Thyroid disorders Medicine and parathyroidism

Development of Thyroid gland

Develops from endodermal cells of the floor

of pharynx (Developing tongue)

Begins as a diverticulum on dorsum of

tongue

This elongation forms the thyroglossal duct

Ultimobranchial body develops into

parafollicular cells

Thyroid status with relevance to this?

Disorders of thyroid (medical) breakdown

MAJOR DEVISIONS 1 Related to anatomy 2 Related to endocrine status 3 A combination of both Anatomical => 1. ectopic thyroid tissue eg lingual thyroid 2. thyroglossal cystsDiseases of the thyroid 1 Graves’ Diseases 2 Thyroiditis *Acute suppurative thyroiditis bacterial infection *Subacute thyroiditis ( see slide 36) 3 Autoimmune thyroiditis ( Hashimoto’s Thyroiditis ) 4 Goiter 5 Malignancies of the thyroid *Papillary Carcinoma of thyroid *Medullary carcinoma of thyroid *Anaplastic Carcinoma of thyroid *Lymphoma Thyroid status with relevance to this?

ANATOMICAL DEFORMITIES OF THYROID PICS and DD

,,,,,,,

both cyst and lingual thyroid move when swallowing

Hormones secreted by thyroid

gland and their actions

Triiodothyronine

Tetraiodothyronine / Thyroxine

Calcitonin ( Para follicular cells)

First two from follicles.

Actions of thyroid hormone

1 Metabolic *Increases metabolism and protein synthesis , reduces cholesterol, increases absorption from gut

2 Cardiovascular *Increases heart rate and blood flow

3 Developmental functions * brain development and maturation and normal development of the nervous system both in utero and in early childhood, and they continue to support neurological function in adults * increases growth rate and needed for fetal and childhood tissue development and growth * Sexual maturation

Endocrine regulation of the thyroid gland description

WHAT IS "GOITER "Just enlargment of the thyroid glandThyroid status is irrelevant, so can beHyperthyroidism (all about)

Causes 1 Graves’ diseases 2 Toxic nodule 3 Toxic nodule in a multinodular goiter

4 TSH producing pituitary adenoma 5 Excessive intake of thyroxine 6 Transient hyperthyroidism

>Sub acute thyroiditis >Drug induced thyroiditis >Radiation induced thyroiditis

Diagnostic radio iodine uptake scans of the thyroid gland

its diagnostic and not therapy (so low dose)MOST COMMON CAUSE => +> Grave's disease What it is? autoimmune disorder antibodies to thyrotropin (TSH) receptorManisfestations of graves? 1. hyperthyrodism

2. ophthalmopathy

3. pretibial myxedemaClinical features of graves?

Weight loss with increased appetite Palpitations Excessive sweating Anxiety and agitation Heat intolerance Tremor Increased gut motility with frequent passage of stools Thyroid eye disease Thyroid dermopathy Thyroid acropathy Clubbing Bruit over the thyroid gland

CVS effects

Increased heart rate

Increased systolic blood pressure

Management of AF in thyrotoxicosis

Control of the hyperthyroid state will usually restore sinus rhythm in the absence of any other cause for AF

Beta blocker propranolol would be the drug of choice as it helps to control some of the other distressing symptoms associated with thyrotoxicosis such as tremor, anxiety, and excessive sweating.

Left top high HR

Atrial flutter has 3:1 heart block

2 Thyroid orbitopathy?

Lid lags = sclera becomes visible between lid and eye ball. Theres a lag.Lid retraction = when looking ahead visible band os sclera over headProptosis = eye ball itself potrudes = go behind and check whether potrude External opthalmoplagia = weakness of the extra ocular muscles..so weakness of muscle movementsClinical features of orbitopathy *May occur before, along with, or after features of hyperthyroidism Or after treatment of hyperthyroidism *conjunctival injection and edema ( chemosis ) and periorbital edema. *Impairment of extraocular muscle function *Lid lag *Lid retraction *Exophthalmos *proptosisGrading of severity of thyroid orbitopathyThe severity therefore ranges from 0 to VI. (not so important..no need to remember) Class 0 No symptoms or signs Class I Only signs, no symptoms ( eg , lid retraction, stare, lid lag) Class II S oft tissue involvement Class III Proptosis Class IV Extraocular muscle involvement Class V Corneal involvement Class VI Sight loss (optic nerve involvement)Risk factors for ophthalmopathy1 Genetics 2 Sex Graves' ophthalmopathy, like hyperthyroidism, is more common in women than men. 3 Smoking 4 Type of treatment for Grave’s disease radio iodine > ant thyroid medication 5 Thyrotropin receptor autoantibodies in high titers Important points = sometimes the eye manifestations can be the forst manifestations of graves/hyper thyroidism. And sometimes pts can develop eye issues after Tx of hyper thyroidism. So keep in mind and doesn't mean.Treatment and management of patients with Graves' orbitopathy

Has three components 1 Reversal of hyperthyroidism if present 2 Symptomatic treatment Treatment with a glucocorticoid, and/or orbital irradiation, and/or orbital decompression surgery to reduce inflammation in the periorbital tissues 3 Orbital decompression surgery

Mild symptoms symptomatic therapy, artificial tears, eye shades, *Red eyes and progressive symptoms Glucocorticoid Selenium *Loss of vision orbital decompression surgery

Dermopathy (acropachy - dermopathy associated with graves) and clinical correlations of Graves

majority of patients have

coexisting

ophthalmopathy (96%). 96%).[7]

Thyroid acropachy

extreme manifestation of Graves’ disease *digital clubbing, *swelling of digits and toes *periosteal reaction of extremity bones *almost always associated with ophthalmopathy and thyroid dermopathy

GERIATRIC HYPERTHYROIDISM

Only 2/3 of such patients have symptoms similar to those

in younger patients

Less prevalent

hyperactivity, heat intolerance, tremor, nervousness and other symptoms of sympathetic overactivity

higher prevalence

of weight loss and shortness of breath of atrial fibrillation

MANAGEMENT OF HYPER THYROIDISM

1 Antithyroid medications Carbimazole Methimazole Propylthiouracil 2 Adjuvant therapy for symptomatic relief Beta blockers propranolol 3 Radioiodine 4 surgery Anti thyroid medication *Methimazole half life 4 6 hours single dose less hepatotoxic quicker achievement of euthyroid state *Carbimazole completely metabolized to methimazole *Propylthiouracil half life 75 minutes divided doses higher failure rates for radio iodine therapy inhibits peripheral conversion of T4 to T3 therefore preferred in thyroid storm and in pregnancy Dose of carbimazole *small goiters with mild hyperthyroidism can be started on 10 to 15 mg once daily *severe hyperthyroidism should be started on 20 to 30 mg daily as a single doseCommon side effects Both Methimazole and PTUMinor

pruritus, rash, urticaria, arthralgias, arthritis, fever, abnormal taste sensation, nausea, or vomiting in up to 13 percent of patients

Serious 1 Potential teratogenicity 2 Agranulocytosis ( PTU > methimazole ) *check blood counts every two weeks for the first two months of therapy *Thereafter at the earliest sign of a sore throat or other infection 3 Hepatotoxicity 4 ANCA-positive vasculitis If huge goiters? (usually surgery) Grave's vs other causes and response to surgery? Graves respond well to medications How to choose modality of Tx? (child bearing age?) Other causes of erthema nodosum? Causes of pyoderma gangrenosum? (IBD) How to Tx when pregnant?? Regimen full story: B blocker until euthyroid Then start with high dose 40mg and reduce with time titrating Measure labs and titrate After eu => continue for 12-18 months Then discontinue and most will be okay If not okay then do another cycle or other TX (surgery or iodine) (cant do iodine if child bearing age) If still not okay after another cycle then other TX Its different from hypo which needs long term Tx All about radioactive iodine? Add from assignment, pharm tute, kumar and clark, and cases

Hypothyroidism (all about)

Causes 1 Primary high TSH Hashimoto’s thyroiditis / chronic lymphocytic thyroiditis Other causes 2 Secondary Low TSH due to pituitary failure 3 Other causes of thyroid dysfunction 1 Subacute thyroiditis subacute granulomatous thyroiditis / subacute nonsuppurative thyroiditis,/ giant cell thyroiditis,/ painful thyroiditis,/ de Quervain's thyroiditis.) Fever, pain over thyroid, painful swallowing, other constitutional symptoms like loss of weight fatigue, elevated ESR, Thyroid antibodies not detected. Initially Hyperthyroid followed by hypothyroidism for a variable period of time to life Management NSAID, Steroids, and Symptomatic management of thyroid status (called dysfunction because at first it increases due to release and then goes back or hypo)

2 Postpartum thyroiditis 3 Drug induced thyroiditis amiodarone and lithium

4 Polyglandular autoimmune syndrome Type IIPolyglandular autoimmune syndrome Type II?More common than Type I In type II syndrome the associated autoimmune endocrine disorders include 1 Autoimmune adrenalitis 2 Autoimmune thyroiditis (resulting in hypothyroidism or hyperthyroidism ) 3 Autoimmune diabetesCLINICAL FEATURES (history taking?)Hypothyroidism fatigue, cold intolerance, weight gain, constipation, dry skin, Periorbital edema myalgia (high CPK) menstrual irregularities oligo or amenorrhea or hypermenorrhea Nonpitting edema myxedemaLoss of hair Peripheral neuropathy Galactorrhea Depression dementia Memory loss Sleep apnea and daytime somnolencePhysical examination findings (nine) **goiter particularly in patients with iodine deficiency or goitrous chronic autoimmune thyroiditis ( Hashimoto’s thyroiditis **bradycardia, **Hypertension ( Typically diastolic hypertension ) **Cold dry rough and scaly skin **Hoarse voice **Macroglossia **delayed relaxation phase of the deep tendon reflexes. **Ataxia **Pericardial and pleural effusionsNeurologic manifestations **Hashimoto's encephalopathy describes a syndrome of altered mental status and seizures that occurs in individuals with serologic manifestations of Hashimoto's thyroiditis. **Carpal tunnel syndrome **Peripheral neuropathy **Proximal myopathyLabsFT4 and FT3 will be reducedSerum TSH will be increasedhypercholesterolemia,macrocytic anemia,elevated creatine kinase,hyponatremiaThyroid antibodiesHashimotos thyroiditis (Thyroid peroxidase antibodies (TPO) / thyroid microsomal are elevatedDiagnosis of Thyroid status hypothyroidism TSH assay

TSH is the screening test Useful except in

1 In the presence of pituitary or hypothalamic disease 2 In hospitalized patients with other illnesses that may have a effect on TSH secretion 3 In patients receiving medicationsDrugs that can decrease TSH secretiondopamine, high doses of glucocorticoids, somatostatin analogues (such as octreotide ).Drugs that increase TSH secretionDopamine antagonists ( metoclopramide or domperidone ), amiodaroneDiagnosis of thyroid Status Highly sensitive TSH assays( 7 stuff )TSH (<0.01 mU /L) overt hyperthyroidismTSH 0.3 mU /L and 0.05 mU / subclinical hyperthyroidism. Most of these patients do not need treatment.TSH 0.4 to 4 euthyroidTSH 4 to 10 with Normal FT3 and FT4 subclinical hypothyroidismTSH >10 overt hypothyroidismTSH < 0.4 with reduced FT3 and FT4 ( Increased rT3 ) sick euthyroid syndrome, nonthyroidal illness (NTI), low T3 syndromeTSH <2.5, First trimester of pregnancy optimum levelThyroid serology 1 Thyroid peroxidase antibodies (microsomal antibodies 2 Thyroglobulin antibodies Both two above used for hashimotors

Do not confuse withTSH receptor antibodies ( Grave’s Disease) and serum thyroglobulin used as marker of tumor recurrence after thyroidectomyTreatment of hypothyroidismUsually a permanent condition requiring lifelong treatment The average replacement dose of T4 in adults is approximately 110 mcg/day range 50 to ≥200 mcg/day T4 should be taken on an empty stomach, ideally an hour before breakfast The initial dose can be the full anticipated dose (1.6 mcg/kg/day) in young, healthy patients, but older patients should be started on a lower dose (25 to 50 mcg daily) and up titrated to the appropriate doseRegimen of thyroxineStart low dose and then increase Measure TSH/T4 like every two weeks until eu Titrate as you go along Then can increase interval to 2 months and then a year Or if sympomatic After eu can only measure TSH But occasionally and if symptoms measure TSH/T4 as well If pregnancy make it morte stringent as should avoid hypo at all costsPlace for t3? (T3 thyrotoxicosis)