Wednesday 16 April 2014

Thyrotoxicosis v\s Hyperthyroidism

Thyrotoxicosis Vs Hyperthyroidism

Thyrotoxicosis refers to the biochemical and physiological manifestations of excessive thyroid hormone.
Hyperthyroidism is a term reserved for disorders that result in the over production of hormone by the thyroid gland. Thyrotoxicosis need not be due to hyperthyroidism.

Causes of hyperthyroidism
Grave's disease
Jod - Basedow's disease
Toxic nodular goiter
Toxic adenoma

Causes of thyrotoxicosis without hyperthyroidism
Subacute thyroiditis
Ectopic functioning thyroid tissue
Struma ovarii
Postpartum thyroiditis
Silent thyroiditis
Metastatic follicular carcinoma
Trophoblastic tumors

Tuesday 15 April 2014

Remanent of Thyroglossal duct


Thyroid Hormones: Scheme of the thyroid hormone production and regulation on the hypothalamus–pituitary–thyroid axis


Iodine is absorbed from the GI tract and is transferred to the thyroid gland where oxidization and incorporation into tyrosyl residues of thyroglobulin occurs. Tyrosine is further oxidized to form monoiodotyrosine (MIT) and diiodotyrosine (DIT). The combination of 2 molecules of DIT forms thyroxine (T4). Triiodothyronine (T3) is made by the combination of MIT and DIT and by the monodeiodination of T4 in the periphery.
T3 is 4 times more active than the more abundant T4. The half-life of T4 is 5-7 days; the half-life of T3 is only 1 day. Approximately 99% of the circulating thyroid hormone is bound to plasma protein and is metabolized primarily by the liver.
Levels of thyroid hormones in the serum are tightly regulated by the hypothalamic-pituitary-thyroid axis. Thyroid-releasing hormone (TRH) is secreted by the hypothalamus, and stimulates the release of thyroid-stimulating hormone (TSH) from the pituitary gland. Mature TSH reaches the thyroid gland and stimulates thyroid hormone production and release. The main hormone secreted from the thyroid gland is T4, which is converted to T3 by deiodinase in the peripheral organs. Secreted thyroid hormone reaches the hypothalamus and the pituitary, where it inhibits production and secretion of TRH and TSH, thereby establishing the hypothalamic-pituitary-thyroid axis.

Difference between TBG and thyroglobulin

Is there a difference between thyroglobulin and thyroxine-binding globulin?

YES!

The two terms are close enough to confuse, so it's worth spelling them out here.Thyroglobulin is the substance that the thyroid follicles make and store in their centres. When thyroid hormones are needed, some of the thyroglobulin protein is pinched off (pinocytosis) and taken into the follicular cell. There it undergoes proteolysis and is ultimately by the converted into the thyroid hormones (mainly T4, but also some T3). In the final step, the thyroid hormones are released into the blood stream.

In the blood, almost all the thyroid hormone is bound to proteins - less than 0.1% of T3 and T4 float freely. The main protein that binds them is thyroxin-binding globulin (TBG), although other proteins also contribute (e.g. albumin).


THYROID GLAND- Biosynthesis of thyroid hormone



Tg is used by the thyroid gland to produce the thyroid hormonesthyroxine (T4) andtriiodothyronine (T3). The active form of triiodothyronine, 3, 5, 3' triiodothyronine, is produced both within the thyroid gland and in the periphery by 5'-deiodinase (which has been referred to as tetraiodothyronine 5' deiodinase). It is presumed that Tg and thyroid are also an important storage of iodine for all body needs, in particular, for many iodine-concentrating organs such as breast, stomach, salivary glands, thymus, choroid plexus and cerebrospinal fluid, etc.[2] (seeiodine in biology).
In fact, the Tg molecule, which contains approximately 120 tyrosyl residues, is able to form only very small amounts of thyroid hormone (5-6 molecules of T4 and T3).
Tg is produced by the thyroid epithelial cells, called thyrocytes, which form spherical follicles. Tg is secreted and stored in the follicular lumen.
Via a reaction with the enzyme thyroperoxidase, iodine is covalently bound to tyrosine residues in thyroglobulin molecules, forming monoiodotyrosine (MIT) and diiodotyrosine(DIT).

Small globules of the follicular colloid (Tg) are endocytosed (hormone (TSH)-mediated) and proteases in lysosomes digest iodinated thyroglobulin, releasing T3 and T4 within the thyrocyte cytoplasm. The T3 and T4 are then transported across (TSH-mediated) the basolateral thyrocyte membrane, into the bloodstream, by an unknown mechanism while the lysosome is recycled back to the follicular lumen.

Examination of Abdominal Lump - Clinical Examination

Sunday 13 April 2014

Lung Sounds - Rales, Rhonchi, Wheezes

Breath Sounds.wmv

Bronchial and Vesicular Breath Sounds

Adventitious Breath Sounds

Breath Sounds

Heart Murmurs- Complete lecture

8-Heart Sounds !!

Heart Murmurs described in the most funniest way !!!

Physiological & pathological breath sounds- best described !!

Breathe Sounds + Heart Sounds

heart and Lung sounds 

Guys ...the link i ve mentioned above shall take u to an awesum site providing a holistic view over all soughts of sounds produced in heart and chest !!

and here's another site :
Heart and chest sounds- made easier


Heart Sounds

Cardiovascular Exam

Respiratory Exam

Respiratory examination



Awesum Video- Do watch it and i ve also added Cardiac and Abdominal examination videos below as no respiratory examination is complete without Cardiac and Abdominal examination !!! Have funn :D



Mediastinal shift: Causes, Conditions and Method of Examination

Mediastinal Position

Position of mediastinum gives important clues to the nature of process in each hemithorax. Trachea is the index of upper mediastinum and heart of the lower mediastinum.

Method of Exam

Examine the position of mediastinum by standing in front of the patient. Make certain that the patient is seated straight or preferably standing erect. Trachea is the index of upper mediastinum. Heart is the index of lower mediastinum. Position of the heart can be used as an index of mediastinum only when it is not enlarged.
  1. Inspect for the symmetry of clavicular insertion of both sternomastoids.
  2. Tracheal Position: Gently bend the head to relax sternomastoids. Assess and compare the space between the trachea and sternomastoid on either side. Keep the tips of your index and ring fingers over the medial end of the clavicles. Then, with the middle finger, assess the space between the trachea and sternomastoid.
    Caution: Make sure that your nails are trimmed.
  3. Position of Heart: Identify the location of apex of the heart by inspection and palpation.
    Caution: Make sure that the heart is not enlarged.

Normal
The right sternomastoid is slightly prominent normally. The trachea is slanted to the right. The apex of the heart is located on the 5th LIC space just internal to the midclavicular line.
Abnormal
Any deviation of the mediastinum is abnormal.

The mediastinum can be either pulled or pushed away from the lesion.
  1. Pull: Loss of lung volume (Atelectasis, fibrosis, agenesis, surgical resection, pleural fibrosis)
  2. Push: Space occupying lesions (pleural effusionpneumothorax, large mass lesions)
  3. Mediastinal masses and thyroid tumors
  4. Kypho-scoliosis
Example:

Let us suppose that you have arrived at a decision that the mediastinum is shifted to left. It could be either due to a pushing lesion from right or a pulling lesion from left. The next step will help us identify which side is abnormal.

Caution :

  1. Do not misinterpret apical impulse to mean deviated mediastinum in the presence of an enlarged Heart.
  2. Difficult to interpret mediastinal position in a patient with Kypho-scoliosis.

Trail Sign






Lamina cribrosa



Haab's striae


Arrangement of optic nerve




Optic nerve cupping


Bupthalmos

Buphthalmos (plural: buphthalmoses) is a medical term that desribes enlargement of the eyeball and is most
commonly seen in infants and young children. It is sometimes referred to as buphthalmia (plural buphthalmias).It
usually appears in the newborn period or the first 3 months of life.121 and in most cases indicates the presence of
congenital (infantile) glaucoma, which is a disorder in which elevated pressures within the eye lead to structural eye
damage and vision loss.

Etiology :
Infantile glaucoma, which often produces the clinical sign of buphthalmos, can be caused when an abnormally narrow
angle between the comeaand ins blocks the outflow of aqueous humor;[3]this causes increased intraocular
pressure and eentual enlargement of the globe (eyeball). Angle closure can be caused by deeIopniental
abnormalities of the eye as well as the presence of abnormal structures within the ‘Âtreous.14]
Symptoms:
Buphthalmos in itself is merely a clinical sign and does not generate symptoms. Patients with glaucoma often
initially hae no symptoms; later, they can exhibit excessie teanng (Iacnmation) and extreme sensitivity to light
(photophobia). On ophthalmologic exam, one can detect increased intraocular pressure, distortion of the optic disc,
and comeal edema, which manifests as haziness.
Prognosis and treatment:
Untreated glaucoma leads to total blindness. Surgical treatment is required. Presently-utilized surgical procedures
include goniotomy, trabeculotomy, or trabeculectomy.

Ectopia Lentis


Ectopia lentis :
Ectopia lentis is a displacement or malposition of the eyes
crystalline lens from its normal location A partial dislocation of a
lens is termed lens subluxation or subluxated lens: a complete
dislocation of a lens is termed lens luxation or luxated lens.


Trabecular meshwork and routes of aqueous flow

Routes of aqueous flow