HYPERTHYROIDISM

1
HYPERTHYROIDISM

• A Practical Approach to Dx. and Rx.
• PROF. BIKHA RAM DEVRAJANI
• MB,FCPS,FACP,FRCP
• LUMHS JAMSHORO

2

• A 27 years unmarried lady presented with the
  history of weight loss increased appetite ,
  sweating and palpitation
• Q what is D/D ?

3
THYROID GLAND
4
Clinical Exam. of Thyroid

• Have patient seated on a stool / chair
• Inspect neck before after swallowing
• Examine with neck in relaxed position
• Palpate from behind the patient
• Remember the rule of finger tips
• Use the tips of fingers for palpation
• Palpate firmly down to trachea
• Pembertons sign for RSG

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Where to look for Thyroid ?
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Clinical Anatomy of Thyroid
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Clinical Exam of Thyroid
8
Clinical Exam of Thyroid
9
Clinical Exam of Thyroid
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Thyromegaly
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Hyperthyroidism

• A hyper metabolic biochemical state
• It is a multi system disease with
• Elevated levels of FT4 or FT3 or both
• What is thyrotoxicosis ?
• What is hyperthyroidism ?
• What are the various causes ?
• How to differentiate the causes ?
• What is the appropriate treatment ?

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Causes of Hyperthyroidism

1. Graves Disease Diffuse Toxic Goiter
2. Plummers Disease Toxic MNG
3. Toxic phase of Sub Acute Thyroiditis - SAT
4. Toxic Single Adenoma STA
5. Pituitary Tumours excess TSH
6. Molar pregnancy Choriocarcinoma (?? ßHCG)
7. Metastatic thyroid cancers (functioning)
8. Struma Ovarii (Dermoid and Ovarian tumours)
9. Thyrotoxicosis Factitia INF, Amiodarone, SSRIs

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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 T4 and T3
• Anti thyro peroxidase (anti-TPO) antibodies
• Anti thyro globulin (anti-TG) Anti Microsomal and
  other
• Autoimmune diseases - Pernicious Anemia, T1DM
• RA, Myasthenia Gravis, Vitiligo, Adrenal
  insufficiency.

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Graves Disease
I 123 or TC 99m Normal v/s Graves
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Graves Disease
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Toxic Multinodular Goiter (TMG)

• TMG is the next most common hyperthyroidism - 20
  
• More common in elderly individuals long
  standing goiter
• Lumpy bumpy thyroid gland
• Milder manifestations (apathetic hyperthyroidism)
• Mild elevation of FT4 and FT3
• Progresses slowly over time
• Clinically multiple firm nodules (called
  Plummers disease)
• Scintigraphy shows - hot and normal areas

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Toxic Multinodular Goiter (TMG)
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Toxic Multinodular Goiter (TMG)
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Sub Acute Thyroiditis (SAT)

• SAT is the next most common hyperthyroidism 15
• T4 and T3 are extremely elevated in this
  condition
• Immune destruction of thyroid due to viral
  infection
• Destructive release of preformed thyroid hormone
• Thyroid gland is painful and tender on palpation
• Nuclear Scintigraphy scan - no RIU in the gland
• Treatment is NSAIDs and Corticosteroids

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Toxic Single Adenoma (TSA)

• TSA is a single hyper functioning follicular
  thyroid adenoma.
• Benign monoclonal tumor that usually is larger
  than 2.5 cm
• It is the cause in 5 of patients who are
  thyrotoxic
• Nuclear Scintigraphy scan shows only a single hot
  nodule
• TSH is suppressed by excess of thyroxines
• So the rest of the thyroid gland is suppressed

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Toxic Single Adenoma (TSA)
Nucleotide Scintigraphy
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Age and Sex

• Age
• Graves disease 20 to 40
• Toxic MNG gt 50 yrs
• Toxic Single Adenoma 35 to 50
• Sub Acute Thyroiditis Any age
• Sex M F ratio
• Graves Disease 1 5 to 110
• Toxic MNG 1 2 to 1 4

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Nucleotide Scintigraphy
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Clinical Features

1. Those that occur with any type of thyrotoxicosis
2. Those that are specific to Graves disease
3. Non specific changes of hyper metabolism

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Common Symptoms

1. Nervousness
2. Anxiety
3. Increased perspiration
4. Heat intolerance
5. Tremor
6. Hyperactivity
7. Palpitations
8. Weight loss despite increased appetite
9. Reduction in menstrual flow or oligo-menorrhea

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Common Signs

1. Hyperactivity, Hyper kinesis
2. Sinus tachycardia or atrial arrhythmia, AF, CHF
3. Systolic hypertension, wide pulse pressure
4. Warm, moist, soft and smooth skin- warm handshake
5. Excessive perspiration, palmar erythema,
   Onycholysis
6. Lid lag and stare (sympathetic over activity)
7. Fine tremor of out stretched hands format's
   sign
8. Large muscle weakness, Diarrhea, Gynecomastia

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Specific to Graves Disease

• Diffuse painless and firm enlargement of thyroid
  gland
• Thyroid bruit is audible with the bell of
  stethoscope
• Ophthalmopathy Eye manifestations 50 of
  cases
• Sand in eyes, periorbital edema, conjunctival
  edema (chemosis), poor lid closure, extraocular
  muscle dysfunction, diplopia, pain on eye
  movements and proptosis.
• Dermoacropathy Skin/limb manifestations 20
  of cases
• Deposition of glycosamino glycans in the dermis
  of the lower leg non pitting edema, associated
  with erythema and thickening of the skin, without
  pain or pruritus - called (pre tibial
  myxedema)

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Clinical Presentations
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MNG and Graves
Huge Toxic MNG
Diffuse Graves Thyroid
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Higher grades of Goiter
(Diffuse) Graves
Toxic MNG
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Grade IV Toxic MNG
Huge Toxic MNG
Huge Toxic MNG
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Thyroid Ophthalmopathy
Proptosis
Lid lag
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Ophthalmopathy in Graves
Periorbital edema and chemosis
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Ophthalmopathy in Graves
Occular muscle palsy
Laka Laka Laka
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Severe Exophthalmia
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Thyroid Dermopathy
Pink and skin coloured papules, plaques on the
shin
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Graves with Acropathy
Graves Goiter
Acropathy
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Thyroid Acropathy
Clubbing and Osteoarthropathy
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Onycholysis
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Non specific changes

1. Hyperglycemia, Glycosuria
2. Osteoporosis and hypercalcemia
3. ? LDL and Total Cholesterols
4. Atrial fibrillation, LVH, ? LV EF
5. Hyper dynamic circulatory state
6. High output heart failure
7. H/o excess Iodine, amiodarone, contrast dyes

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Nine Square Approach



PRIMARY HYPERTHYROID
LOW NORMAL HIGH
FREE THYROXINE or FT4
LOW NORMAL
HIGH
THYROID STIMULATING HORMONE - TSH
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Nine Square Approach



SUB CLINICAL HYPERTHYROID
LOW NORMAL HIGH
FREE THYROXINE or FT4
LOW NORMAL
HIGH
THYROID STIMULATING HORMONE - TSH
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Diagnosis

1. Typical clinical presentation
2. Markedly suppressed TSH (lt0.05 µIU/mL)
3. Elevated FT4 and FT3 (Markedly in Graves)
4. Thyroid antibodies by Elisa anti-TPO, TSI
5. ECG to demonstrate cardiac manifestations
6. Nuclear Scintigraphy to differentiate the causes

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Algorithm for Hyperthyroidism
Measure TSH and FT4
? TSH, FT4 N
? TSH, ? FT4
N TSH, FT4 N
? TSH, ? FT4
FNAC, N Scan
Primary (T4) Thyrotoxicosis
Pituitary Adenoma
Measure FT3
High
T3 Toxicosis
Features of Graves
Normal
Sub-clinical Hyper
Yes
No
? RAIU
Low RAIU
F/u in 6-12 wks
Rx. Graves
Sub Acute Thyroiditis, I2, ? Thyroxine
Single Adenoma, MNG
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Laboratory Diagnosis

• Serum T3, T4, FT3, FT4
• Sensitive TSH assay
• Serum TRAb
• Test of TRH irritation
• Radioactive iodine uotake
• Normal 3h 5-25, 24h 20-45, peak at 24h
• Thyroid scan 131I, 99mTc

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Diagnosis

• Symptoms
• Signs
• Laboratory examination

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Differential diagnosis

• Other causes of thyrotoxicosis
• Anxiety neurosis or mania
• Some states of hypermetabolism without
  thyrotoxicosis severe anemia, leukemia, etc.
• Cardiac disease atrial fibrillation, angina
• Pheochromocytoma
• Other causes of ophthalmoplegia (myasthenia
  gravis) and exophthalmos (orbital tumor)
• Others COPD, DM, cirrhosis of the liver.

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Treatment Options

• Symptom relief medications
• Anti Thyroid Drugs ATD
• Methimazole, Carbimazole
• Propylthiouracil (PTU)
• Radio Active Iodine treatment RAI Rx.
• Thyroidectomy Subtotal or Total
• NSAIDs and Corticosteroids for SAT

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Symptom Relief

• Rehydration is the first step
• ß blockers to decrease the sympathetic excess
• Propranalol, Atenelol, Metoprolol
• Rate limiting CCBs if ß blockers
  contraindicated
• Treatment of CHF, Arrhythmias
• Calcium supplementation
• SSKI or Lugol solution for ? vascularity of the
  gland

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Anti Thyroid Drugs (ATD)
Imp. considerations Methimazole Propylthiouracil
Efficacy Very potent Potent
Duration of action Long acting BID/OD Short acting QID/TID
In pregnancy Contraindicated Safely can be given
Mechanism of action Iodination, Coupling Iodination, Coupling
Conversion of T4 to T3 No action Inhibits conversion
Adverse reactions Rashes, Neutropenia Rashes, ?Neutropenia
Dosage 20 to 40 mg/ OD PO 100 to 150mg qid PO
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How long to give ATD ?

• Reduction of thyroid hormones takes 2-8 weeks
• Check TSH and FT4 every 4 to 6 weeks
• In Graves, many go into remission after 12-18
  months
• In such pts ATD may be discontinued and followed
  up
• 40 experience recurrence in 1 yr. Re treat for 3
  yrs.
• Treatment is not life long. Graves seldom needs
  surgery
• MNG and Toxic Adenoma will not get cured by ATD.
• For them ATD is not the best. Treat with RAI.

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Radio Active Iodine (RAI Rx.)

• In women who are not pregnant
• In cases of Toxic MNG and TSA
• Graves disease not remitting with ATD
• RAI Rx is the best treatment of hyperthyroidism
  in adults
• The effect is less rapid than ATD or
  Thyroidectomy
• It is effective, safe, and does not require
  hospitalization.
• Given orally as a single dose in a capsule or
  liquid form.
• Very few adverse effects as no other tissue
  absorbs RAI

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Radio Active Iodine (RAI Rx.)

• I123 is used for Nuclear Scintigraphy (Dx.)
• I131 is given for RAI Rx. (6 to 8 milliCuries)
• Goal is to make the patient hypothyroid
• No effects such as Thyroid Ca or other
  malignancies
• Never given for children and pregnant/ lactating
  women
• Not recommended with patients of severe
  Ophthalmopathy
• Not advisable in chronic smokers

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Surgical Treatment

• Subtotal Thyroidectomy, Total Thyroidectomy
• Hemi Thyroidectomy with contra-lateral subtotal
• ATD and RAI Rx are very efficacious and easy so
• Surgical treatment is reserved for MNG with
• Severe hyperthyroidism in children
• Pregnant women who cant tolerate ATD
• Large goiters with severe Ophthalmopathy
• Large MNGs with pressure symptoms
• Who require quick normalization of thyroid
  function

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Preoperative Preparation

• ATD to reduce hyper function before surgery
• ßeta blockers to titrate pulse rate to 80/min
• SSKI 1 to 2 drops bid for 14 days
• This will reduce thyroid blood flow
• And there by reduce per operative bleeding
• Recurrent laryngeal nerve damage
• Hypo parathyroidism are complications

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Dietary Advice

• Avoid Iodized salt, Sea foods
• Excess amounts of iodide in some
• Expectorants, x-ray contrast dyes,
• Seaweed tablets, and health food supplements
• These should be avoided because
• The iodide interferes with or complicates the
  management of both ATD and RAI Rx.

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Summary of Hyperthyroidism
Hyperthyroidism Age Enlarged Pain RAIU Treatment
Graves (TSI Ab eye, dermo, bruit) 20 - 40 60 Diffuse None ?? ATD 18 m
Toxic MNG gt 50 20 Lumpy Pressure ? RAI, Surgery
Single Adenoma 35 - 50 5 Single None RAI, ATD
S Acute Thyroiditis Any age 15 None Yes ?? NSAID, Ster.
TSH is markedly low, FT4 is elevated
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Thyrotoxicosis Factitia

• Excessive intake of Thyroxine causing
  thyrotoxicosis
• Patients usually deny it is willful ingestion
• This primarily psychiatric disorder
• May lead to wrong diagnosis and wrong treatment
• They are clinically thyrotoxic without eye signs
  of Graves
• High doses of Thyroxine lead to TSH suppression
• This causes shrinkage of the thyroid
• Stop Thyroxine and give symptom relief drugs

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• A 27 years unmarried lady presented with the
  history of weight loss increased appetite ,
  sweating and palpitation
• Q what is D/D ?

61
Case 1

• A patient complains of sandy sensation in
  his eyes,weight loss, and a tremor. His
  extraocular muscles are inflammed. His thyroid is
  diffusely enlarged and non tender.
• The most likely diagnosis is
• a. Iodine deficiency
• b. Sub-acute thyroiditis
• c. Multinodular goiter
• d. Graves disease
• e. Silent thyroiditis

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Case 2

• A 55 year old woman is anxious, irritable,
  frequent semi solid stools and she reports weight
  loss of 5 kgs in the past six months. She was
  having a lumpy bumpy painless swelling in her
  neck for past 20 years.
• The most likely diagnosis is
• a. Iodine deficiency goiter
• b. Sub-acute thyroiditis
• c. Multinodular goiter
• d. Graves disease
• e. Solitary toxic adenoma

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Case 3

• A 60 year patient from a mountain region
  complains of
• constipation. He has a heart rate of 60, dry
  thick skin,
• and a tongue that has scalloped edges from
  teeth
• indentation. He has a goiter.
• The most likely diagnosis is
• a. Iodine deficiency
• b. Subacute thyroiditis
• c. Graves disease
• d. Silent thyroiditis

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Case 5

• A 72 year old man complains of tremor and
  inability to
• concentrate. On exam, he has a heart rate of 100
  beats
• per minute. He has a large goiter with many
  nodules. He
• has a fine tremor. His serum T4 is very high and
  TSH is
• very low.
• Treatments that are likely to improve his
  symptoms are
• a. Iodine therapy
• b. Ethanol injection of his thyroid (PEI)
• c. 6 weeks of Methimazole
• d. Radio Active Iodine therapy

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Case 6

• In Nuclear Scintigraphy Scan I123 uptake is
  very high in
• the thyroid of patients with
• a. Silent thyroiditis
• b. Single functional adenoma
• c. Sub-acute thyroiditis
• d. Acute ingestion of animal thyroid extract
• e. Graves disease

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Hypothyroidism and Myxedeam Coma

• PROF.BIKHA RAM DEVRAJANI
• MB,FCPS,FACP
• INCHARGE MEDICAL UNIT IV
• LUMHS JAMSHORO

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Normal Thyroid State

• Synthesis and release of thyroid hormone is
  controlled by TSH relaesed form the anterior
  pituitary
• TSH is controlled by the release of thyroid
  releasing hormone (TRH) from the hypothalmus and
  a negative feedback loop to the pituitary
• Thyroid hormone production s dependent on
  adequate adequate iodine intake

68
Normal Thyroid State

• Thyroid hormone is reversible bound to various
  proteins including thyronine-binding globulin
  (TBG)
• Free unbound portions are biologically active
• T4 is the predominant circulating hormone
• T4 is deiodinated to t3
• T3 is biologically more active than T4 but has a
  shorter half-life

69
Hypothyroidism

• Occurs when there is insufficient hormone
  production or secretion
• Occurs more frequently in women (0.6 to 5.9 )
• The most common etiologies are
• Primary thyroid failure due to autoimmune
  diseases (Hashimoto thyroiditis is the most
  common)
• Idiopathic causes
• Ablative therapy
• Iodine deficiency
• May be transient
• Pathophysiology is unclear but may be viral in
  nature

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Hypothyroidism

• Etiologies of Hypothyroidism
• Primary
• Autoimmune etiologies
• Hashimotos is the most common
• Idopathic
• Post ablation (surgical, radioiodine)
• Post external radiation
• Thryoiditis (subacute, silent, postpartum)
• Postpartum thyroiditis occurs within 3-6 months
  and occurs in 2- 16 of women
• Self limited etiologies, often prededed by
  hyperthroid phase
• Infiltrative disease (lymphoma, sarcoid,
  amyloidosis, Tuberculosis
• Congenital

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Hypothyroidism

• Etiologies of Hypothyroidism
• Post Partum
• Occurs 3-6 months post partum and occurs in 2-16
  of women
• Secondary (pituitary)
• Neoplasm
• Infiltrative Dz.
• Hemorrhage
• Tertiary (hypothalamic)
• Neoplasm
• Infiltrative Dz.

72
Hypothyroidism

• Etiologies of Hypothyroidism
• Drugs
• Amiodarone
• Occurs in 1-32 of patients
• Most likely due to the large amount of iodine
  released in the metabolism of the drug which
  inhibits thyroid hormone synthesis, release, and
  conversion of T4 to T3
• Lithium
• Acts similarly to iodine and inhibit thyroid
  hormone release
• Iodine (in patients with pre-existing autoimmune
  disease)
• Antithyroid medication

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Hypothyroidism

• Clinical Features
• The typical symptoms of hypothyroidism include
  fatigue, weakness, cold intolerance,
  constipation, weight gain, and deepening of
  voice.
• Cautaneous signs include dry, scaly, yellow skin,
  non-pitting, waxy edema of the face and
  extremities (myxedema) and thinning eyebrows

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Hypothyroidism

• Clinical Features cont.
• Cardiac findings include bradycardia, enlarged
  heart, and low-voltage electrocardiogram
• Paresthesia, ataxia, are characteristic
  neurologic findings
• See table below for more complete list

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Hypothyroidism

• Symptoms and Signs or Hypothyroidism

Symptoms Signs
Fatigue Hoarseness
Weight Gain Hypothermia
Cold intolerance Periobital puffiness
Depression Delayed relaxation of ankle jerks
Menstrual irregularities Loss of outer third of eyebrow
Constipation Cool, rough, dry skin
Joint Pain Nonpitting edema
Muscle cramps Bracycardia
Infertility Peripheral Neuropathy
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Hypothyroidism

• Treatment
• Most patient with uncomplicated symptomatic
  Hypothyroidism may be referred to the primary
  physician for further evaluation and initiation
  of treatment
• If hypothyroidism is due to a secondary etiology
  initiation of thyroid hormone therapy may
  exacerbate preexisting adrenal insufficiency

77
Myxedema

• Myxedema is a rare life threatening
  decompensation of hypothyroidism
• Usually in individuals with long-standing
  hypothyroidism
• Most often seen in the winter months
• More common in elderly women with underdiagnosed
  or undertreated hypothyroidism

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Myxedema

• Precipitating events include
• Infection
• CHF
• Trauma
• CVA
• Exposure to cold
• Drugs
• Sedatives
• Lithium
• Amiodarone

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Myxedema

• In addition to the clinical features of
  hypothyroidism patients may present with
• Hypothermia
• Altered metal status
• Coma, delusions, and psychosis (myxedema
  maddness)
• Hyponatremia
• Dilutional secondary to decreased free-water
  clearance
• Hypoglycemia
• Secondary to impaired gluconeogenesis
• Hypotension
• Bradycardia
• Respiratory Failure
• Secondary to decreased strength of respiratory
  muscle
• Hypercapnia and hypoxia is common

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Myxedema

• Diagnosis
• Must have high clinical suspicion
• Commonly has Hx. Of hypothyroidism
• Delcine in function is usually insidious in onset

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Myxedema

• Diagnosis cont
• Laboratory evaluation may reveal
• Anemia
• Hyponatremia
• Hypoglycemia
• ? Transaminases
• ? CPK
• ? LDH
• ?Po2 and ?PCo2 on ABGs

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Myxedema

• Diagnosis cont.
• EKG may reveal
• Sinus Bradycardia
• Prolonged QT interval
• Low voltage
• Flattened or inverted T waves

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Myxedema

• Treatment
• No prospective studies on optimal therapy have
  been done thus treatment recommendations are not
  uniform
• Airway stabilization with adequate oxygenation
  and ventilation or vital
• Cardiovascular status must be monitored closely
• Hypothermic patients should be gradually rewarmed
  with gentle passive external rewarming
• Hypotension from reversal of hypothermic
  vasoconstriction should be avoided

84
Myxedema

• Treatment cont.
• Hyponatremia typically responds to fluid
  restrictions. Severe cases may require hypertonic
  saline with lasixs
• Vasopressors are usually ineffective and should
  only be used in severe hypotension
• Lovothyroxine 300-500 mcg slow IVP followed by
  50-100 mcg daily

85
Myxedema

• Treatment cont.
• L-triiodothyronine 25 mcg IV or orally q 8 h is a
  alternative
• This dose should be halved in patients with
  cardiovascular disease
• Hydrocortisone 100 mg IV q 8 hours should be
  given
• Send baseline cortisol level to lab if possible
• Precipitating causes should be sought and treated

86
Myxedema

• Treatment of Myxedema Coma
• Recognition
• Supportive therapy including ventilatory support
• Thyroid replacement
• Lovothyroxine 300-500 mcg slow IVP followed by
  50-100 mcg daily or
• T3 25 mcg IV or PO q 8 hrs
• Glucocorticoid
• Hydrocortisone 100 mg IV q8h
• Hypothermia
• Prevent additional loss
• Passive external rewarming
• Electrolyte correction
• Gentle fluid restriction for dilutional
  hyponatremia
• Hypertonic saline for severe hyponatremia
• Hypoglycemia
• Dextrose-containing IV fluids
• Monitoring
• Aggressive treatment of presipitating causes
• Admit patient to a monitored setting

87
Myxedema

• Disposition
• Admit to appropiately monitored bed

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Myxedema Coma
89
Introduction

• Myxedema coma still has a high mortality rate
  (despite intensive treatment).

90
Clinical Manifestations

• Reduced level of consciousness.
• Seizures.
• Other features of hypothyroidism.
• Hypothermia (up to 74oF).
• There may be a history of treated hypothyroidism
  with poor compliance, or the patient may be
  previously undiagnosed.

91
Clinical Manifestations

• Myxedema coma almost always occurs in the elderly
  and is usually precipitated by factors that
  impair respiration, such as
• Drugs (esp. sedatives, anaesthetics,
  antidepressants).
• Pneumonia.
• Congestive heart failure.
• Myocardial infarction.
• Gastrointestinal bleeding.
• Cerebrovascular accidents.
• Sepsis.
• Exposure to cold.

92

• Elevated TSH

Measure Free T4
Normal
Low
Subclinical hypothyroidism
Primary hypothyroidism
TPOAb or symptomatic
TPOAb, no symptoms
TPOAb
TPOAb
Rule out other causes of hypothyroidism
Autoimmune hypothyroidism
T4 treatment
Annual follow up
T4 treatment
93

• Normal TSH

Pituitary disease suspected?
No
Yes
No further testes
Measure free T4
Normal
Low
No further tests
Rule out drug effects, sick euthyroid syndrome,
then evaluate anterior pituitary function
94
Pathogenesis

• Hypoventilation, leading to hypoxia and
  hypercapnia, plays a major role in pathogenesis.
• Hypoglycemia and dilutional hyponatremia also
  contribute to the development of myxedema coma.

95
Treatment

• Levothyroxine single intravenous bolus of 500
  ?g, and usually continued at a dose of 50100 ?g.
• OR
• Liothyronine (T3) intravenously or via NG tube,
  dose range from 10 25 ?g every 8 to 12 h.
• T4 ? T3 conversion is impaired.
• Excess dose has the potential to provoke
  arrhythmias.
• OR

96
Treatment

• Combine levothyroxine (200 ?g/d) and liothyronine
  (25 ?g) as a single, initial intravenous bolus
  followed by daily treatment with levothyroxine
  (50 to 100 ?g/d) and liothyronine (10 ?g every 8
  h).
• Supportive therapy should be provided to correct
  any associated metabolic disturbances.
• External warming is indicated only if the
  temperature is lt30oC, as it can result in
  cardiovascular collapse.

97
Treatment

• Space blankets should be used to prevent further
  heat loss.
• Parenteral hydrocortisone (50 mg every 6 h), as
  there is impaired adrenal reserve in profound
  hypothyroidism.
• Any precipitating factors should be treated,
  including the early use of broad-spectrum
  antibiotics, pending the exclusion of infection.

98
Treatment

• Ventilatory support with regular blood gas
  analysis is usually needed during the first 48 h.
• Hypertonic saline or intravenous glucose may be
  needed if there is hyponatremia or hypoglycemia.
• Hypotonic intravenous fluids should be avoided
  because they may exacerbate water retention
  secondary to reduced renal perfusion and
  inappropriate vasopressin secretion.

99
Treatment

• The metabolism of most medications is impaired,
  and sedatives should be avoided if possible or
  used in reduced doses.
• Blood levels should be monitored, when available,
  to guide medication dosage.

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101
Algorithm for Thyroid Nodule
Thyroid Nodule
Low TSH
Normal TSH
TC 99 Nuclear Scan
FNAC or US guided biopsy
Hot Nodule
Cold Nodule
4
10
69
17
RAI Ablation, Surgery or ATD
Non diagnostic repeat FNAC
Suspicious or follicular Ca
Cyst
Malignant
Benign
Surgery or Cytology
T4 suppression
Surgery
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103

• A 27 years unmarried lady presented with the
  history of weight loss increased appetite ,
  sweating and palpitation
• Q what is D/D ?

104
Case 4

• A 25 year old woman is three months pregnant.
  She has a large goiter. Her exam is otherwise
  normal. Her thyroid tests are normal.
• You recommend
• a. Cassava five times weekly
• b. Fish three times weekly
• c. Formula milk for the baby when it is born
• d. A very low salt diet

105
THYROID DISEASEIN PREGNANCY
106
Physiologic Changes in Pregnancy

• Free thyroxine levels remain within the normal
  range during pregnancy (though total thyroxine
  levels are increased secondary to increased TBG.)
• TSH decreases slightly in first trimester.
• The thyroid gland increases slightly in size
  during pregnancy.

107
Hypothyroidism

• Untreated patients with hypothyroidism rarely
  conceive and carry a pregnancy.
• Treated hypothyroidism usually has no associated
  pregnancy complications.

108
Hypothyroidism

• Some patients will require increased
  levothyroxine doses during their pregnancies.
• Monitor thyroid function tests each trimester
  and at other clinically indicated times.
• Prenatal vitamins can decrease the absorption of
  levothyroxine.

109
Hyperthyroidism

• 95 of hyperthyroidism in pregnancy is secondary
  to Graves Disease.
• A good pregnancy outcome can be expected in
  patients with good control.

110
Hyperthyroidism

• Untreated hyperthyroidism is associated with
  decreased fertility, an increased rate of
  miscarriage, intrauterine growth retardation
  (IUGR), premature labor, and perinatal mortality.
• Poorly controlled thyrotoxicosis is associated
  with thyroid storm especially at labor and
  delivery.

111
Hyperthyroidism

• Beta Blockers and PTU can be safely used in
  pregnancy and in nursing mothers.
• PTU crosses the placenta but does not usually
  cause fetal hypothyroidism and goiter unless
  used in high doses.
• Treatment goals favor mild hyperthyroidism over
  hypothyroidism.

112
Hyperthyroidism - Graves Disease

• Like other immune mediated diseases in
  pregnancy, Graves disease tends to improve in
  the third trimester.
• Exacerbations may occur in the first trimester
  and postpartum.

113
Hyperthyroidism - Graves Disease

• Neonatal and fetal thyrotoxicosis may occur
  because of transplacental passage of thyroid
  stimulating antibodies.

114
Postpartum Thyroiditis

• Postpartum thyroiditis is a destructive
  autoimmune thyroiditis that begins with a
  period of hyperthyroidism followed by a period
  of hypothyroidism. The gland is often enlarged.
• There is usually complete recovery but a chance
  of recurrence in subsequent pregnancies exists.

115
Postpartum Thyroiditis

• 80-85 of patients will have positive
  antithyroid antibodies.
• A radioactive iodine uptake scan can
  differentiate postpartum thyroiditis from an
  exacerbation of Graves Disease.

116
Postpartum Thyroiditis

• Postpartum thyroiditis in an important
  consideration in women with postpartum depression.

117
Hyperemesis Gravidarum

• Hyperemesis is associated with abnormal thyroid
  function tests in a significant number of cases.
• Hyperthyroidism may be the cause of hyperemesis
  or hyperemesis may be the cause of the
  hyperthyroidism.

118
Thyroid Nodules

• New thyroid nodules should be aggressively
  investigated during pregnancy because of a high
  incidence of malignancy.

119
Thyroid Investigations

• Radioactive Iodine is contraindicated in
  pregnancy.
• Nursing mothers who have radioactive iodine
  uptake scans should pump and discard their milk
  for 48-72 hours after the test.

120
Thyroid Storm

• A life threatening hypremetabolic state due to
  hyperthyroidism
• Mortality rate is high (10-75) despite treatment
• Usually occurs as a result of previously
  unrecognized or poorly treated hyperthyroidism
• Thyroid hormone levels do not help to
  differentiate between uncomplicated
  hyperthyroidism and thyroid storm

121
Thyroid Storm

• Preciptatnts of Thyroid Storm (tabel 215-4)

Infection Trauma
DKA MI
CVA PE
Surgery Withdrawal of thyroid med
Iodine administration Palpation of thyroid gland
Ingestion of thyroid hormone Unknown etiology (20-25)
122
Thyroid Storm

• Clinical features
• The most common signs are fever, tachycardia out
  of proportion to the fever, altered mental
  status, and diaphoresis
• Clues include a history of hyperthyroidism,
  exophthalmoses, widened pulse pressure and a
  palpable goiter
• Patients may present with signs of CHF

123
Thyroid Storm

• Clinical features cont.
• Common GI symptoms include diarrhea and
  hyperdefication
• Apathetic thyrotoxicosis is a distinct
  presentation seen in the elderly
• Characteristic symptoms include lethargy, slowed
  mentation, and apathetic facies
• Goiter, weight loss , and proximal muscle
  weakness also present

124
Thyroid Storm

• Diagnosis
• Thyroid storm is a clinical diagnosis based upon
  suspicion and treated empirically
• Lab work is non specific and may include
  Leukocytosis, hyperglycemia, elevated
  transaminase and elevated bilirubin

125
Thyroid Storm

• Treatment
• Initial stabilization includes airway protection,
  oxygenation, fluids and cardiac monitoring
• Treatment can then be divided into 5 areas
• General supportive care
• Inhibition of thyroid hormone synthesis
• Retardation of thyroid hormone release
• Blockade of peripheral thyroid hormone effects
• Identification and treatment of precipitating
  events

126
Thyroid Storm

• Drug Treatment of Thyroid Storm (table 216-6)
• Decrease de novo synthesis
• Porpythiouracil 600-1000mg PO initially, followed
  by 200-250 mg q 4 hrs
• Methimazole 40 mg PO initial dose, then 25 mg PO
  q6h
• Prevent relases of hormone (after synthesis
  blockade intiated)
• Iodine Iaponoric acid (Telepaque) 1 gm IV q8h for
  the first 24 h, then 500 mg bid or Potassium
  iodide (SSKI) 5 drops PO q6h or Lugol solution
  8-10 drops PO q6h
• Lithuim 800-1200 mg PO every day
• Prevent peripheral effects
• B-Blocker Propanolol (IV) titrate 1-2 mg q 5min
  prn (may need 240-480mg PO q day) or Esmolol
  (IV) 500 mcg/kg IV bolus, then 50-200 mcg/kg per
  min maintenance
• Guanethidine 30-40 mg PO q 6 h
• Reserpine 2.5-5 mg IM q4-6h
• Other consideration
• Corticosteroids Hydrocortisone 100 mg IV q 8 h or
  dexamethosone 2 mg IV q 6 hr
• Antipyretics Cooling blanket
  acteaminophen
  650 mg PO q 4-6h

127
Thyroid Storm

• Treatment cont
• Propranolol has the additional effects or
  blocking perpheral conversion of T4-T3
• Avoid Salicylates because it may displace T4
  from TBG
• If the patient continues to deteriorate despite
  appropriate therapy circulating thyroid hormone
  may be removed by plasma transfusion,
  plasmapheresis, charchoal plasmaperfusion
• Remember you must not administer iodine until the
  synthetic pathway has been blocked

128
Thyroid Storm

• Disposition
• Admit to the ICU

129
Questions

• 1. Hyperthyroidism is Characterized by which of
  the following
• A. Fatigue
• B. Palpitations
• C. Weight Loss
• D. Heat intolerance
• E. All the above

130

• 2. The most common etiology of hyperthyroidism
  is
• A. Toxic Multinodular
• B. Graves
• C. Toxic Nodular
• D. Amiodarone induces

131

• 3. Typical Feature of Hyperthyroidism include
• A. Fatigue
• B. Weakness
• C. Constipation
• E. Cold Intolerance
• F. All the above

132

• 4. T or F Hyperthyroidism is more common in women
• 5. T or F Hypothyroidism is more common in women
• 6. T or F Mild hyperthyroidism may be treated
  with B-blockers
• Answers 1. E 2. B 3. F 4.T 5.T 6.T

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