Medicine II f.
FNAB of the thyroid
ENDOCRINOLOGY
Prelim Coverage – Dr. Ligon
AMS 204
Coverage of Preliminary Examination:
I. Basic Aspect of Thyroid Gland
II. Clinical Disorders of Thyroid Gland
III. Diagnosis and Management of Thyroid Diseases
IV. Parathyroid Gland Disorders
V. Pituitary Gland Disorders
BASIC ASPECT OF THYROID GLAND
Modified True or False
A 23-year old female, G1P0 came to your clinic because of an
enlarging neck mass. She denies symptoms of either hypothyroidism
or hyperthyroidism. PE disclosed an enlarging thyroid, nodular, firm,
non-tender, widest diameter of the said mass is about 4cm. No bruit
nor Pemberton’s sign (physical examination tool used to
demonstrate the presence of latent pressure in the thoracic
inlet. The maneuver is achieved by having the patient elevate both
arms until they touch the sides of the face. A positive Pemberton's
sign is marked by the presence of facial congestion and cyanosis, as
well as respiratory distress after approximately one minute. It is
indicative of superior vena cava syndrome (SVC), commonly the
result of a mass in the mediastinum. Rationale: thyroid gland is very
large compressing the thoracic inlet. It is a manifestation of
intrathoracic goiter) elicited. The following tests are appropriate:
a. TSH
- Appropriate
- TSH determination is done in this setting to determine
the metabolic status of the patient
- Most specific, sensitive test
b. T3 and T4
- Not appropriate
- This is a reflection of your total hormone concentration
bound to proteins.
- In hyperestrogenic states like pregnancy, you expect
the TSH levels to be high. During pregnancy, hCg
levels are high so the TSH is depressed because it
has a slight thyromimetic activity because of the alpha
subunit similar to TSH which can mimic the actions of
TSH. If the action of the hCG is markedly elevated,
the TSH level is low due to the negative feedback
hCG produces.
- Increase hCG levels  decrease in TSH level
- Do a FT3 FT4/ Free Hormone assay
c. Thyroid Ultrasound
- Appropriate
- To know the consistency of the nodules and the
accurate size of the neck
d. MRI of the neck
- Not appropriate
- Patient is negative for Pemberton sign
e. 24hr RAIU
- Not appropriate
- Pregnant – absolute contraindication because it may
destroy the thyroid gland of the fetus
- Most definitive test
Thyroid Gland
- Second largest endocrine organ in the body (the fats being
the largest – an active endocrine gland because it is
capable of producing hormones like adiponectin and all the
other hormones) weighing about 15-20 grams in human
adults
- It consists of two lobes, the right and left lobe joined by an
isthmus. At the anterior median of the isthmus sometimes
would arise a pyramidal lobe thereby assuming a butterfly
configuration. The right lobe is larger than the left lobe so
that in diffuse thyroid enlargement, you expect the right
lobe to be larger than the left.
- There are two pairs of parathyroid glands that lie at the
back of the thyroid gland. This is the one that mediates the
metabolism of your calcium ion.
- Another anatomical consideration is its close relation with
other structures such as the esophagus, trachea, and
parathyroid gland. Compression of these structures would
result to difficulty of swallowing, breathing, or manifesting
signs and symptoms of hypocalcemia.
- The widest diameter of the thyroid gland is about 4cm long,
2cm width, and 2cm thickness. This is why the thyroid
ultrasound is the most sensitive test to measure the gland
accurately because it views the gland in three dimensions.
In contrast to other localizing procedures like the thyroid
scan, MRI, and others that views the gland as flat (height
and width only but not the thickness)
Blood supply
- Arterial
o Superior thyroid artery from the common or external
carotid artery
o Inferior thyroid artery from subclavians
o Accessory thyroid artery
o Thyroid ima artery from the brachiocephalics
o Blood flow is about 5ml/gm/min (much higher than the
renal blood flow which is 3ml/gm/min)
 In cases of diffuse toxic enlargement, this blood
flow can increase to 1 liter/gm/min such that in
this setting you will be able to appreciate a bruit
(the bell of the stethoscope is used because it is
a low pitch sound because the thyroid artery is
a small vessel. High pitch sounds are only
produced by large vessels like the abdominal
aorta). To check for bruit, ask the patient to hold
his or her breath.
- Venous
o Superior, middle, and inferior veins
Histology of the thyroid gland
- The thyroid gland consists of two types of cells: follicular cells
and parafollicular cells or C cells which is the one responsible
for the production of calcitonin.
- The thyroid hormones are only being produced by the follicular
epithelium
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Follicles: the functional units of the thyroid gland Summary of Steps in the production of thyroid hormones
- Follicles are the sites where key thyroid elements function: 1. Dietary Iodine (I) ingestion
o Thyroglobulin (Tg) 2. Active transport and uptake of Iodide (I-) by thyroid
 glycoprotein that is only produced by follicular gland
tissues 3. Oxidation of I- and iodination of thyroglobulin (Tg)
o Tyrosine tyrosine residue
 Amino acid 4. Coupling of iodotyrosine residues (MIT and DIT) to
o Iodine (I) form T3 and T4
o Thyroxine (T4) 5. Proteolysis of Tg with release of T4 and T3 into the
 Hormonally active circulation.
o Triiodothyronine (T3)
Thyroid Hormone
Iodine Sources
- Iodine is a major substrate of thyroid hormone production L-thyroxine (T4) Triiodothyronine (T3)
- Available through certain foods: seafood, bread, dairy product, Produced only in the thyroid 80% are from peripheral
iodized salt, or dietary supplement gland conversion of T4 (T4 released in
- The recommended minimum intake is 150ug/day for adult and circulation will be iodinated to
200ug/day for pregnant women produce T3)
t ½ = 7 days t ½ = 1 day
99.97% protein-bound 99.7% protein-bound
Excess Iodine (Thyroxine Binding Globulin
- In normal patients, it usually induces a “Wolff Chaikoff effect” (TBG), pre-albumin, albumin)
where there is a transient shut down of thyroid hormone Only free hormones are active 3x more potent than T4
production.
o If you saturate the thyroid gland with too much iodine, Distribution of Thyroid Hormones
it would result to temporary inhibition of thyroid - It consists of two circulating forms:
hormone production. o Free hormones – result to different biological effects of
- In some patients like Hashimoto’s thyroiditis (autoimmune your thyroid hormones (tissue action, hormone
problem leading to hypothyroidism), they may stay hypothyroid metabolism)
because of inability to escape this effect (Wolff Chaikoff effect) o Protein-bound
- In some patients with quiet Grave’s disease (autoimmune - Three circulating carrier proteins for T4:
problem leading to hyperthyroidism) or autonomous nodules, o 70-75%  Thyroxine binding globulin (TBG)
hyperthyroidism may be induced by too much iodine (Jod o 15-20%  Thyroxine binding pre-albumin
basedow phenomenon) or Iodine induced hyperthyroidism o 5-10%  albumin
- Two carrier proteins for T3
Thyroid hormone biosynthesis o 70-75%  TBG
- For thyroid hormone production, initially it starts with o 25-30%  albumin
extrathyroidal production of Iodine towards the thyroid cell
known as _____________. This iodine will enter thyroid cell Factors that increase/decrease thyroxine binding concentration
and this will be acted upon by hydrogen peroxide and thyroidal A. Increased TBG concentration
peroxidase to produce the oxidized form. This oxidized form of 1. Congenital
iodine will iodinate tyrosine residues found in thyroglobulin. 2. Hyperestrogenic states: pregnancy, estrogen
- Iodination of thyroglobulin would produce your hormonally intake
inactive thyroid hormones in the form of diiodotyrosine and 3. Diseases: acute infectious hepatitis,
monoiodotyrosine. hypothyroidism
- After the odination is the coupling of these iodotyrosines such B. Decreased TBG concentration
that two diiodotyrosine would result to the formation of T4 and 1. Congenital
the combination of monotyrosine and diiodotyrosine will 2. Drugs: Androgenic steroids, glucocorticoids
produce T3. T4 and T3 are the hormonally active thyroid 3. Major systemic illness: protein malnutrition,
hormones. nephrotic syndrome, cirrhosis
- Once this process has been completed, lysozymes would act (hypoalbuminemia), hyperthyroidism
on these iodinated thyroglobulin (MIT, DIT, T3 and T4) so that C. Drugs affecting TH binding to normal concentration of
the T3 and T4 would be released to the general circulation to binding protein (competitive agonist)
serve its biological function while the MIT and DIT’s iodine will 1. Phenytoin (aspirin, NSAIDS)
be conserved to be used for the organification process. There 2. ‘Salicylates
is a small portion of the iodine that would leak outside the 3. Phenylbutazone
thyroid cell called the iodine leak. 4. Mitotane (Lysodren) – anti-cancer drug
5. Diazepam (benzodiazepine)
6. FFA released by heparin stimulation of
lipoprotein lipase

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Decreased conversion of T4 to T3 o Type 3
1. Fetal life  only found in pregnant women
2. Caloric restriction - It is important to know the deiodinase system (it is the one that
3. Hepatic diseases converts T4 to T3, T3 to T2 and rT3 which are all inactive
4. Major systemic illnesses hormones) because this can greatly modify the action of T3
5. Drugs and T4. It operates to regulate the level of thyroid hormones:
a. Anti-thyroid drug: PTU (Prophylthiouracil) o In hypothyroid state, you expect the level of the
b. Glucocorticoids hormones to be low:
c. Beta-blocker: propranolol  Type 1 activity is decreased.
d. Iodinated X-ray contrast agent:  We do not want inactive hormones in
e. Cardiovascular drug: Amiodarone hypothyroid states so there will be
6. Selenium deficiency inhibition of the activity of type 1 to
preserve the low level of circulating T4.
Control of thyroid function  Type 2 activity is increased
- Regulated by several mechanisms:  To ensure that there will be an enzyme
1. Hypothalamic-pituitary-thyroid axis that will convert T4 to T3 which is the one
2. Deiodinase system that sends the negative feedback loop.
3. Thyroidal autoregulation o The opposite is true in Hyperthyroid state
4. Autoimmune regulation  Type 1 activity is increased
 in order to increase the conversion of T4
TSH to T3 and inactive hormones to get rid of
- Regulates thyroid hormone production, secretion, and growth. excess thyroid hormones
o It is the #1 growth promoting factor of thyroid gland  Type 2 activity is decreased
- Regulated by the negative feedback action of T4 and T3  In order to prevent the oversaturation of
Any stimulus from the hypothalamus would stimulate the production T3 to your higher center
of TRH  TRH would reach the anterior pituitary gland by way of the
hypothalamic hypophyseal portal system  Once it stimulates the Thyroidal Autoregulation
release of TSH, this would be released to the circulation to stimulate - Definition: the capacity of the thyroid gland to modify its
the target gland (thyroid gland) to produce T3 and T4. function to adapt to changes in the availability of iodine,
independent of pituitary TSH (axis).
Intrathyroidal production of T4 is greater than that of T3. Once T4 is - Example: Wolff Chaikoff effect – initially inhibitory but will
released to the general circulation, this would be further deiodinated escape eventually independent of the axis to make thyroid
to produce T3. T3 is the one that would send a negative feedback hormones
loop to higher center to switch off the production of TRH and TSH.
Autoimmune Regulation
Two types of feedback loop: - Definition: the ability of the immune system, particularly the B
1. Long negative feedback loop lymphocyte, to produce certain antibodies. There are two types
o Exerted by T3 of these antibodies:
o Inhibits TRH and TSH in pituitary 1. TSH receptor stimulating antibodies
2. Short negative feedback loop  can mimic the action of TSH
o Production of TSH would also inhibit the production of  Metabolic function: increase hormones
TRH  Too much TSH receptor stimulating antibodies
is the pathology of Graves disease
Deiodinase System (hyperthyroidism)
- The specific enzymes that would inhibit the conversion of T4 2. TSH receptor blocking antibodies
and T3  Too much TSH receptor blocking antibodies that
- There are three types: can antagonize the action of TSH is the
o Type 1 pathology of Hashimoto’s thyroiditis
 operational in adults. (hypothyroidism)
 Located in the peripheral tissues: liver, kidney,
muscle, and thyroid Control of thyroid function
 The activity of type 1 is inhibited by PTU - can occur at three different levels:
o Type 2 1. Hypothalamic level – modifying the secretion of TRH
 operational in adults. 2. Pituitary level – modifying the secretion of TSH
 Located in the higher centers: CNS, pituitary, 3. Thyroidal level
brown fat (brown adipose tissues are intended  Through two types:
for thermogenesis unlike the white adipose  autoregulation
tissues that functions for storage), placenta of  Production of antibodies
pregnant women
 The activity of Type 2 is not inhibited by PTU
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Factors controlling thyroid function
1. Hypothalamic: synthesize and release of TRH
 Stimulatory: decreased serum T4 and T3,
neurogenic, exposure to cold, a-adrenergic
cathecolamines, vasopressin or ADH
 Inhibitory: increased serum T4 and T3, a-
adrenergic blockers, certain hypothalamic
tumors that can compress thyrotrops cell to
produce TRH
2. Anterior pituitary: synthesize and release of TSH
 Stimulatory: TRH, decreased serum T4 and T3,
decrease activity type II deiodinase, and
estrogen.
 Inhibitory: increased serum T4 and T3, increase
activity type II deiodinase, somatostatin,
dopamine, dopamine agonist, glucocorticoids
(androgen), chronic illness, pituitary tumors
3. Thyroid: synthesis and release of thyroid hormones
 Stimulatory: TSH and TSH-Receptor stimulating
antibody
 Inhibitory: TSH-R blocking antibody, iodine
excess, and ____________
Endocrine Rule:
- For every hormone before it could exert its biological effects it
must first bind to a specific receptor.
o Example: Insulin and Insulin receptor
Thyroid hormone receptor
- There are four types of receptors:
o a1 – stimulatory to thyroid hormones
o a2 – it is the only one that would result to
hypothyroidism because this would not result to
binding of your thyroid hormones
o b1 – stimulatory to thyroid hormones
o b2 – stimulatory to thyroid hormones
Effects of Thyroid hormone
- Fetal effects:
o Fetal growth and development
o Fetal brain development
o Fetal skeletal maturation
Note: Common congenital hypothyroidism condition
associated with mental and growth retardation - Cretinism
- Oxygen consumption, heat production, and free radical
formation effects:
o Increased basal metabolic rate
o Increased sensitivity to heat
o Increased superoxide anion free radical formation
Note: Hypothyroidism  toxic effects due to the formation
of free radicals, tachycardic, heat intolerance. TH will inhibit
the enzyme superoxide dismutase that will prevent the
production of free radicals
- Cardiovascular effects
o + inotropic effects – increase contraction
o + chronotropic effects – increase rate
o +dromotropic effects – increase conduction of impulse
- Sympathetic effects
o Increased beta-adrenergic receptors in heart muscle,
skeletal muscle, adipose tissue, and lymphocytes
 No direct action to catecholamines. It increases
the receptors.
o Decreased myocardial a-adrenergic receptor
o Amplify catecholamine action
Note: Hyperthyroidism  tachycardia; Hypothyroidism 
bradycardia
- Pulmonary effects
o Maintain normal hypoxic and hypercapnic drive in the
respiratory center
Note: No TH  hypoventilation  respiratory failure
- Hematopoietic effects
o Increased production of erythropoietin and increased
erythropoiesis
o Blood volume is not increased because of
hemodilution and increased red cell turn over.
o Increased oxygen dissociation increasing oxygen
availability to tissues due to increased 2,3
diphosphoglycerate levels.
Note: production and destruction of cells are both affected
by TH but the destruction is greater than production  net
effect is anemia
- GIT effects
o Stimulate gastric motility
o Hyperdefecation and weight loss
- Skeletal effects
o Increased bone turnover
o Increase bone resorption and to a lesser degree bone
formation
o Hypercalcemia, hypercalciuria, and increased
excretion of urinary hydroxyproline and ___________
which are markers of bone destruction
- Neuromuscular effects
o Increase synthesis of structural proteins
o Increase protein turnover
o Loss of muscle tissue
o Increase muscle contraction and relaxation
Note: Hyperthyroidism  increase deep tendon reflex;
Hypothyroidism  hyporeflexia
- Lipids and CHO metabolism effects
o Increase hepatic gluconeogenesis (production of
glucose from non-carbohydrate substrate – amino
acid to glucose) and glycogenolysis and intestinal
glucose absorption
o Increase cholesterol degradation and to lesser
degree, cholesterol synthesis.
Note: Hyperthyroidism  secondary diabetes;
Hypothyroidism  hypoglycemia, hypercholesterolemia
- Endocrine effects
o Increase degradation of cortisol
 Patient may die of Adrenal insufficiency/crisis
o Ovulation may be impaired resulting in infertility
o Decreased levels of prolactin
Note: Hypothyroidism  galactorrhea or nipple discharge
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Physiologic changes
- Thyroid function in the fetus:
o Highly dependent on maternal thyroid hormone prior
to independent fetal thyroid function
o Hypophyseal portal system has developed during the
11 weeks AOG.
o Secretion of thyroid hormone begins in mid gestation
(18-20w AOG)
o Peak levels of TSH at 24 to 28 weeks, T4 at 35-40w,
while T3 remain low during AOG.
o At birth, there is a sudden rise in TSH due to exposure
to cold environment  transient elevation of TSH.
This is the reason why congenital screening for
hypothyroidism is done after 24-48 hours of life.
o These parameters return to normal after the 1 st month
of life
- Thyroid function in pregnancy
o The striking change is the rise of TBG
 FT4 and FT3 are normal
 It is not elevated as a result of
hyperestrogenic state. Evaluating the
thyroid function of pregnant women, rely
on free hormone assay
 Iodide clearance is increased there is a relative
iron deficiency anemia of pregnancy
 hCG (due to slight thyromimetic effect) results
to physiologic goiter
 Maternal iodide, TSH-R antibodies, and Anti
Thyroid Drugs (ATDs) can cross the placenta
while most of the maternal thyroid hormones
are acted upon by Type III (rendering increase
level of rT3 and T2) deiodinase and do not
reach the fetus.
 During pregnancy, you need to double the
dose of thyroid drugs
- Thyroid function with aging
o Thyroxine turnover is highest in infants and children,
gradually falls to adult levels after puberty, becomes
stable after age 60 and drops at age 90
- Thyroid function in acute and chronic illness (non-thyroidal
illness – thyroidal abnormalities are only the effect of the
sickness)
o In a hospital setting, you request for a free hormone
assay due to these comorbidities to assess whether it
requires replacement therapy (true hypothyroidism)
o Two types:
 Low T3 syndrome resulting from the inhibition of
Type I (convert T4 to T3) and activation of type
III deiodinase system (convert T3 to rT3 and
T2).
 Low T3-T4 syndrome due to inhibition of the
binding of T4 to TBG (because of the hypoxic
tissues it will release the cytokines which
inhibits the binding of T4 to TBG)
o These abnormalities normalize when the patient
recovers.
Note: Normal level of TSH is from 0.5 to 5miu/L. If TSH is
more than 14 it is more of hypothyroidism, 14 and below is
more of non-thyroidal illness.
Non-thyroidal Illness
- Low T3-T4 syndrome is just a prognostication. The higher the
low T3-T4, the higher the mortality
Thyroidal autoimmunity
- Autoimmune mechanisms are involved in the pathogenesis of
many thyroid diseases: Post-partum thyroiditis, silent
thyroiditis, Grave’s disease, Hashimoto’s thyroiditis.
o 3 major thyroidal antigen:
 Tg (thyroglobulin)
 TPO (Thyroid peroxidase)
 TSH-R antibodies (stimulatory or blocking)
o Thyroid cells have the capacity to digest antigen and
when stimulated by cytokines will express cell surface
class II molecules that will present this antigen to T
lymphocyte
TH1 subset when it interacts with interferon gamma will be
recognized by thyrocytes such that the HLA class II molecules found
in the lungs can be attached to thyrocytes. As a result of
costimulation, this would result to the production of TH2 subset or
stimulated T cells. TH2 by the action of cytokines would activate beta
cells to produce anti-bodies.
ATDs have some immunosuppressive effects because it will stop the
costimulation (despite production of HLA, there will be no production
of TH2. TH2, due to the ATDs, will not bind to cytokines therefore
cells will not be activated)
Thyroid function tests
- Tests of thyroid hormone in blood
- Evaluation of the hypothalamic-pituitary-thyroid axis
- Assessment of iodine metabolism
- Estimation of gland size
- Thyroid biopsy
- Observation of the effects of thyroid hormones in peripheral
tissues (most definitive test for Thyroid Function)
- Measurement of thyroid antibodies because most thyroid
problems has autoimmunity as etiology
Tests of TH in blood
- Total serum T3/T4 assay
o Free serum T3/T4 assay
o Thyroglobulin (Tg) – glycoprotein produced by
follicular tissues/thyroid tissues so this has
revolutionized the evaluation of diagnosis of thyroid
carcinoma who underwent total thyroidectomy and
consequent radioactive ablation. It confirms a
functioning distant metastasis or progressive disease
- Bound form can also be a sensitive reflection of metabolic
status, there are three cases where in you don’t want to use
this test:
o Pregnancy
o Acute illness
o Chronic illness
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 - Most sensitive and most reliable method of getting the true
metabolic function, do the Free hormone assay
Evaluation of the hypothalamic-pituitary-thyroid axis
- TRH assay
o Has a very short half-life; not really feasible
- TSH assay
o Most sensitive, most specific biological test to confirm
hypo or hyperthyroidism and to evaluate the thyroid
tissue
- TRH test
o Procedure: inject a synthetic analog of TRH then after
30min to 1hour, check for TSH.
 High: Lesion is in hypothalamus
 Low: Lesion is in pituitary
Estimation of gland size
- There are several ways of doing imaging studies:
o Radionuclide imaging
 Use a radioisotope in the form of 123I or
technetium Tc99m pertechnetate
 This would only give the functional activity of the
thyroid gland (hypofunctioning/hyperfunctioning
nodules/areas that is consistent with a cold/hot
nodules/areas and a normal functioning thyroid
gland consistent with warm nodules/areas)
o Fluorescent scanning
 Give the same information without using any
radioisotope which is safe; costly
o Thyroid ultrasonography
 Most sensitive test to measure the gland in
three dimension and also help in determining
the consistency of the nodule whether it is solid
(increase risk for malignancy), cystic (less
malignancy except if the size of the nodule is
more than 4cm), or complex lesions
(combination of solid and cystic lesions, lesser
risk for malignancy)
 Limitation: Sensitive to thyroid tissue in the
neck. Beyond the neck, it will not be detected by
the ultrasound (substernal, intrathoracic goiter)
o Magnetic resonance imaging
 Detects thyroid tissues beyond the neck
(substernal, intrathoracic goiter – If (+)
Permberton sign, consider these conditions)
Assessment of Iodine metabolism
- Radioactive iodine uptake (RAIU)
o Just an assessment of iodine stores. It does not
correlate with metabolic activity.
o Example: the most common cause of hypothyroidism
is iodine deficiency. RAIU in these patients with iodine
deficiency is still high. Iodine scan in patients with
Grave’s disease will show low results. So if you want
to assess the functional activity of the thyroid gland,
do not perform RAIU because you only evaluate the
iodine stores.
o This is most helpful in differentiating the thyrotoxicosis
of Grave’s disease versus thyroiditis. Patients with
subclinical thyroiditis will present clinically as
hyperthyroid patients but the uptake is low so as to
differentiate from a true Grave’s disease do a RAIU.
o Differentiates between a low versus a high cause of
thyroid disease
- Perchlorate discharge test
o No longer done clinically because of the sensitivity of
TSH
o Done if you are suspecting an organification defect
Thyroid biopsy
- Most sensitive from differentiating a benign from a malignant
lesion. Done for nodular form of goiter. Sensitivity is for
solitary, if multiple the sensitivity decreases for biopsy
- Results:
o Benign (lymphocytic thyroiditis, subacute
granulomatous thyroiditis, benign thyroid nodule
o Indeterminate (cellular follicular lesions) – false or lack
specimen so repeat the procedure
o Suspicious (follicular neoplasm) – biopsy is only
cytological so it will not differentiate between a
follicular adenoma from a carcinoma because in order
to differentiate that is to demonstrate tumor or
vascular nutrition which cannot be seen in cytological
examination.
o Positive (papillary carcinoma (Orphan Annie Nuclei,
Psammomma bodies), medullary carcinoma
(Amyloids), anaplastic carcinoma, lymphoma) -
definitive
Observation of the effects of thyroid hormones on peripheral tissue
(most definitive test to evaluate)
- All the available tests are non specific
o Basal metabolic rate (BMR)
 Increase  hyperthyroidism
 Decrease  hypothyroidism
o Photomotogram - Assess the contraction of Achilles
tendon
 Hyporeflexia  Hypothyroidism
o Cardiac muscle contractility (PEP or LVET)
 Shortened  hyperthyroidism
o Serum cholesterol, creatine kinase, LDH, ACE, SHBG
 Hypercholesterolemia  hypothyroidism
 CDKMN elevation
Measurement of Thyroid Autoantibodies
- Two antibodies:
o Thyroglobulin antibody
o Thyroid peroxidase antibody
- If the TSH-R antibodies are high, consistent with Grave’s
disease
- If the thyroid peroxidase antibody is markedly elevated,
consistent with Hashimoto’s disease
Who needs a TFT?
- Symptoms of frank hypothyroidism/hyperthyroidism
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 - Suspicion of thyroid function abnormality such as atrial
fibrillation, depression, weight problem, dyslipidemia, or mental
abnormalities
- In patients with nodular lesions
- Assess the adequacy of treatment
CLINICAL DISORDERS OF THE THYROID GLAND
CASE 1:
A 23 year old female complains of progressive weight loss
in spite of a good appetite of 2 months duration. This is
associated with heat tolerance, increased sweating and tremors
at rest.
Above symptoms become exaggerated now associated
with palpitations, easy fatigability even at rest. Progressive
jaundice and hyperdefecation were also noted, a week prior to
consult.
PE showed a very restless and combative woman. BP is
170/80, tachycardic at 120/min with irregularly irregular rhythm,
temp. of 40OCand BMI of 14 kg/m2. Generalized icteresia and
exopthalmos were noted with hyperreflexic DTRs and tremors
on outstretched hands.
The thyroid gland is diffusely enlarged, doughy in character,
non-tender, weighing about 60 grams. Presence of thyroid
bruits was appreciated.
DIAGNOSIS: Thyroid Storm Secondary to Diffuse Toxic Goiter
Secondary to Graves’ disease
Thyroid Storm – life threatening condition, exaggeration of
hyperthyroidism resulting to target organ damage
Clinical Manifestations: comatose, stuporous, restless,
unexplained jaundice, intractable heart failure
Management: Admit patient.
CASE 2:
Two months after above patient was stabilized medically,
she underwent subtotal thyroidectomy. After which, she was
lost to follow-up.
Ten years later, she noticed progressive weight gain in
spite of a poor appetite associated with constipation, cold
intolerance and somnolence. Her voice became deep,menses
are irregularand became very forgetful. She was rushed to the
ER due to unresponsiveness.
At the ER, she was noted to be unresponsive to painful
stimuli, BP at 80/60, CAR at 47/min and regular, RR at 6/min.,
temp. at 35OC and markedly obese by eye balling. Theskin is
sallow, coarse and dry with puffy face and eyelid. There is
visible neck scarand thyroid gland is nodularly enlarged on the
right lobe. The lung fields are dull with diminished breath
sounds, apex beat at 6th ICS MCL with very faint heart sounds,
ascitis and bipedal edemawere noted. Slow DTRs on the
elbowswere elicited.
DIAGNOSIS: Myxedema Coma Secondary to Postsurgical
Hypothyroidism
Management: Admit patient
CASE 3:
A 33 year old male presented with high grade fever, body
malaise, sore throat, and soreness in the neck of 3 days
duration. This was associated with palpitations, agitation,
sweating and tremors.
PE disclosed a very acutely-ill looking man, tachycardic at
120/min. and regular, body temp. of 39.5 OC, and BMI of 21
kg/m2. The thyroid gland is visiblewith no erythemaand
exquisitely tender to the point the patient refused that it will be
touched. Hyperreflexiaand tremorswere noted.
DIAGNOSIS: De Quervain’s Thyroiditis (Subacute Thyroiditis)
Subacute Thyroiditis – viral in origin unless proven otherwise
De Quervain’s Thyroiditis – very tender thyroid with subtle
manifestation of hyperthyoidism
Management: if febrile =admit patient = might end up with
sepsis;
If nonfebrile= send home, prescribe analgesic
CASE 4:
A 28 year old female came to your clinic due to a grade 2
goiter. This was not associated with manifestations of either
hypo/hyperthyroidism nor compressing symptoms. She is
presently residing inCaviteand denies family history of goiter.
Except for a diffusely enlarged thyroid that is firm, non-
tender, weighing approximately 45 grams with absent
Pemberton’s sign and bruit, the rest of the PE findings were
essentially normal.
DIAGNOSIS: Diffuse Nontoxic goiter (Simple goiter)
Grade1 goiter – palpable
Grade 2 goiter – visible from a distance
Living in Cavite – iodine sufficient
CASE 5:
A 55 year old malewas referred at the OPD because of a
neck mass. He works as a technician in a nuclear medicine lab
for the last 25 years. He noticed sudden hoarseness of voice,
dysphagia on solid foods and effort-related SOB. He has a
strong family history of lung and nasopharyngeal CA. He is a
smoker.
Pertinent neck exam revealed the presence of cervical
lymph adenopathies, dominant solitary, firm, non-tender thyroid
nodule on the right lobe that is fixated on deglutition. The widest
diameter of the said nodule isabout 5.7 cm. Pemberton’s sign is
present.
DIAGNOSIS: Thyroid CA (highly considering Papillary CA)
Risk Factors
-Age = extremes
-Gender = male (when there is presence of nodules)
-Exposure = radiation
-Hoarseness = invasion of recurrent laryngeal nerve
-SOB = invasion of trachea
-Dysphagia = invasion of esophagus
7|J K C P a l o m a r e s
 -nodule >4cm Classification of Goiters (ICD)
 DTG – Diffuse Toxic Goiter
DEFINITION OF TERMS  DNTG – Diffuse Non-Toxic Goiter
 NTG – Nodular Toxic Goiter
Goiter/ Struma  NNTG – Nodular Non-toxic Goiter
- Enlarged thyroid gland  MNTG – Multi-nodular Toxic Goiter
 MNNTG – Multi-nodular Non-toxic Goiter
Nodular goiter  Goitrous hypothyroidism
- Regular or lumpy enlargement on one site  Thyroiditis
 Thyroid tumors
Diffuse goiter
- General form of thyroid enlargement both the right and left Patients with thyroid disease
lobe and isthmus uniformly enlarging
 Thyroid enlargement (Goiters)
 Symptoms of thyroid deficiency (Hypothyroidism)
Toxic goiter
- Thyroid enlargement associated with high levels of  Symptoms of thyroid hormone excess (Thyrotoxicosis)
circulating thyroid hormones  Complications of specific form of hyperthyroidism (Graves’
Disease)
Goitrous hypothyroidism
- Thyroid enlargement resulting from a deficiency of thyroid Clinical history
hormones  Evaluation of symptoms related to the complaints
*results from the alteration in the 6 sequential steps of  Exposure to ionizing radiations
thyroid hormone synthesis  History of drug intake
 Residence in an area of low dietary iodide
Nontoxic goiter  Family history (goiter, hyper/hypothyroidism, and other
- Thyroid enlargement not associated with thyrotoxicosis and immunologic disorders such as DM, rheumatoid disease,
does not result from an autoimmune or inflammatory pernicious anemia, alopecia, vitiligo or myasthenia gravis,
process etc.)
(Simple goiter)
Mechanisms of Goiters
Endemic goiter  Compensatory hypertrophy/hyperplasia
- When goiter prevalence in children 6-12 years of age within  Hyperfunctioning gland
a population is more than 10% (iodine deficiency goiter)  Inflammation
 Post-degenerative changes
Sporadic Goiter  Infiltrative diseases
- (simple) when the prevalence is 10% or less  Neoplasia
Thyroid tumors Compensatory Hypertrophy/Hyperplasia
- Thyroid enlargement resulting from neoplastic process  Iodine deficiency
*Most common cause of hyperthyroidism in developed
Hypothyroidism countries= HASHIMOTO’S THYROIDITIS
- Is a crucial syndrome resulting from a deficiency of thyroid **Most common cause of hyperthyroidism in the Phils =
hormones characterized by generalized slowing down of IODINE DEFICIENCY
metabolic processes
 Iodine excess (Jodbasedow phenomenon)
*T3 and T4 induced thyrotoxicosis
Myxedema
 Dyshormonogenesis
- Is the non-pitting edema due to accumulation of
glycosaminoglycans in subcutaneous and interstitial  Goitrogens (drugs/food)
tissues seen in hypothyroid patients
*check edema in bony prominences Goitrogens
- Substances that can lead to the inhibition of thyroid
Thyrotoxicosis hormone transport, hormonogenesis, or release resulting in
- Clinical syndrome resulting when tissues are exposed to a rise of TSH and the induction of goiter.
high levels of thyroid hormones
*elevated thyroid hormone regardless of the cause – could Goitrogens (drugs)
be example, from the higher centers, or ectopic ovary,etc. o Block iodide transport into the thyroid gland
 SCN, ClO4, NO3, monofluorosulfonate,
Hyperthyroidism difluorophosphate, fluoroborate, minerals,
- Thyrotoxicosis due to hyperactivity of the thyroid gland lithium, ethionamide
*elevated thyroid hormone comes from the thyroid gland
o Impair TG iodination and iodotyrosine coupling
8|J K C P a l o m a r e s
  ATD’s, sulfonamides, sulfonylureas, - Hemochromatosis
salycylamides, ethionamides, resorcinol, - Scleroderma
SCN, aminoglutethimide, amtipyrine,
amphenidione, ketoconazole, Neoplastic Process/Neoplasia
dimercaptopropanol - Benign(>95% of Thyroid Neoplasms)
o Inhibit thyroid hormone secretions o Colloid adenoma
 Iodide, lithium - Malignant
o Unknown MOA o Primary
 Phenylbutazone, Ca, Co, interleukin-1,  Papillary(most common), follicularI(most
gamma interferon invasive), medullary(associated with
increased calcitonin), anaplastic(poor
Goitrogens (food) prognosis)
o Cruciferous plants o Miscellaneous
 Cabbage, cauliflowers, turnips, carrots  Lymphoma, squamous cell, fibrosarcoma,
o Cyanoglocosides teratomas, hemangioendothelioma
 Cassava, corn, bamboo shoots, sweet o Metastatic CA
potatoes, lima beans
o Soya beans HYPOTHYROIDISM

Hyperfunctioning gland Manifestations of Hypothyroidism

- Diffuse toxic goiter (Graves’ Disease)
- Toxic autonomous goiters
o Nodular toxic goiter (Plummer’s Disease)
o Multi-nodular toxic goiter
*from longstanding multi-nodular nontoxic goiter
example- inhabitants of Mountain provinince – through
the years, they become autonomous in producing
thyroid hormones
Inflammation
- Acute suppurative thyroiditis
o Bacterial, fungal, mycobacterial, parasitic, syphilitic
- Subacute thyroiditis
o De Quervain’s, silent or post partum thyroiditis
*De Quervain’s – painful, viral in origin
*Post partum thyroiditis – not painful
- Chronic thyroiditis
o Hashimoto’s Disease
- Riedel’s struma–rare form of thyroiditis, thyroid tissue
replaced by fibrosis, becomes rock-hard
Post-degenerative changes
- Post thyroidectomy
 Difficult to remove 100% of thyroid tissue-
remnants trigger the higher centers to release
TSH which results to thyroid enlargement
- Post RAI ablation
 Responsive/successful if after 6 months, not
hyperthyroid anymore
 Failure of RAI ablation if after 6 months, still
hyperthyroid – give 2nd dose
- Large doses of neck radiation
 example - in the early 1950s, recommended
procedure for treatment of Acute
Tonsillopharyngitis was neck radiation
Infiltrative diseases
- Amyloidosis
- Sarcoidosis
- The skin and connective tissue
o Surface alterations: cool, dry, pale, keratoderma
o Vascular signs: vasoconstriction, purpura,
ecchymoses
o Hair alterations: dry, coarse, brittle, diffuse or partial
alopecia, madarosis
o Nail changes: thick, britlle, slow growing, pits and
tachyonychia
o Dermal pathology: generalized edema
o Pigmentary changes: sallow color, carotenemia
In hyperthyroidism, there is activation of the Na K ATPase that
causes liberation of heat ->explains heat intolerance, sweating
In hypothyroidism, there is NO activation of the Na K ATPase, no
libreration of heat -> cold intolerance
- The cardiovascular system
o Cardiovascular hemodynamics: increased systemic
vascular resistance, increased or normal diastolic BP,
decreased or normal systolic BP and heart rate,
decreased CO, cardiac contractility, cardiac mass and
blood volume
*Increased systemic vascular resistance – a
compensatory mechanism to maintain BP in the
setting of bradycardia associated with hypothyroidism
- The pulmonary system
o Direct effects: altered PFT’s (increased A-a O 2
gradient, decreased DLCO and maximal exercise
capacity), decreased ventilatory drives, pleural
effusions, upper airway obstruction, sleep apnea
syndrome, low surfactant production (neonate)
o Indirect effects: phrenic nerve paralysis,
neuromuscular weakness or dyscoordination,
atelectasis (obesity), pulmonary edema (CHF),
difficulty in weaning (mechanical ventilation), risk for
theophylline intoxication
- The GIT and liver

9|J K C P a l o m a r e s
 o Prominent findings: severe constipation unresponsive
to laxatives, paralytic ileus, intestinal
pseudoobstruction, myxedema ascites, hepatic
lesions may be associated with autoimmune liver
disease
*Paralytic Ileus –(hypothyroidism causes hypokalemia
that results to distention and dilatation of the
intestines)
- The blood
o Hematologic findings: anemia, bleeding problems
such as easy bruising, prolonged bleeding and
menorrhagia
- The kidney and electrolyte metabolism
o Hemodynamics: decreased GFR and renal plasma
flow, increased mean serum creatinine and urea,
reduced renal tubular absorption, hyponatremia,
edema
- The neuromuscular system
o Neurologic features: cretinism, pseudohypertrophy of
muscles, entrapment neuropathy, peripheral
neuropathy, cerebellar ataxia, hearing loss, seizures,
mental dysfunctions, sleep apnea, myxedema coma,
problems related hypothalamic-pituitary dysfunctions,
Hashimoto’s encephalopathy
- The pituitary
o Clinical consequences: decreased GH secretion
resulting to growth retardation, hyperprolactinemia
resulting to galactorrhea
*Galactorrhea- due to TRH stimulation of prolactin
- The adrenals
o Features: decreased cortisol secretion and
metabolism manifesting as AI, diminished response to
catecholamines leading to depression of sympathetic
activity
*Give glucocoticoids first before replacing with thyroid
hormones
- The reproductive system
o Effects: delay sexual maturity and short stature,
menorrhagia, increased fetal wastage in females; less
clear-cut effect on the reproductive system of males
- The skeletal system
o Effects: decreased bone growth and maturation
resulting to articular and muscular pains, joint effusion,
carpal tunnel syndrome, and avascular necrosis
- The metabolic process
o Effects: decreased energy expenditure, oxygen
consumption, and heat generation, hyperlipidemia
- The psychiatric and behavioral aspect
o Effects: inattentiveness, inability to concentrate,
slowing of thought and speech process, inability to
calculate and to understand complex questions, poor
memory, slow motor functions, and psychosis
Causes of Hypothyroidism
- Primary hypothyroidism
o Destruction of thyroid tissue
 Chronic autoimmune thyroiditis, radiation,
thyroidectomy, infiltrative diseases
o Defective thyroid hormone biosynthesis
 Iodine deficiency, drugs with anti-thyroid
actions
- Central hypothyroidism
o Pituitary and hypothalamic diseases
- Transient hypothyroidism
o Silent thyroiditis, subacute thyroiditis, thyroid hormone
withdrawal
HYPERTHYROIDISM
Manifestations of Thyrotoxicosis
- The skin
o Surface alterations: warm, moist, smooth, dermopathy
o Vascular changes: vasodilatation, palmar erythema
o Sweat gland effects: generalized and localized
hyperhidrosis
o Hair alterations: fine, soft, diffuse and non-scarring
alopecia
o Nail changes: Plummer’s nail, pits and tachyonychia
o Pigmentary signs: localized or Addisonian distribution
o Dermal changes: pretibial myxedema –hardening of
the skin on the anterior leg (=shin)
Myxedema (Interstitial Myxedema) is usually associated with
hypothyroidism
Pretibial myxedema is associated with hyperthyroidism
Hypertension is both associated with hyper and hypothyroidism
-Hyperthyroidism – systolic HPN
-Hypothyroidism – diatolic HPN
- Other organ and system effects are just the opposite of
hypothyroidism…
- Life threatening emergency
o Thyroid crisis or storm
 Exaggerated signs and symptoms of
thyrotoxicosis
 Tachycardia out of proportion to the fever
 Cardiac, GI, and NS dysfunction
*Cardiac – Heart Failure
*GI – unexplained jaundice, hyperdefecation
*NS – restlessness, combativeness,
comatose
 Diffuse goiter
Causes of Thyrotoxicosis
- Thyrotoxicosis with hyperthyroidism
o Graves’ disease, toxic adenoma, MNTG
o TSH hypersecretion, trophoblastic tumor, hyperemesis
gravidarum, thyroid CA, strumaovari, drug-induced
10 | J K C P a l o m a r e s
 (iodine, iodine containing drugs and radiographic - Many of these tumors secrete thyroglobulin which can be
contrast agents) used as a marker for recurrence or metastasis of the
- Thyrotoxicosis without hyperthyroidism cancer
o Silent/subacute thyroiditis, thyrotoxicosis factitia *thyroglobulin – most reliable test for evidence of
o Drug-induced thyroiditis, radiation thyroiditis, infarction metastasis
of thyroid adenoma
Follicular Carcinoma
Complications of Graves’ Disease - Differs from follicular adenoma by the presence of capsular
- Graves’ophthalmopathy or vascular invasion
- Graves’dermopathy *Routine cytology cannot differentiate benign from
- Thyroid crisis malignant neoplasm
*2 out of 3 signs= sae to make a clinical diagnosis of
Graves’ Disease - More aggressive than papillary CA and can spread either
*But the most definitive test is TSI (Thyroid Stimulating by local invasion of lymph nodes or by blood vessel
Immunoglobulin) invasion with distant metastases to bone or lung
- Death is due to local extension or to distant bloodstream
metastasis with extensive involvement of bone, lungs and
viscera
Benign Thyroid Nodules - These tumours often retain the ability to concentrate RAI
- Thyroid nodules are common especially among older - A variant of follicular carcinoma is the “Hurthle cell”
women carcinoma. These tumours behave like follicular cancer
- Etiology: except that they rarely take up RAI*not responsive to RAI
o Focal thyroiditis therapy
o Dominant portion of multinodular goiter - Thyroglobulin secretion by follicular carcinoma can be used
o Thyroid, parathyroid, or thyroglossal cysts to follow the course of the disease
o Agenesis of a thyroid lobe
o Post-surgical remnant hyperplasia or scarring Medullary Carcinoma
o Post-radioiodine remnant hyperplasia - A disease of the C cells (parafollicular cells)
- More aggressive than papillary or follicular carcinoma but
o Benign adenomas:
not as aggressive as undifferentiated thyroid cancer
 Follicular
- It extends locally, and may invade lymphatics and blood
 Colloid
vessels
 Hurthle Cell
- Calcitonin and CEA are clinically useful markers for DX and
 Embryonal
F/U
 Rare: Teratoma, lipoma, hemangioma
- 80% of medullary CA are sporadic and the rest are familial.
Thyroid Cancer There are 4 familial patterns:
Approximate frequency of malignant thyroid tumors: o FMTC without endocrine disease
- Papillary carcinoma (including 75% o MEN 2A: medullary CA + pheochromocytoma +
mixed papillary and follicular hyperparathyroidism
- Follicular carcinoma 16% o MEN 2B: medullary CA + pheochromocytoma +
- Medullary carcinoma 5% multiple mucosal neuromas(von recklinghausen
- Undifferentiated carcinoma 3% disease)
o MEN 2 with cutaneous lichen amyloidosis
- Miscellaneous (e.g. lumphoma, 1%
Fibrosarcoma, squamous cell CA, - The familial syndromes are associated with mutations in
Teratoma, and metastatic CA) the ret protooncogene (a receptor protein kinase gene on
chrom. 10)
- Diagnosis is by FNAB. Patient needs to be screened for
Papillary Carcinoma other endocrine abnormalities found in MEN 2. Family
- Usually presents as a nodule that is firm, solitary, “cold” on members need to be screened for medullary CA and MEN
isotope scan, and usually solid on thyroid US 2 as well.
- In MNG, the cancer is usually a “dominant nodule” that is
Undifferentiated (Anaplastic) Carcinoma
larger, firmer and different from the rest of the gland
- This tumour usually occurs in older patients with a long
- 10% of papillary CA present with enlarged cervical nodes
history of goiter in whom the gland suddenly- over weeks
- Grows very slowly and remains confined to the thyroid
or months- begins to enlarge and produce pressure
gland and local lymph nodes for many years
symptoms, dysphagia, or vocal cord paralysis
- In later stages they can spread to the lung
- Death from massive local extension usually occurs within
- Death usually from local disease or lung metastases
6-36 months
- Many convert to undifferentiated CA - These tumours are very resistant to therapy

11 | J K C P a l o m a r e s
Diagnosis of Thyroid Disorder
- Carefully taken history
- Thorough search of physical signs
- Appraisal of laboratory tests
DIAGNOSIS AND MANAGEMENT OF THYROID GLAND
DISORDERS
CASE 1:
A 23 year old female complains of progressive
weight loss in spite of a good appetite of 2 months
duration. This is associated with heat tolerance, increased
sweating and tremors at rest.
Above symptoms become exaggerated now
associated with palpitations, easy fatigability even at rest.
Progressive jaundice and hyper defecation were also
noted, a week prior to consult.
PE showed a very restless and combative
woman. BP is 170/80, tachycardic at 120/min with
irregularly irregular rhythm, temp. of 40OC and BMI of 14
kg/m2. Generalized icteresia and exopthalmos were noted
with hyperreflexic DTRs and tremors on outstretched
hands.
The thyroid gland is diffusely enlarged, doughy in
character, non-tender, weighing about 60 grams. Presence
of thyroid bruits was appreciated.
DIAGNOSIS: Thyroid storm (or thyroid crisis) secondary to
Grave’s disease
DDX:
Uncontrolled hyperthyroidism or uncontrolled thyrotoxicosis
Thyroid Crisis- Tsh is elevated
Uncontrolled hyperthyroidism or thyrotoxicosis- Tsh is
normal
Note:
1. Total hormone concentration is NOT a reliable metabolic
index if your patient is UNDER STRESS in ACUTE OR
CHRONIC ILLNESS” exceptions: Hospitalized patients,
Pregnancy state, Acute or chronic comorbidities. They are
dependent on your protein, pag malnourished ang patient
automatic mababa ang total hormone pero wlang
confirmation sa metabolic.
2. There are no lab test that will differentiate thyroid storm
from uncontrolled hypethyroidism. Clinical manifestations
lang ang differentiation base sa symptoms and end organ
damage. End organ damage nakikita lang po sa thyroid
crisis
3. BUT your TSH and Free hormones are essential because if
that test is normal you will rule out Thyroid crisis. Di sya
pwedeng maging thyroid crisis kung hindi mababa ang TSh
nia at hindi mataas ang Free hormones niya.. it will not
confirm the dx but it will support the dx mo po..
Things you will do to your patient after confirmation of your Dx:
- Admit patient in ICU-kasi life threatening condition ang
Thyroid storm
Precipitating events para sa endocrine manifestations:
1. INFECTION
2. Adrenal Crisis- ang statistically present,decrease cortisol,
glucocorticoids kasi increase ang metabolic degradation
pag hyperthy..
Tests that you will request:
1. TSI-Thyroimmunoglobulin test –to intensify the cause of
your hyperthyroidism kung grave’s disease ba pero wla
naman sya dito for research lang pero pwede siya
2. CBC-increase WBC
3. Urinalysis- kung GUT ba ang cause ng infection, Pus in
urine will not denote infection agad agad.. cast will tell you
glomerulonephritis, Look for pyuria + elevated esterase and
nitrate para maconfirm kung +infection
4. Chest Xray-look for infiltrates or consolidation that will
suggest pneumonic or tuberculosis process
5. ECG- look at conduction abnormalities plus presence of
ischemia
6. UTZ
7. Electrolytes-hypokalemia, hypomagnesemia…. Ung iba pa
na nagcacause ng cardiac problem
8. CBG- idea of glucose levels
9. O2sat-pulse oximetry-for hypoxia
10. ABG-for hypoxia din
11. Liver function test-most important drug that you will
administer in this patient is metabolize in the liver para
maprevent ang toxic hepatitis
12. Renal function test-might compromise ang renal blood flow
baka mag AKI, determine baseline crea level
Treatment:
- Stabilize patient by:
o 3/4 standard regimens
 Antithyroid drug
 PTU (DOC) - Shortest acting antithyroid
drug; added benefit of inhibiting peripheral
conversion of T4 to T3
 Other anti thyrod drugs like Methimazole -
action is mainly intrathyroidal inhibition of
production pero meron din naman to sa
PTU. Ideal lang ang PTU pero pwede din
naman ung ibang anti thyroid drug lalo na
kung hindi available ang PTU
o Virgin case: Loading dose: 800-1200mg of PTU
12 | J K C P a l o m a r e s
PTU available in 50mg/tab so mga 16tabs single loading dose ang
ibibgay mo tapo maintain it sa 200mg every 4hours.. pag +clouding
in sensoriumtutulog tulog via NGT po ang administration
 Propranololshort acting b-blockers, for
sympathetic overactivity (Inc HR,
anxiousness, palpitations, etc). Also High
doses of propranolol cause peripheral
inhibition of thyroid hormones
 Steroids(glucocorticoids)thyroid hormones
increase metabolic degradation of
exogenous steroids so there is adrenal
insufficiency in the setting so give steroids
for adrenal support, inhibit peripheral
conversion of T4 to T3. Long acting
dexamethasone
Iodine preparation(Lugose solution)doesn’t affect the release of the
hormone, it inhibit release of free hormones; optional because it
delays RAIU for 6 months;
High dose of iodine cause inhibition of secretion pero not given
routiunely, pag hindi lang nagrespond within 24hours sa 3drugs na
nauna..
Post pone ang definitive treatment so walang RAIU for 6months hindi
mo masisira ang gland nia
Iodine use as a substrate for hormone production so give PTU
 Earliest manifestation of pleural effusion seen in chest xray is
For other symptoms, supportive measures
o Fever: give analgesic
don’t give aspirincompetitively binds with carrier protein thus
increases the free hormone assay
o Seizuresbarbiturates don’t give benzodiazepines and
phenobarbital kasi ang problem is rapid firing in foci
o Multivitamins-for electrolyte hydration
o PneumoniaAB
Treatment of choice is RAIU
For pregnantsurgery
o Subtotal thyroidectomy (Grave’s disease to control hypothyroidism)
o Nodular
o Unilateral lobectomy
o Total lobectomy with isthmutectomy
o Near total thyroidectomy (<5gm left)
Most important advice to the patient after stabilizing her medically:
Definitive treatment: RAIU or surgery kasi you may not be lucky for
the second time around..
Watch out for:
Complications like hypothyroidism
CASE 2:
Two months after above patient was stabilized
medically, she underwent subtotal thyroidectomy. After
which, she was lost to follow-up.
Ten years later, she noticed progressive weight
gain in spite of a poor appetite associated with
constipation, cold intolerance and somnolence. Her voice
became deep, menses are irregular and became very
forgetful. She was rushed to the ER due to
unresponsiveness.
At the ER, she was noted to be unresponsive to
painful stimuli, BP at 80/60, CAR at 47/min and regular, RR
at 6/min., temp. at 35OC and markedly obese by eye
balling. The skin is sallow, coarse and dry with puffy face
and eyelid. There is visible neck scar and thyroid gland is
nodularly enlarged on the right lobe. The lung fields are dull
with diminished breath sounds, apex beat at 6th ICS MCL
with very faint heart sounds, ascitis and bipedal edema
were noted. Slow DTRs on the elbows were elicited.
DIAGNOSIS: Myxedema Coma secondary to post
operative hypothyroidism
Test to strengthen the diagnosis:
TSH-dapat elevated ang result because ang main pathology natin ay
ang thyroid gland dahil di na gumagawa ng thyroid hormones
binobomba niya ang higher center mo to produce too much TSH.
Pero intact ang higher center mo
Admit in ICU
Respiratory failure-most common cause of death in hypothy
Precipitating factor:
Long standing untreated hypothyroid state
Request for :
ABG - respiratory acidosis with hypoxemia
ECG-bradyarrythmias, conduction defect, 1st,2nd,3rd degree AV
block
X-ray - risk for pleural effusion, pericardial effusion dahil daw matagal
na sya may hypothyroidism na di nagagamot
blunting of costophrenic angle +white portion in lungs
Pericardial effusion-+watter bottle sign
(hala pati radiology)
Electrolytes-check for hyponatremia resulting to pleural effusion, risk
of developing cardiac arrhythmia
Liver function test
Renal function test
CBC- check for concomitant infection
Treatment
o Give glucocorticoids muna like Hydrocortisonefor adrenal support
before giving L-thyroxine , kasi sanay siya na hypothy para di sya
mabigla. Hydrocortisone kasi sya ang shortest acting steroid and life
threatening condition to
o 1st druglevothyroxineT4 predictable to kung kelan babalik sa
euthyroid state (levothyronine is not available)
o TestTSHincrease because primary in nature(thyroid gland)
Supportive Treatment:
o Cooling blankets
o Mechanical ventilator
Long term and most important advice:
o Patient to take thyroid hormone replacement for life kasi high risk
sya to develop myxedema again
CASE 3:
A 33 year old male presented with high grade
fever, body malaise, sore throat, and soreness in the neck
of 3 days duration. This was associated with palpitations,
agitation, sweating and tremors.
PE disclosed a very acutely-ill looking man,
tachycardic at 120/min. and regular, body temp. of 39.5OC,
and BMI of 21 kg/m2. The thyroid gland is visible with no
erythema and exquisitely tender to the point the patient
13 | J K C P a l o m a r e s
 refused that it will be touched. Hyperreflexia and tremors
were noted.
DIAGNOSIS: Subacute Thyroiditis a.k.a. De Quervin’s
Thyroiditis (probably granulomatous type)
Confirmation of diagnosis24RAIU uptakelow because destroyed
na ang tghyroid tissue kaya di na niya makuha ang hormones (De
Quervin’s), high (Grave’s)
Admit the patient kasi may fever pa ang patient baka mag convulsion
pa ang patient. If ok ang VS without fever manage patient in OPD
basis
Treatment
o Paracetamol-fever
o Thyrotoxicosis is transient, not a result of overactivity of gland
o NSAIDS for pain
o B-blockers to control the increase sympathetic activity
o Antithyroid drug contraindicted kasi hindi sya due to overactivity of
thyroid gland, kaya alng sya hyperthy kasi nasira tapos niliberate
niya ung free hormonesonce naubos na ang free hormones wala na
syang hyperthyroidism kaya kung nagbigay ka ng antithyroid drug
lalo lang sya mag hhypothy kasi hindi na nga sya gagawa ng thyroid
hormones dahil sira na nga tapos naka antithyroid drug ka pa.
o Metabolic stage depends on what stage u catch the disease (initial
thyrotoxicosis, euthyroid, permanent hypothyroidism)
o Hypothyroidism is permanent if 3-6 mos
CASE 4:
A 28 year old female came to your clinic due to a
grade 2 goiter. This was not associated with manifestations
of either hypo/hyperthyroidism nor compressing symptoms.
She is presently residing in Cavite and denies family
history of goiter.
Except for a diffusely enlarged thyroid that is firm,
non-tender, weighing approximately 45 grams with absent
Pemberton’s sign and bruit, the rest of the PE findings
were essentially normal.
sudden hoarseness of voice, dysphagia on solid foods and
effort-related SOB. He has a strong family history of lung
and nasopharyngeal CA. He is a smoker.
Pertinent neck exam revealed the presence of
cervical lymph adenopathies, dominant solitary, firm, non-
tender thyroid nodule on the right lobe that is fixated on
deglutition. The widest diameter of the said nodule is about
5.7 cm. Pemberton’s sign is present.
DIAGNOSIS: Primary Thyroid Malignancy
OPD management with close follow up monitoring,
pero pag severe respiratory failure na admit na
Malignancy is always euthyroid
Follicular Ca lang ang pwedeng magpresent ng hyperthyroidism
Follicular Ca- follicular tumor as reported pro hindi madodocument as
vascular or tumor lesion
Papillary Ca-orphan annie nuclei or psamomma bodies
After madocument kung may malignancy nga ang patient then
pwede na iadmit ang patient for surgery
For monitoring – Thyroglobulin test
Diagnosis by
o Biochemical (TSH)to check thyroid state
o FNABconfirm malignancy
Treatment
o Near total thyroidectomy5gm of thyroid tissue left (N15-20 gm)
o Total thyroidectomy
For monitoring purposes
Thyroglobulinto monitor thyroid tissue, this is produced only by
thyroid tissue
o Radioactive ablation
o L-thyroxine replacement and suppressive
Maintain TSH level 0.01-0.1 level

DIAGNOSIS: Diffused non-toxic goiter (simple goiter)

OPD management lang siya kasi wala syang compressing symptoms

Treatment
UTZmost important diagnosiskasi gusto mo Makita kung solid,
cystic ang lesion and to examine the TSH and FT4 to determine if it
is apathetic form of thyrotoxicosis, to assess the efficacy of
suppression therapy and to monitor progression of therapy
 L-thyroxinegiven as suppression therapy, euthyroid
state(indication of suppressionDNTG and thyroid malignancy)

Suppess TSH because it is the no 1 growth promoting factor kasi

baka pag bumaba ang TSH baba ang hyperthy lililiit ang gland
Efficacy is <20% respond
Take basal UTZ and check after 6mos. –if there is significant
change in size of goiter

CASE 5:
A 55 year old male was referred at the OPD
because of a neck mass. He works as a technician in a
nuclear medicine lab for the last 25 years. He noticed
14 | J K C P a l o m a r e s