5 Thyroid Disorders A Practical Approach to Diagnosis & Treatment.ppt

5 Thyroid Disorders A Practical Approach to Diagnosis & Treatment

1. Thyroid Disorders
A Practical Approach to Diagnosis & Treatment
Dr. Kamal Kishore MD
Consultant Physician
Geetanjali Hospital Hisar
Life Member: Indian Thyroid Society

2. GENERAL ASPECTS OF THYROID GLAND
–Anatomy: weight range from 12 to 20g
–Located anterior to the trachea
between the cricoid cartilage and
suprasternal notch
–Produces: T4 & T3 (active hormone)
–Regulation: is a classical example of
an endocrine feed back loop : “negative
Feed-back axis”
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3. Hormonogenesis
–THYROID GLAND REGULATION
“negative Feed-back” axis
–Hypothalamus
(TRH positive effect)
–Pituitary gland
(TSH, positive effect)
–Thyroid gland
T3 & T4
(negative
effect)
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4. THYROID GLAND HORMONES
Thyroid hormones:
–T4: (Thyroxine) is made exclusively in
thyroid gland
Ratio of T4 to T3 : 20 : 1
Relative Potency of T4 to T3: 0.3 : 1
T4 is the most important source of T3 by
peripheral tissue deiodination “ T4 to T3 “
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5. THYROID GLAND HORMONES
Thyroid hormones:
–T3: (Triiodothyronine) Main source is
peripheral deiodination:
T3 is the most important because more than
90% of the thyroid hormones physiological
effects are due to the binding of T3 to
Thyroid receptors in peripheral tissues.
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6. THYROID HORMONE EFFECTS:
–Affects every single cell in the body
Modulates:
–Oxygen consumption
–Growth rate
–Maturation and cell differentiation
–Turnover of Vitamins, Hormones, Proteins,
Fat, CHO
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7. MECHANISMS OF THYROID
HORMONE ACTION
–ActbybindingtoNuclearreceptors,
termed ThyroidHormone Receptors
(TRs),Increasingsynthesisofproteins
–Atmitochondrial levelincreases
numberandactivityofATP
–AtCellmembrane increasesionsand
substratestransmembrane flux
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8. THYROID HORMONE EFFECTS
–CALORIGENESIS
–GROWTH & MATURATION RATE
–C.N.S. DEVELOPMENT & FUNCTION
–CHO, FAT & PROTEIN METABOLISM
–MUSCLE METABOLISM
–ELECTROLYTE BALANCE
–VITAMIN METABOLISM
–CARDIOVASCULAR SYSTEM
–HEMATOPOIETIC SYSTEM
–GASTROINTESTINAL SYSTEM
–ENDOCRINE SYSTEM
–PREGNANCY
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9. 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
Pemberton’s sign for RSG
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10. THYROID GLAND DISORDERS
DIVIDED INTO:
–THYROTOXICOSIS (Hyperthyroidism)
Overproduction of thyroid hormones
–HYPOTHYROIDISM (Gland destruction)
Underproduction of thyroid hormones
–NEOPLASTIC PROCESSES
Beningn
Malignant
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11. THYROID GLAND DISORDERS
LABORATORY EVALUATION
TSH normal, practically excludes primary Thyroid
abnormality
–If TSH is abnormal, next step: Total & Free T4 & T3
-TSI (Thyroid Stimulating Ig)
-TPO (Thyroid Peroxidase Ab)
-Serum Tg (Thyroglobulin)
-RAIU (Radioiodine uptake) & Thyroid scaning
-FNAC
-Thyroid ultrasound
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12. TSH High usually means Hypothyroidism
–Rare causes:
TSH-secreting pituitary tumor
Thyroid hormone resistance
Assay artifact
Severe non thyroidal illness
TSH low (particularly <0.1 mU/L) usually indicates
Thyrotoxicosis
–Other causes
First trimester of pregnancy
After treatment of hyperthyroidism
Some medications (glucocorticoids & dopamine)
Severe non thyroidal illnes
TSH should not be used as an isolated Lab test to
assess thyroid function in patients with suspected or
known pituitary disease
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13. Thyrotoxicosis/ Hyperthyroidism
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14. Thyrotoxicosis
Defined as the clinical,physiologic,and
biochemical findings that result when the
tissues are exposed to, and respond to, excess
thyroid hormone.
Rather than being a specific disease ,
thyrotoxicosis can originate in a variety of
ways.
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15. Hyperthyroidism
Denotes only those conditions in which
sustained hyperfunction of the thyroid gland
leads to thyrotoxicosis.
Increased RAIU is the hallmark.
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16. 16
While many patients with
thyrotoxicosis have
hyperthyroidism, it is not so in
others such as-those in whom it
is caused by thyroiditis or
exogenous thyroid hormone
administration.
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17. Causes of Thyrotoxicosis??
Primary Thyrotoxicosis Secondary
hyperthyoridism without hyperthyroidism hyperthyroidism
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18. Primary Hyperthyroidism
Graves disease (most common cause; 50-60%)
Toxic Multi Nodular Goitre (20%)
Toxic adenoma (5%)
Functioning thyroid metastasis
Struma ovarii
Activating mutation of TSH receptor
Activating mutation of G
s
(McCune-Albright
syndrome)
Drugs: iodine excess (Jod-Basedow phenomenon)
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19. Thyrotoxicosis without
hyperthyroidism
Sub acute Thyroiditis (15%)
Silent Thyroiditis
Thyrotoxicosis factitia
Thyroid destruction: use of amiodarone,
lithium, interferon-alpha & beta, interleukin-2,
radiation & infarction of adenoma
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20. Secondary hyperthyroidism
(Non Suppressed TSH levels)
TSH-secreting pituitary adenoma (Diffuse Goitre)
Thyroid hormone resistance syndrome
Chronic gonadotropin secreting tumors
Gestational thyrotoxicosis.
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21. Graves Disease
(Parry's disease, Basedow disease)
The most common cause of thyrotoxicosis (50-60%).
The most important autoantibody is
–Thyroid Stimulating Immunoglobulin (TSI)
–TSI acts as proxy to TSH and stimulates T
4and T
3
Anti thyro peroxidase (anti-TPO) antibodies
Anti thyro globulin (anti-TG)
Autoimmune diseases -Pernicious Anemia, Type 1
DM, Myasthenia Gravis, Vitiligo, Adrenal
insufficiency.
In long term, spontaneous auto immune hypothyroidism can
develop in up to 15% of patients.
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22. Toxic Multi Nodular Goiter (TMG)
TMG is the next most common hyperthyroidism -
20%
More common in elderly individuals –long standing
goiter
Mild elevation of FT
4and FT
3
Progresses slowly over time
Clinically multiple firm nodules (called Plummer’s
disease)
Scintigraphy shows -hot and normal areas
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23. Age and Sex
Age
–Graves disease 20 to 40
–Toxic MNG > 50 yrs
–Toxic Single Adenoma35 to 50
–Sub Acute ThyroiditisAny age
Sex M : F ratio
–Graves Disease 1: 5 to 1:10
–Toxic MNG 1: 2 to 1: 4
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24. Clinical Features
1.Those that occur with any type of
thyrotoxicosis
2.Those that are specific to Graves disease
In the elderly, features of thyrotoxicosis may be
subtle or masked, and patients may present
with fatigue and weight loss, known as
APATHETIC THYROTOXICOSIS. It can
be mistaken for depression in elderly.
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25. Clinical features of
thyrotoxicosis
Neuromuscular:
Nervousness, irritability, emotional liability,
psychosis
Tremor
Hyperreflexia,ill sustained clonus
Muscle weakness, proximal myopathy,bulbar
myopathy
Reproductive:Amenorrhoea,Oligomenorrhoea
Infertility, impotence
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26. Thyrotoxicosis..
Gastrointestinal:
Weight loss despite increased appetite
Hyper defecation
Diarrhea and steatorrhoea
Vomiting
Cardio respiratory:
Palpitations, Sinus tachycardia, atrial fibrillation
Increased pulse pressure
Dyspnea on exertion
Angina, cardiomyopathy and heart failure
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27. Thyrotoxicosis..
Others:
Heat intolerance
Increased sweating
Fatigue
Gynaecomastia
Palmar erythema, Onycholysis
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28. Common Signs
1.Sinus tachycardia or PAC, AF, Thyrotoxiccardiomyopathy, ppt
of CHF & angina in elderly patients and in those with pre
existing heart disease
2.Systolic hypertension, wide pulse pressure
3.Diffuse toxic Goitrewith +bruit over goitre
4.Warm, moist skin
5.Fine hair echo texture & Onycholysis
6.Fine tremor of out stretched hands –format's sign
7.Hyperreflexia, proximal myopathywithout fasciculation, chorea
(rare).
8.Hypokalemicperiodic paralysis
9.Gynecomastia
10.Osteopenia
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29. Common Eye Signs
Dalrymple sign-Upper eyelid retraction
Von Graefe sign-lid lag with downward gaze
Kocher sign-staring appearance
These signs can occur with thyrotoxicosis of any
etiology
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30. Specific to Graves Disease
1.Diffuse painless goitre with audible bruit.
2.Ophthalmopathy –Eye manifestations –20-40% of cases
Sense of sand in eyes (grittiness), periorbital edema,
conjunctival edema (chemosis), proptosis , extraocular
muscle dysfunction leading to diplopia
Weakness of upward gaze ( Stellwag sign )
Weakness of convergence ( Moebius sign )
Optic nerve compression leading to papilledema, field
defect and permanent loss of vision
Eye changes are unilateral in 10% of cases.
Severity of eye disease does not correlate with severity of
thyrotoxicosis. some cases are EUTHYROID.
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31. Thyroid Ophthalmopathy
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Proptosis Staring
appearance
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32. Ophthalmopathy in Graves
32Periorbital edema and chemosis
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33. Dermopathy
Usually occurs over the dorsum of the legs or feet
and is termed localized or pretibial myxedema.
It is usually a late phenomenon
The affected area is usually demarcated from the
normal skin by being raised and thickened and
having a peau d’ orangeappearance; it may be
pruritic and hyperpigmented.
The most common presentation is non pitting
oedema, but lesions may be plaque like, nodular or
polypoid.
Clubbing of the fingers and toes accompanies and
is termed thyroid acropachy
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34. Thyroid Dermopathy (<5% of
patients with Grave’s disease)
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Deep Pink and skin coloured papules, plaques on the shin
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35. Thyroid Acropachy (<1%)
Presents with clubbing & swelling of fingers
and toes.
It is so strongly associated with thyroid
dermopathy that an alternative cause of
clubbing should be sought in Graves patient
without coincident skin and orbital
involvement.
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36. Sub Acute Thyroiditis (SAT)
Also called as De-Quervain Thyroiditis or viral Thyroiditis.
SAT is the next most common hyperthyroidism –15%
T
4 and T
3are 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
Hyperthyroidism (3-6 weeks) is followed by transient
hypothyroid phase(4-6 months)
If the gland is non-tender, called as silent thyroiditis
Disease is self limiting with 95% remission rate.
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37. 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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38. Toxic Single Adenoma (TSA)
Single hot nodule
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Nucleotide
Scintigraphy

39. Thyrotoxicosis Factitia
Excessive intake of Thyroxine causing thyrotoxicosis
Patients usually deny –it is willful ingestion
This is a 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, so impalpable thyroid
gland
Stop Thyroxine and give symptom relief drugs
Epidemic of thyrotoxicosis has been caused by consumption of
ground beef contaminated with bovine thyroid gland.
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40. Differential Diagnosis in Hyperthyroidism
Type of Goiter Diagnosis
Diffuse, nontender goiterGraves’ disease of painless thyroiditis
Multiple thyroid nodules Toxic multi nodular goiter
Single thyroid nodules Thyroid adenoma
Tender painful goiter Sub acute thyroiditis
Normal thyroid gland Graves’ disease, painless thyroiditis, or
factitious hyperthyroidism
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41. Differential diagnosis
Anxiety
Pheochromocytoma
Hydatidiform mole
Ectopic thyroid tissue(struma ovarii)
Factitious thyrotoxicosis
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42. Diagnosis
1.Typical clinical presentation
2.Markedly suppressed TSH (<0.05 µIU/mL)
3.Elevated FT
4
and FT
3
(Markedly in Graves)
4.In 2-5% cases, only T3 increased (T3 toxicosis)
5.T4 toxicosis (seen when hyperthyroidism is induced
by excess iodine)
6.Thyroid antibodies –by Elisa –anti-TPO, TSI, TB II
7.ECG to demonstrate cardiac manifestations
8.Nuclear Scintigraphy to differentiate the causes
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43. 43
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44. 44
FREE THYROXINE or FT4
PRIMARY
HYPERTHYROID
LOW NORMAL HIGH
THYROID STIMULATING HORMONE -TSH
BASIC THYROID EVALUATION
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45. 45
FREE THYROXINE or FT4
SECONDARY
HYPERTHYROID
LOW NORMAL HIGH
THYROID STIMULATING HORMONE -TSH
BASIC THYROID EVALUATION
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46. 46
FREE THYROXINE or FT4
SUB-CLINICAL
HYPERTHYROID
LOW NORMAL HIGH
THYROID STIMULATING HORMONE -TSH
BASIC THYROID EVALUATION
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47. T3/T4 RATIO
Graves disease and toxic nodular goitre
typically present with increased T3 production,
with T3/T4 ratio greater than 20.
While thyrotoxicosis caused by thyroiditis,
iodine exposure or exogenous levothyroxine
intake, T4 is the predominant hormone and
T3/T4 ratio is usually less than 15.
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48. Thyroid Antibodies
Anti Thyroid Peroxidase (TPO)
Anti Thyroglobulin (TG)
TSH-R antibodies
TSH-R Ab are helpful in diagnosis &
management of Grave`s disease.
It also helps in prediction of post-partum
grave`s disease & neonatal thyrotoxicosis.
Helps in identification of orbitopathy in
absence of features of Thyrotoxicosis.
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49. Differential Diagnosis of Hyperthyroidism
Type of Goiter Diagnosis
Diffuse, nontender goiterGraves’ disease of painless thyroiditis
Multiple thyroid nodules Toxic multi nodular goiter
Single thyroid nodules Thyroid adenoma
Tender painful goiter Sub acute thyroiditis
Normal thyroid gland Graves’ disease, painless thyroiditis, or
factitious hyperthyroidism
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50. Algorithm for Hyperthyroidism
Measure TSH and FT4
TSH, FT4
Measure FT3
Primary (T4)
Thyrotoxicosis
High
Pituitary AdenomaFNAC, N Scan
Normal
TSH, FT4 N TSH, FT4 NTSH, FT4 N
T3 Toxicosis
Sub-clinical Hyper
Features of Grave’s
Yes
Rx. Grave’s
No
Single Adenoma, MNG
Low RAIURAIU
Sub Acute Thyroiditis, I
2
, ↑ Thyroxine
F/u in 6-12 wks
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51. Thyrotoxicosis
Treatment:
–Reducing thyroid hormone synthesis:
Antithyroid drugs (Methimazole, Propylthyouracil)
Radioiodine (
131
I)
Subtotal thyroidectomy
–Reducing Thyroid hormone effects:
Propranolol
Glucocorticoids
Benzodiazepines
–Reducing peripheral conversion of T4 to T3
Propylthyouracil
Glucocorticoids
Iodide (Large oral or IV dosage) (Wolf-Chaikoff
effect)
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52. Anti thyroid drugs
Chemically block hormone synthesis
Enhance evolution to remission
Best indicated for children,adolescents,young adults
and pregnant women.
Propylthiouracil-100-150mg every 6or 8 hrs
Carbimazole-40-60mg daily initially for 3
weeks,then reduce to 20-40mg for another 8 weeks
and maintain at 5-20mg daily for 18-24 months.
Methimazole-active metabolite of Carbimazole
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53. How long to give ATD ?
Reduction of thyroid hormones takes 2-8 weeks
Check TSH and FT
4every 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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54. Adverse effects of Thionamides
Abnormal taste, fever (<1%) arthralgias,
pruritis, urticaria (1-5% of patients)
Agranulocytosis-usually occurs in first three
months, related to dose of methimazole
(>30mg/day) and not of PTU.
Routine assessment of blood counts has not
been useful and is not recommended.
Hepatitis
Vasculitis, SLE like syndrome
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55. β–Blocking Drugs
Control cardiovascular and hyperadrenergic
manifestations.
There is also rapid metabolism of propranolol
in thyrotoxicosis hence larger doses are
needed.
In addition to βblocking effect, propranolol in
doses greater than 160mg/day decreases T3
generation by inhibiting 5-monodeiodinase
enzyme (T4T3).
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56. Role of Iodine
Iodine in high concentrations, blocks release of
pre-stored hormone and decrease iodide transport
and oxidation called as WOLF-CHAIKOFF
EFFECT.
But this effect is transient and within 1-2 weeks
complete escape from inhibition occurs.
So while treating thyrotoxicosis with iodine,
addition of thionamides is essential to prevent
aggravation of symptoms with loss of Wolf-
chaikoff effect.
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57. Radio Active Iodine (RAI Rx.)
indications
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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58. Radio Active Iodine (RAI Rx.)
I
123
is used for Nuclear Scintigraphy (Dx.)
I
131
is given for RAI Rx. (6 to 8 milliCuries)
Goal is to make the patient hypothyroid
No side 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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59. Surgical Treatment
Subtotal Thyroidectomy, Near Total Thyroidectomy
Hemi Thyroidectomy with contra-lateral subtotal
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60. Surgical Treatment
ATD and RAI Rx are very efficacious and easy –so
Surgical treatment is reserved for MNG with
1.Severe hyperthyroidism in children
2.Pregnant women who can’t tolerate ATD
3.Large goiters with severe Ophthalmopathy
4.Large MNGs with pressure symptoms
5.Who require quick normalization of thyroid function
6.Suspicious of biopsy proven malignant nodules
7.Co-morbidity requiring surgery like
hyperparathyroidism.
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61. Preoperative Preparation
Careful control of Thyrotoxicosis withATD to
reduce hyper function before surgery
βeta blockers to titrate pulse rate to 80/min
SSKI 3 drops orally TDS
This will reduce thyroid blood flow & there by
reduce per operative bleeding
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62. Complications of ablative
therapy
Immediate complications of surgery:
Bleeding, injury to recurrent laryngeal nerve
and thyroid crises.
Other complications
Hypothyroidism
Radiation thyroiditis
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63. Complications of
thyrotoxicosis
1)Cardiac-Heart failure
Atrial fibrillation
2)Thyrotoxic crisis: or ‘storm’:
Fulminating increase in signs and symptoms of
thyrotoxicosis.
Occurs in medically untreated or inadequately treated
patients. May be precipitated by surgery or sepsis
The syndrome is characterized by extreme
irritability,delirium or coma, fever 41°C or more,
tachycardia, restlessness, hypotension,vomiting and
diarrhea.
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64. Treatment of thyroid crisis
Provide supportive care, oxygen , antibiotics (if
infection), cooling
Treat dehydration
Administer iv fluids
Digitalization is required in those with atrial
fibrillation
Immediate and large doses of anti thyroid agents(eg–
PTU (propylthiouracil) 600 mg loading f/b 200-300
mg every 6 hrly)
Iodine 1hour after PTU dose to block thyroid hormone
synthesis
Propranolol(40-80 mg every 4h)
Dexamethasone(2mg every 6h) and to be tapered later.
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65. Hypothyrodism
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67. HYPOTHYROIDISM
–Primary
Autoimmune (Hashimoto ´s)
Iatrogenic Surgery or
131
I
Drugs: amiodarone, lithium
Congenital (1 in 3000 to 4000)
Iodine defficiency
Infiltrative disorders
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68. THYROID GLAND DISORDERS
HYPOTHYROIDISM
–Secondary
Pituitary gland destruction
Isolated TSH deficiency
Bexarotene treatment
Hypothalamic disorders
–Peripheral:
Rare, familial tendency
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69. THYROID GLAND DISORDERS
Hashimoto´s Thyroiditis or
Goitrous thyroiditis

–Mean anual incidence:
Women 4:1000 Men 1:1000
Risk factors; TPO antibodies (90%)
Japanese, previous history, high I
intake
Average age: 60
Frequently associated toother
autoimmune disorderssuchas:AR,
SLE,Sjogren´sso-on.
Treatment: Levothyroxine
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70. THYROID GLAND DISORDERS
CONGENITAL HYPOTHYROIDISM
Prevalence: 1 in 3000 to 4000 newborns
–Cause: Dysgenesis 85%
–Dx: Blood screning (TSH &/or T4)
Treatment:
–SupplementalTx.WithLevothyroxineis
“essential” foranormal C.N.S.
Development andpreventionofmental
retardation
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71. HYPOTHYROIDISM
Symptoms:
–Tiredness
–Weakness
–Dry skin Sexual
dysfunction
–Dry skin
–Hair loss
–Difficulty
concentrating
Signs:
–Bradycardia
–Dry coarse skin
–Puffy face, hands and
feet
–Diffuse alopecia
–Peripheral edema
–Delayed tendon reflex
relaxation
–Carpal tunel
syndrome
–Serous cavity
effusions.
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72. THYROID GLAND DISORDERS
SPECIAL TREATMENT CONSIDERATIONS
Myxedema coma
–Reduced level of consciousness, seizures
–Hypotension/shock
–Hypothermia
–Hyponatremia
Usually in elderly hypothyroid pts.
Usually precipitated by intercurrent illnesses that
impairs ventilation
It´s an Emergency with a high mortality rate
Treatment: Lyotironine(T3) or T4, Hydrocortisone,
external warming, IV fluids
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73. Treatment of Hypothyroidism:
starting doses of LT4
If no significant thyroid reserve:
1.6microgram/kg/day (typical dose 100-150)
If some thyroid reserve present: lower dose is sufficient
Older persons without heart disease is 50-100 microgram/day
Older persons with heart disease is 12.5-25 microgram/day
Patients with grave’s disease who develops hypothyroidism
dose is 75-125 microgram/day
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74. Follow up TSH measurements
Ongoing adherence counseling is most
important part of treatment.
Once TSH levels are stable, followup
measurements of TSH is recommended at
annual intervals and even may be extended to
2 to 3 years if a normal TSH is maintained
over several years
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75. If LT4 dose is ≥ 200µg/d in normal body
weightpatients and TSH is still high
Causes are
Poor adherence
Malabsorption disorder
Estrogen therapy
Drugs
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76. Targets of control
TSH responses are gradual and should be measured
about two months after instituting treatment or after
any subsequent change in levothyroxine dosage
The dose is adjusted on the basis of TSH levels, with
the goal of treatment being a normal TSH, ideally in
the lower half of refernce range.
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77. In Secondary Hypothyroidism
TSH levels should not be used for monitoring
therapy.
The goal of treatment is to maintain FT4 levels
in the upper half of the reference range.
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78. Special situations
The elderly patients may require 20% less
thyroxine than younger patients
Pregnant patient requires aprox. 30% increase
dose of thyroxine as compare to non pregnant
status.
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79. Surgery and Hypothyrodism
Emergency surgery is generally safe in patients
with untreated hypothyroidism.
Routine surgery in a hypothyroid patient
should be deferred until euthyroidism is
achieved.
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80. Hypothyroidism
SPECIAL TREATMENT CONSIDERATIONS
Elderly patients
Coronary Artery Disease
Poor adrenal gland reserve
Childrens
Pregnancy
Emergency surgery (Non thyroid related)
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81. Algorithm for Hypothyroidism
Measure TSH
Elevated TSH
Measure FT4
Normal Low
Sub-clinical hypo
TPO + TPO -
T4 replAnnual FU
Primary hypothyroid
TPO + TPO -
Hashimoto
Others
Normal TSH
TPO: Thyroid Peroxidise
FU: Follow Up
Next Slide
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82. Algorithm for Hypothyroidism
Measure TSH
Elevated TSH Normal TSH
Considering Pituitary
No Yes
No tests Measure FT4
Low Normal
No tests
Evaluate Pituitary
Sick Euthyroid
Drugs effect
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83. 83
THANKS
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