevated Total T-4(TT-4) may indicates Hyperthyroidism and a dippressed T-4 may indicate Hypothyroidism
Serum total T-3 Test
This sensitive and most specific test indicates measure of TT-3.
This test is more accurate and help early detection in hyperthyroidsm as the elevation of TT-3 is immediate and more quicker than TT-4.Many of the symptoms of hyperthyroidsm is due to the elevation of TT-3.
But on the contrary in hypothyroidism this test is not reliable as even though there is a fall in TT-3 but will stay at the normal level.In rare case the TT-3 may be low.These test may also mislead by those factors which affect the test result of TT-4.
Resin T-3 uptake(RT,U)
This test will clarify whether the abnormal T-4 levels are due to thyroid disorder or a disorder by protein uptake because it evaluate the binding capacity of TBG
This test read more accurate changes of the abnormal levels of the hormone in the blood.
Serum Thyrotropin(TSH) and Sensitive TSH Assays
a)Serum Assay This assay results are more reliable and sensitive as the hypothalamus - pituitary axis is more sensitive in responding even a minute variations of the circulating blood thyroid hormones to release or stop the TSH.This axis is very sensitive to indicate hypothyroidsm as a small dip in the blood hormone will receive a quick compensatory response from the hypothalamus - pituitary axis.
The TSH levels may be elevated even much before the TT levels are dipped and very useful and easy to detect Hypothyroidsm in advance.
This test is not reliable to asses Hyperthyroidsm as the hypothalamus-pituitary axis is varyingly responding to the elevated TT in plasma
Sesitive Assay This is an advanced technology using immunoradiometric methods instead of the old radioimmune assay and is very expensive.This is the most occurate method of detecting thyroid defects.
This is a very useful test to monitor paients receiving hormone replacement therapy to control hormone over exposures,since over exposure to thyroid hormones may precipitate unwanted elevation of liver enzymes,bone demineralizations and ECG effects.