Endocrine Disorders

Clinical & Laboratory Studies

Liong Boy Kurniawan, Ruland Pakasi

Department of Clinical Pathology, Hasanuddin University
Makassar
2 Diabetes Mellitus (DM)

OVERVIEW

refers to a group of disorders of abnormal carbohydrate metabolism sharing in common the

clinical finding of hyperglycemia.
DM is associated with a relative or absolute impairment in insulin secretion, along with
varying degrees of peripheral resistance to the action of insulin.

LB Kurniawan, RDN PAKASI - UNHAS TEACHUNG HOSPITAL, MAKASSAR 5/16/17

3 Diabetes Mellitus (DM)

TYPES &
CLASSIFICATIO
N

1.Type 1: immune mediated, results in an absolute insulin deficiency

2.Type 2: relative insulin deficiency due to abnormalities of both insulin secretion and insulin
action. Insulin levels are sufficient to prevent lipid mobilization & ketosis.
3.Gestational diabetes: diagnosed during pregnancy. Only 2% of patients with gestational
diabetes remain diabetic after delivery. 40% patients will develop overt diabetes within 15
years, mostly type 2, but occasionally type 1.

5/16/17
4 Diabetes Mellitus (DM)

TYPES &
CLASSIFICATIO
N
4.Specific types of diabetes:

a. Genetic defects of beta cell functionb.

b. Genetic defects in insulin action
c. Diseases of the exocrine pancreas, such as
pancreatitis, trauma, pancreatectomy,
neoplasia, cystic fibrosis (CF)
5.Associated with endocrinopathies (i.e., Cushings syndrome), drugs (i.e., corticosteroids),
or chemicals

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5 Diabetes Mellitus (DM)

Screening for A.In the absence of specific

Diabetes
Mellitus
symptoms:
Routine screening for
type 1 DM : not recommended,
type 2 DM: (ADA recommends)
screening for diabetes or
prediabetes
all adults with BMI 25 kg/m2
& one or more additional risk factors
for diabetes

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6 Diabetes Mellitus (DM)

Screening for
Diabetes A.In the absence of specific
Mellitus symptoms :

In individuals without risk factors,

testing should begin at age 45
years.
Fasting plasma glucose is the
recommended screening test, since
it is faster, easier to perform, more
convenient, acceptable to patients,
and less expensive.

5/16/17
7 Diabetes Mellitus (DM)

Screening for B.Risk factors for diabetes:

Diabetes
1. Age 45 years
Mellitus
2. Overweight (body mass index 25
kg/m2)
3. Family history diabetes mellitus in a
first-degree relative
4. Habitual physical inactivity
5. Belonging to a high-risk ethnic or racial
group (e.g., African American, Hispanic,
Native American, Asian American, and
Pacific Islander)

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8 Diabetes Mellitus (DM)
B.Risk factors for diabetes:
Screening for 6. History of delivering a baby weighing >4.1
kg (9 lb) or of gestational DM
Diabetes
Mellitus 7. Hypertension (blood pressure 140/90
mm Hg)
8. Dyslipidemia defined as a serum high-
density lipoprotein cholesterol
concentration 35 mg/dL (0.9 mM) and/or
a serum triglyceride concentration
mg/dL (2.8 mM)
9. Previously identified impaired glucose
tolerance (IGT) or impaired fasting glucose
(IFG)
10.Polycystic ovary syndrome
11. History of vascular disease 5/16/17
9 Diabetes Mellitus (DM)

How to ADA Criteria for the diagnosis of diabetes

Confirm the mellitus:
Diagnosis a.a. Symptoms of diabetes and a casual
plasma glucose 200 mg/dL. Casual is
defined as any time of day without regard
to time since the last meal. The classic
symptoms of diabetes include polyuria,
polydipsia, and unexplained weight loss.
OR
b.Fasting plasma glucose 126 mg/dL
(7.0 mM). Fasting is defined as no caloric
intake for at least 8 hours. Or

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10 Diabetes Mellitus (DM)

How to
Confirm the ADA Criteria for the diagnosis of diabetes
Diagnosis mellitus:
c.Two-hour plasma glucose 200 mg/dL
during an oral glucose tolerance test
(OGTT). The test should be performed
using a glucose load containing the
equivalent of 75 g anhydrous glucose
dissolved water.
OR
d.Glycosylated hemoglobin A1c (HbA1c)
6.5%.

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11 Diabetes Mellitus (DM)

How to Diagnostic Thresholds for Diabetes and

Confirm the Prediabetic Conditions
Diagnosis Glycosylate
Fasting 2-hour d
Category plasma plasma hemoglobin
glucose glucose A1C

Normal <100 <140

<5.7%
mg/dL mg/dL
Impaired
100125
fasting
mg/dL
glucose
Impaired
140199
glucose
mg/dL
tolerance
Increased 5/16/17
5.7 6.4%
risk
12 Diabetes Mellitus (DM)

circulating lifespan of 90 days, thus

Glycated-Hb measurement of HbA1c provides
(HbA1c) information about the level of glycemic
control over a 3-month period
if RBCs have abnormal survival
timevalue of HbA1c may not be
reliablefalsely low in patients with
hemolytic anemias, & may be falsely
elevated in patients with polycythemia
vera or postsplenec tomy.
It cannot be used as reliable index for
glycemic control in patients with chronic
liver diseases due to increased
erythrocyte turnover.
5/16/17
13 Diabetes Mellitus (DM)

Absence of
unequivoval Diagnosis of DM must be confirmed
hyperglydemi on
a
a subsequent day by measuring any
one of the three criteria (b, c, and d).
In symptomatic patients with blood
glucose 200 mg/dL or patients with
ketonuria and clear manifestations of
type 1 DM, the diagnosis is
established and further evaluation is
not needed.

5/16/17
14 Diabetes Mellitus (DM)

prediabetic
conditions Should be counseled on
lowering their risk for
macrovascular diseases (smoking
cessation, use of aspirin, diet,
and exercise)
should have measurements of
blood pressure & serum lipids,
be encouraged to modify their
lifestyle and reduce their weight.

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15 Diabetes Mellitus (DM)

Acute
Complication
s

Excessive & prolonged hyperglycemia

associated with uncontrolled diabetes can
cause fluid and electrolyte imbalance, life-
threatening.
Diabetic ketoacidosis (mostly in type 1 DM,)
Hyperglycemia (generally 300 mg/dL), glucosuria, ketonemia & , HCO 3 -,
BUN, creatinine,pH usually <7.3 2.
total body potassium & phosphorus , serum levels may be normal due to acidosis &shifts to the
extracellular space

5/16/17
16 Diabetes Mellitus (DM)

Chronic
Complications

Diabetic nephropathy
The earliest evidence of nephropathy is the appearance of low levels of albumin (30 mog/day or 20
g/min) in the urine, termed microalbuminuria.
microalbuminuria will progress to overt nephropathy ( 300 mg/day or 200 g/min) over a period
of 1015 years if not treated.
Patients who develop overt nephropathy, develop ESRD in 75% of DM-typ1 0%, in 20% DM-type1
over 20 years.

Retinopathy and neuropathy

5/16/17
DIABETIC KETOACIDOSIS (DKA)

BACKGROUND
Diabetic ketoacidosis (DKA) is an acute,
major, life-threatening complication of
diabetes that mainly occurs in patients
with type 1 diabetes, but it is not
uncommon in some patients with type 2
diabetes. This condition is a complex
disordered metabolic state characterized
by hyperglycemia, ketoacidosis,
&ketonuria

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DIABETIC KETOACIDOSIS (DKA)

LABORATORY
STUDY
The blood glucose
usually exceeds 250 mg/dL.
BLOOD GLUCOSE Urine dipstick test

URIN GLUCOSE & is highly positive for glucose & ketones. Rarely,
KETONES urine is negative for ketones, due to the fact
that most available laboratory tests can detect
only acetoacetate, while the predominant
ketone in severe untreated DKA is -hy
droxylbutyrate

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DIABETIC KETOACIDOSIS (DKA)

LABORATORY
STUDY

Serum or capillary -hydroxybutyrate

- can be used to follow response to treatment in
HYDROXYBUTYRAT
patients with DKA.
E
Levels >0.5 mmol/L: considered abnormal,
Levels of 3 mmol/L correlate with the need for
treatment for DKA

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DIABETIC KETOACIDOSIS (DKA)
Serum K levels initially or within the reference range in
patients with DKA. This is due to the extracellular shift of
LABORATORY potassium in exchange of hydrogen, which is
STUDY accumulated in acidosis, in spite of severely depleted
total body potassium. This needs to be checked
Electrolyte frequently, as values drop very rapidly with treatment.
panel An ECG may be used to assess the cardiac effects of
extremes in potassium levels.
Serum Na level usually in affected patients.
The osmotic effect of hyperglycemia moves
extravascular water to the intravascular space. For each
100 mg/dL of glucose over 100 mg/dL, the serum
sodium level is lowered by approximately 1.6 mEq/L.
When glucose levels fall, the serum sodium level rises
by a corresponding amount.
Additionally, serum Cl levels and P levels always in
these patients.
5/16/17 20
LABORATORY DIAGNOSIS OF THYROID
DISEASE:

LIONG BOY KURNIAWAN

Clinical Pathology Department-Medical Faculty of

Hasanuddin University/ Dr. Wahidin Sudirohusodo Hospital
Makassar
INTRODUCTION
Diseases of the thyroid among the most
prevalent of medical disorders
The symptoms can be non specific or mild
so the clinicians uses laboratory tests for
diagnosing thyroid disorder
INTRODUCTION
In the 1950s the only thyroid test available
protein-bound iodine (T4) poor sensitivity and
specificity
Nowadays thyroid testing serum specimens
manual/automated methods employing
specific antibodies
INTRODUCTION
Several tests currently available :
Pituitary thyroid stimulator
Thyrotropin (TSH)
Thyroglobulin (Tg)

Thyroid autoantibodies
Thyroid peroxidise antibodies (TPOAb),
Thyroglobulin antibodies (TgAb)
TSH receptor antibodies (TRAb)
INTRODUTION
Several tests currently available :
Serum based methods
TT4 and TT3
FT4 and FT3
Thyroid hormone binding proteins
Thyroxine Binding Globulins (TBG)
Transthyretin (TTR)/Prealbumin (TBPA)
REFERENCE VALUES OF THYROID
FUNCTION TEST

JAPI Supplement Jan 2011;59:14-20.

PRINCIPLES OF LABORATORY TESTING
USED FOR THYROID TESTING

Most thyroid tests are performed

competitive immunoassays
Sandwich immunoassays
 PRINCIPLES OF LABORATORY TESTING
USED FOR THYROID TESTING

Thyroid hormones competitive immunoassays

A limited amount of antibody to thyroid hormone + patients serum +
a known amount of the same thyroid hormone is labeled
The labeled and the unlabeled hormone compete for binding by the
antibody
The amount of label bound to antibody is inversely proportional to the
amount of hormone in the patients serum.
 PRINCIPLES OF LABORATORY TESTING
USED FOR THYROID TESTING

Thyroid hormones competitive immunoassays

Subject interference by compounds that are similar in structure to
the compound of interests
Patients with antibodies to the compound of interest falsely
increased results
 PRINCIPLES OF LABORATORY TESTING
USED FOR THYROID TESTING

Peptide hormones (TSH, calcitonin, thyroglobulin) sandwich

immunoassays
a large amount of antibody to the hormone is bound to a solid support
patient serum is added
After incubation + washing a second labeled antibody to the
hormone is added (sandwich assay)
After washing the amount of labeled antibody remaining directly
proportional to the amount of hormone in serum
 PRINCIPLES OF LABORATORY TESTING
USED FOR THYROID TESTING

Peptide hormones (TSH, calcitonin, thyroglobulin) sandwich

immunoassays
Human antibodies to antibodies used in the assays may lead to
attachment of the indicator antibody to the solid support even in the
absence of hormone
The most commonly occurs with human antibodies to mouse proteins
mouse monoclonal antibodies are most widely used (heterophile
antibodies)
 THYROID STIMULATING
HORMONE
Thyroid stimulating hormone glicoprotein hormone secreted by
the anterior pituitary
Serum TSH exhibits a diurnal variation
A peak shortly after midnight
A nadir in late afternoon
At the peak TSH can be double the value at the nadir
 THYROID STIMULATING
HORMONE
In acutetely ill individuals the range of TSH in euthyroid
changes markedly
Cortisol, dopamine and cytokines affect TSH production
Central hypothyroidism decreased sialylation results in
reduced bioactivicity and increased TSH half life
Measurement of TSH subject to interference (heterophile
antibodies/rheumatoid factor) falsely increased results
CAUSES OF MISLEADING THYROID-
STIMULATING HORMONE RESULTS

Endocrinol Metab Clin N Am 2007;36:579-594

 TOTAL THYROXINE AND
TRIIODOTHYRONINE
Over 99% of T4 and T3 bound to binding proteins (TBG,
albumin, and transthyretin, also termed thyroxine binding
prealbumin)
Total thyroid hormone levels affected by changes in binding
protein levels or binding affinity
Total thyroid hormone levels more often abnormal due to
binding protein changes than to thyroid dysfunction
THYROTOXICOSIS/HYPERTHYROIDISM
physiologic manifestations of excessive
quantities of the circulating thyroid
hormones. The term hyperthyroidism is
reserved for disorders that result from
sustained overproduction of the hormone
by the thyroid itself.
OVERVIEW
Thyrotoxicosis can be caused by
hyperthyroidism, or by exogenous thyroid
hormone, iatrogenic, or self-administered
manifestations of thyrotoxicosis are largely
independent of its cause
The most common form is Graves disease,
comprising 7080% of the cases.
5/16/17 42
THYROTOXICOSIS/HYPERTHYROIDISM
Common causes
Graves disease
(diffuse toxic goiter)
Toxic multinodular goiter
Toxic adenoma
Chorionic gonadotropininduced
OVERVIEW hyperthyroidism
Iodide-induced hyperthyroidism.
Hashimotos thyroiditis
Subacute thyroiditis

5/16/17 43
THYROTOXICOSIS/HYPERTHYROIDISM

radioactive iodine uptake (RAIU) is typically

unless the patient has been exposed to
excess iodine or acutely to large dose of
COMMON CAUSES glucocorticoids.
1. Graves disease
(diffuse toxic goiter)
The circulating autoantibodies specific to
Graves disease are directed against the
thyroid-stimulating hormone (TSH) receptor
and can be measured directly.

5/16/17 44
THYROTOXICOSIS/HYPERTHYROIDISM

is a disorder in which hyperthyroidism

COMMON CAUSES
2. Toxic multinodular goiter (MNG)
arises in a mul-tinodular goiter, usually of
long standing.
The overproduction of thyroid hormone is
usually less than in Graves disease and is
almost never accompanied by infiltrative
ophthalmopathy.
All patients with MNG should be screened
annually with a serum TSH. .

5/16/17 45
THYROTOXICOSIS/HYPERTHYROIDISM

is usually caused by a single adenoma

sometimes referred to as hyperfunctioning
solitary nodule or toxic nodule.
COMMON CAUSES
3. Toxic adenoma
It often shows a suppressed TSH, which
appears in a radioiodine thyroid scan as a
localized area of increased radioiodine
accumulation.

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THYROTOXICOSIS/HYPERTHYROIDISM
can be physiologic during pregnancy
(transient gestational thyrotoxicosis) or
associated with trophoblastic tumors.

COMMON CAUSES
4. Chorionic gonadotropininduced
hyperthyroidism
Administration of supplemental iodine to
5. Iodide-induced hyperthyroidism.
subjects with endemic iodine-deficiency
goiter can result in iodide-induced
hyperthyroidism. Amiodarone, an
antiarrhythmic medication, is the most
common drug that has been reported to be
associated with iodine-induced
thyrotoxicosis.
5/16/17 47
THYROTOXICOSIS/HYPERTHYROIDISM
can associate with transient thyrotoxicosis,
which is caused by thyroid cell breakdown,
and the hyperthyroid symptoms are of abrupt
COMMON CAUSES onset and short duration.
6. Autoimmune an acute infl ammatory disorder of the
(Hashimotos)
thyroid gland, which is caused directly or
thyroiditis
indirectly by a viral infection.

7. Subacute
The symptoms of fever, malaise, and neck
thyroiditis
soreness frequently overshadow the
symptoms of hyperthyroidism.
Characteristic findings are of a tender thyroid
gland, an elevated ESR, and a low RAIU.
5/16/17 48
THYROTOXICOSIS/HYPERTHYROIDISM
Serum TSH is the most cost-effective
screening test. If the value is normal, the
patient is very unlikely to have
hyperthyroidism.
Laboratory In hyperthyroidism, serum TSH is < N and
Findings frequently <0.1 uIU/mL.
TSH may remain decreased for many
TSH months in treated formerly hyperthyroid
patients; therefore, thyroid hormone levels
more accurately reflect the clinical situation.

5/16/17 49
THYROTOXICOSIS/HYPERTHYROIDISM
Serum free T4 is important to confirm and
determine the degree of hyperthyroidism in
a patient with a low TSH.
Serum T3 is usually elevated with
Laboratory hyperthyroidism. Assessment of T3 levels is
Findings important to determine the severity of the
hyperthyroidism and to monitor the
response to treatment.
T4, T3

5/16/17 50
THYROTOXICOSIS/HYPERTHYROIDISM
Laboratory Findings
Radio Active Iodine Uptake (RAIU)
5/16/17
RAIU is often in Graves disease. However,
the diagnostic accuracy of RAIU in
hyperthyroidism does not approach that of
the serum TSH plus free T4 measurement.
Therefore, determining RAIU is not useful in
the diagnosis of straightforward Graves
disease but is useful in excluding
thyrotoxicosis not caused by hyperthyroidism.
values of RAIU in association with
thyrotoxicosis signal the presence of
factitious thyrotoxicosis, ectopic thyroid
tissue, subacute thyroiditis, or the thyrotoxic
phase of autoimmune thyroiditis.
51
THYROTOXICOSIS/HYPERTHYROIDISM
Thyrotropin receptor autoantibodies are
present in 70100% of the patients with
Graves disease, their measurement is not
usually necessary for diagnosis, but it may
be helpful in prognosis because patients
Laboratory who have high titers that do not decrease
Findings with antithyroid drug treatment are unlikely
Autoantibodies to go into remission.
Measurement of thyrotropin receptor
autoanti-bodies is important in pregnancy,
because a high titer at the end of
pregnancy correlates with an increased risk
of neonatal hyperthyroidism.

5/16/17 52
THYROTOXICOSIS/HYPERTHYROIDISM
Abnormal TSH can also been seen in
various nonthyroidal disease.
Simultaneous measurement of TSH with
free FT4 is useful in evaluating the
differential diagnoses.
Laboratory
Findings

5/16/17 53
HYPOTHYROIDISM

OVERVIEW

Hypothyroidism refers to a condition in which the amount of thyroid hormones in the body is <
normal.
The diagnosis of hypothyroidism relies heavily upon laboratory tests because of the lack of
specificity of the typical clinical manifestations.

5/16/17 54
 HYPOTHYROIDISM

COMMON CAUSES
1) Hashimotos thyroiditis
2) Iatrogenic:
Thyroidectomy and
radioiodine therapy 5.
6.
Infiltrative diseases
Transient hypothyroidism
7. Congenital thyroid agenesis
3) Iodine deficiency 8. Subclinical hypothyroidism

(endemic goiter)
4) Drugs

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HYPOTHYROIDISM

COMMON CAUSES
1) Hashimotos
thyroiditis
2) Iatrogenic: most common cause of hypothyroidism in areas of the world in which dietary
iodine is sufficient.
Thyroidectomy It usually presents with goiter, hypothyroidism, or both. Goiter usually develops
gradually.
and radioiodine The diagnosis of Hashimotos thyroiditis is confirmed by the presence of
thyroid autoantibodies, including thyroid peroxidase (TPO) antibody &
therapy thyroglobulin antibody

3) Iodine deficiency
(endemic goiter)
4) Drugs

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HYPOTHYROIDISM

COMMON CAUSES
1) Hashimotos
thyroiditis
2) Iatrogenic:
Thyroidectomy Thyroidectomy and radioiodine therapy or external irradiation for treatment of
and radioiodine carcinoma, hyperthyroidism, or goiter can lead to hypothyroidism.

therapy
3) Iodine deficiency
(endemic goiter)
4) Drugs:

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HYPOTHYROIDISM

COMMON CAUSES
1) Hashimotos
thyroiditis
2) Iatrogenic:
Thyroidectomy almost always occurs in areas of environmental iodine deficiency.
The incidence of endemic goiter has been greatly reduced by the introduction
and radioiodine of iodized salt.

therapy
3) Iodine deficiency
(endemic goiter)
4) Drugs:

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HYPOTHYROIDISM

COMMON CAUSES
1) Hashimotos
thyroiditis
2) Iatrogenic:
Thioamides
Thyroidectomy Lithium
amiodarone
and radioiodine Interferon
interleukin-2
therapy
3) Iodine deficiency
(endemic goiter)
4) Drugs:

5/16/17 59
HYPOTHYROIDISM

COMMON CAUSE
5. Infiltrative
diseases
6. Transient
hypothyroidism Fibrous thyroiditis
Hemochromatosis
sarcoidosis
7. Congenital
thyroid agenesis
8. Subclinical
hypothyroidism

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HYPOTHYROIDISM

COMMON CAUSE
5. Infiltrative
diseases
6. Transient
a period of reduced free T4 with suppressed, normal, or elevated TSH levels
hypothyroidism that are eventually followed by an euthyroid state.
This form of hypothyroidism usually occurs in the clinical context of subacute
(postviral) thyroiditis, lymphocytic (painless) thyroiditis, or postpartum
7. Congenital thyroiditis.

thyroid agenesis
8. Subclinical
hypothyroidism

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HYPOTHYROIDISM

COMMON CAUSE
5. Infiltrative
diseases
6. Transient
hypothyroidism Agenesis
Dysgenesis
or defect in hormone synthesisidism.
7. Congenital
thyroid agenesis
8. Subclinical
hypothyroidism

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HYPOTHYROIDISM

COMMON CAUSE
5. Infiltrative
diseases
6. Transient
hypothyroidism defined as a normal serum free T4 concentration and a slightly high serum TSH
concentration.
These patients usually have nonspecific symp-toms and a substantial
7. Congenital proportion of them eventually develop overt hypothyroidism.

thyroid agenesis
8. Subclinical
hypothyroidism

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HYPOTHYROIDISM

LABORATORY
FINDINGS
Laboratory confirmation of the diagnosis
TSH & FT3 of hypothyroidism consists of measuring
serum TSH and free T4.
Primary hypothyroidism: serum TSH
concentration & free T4 concentration.
Secondary hypothyroidism: serum TSH
concentration as well as serum T4
concentration.

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HYPOTHYROIDISM

LABORATORY
FINDINGS Total T4, RAIU, and free T4 index are
usually decreased in hypothyroidism, but
T4 they are less sensitive than TSH and free
RAIU T4 measurement.
Antithyroid peroxidase (TPO) antibodies
FT4i are detected in almost all patients with
Hashimotos disease and its variants, in
70% of patients with Graves disease, and
Anti-TPO in a smaller number of patients with
various other thyroid disorders such as
MNG, nontoxic goiter, and thyroid
carcinoma.

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GOITER AND THYROID NODULES

OVERVIEW
enlargement of thyroid gland.
It can be classified in different
ways.
Toxic goiter refers to goiter with
hyperthyroidism.
Nontoxic goiter refers to enlarged
thyroid gland with normal or low
thyroid hormone levels.
A thyroid nodule is defined as a discrete lesion within the thyroid gland that is
due to an abnormal focal growth of thyroid cells.

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GOITER AND THYROID NODULES

COMMON CAUSES I. Diffuse enlargement of the

thyroid gland is seen in the
following conditions:
Diffuse toxic goiterGraves disease;
most common cause of endogenous
hyperthy-roidism
Diffuse nontoxic (simple) goiter
relative deficiency of thyroid hormone
Hashimotos thyroiditis
Organification defect (abnormality in
the incorporation of iodine into thyroid
hormone precursors)

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GOITER AND THYROID NODULES

COMMON CAUSES
II. Nodular enlargement of the
thyroid gland is seen in the
following situations:
A. Benign solid nodule
Hyperplastic (or colloid) nodule
Follicular adenoma
B. Malignant tumors
Thyroid carcinomas, including
papillary, follicular, anaplastic,
and medullary carcinomas

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GOITER AND THYROID NODULES

COMMON CAUSES

II. Nodular enlargement of the

thyroid gland is seen in the
following situations:
C. Multinodular goiter can
present with or without
thyrotoxicosis.
D. Simple cyst

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GOITER AND THYROID NODULES

COMMON CAUSES

II. Nodular enlargement of the

thyroid gland is seen in the
following situations:
C. Multinodular goiter can
present with or without
thyrotoxicosis.
D. Simple cyst

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GOITER AND THYROID NODULES

LABORATORY
FINDINGS
TSH
1. Serum TSH should be measured in any patient with a goiter or
nodules. It may be used as a first-line screening test. In
multinodular goiter, TSH usually is in normal or low-normal range;
it is rarely increased.
2. Calcitonin level in virtually all patients with clinical medullary
carcinoma. However, it is not cost-effective or necessary in patients
without clinical suspicion due to rarity of the disease and high
frequency of false-positive results.

CALCITONIN

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GOITER AND THYROID NODULES

LABORATORY
FINDINGS
Anti-TPO
Anti-TGB
3. Measurement of serum antithyroid peroxidase antibody &
antithyroglobulin antibody levels may be helpful in diagnosis of
chronic autoimmune thyroiditis, especially if the serum TSH level is

4. Fine-needle aspiration (FNA) biopsy of the nodule is the most time-
and cost-effi cient evaluatio

FNA

5/16/17 RDN PAKASI - UNHAS TEACHUNG HOSPITAL, MAKASSAR 72

 THANK YOU

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