Download Free Medical Thyrotoxicosis PowerPoint Presentation

Thyrotoxicosis PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Thyrotoxicosis" by Dr Amit Gupta.

This medical PowerPoint presentation talks about thyrotoxicosis, a medical condition characterized by an excessive amount of thyroid hormones in the bloodstream. This is usually caused by an overactive thyroid gland, also known as hyperthyroidism. Thyroid hormones play an essential role in the bodys metabolism and affect many body functions, such as heart rate, body temperature, and energy levels.

The most common cause of thyrotoxicosis is Graves disease, an autoimmune disorder that causes the thyroid gland to produce too much thyroid hormone. Other causes of thyrotoxicosis include thyroid nodules, thyroiditis, and excess iodine intake.

Symptoms of thyrotoxicosis can vary depending on the severity of the condition, but some common signs include weight loss, increased appetite, rapid or irregular heartbeat, trembling hands, sweating, and nervousness. In severe cases, thyrotoxicosis can lead to heart failure, osteoporosis, and other health complications.

Treatment for thyrotoxicosis depends on the underlying cause and the severity of the symptoms. Options include medications to block the production of thyroid hormones, radioactive iodine therapy to destroy overactive thyroid cells, and surgery to remove part or all of the thyroid gland. With proper treatment, most people with thyrotoxicosis can manage their condition and lead healthy lives.

Tags : thyrotoxicosis, thyroid gland, hyperthyroidism, Thyroid hormones, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 24, 2023 | Views : 2504 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Thyrotoxicosis Dr Amit Gupta Associate Professor Dept Of Sugrery
Slide 2-

Etiology Hyperthyroidism with high RIU - Grave’s Disease - Toxic Multinodular Goitre - Toxic Adenoma - TSH- producing Pituitary Adenoma
Slide 3-

Etiology Hyperthyroidism with low/ normal RIU - Sub-Acute Thyroiditis - Exogenous Hormone intake - Struma Ovarii - Metastatic Follicular Thyroid CA - Amiodarone induced
Slide 4-

Diffuse toxic goitre ( Graves’) Autoimmune Disease Abnormal Thyroid Stimulating Antibodies to TSH receptors 50% familial, with other autoimmune endocrine diseases Younger females Primary thyrotoxicosis with eye signs
Slide 5-

Toxic Multinodular Goitre Only 5% of all cases 10 times more common in iodine deficient area Typically occurs in patients older than 40 with long standing goitre Secondary thyrotoxicosis, eye signs rare
Slide 6-

Toxic Adenoma ( Plummers’) More common in young patients Autonomous functioning single nodule Somatic mutations in the TSH receptor gene Size usually > 3 cm Visualized as a hot nodule on RAI uptake scan
Slide 7-

Sub-acute Thyroiditis ( De Quervain) Abrupt onset due to leakage of preformed hormones following injury to gland Follows viral infection Resolves within eight months Rapid response to Prednisone Can re-occur
Slide 8-

Treatment Induced Hyperthyroidism Iodine induced Radiographic contrast media Medication Amiodarone Induced Jod-Basedow thyrotoxicosis Thyroid Hormone Induced Metastatic thyroid cancer Struma ovarii TSH secreting tumor
Slide 9-

Pathology
Slide 10-

Clinical symptoms (Skin) Warm, Erythematous Smooth- due to decrease in keratin Sweaty and heat intolerance Infiltrative dermopathy on shins Onycholysis –softening of nails and loosening of nail beds Thinning of hair
Slide 11-

Clinical symptoms Graves disease has ophthalmopathy Antibody mediated effect on ocular muscles Exophthalmos Infiltration of retro-bulbar tissues with fluid & round cells with lid retraction/spasm* *Due to sympathetic over activity
Slide 12-

ppt slide no 12 content not found
Slide 13-

Clinical symptoms (Eye) Impaired extraocular eye muscle function (Diplopia) Periorbital and conjunctival edema Corneal ulceration due to lid lag and proptosis Optic neuritis and even blindness Gritty feeling or pain in the eyes
Slide 14-

Eye signs Lid retraction ( Dalrymple’s sign) Lid lag ( von Graefe’s sign ) Periorbital puffiness* (Enroth’s sign) Difficulty in eversion of upper lid (Gifford’s sign) Infrequent blinking (Stellwag’s sign) Absent creases on forehead on superior gaze (Goffroy’s sign) Difficulty in convergence (Moebius sign)
Slide 15-

Long-standing thyroid ophthalmopathy with typical features of lid retraction (upper & lower) and visible sclera with proptosis.
Slide 16-

Lid lag ( von Graefe’s sign )
Slide 17-

Periorbital puffiness (Enroth’s sign)
Slide 18-

Difficulty in convergence (Moebius sign)
Slide 19-

Clinical symptomsCardiovascular System Increased cardiac output (due to increased oxygen demand and increased cardiac contractibility. Tachycardia persists in sleep Stages of thyrotoxic arrhythmias Multiple extrasystoles Paroxysmal atrial tachycardia Paroxysmal atrial fibrillation Persistent atrial fibrillation
Slide 20-

Clinical symptoms (GI System) Weight loss due to increased calorigenesis Hyperphagia (weight gain in younger patient) Hyperdefecation Malabsorption Steatorrhea Celiac Disease (in Grave’s Disease)
Slide 21-

Neuromuscular System Tremors-outstretched hand and tongue Hyperactive tendon reflexes
Slide 22-

Psychiatric Hyperactivity Emotional lability Anxiety Decreased concentration Insomnia
Slide 23-

Muscle Weakness Proximal muscle weakness in 50% pts. Decreased muscle mass and strength May take up to six months after euthyroid state to gain strength Myesthenia Gravis, especially in Grave’s disease.
Slide 24-

Thyroid function test TSH level Low TSH High TSH (rare) Measure T4 High Secondary hyperthyroidism Image pituitary gland
Slide 25-

Low TSH Measure Free T4 Level Normal High Measure Free T3 Level Normal High -Subclinical hyperthyroidism -Resolving Hyperthyroidism -Medication -Pregnancy T3 Toxicosis Primary hyperthyroidism Thyroid uptake Low High Measure thyroglobulin decreased Increased Exogenous Thyroiditis Iodide exposure Exrtraglandular production DIffuse Nodular hormone Graves disease Multiple areas One “hot” area Toxic multinodular goiter Toxic adenoma
Slide 26-

Treatment Goal: To correct hyper-metabaolic state with least side effects and lowest incidence of hypothyroidism. Treatment depends upon -Cause and severity of disease -Patients age -Goiter size -Comorbid condition -Treatment desired
Slide 27-

Options Anti-thyroid drugs Radioactive iodine Surgery Beta-blocker and iodides are adjuncts to above treatment
Slide 28-

Anti-thyroid Drugs They interfere with uptake and organification of iodine—suppress thyroid hormone levels Two agents: -Carbimazole -PTU (Propylthiauracil)
Slide 29-

Anti-thyroid Drugs Short term therapy: Prepare patients for RAI/ Surgery Medium term therapy: For remission in Graves Disease Relapse more common in -smokers -elevated TS antibodies at end of therapy
Slide 30-

Anti-thyroid Drugs Carbimazole Drug of choice for non-pregnant patients because of : Dose 20 mg/day Low cost Lower incidence of side effects Can be given in conjunction with beta-blocker Beta-blockers can be tapered off after 4-8 weeks of therapy
Slide 31-

Anti-thyroid Drugs PTU Preferred for pregnant patients Carbimazole is associated with genetic abnormalities like aplasia cutis Dose 100 mg t.i.d Inhibit peripheral deiodination of T4 to T3 Breast feeding is not contraindicated
Slide 32-

Anti-thyroid Drugs Complications Agranulocytosis up to 0.5% cases High with PTU Advised to stop drug if they develop sudden fever or sore throat Hepatitis Skin rashes Lupus like syndromes
Slide 33-

Beta Blockers Prompt relief of adrenergic symptoms Propranolol widely used Start with 10-20 mg q6h Increase progressively until symptoms are controlled Most cases 80-320 mg qd is sufficient CCB can be used if beta blocker not tolerated or contraindicated
Slide 34-

Iodides Iodide blocks peripheral conversion of T4 to T3 and inhibits hormone release. These are used as adjunct therapy Before emergency non-thyroid surgery Beta blockers cannot curtail symptoms Decrease vascularity before surgery for Grave’s disease
Slide 35-

Radioactive Iodine Treatment of choice for Grave’s disease and toxic nodular goiter Inexpensive Highly effective Easy to administer Safe Dose depends on estimated weight of gland Higher dose increases success rate but higher chance of hypothyroidism
Slide 36-

Radioactive Iodine Higher dose is favored in older patient Dose individualization is difficult Arbitrary dosage of 200-600 MBq Effective for both Graves Disease and Toxic MNG Transient thyroiditis is side effect
Slide 37-

Surgery Radioactive iodine has replaced surgery for Tx of hyperthyroidism Indications: Large Toxic MNG Large Diffuse Toxic Goitre Toxic adenoma Childhood Graves’ Disease Thyrotoxicosis in pregnancy
Slide 38-

New Treatment Minimally invasive subtotal thyroidectomy Embolization of thyroid arteries Plasmapheresis Percutaneous ethanol injection into toxic nodule L-Carnitine supplementation may improve symptoms and may prevent bone loss