Transcript HIPOTIROIDISMUL

HYPERTHYROIDISM
(THYROTOXICOSIS)
THYROTOXICOSIS &
HYPERTHYROIDIDM
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Thyrotoxicosis = the clinical sdr that results when
tissues are exposed to high levels of circulating
TH
Hyperthyroidism = the manifestations result from
overproduction of hormone by the thyroid gland
itself
Classification of Thyrotoxicosis
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Thyrotoxicosis with Hyperthyroidism
Grave’s disease
Toxic multinodular goiter
Toxic adenoma
Iodine-induced (Jod-Basedow)
TSH-secreting pituitary adenoma
Thyrotoxicosis without Hyperthyroidism
Thyrotoxicosis factitia (← iatrogenic or voluntary ingestion of ↑ T4 or TH
preparation )
Subacute thyroiditis
Thyroiditis with transient thyrotoxicosis
(silent, postpartum thyroiditis, Hashytoxocosis)
Ectopic thyroid tissue (struma ovari )
Forms of hyperthyroidism
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BASEDOW-GRAVES’ DISEASE
 the most common form of thyrotoxocosis
 =diffuse goiter, thyrotoxicosis, infiltartive ophtalmophathy +/_ infiltrative
dermopathy (5-10%)
 Is an autoimmune disease of unknown cause
 Pathogenesis : the major atg of Grave’s disease is TSH-R
 T- Ly become sensitized to atgs within the thyroid gland and (+) B-Ly to
synthesize antibodies (Abs ) to these antigens; TSHRAbs (Abs directed
against the TSH rec- the thyroid cell membrane = TSI )→ thyroid growth, ↑
vascularity, ↑ rate of thyroid hormone production and secretion
1.
! There is an underlying genetic predisposition, but it is not clear what “
triggers “the acute episode
Some factors that may incite the acute episode : psychological stress,
pregnancy, particularly the postpartum period
FORMS OF THYROTOXICOSIS
2. TOXIC ADENOMA (Plummer’s disease)
= a functioning adenoma hypersecreting T3, T4; these
lesions start out as a small autonomously functionig nodule that
slowly increases in size to produce excessive quantities of
TH→gradually suppresses endogenous TSH secretion → reduced
function of the contralateral lobe of the gland
Pathogenesis: several mutations in the TSH-rec gene →
constitutive activation of the TSH rec in the absence of TSH
 The tipical patient is an older individual (usually> 40)
 tyrotoxicosis + palpable /not palpable thyroid lump
 The cardiovascular manifestations may be prominent;
infiltrative ophatalmopathy or dermopathy are never present!!!
 Physical examination reveals a definite nodule on one side, with
very little thyroid tissue on the other side
FORMS OF THYROTOXICOSIS
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3. TOXIC MULTINODULAR GOITER
Usually occurs in older patients with long standing euthyroid multinodular goiter,
from which it emerges slowly ; the increase in the extent of autonomous function
cause the disease to move from the nontoxic to the toxic phase
Physical examination : reveals a multinodular goiter + manifestations of
hyperthyroidism, without signs of autoimmunity
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→ older individuals
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4. IODINE-INDUCED HYPERTHYROIDISM
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→ adm. of supplemental iodine to subjects with endemic iodine deficiency goiter →
in iodine-induced hyperthyroidism and even Grave’s disease
Causes :amiodarone ( contains 37% iodine), coronarography , IVU, CT (
radiographyc contrast media)
Thyrotoxicosis + diffuse or multinodular goiter
Confirmation that the patient has been exposed to large quantities of iodine :
↓ RAIU
↑urinary iodine excretion (>several mg/day)
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5. TSH-SECRETING PITUITARY ADENOMA
rare
goiter + hyperthyroidism
FORMS OF THYROTOXICOSIS
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6. SUBACUTE AND SILENT, POSTPARTUM
THYROIDITIS
mild→ severe thyrotoxicosis, following an acute release of
T4, T3 into circulation
!!! These illness can be differentiated from others forms of
thyrotoxicosis in that RAIU is ↓↓ and the symptoms usually
subside spontaneously over a period of weeks or month
7. STRUMA OVARY
A teratoma of the ovary contains thyroid tissue that becomes
hyperactive
! No goiter or eye signs
RAIU over the neck is ↓; total body scan reveals uptake of I131 in the
pelvis
Clinical features
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Effects on – cardiovascular system, CNS, gastrointestinal tube , neuromuscular system, lipid,
protein, carbohydrate metabolisms
1.GENERAL MANIFESTATIONS
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The stimulation of energy metabolism and heat production is reflected in the ↑ basal metabolic rate. ↑
appetite and heat intolerance and in a sometimes slightly elevated basal body temperature ( 3737.5°C), sweating
2. Nervous system
Alterations in NS function are manifested by:
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Emotional lability, nervousness, irritability
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Insomnia, restlessness, shortness of attention span
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Fine, rhytmic tremor of the hands, tongue, or slightlly closed eyelids
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Hyperkinesia
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hyperreflexia (  an increase in the speed of muscle contraction and relaxation)
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3. CARDIOVASCULAR SYSTEM
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! TH have marked positive inotropic and chronotropic effects on the heart → accounts for the increased
cardiac output and ↑↑ in heart rate in hyperthyroidism; TH increase the number of beta-adrenergic receptors
in heart muscle ( and also skeletal muscle, adiposse tissue)  the most common complaints:
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palpitations
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tachycardia is almost always present.
heart sounds are loud and ringing; functional systolic murmurs may also be heard in different areas
of ausculatation (mostly at the apex) (usually abate when a normal metabolic state is restored)
cardiac arrhythmias are almost invariably supraventricular (extrasistolia, atrial fibrillation, paroxysmal
supraventricular tahycardia, )
widening of pulse pressure ( ↑ systolic TA ← ↑cardiac output; ↓ diastolic pressure  ↓ peripheral
vascular resistance )
hyperkinetic cardiovascular syndrome ↑ cardiac output , ↑ heart rate ( ↑ TA) and ↓peripheral
vascular resistance → ↓diastolic pressure
Clinical features
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4. DIGESTIVE MANIFESTATIONS
 An increase in appetite but with weight loss( ← because of the
increased basal metbolic rate)
 TH (+) gut motility increased motility ( stools are frequently soft ,
but diarrhea is rare)
 Hepathic dysfunction occurs, particularly when thyrotoxicosis is
severe
5. MUSCULAR EFFECTS
! Although TH (+) increased synthesis of many structural proteins, in
hyperthyroidism there is increased protein turnover and loss of
muscle tissue or myopathy
 Weakness and fatigability ; weakness is most prominent in the
proximal muscles of limbs, causing difficulty in climbing stairs ( “ chair
sign”)
 In severe untreated cases, muscle wasting (proximal) develops out of
proportion = thyrotoxic myopathy
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6. ENDOCRINE manifestation
 Menstrual abnormalities: ovulation may be impaired, oligomenorrhea,
secondary amenorrhea
 In M: erectile dysfunction, gynecomastia
Clinical manifestations
7. EYES
Retraction of the upper eyelid that lead to widening of the palpebral
fissure so that the sclera are exposed above the superior margin of
limbus (  adrenergic stimulation of the upper eyelid)= common in all
forms of thyrotoxicosis, regardless of the underlying cause and is
responsible for the bright-eyed “ stare” of the patient with
thyrotoxicosis
Lid lag= the upper lid lags behind the globe when the patient is asked to
gaze slowly downward
Globe lag= when the globe lags behind the upperlid when the patient
gazes slowly upward
A fine tremor of the lightly closed lids can often be observed=
Rosenbach’ s sign
= Class 1 (O) of the Werner’s classification of eye signs in Graves’
disease
! These ocular manifestations appear to be the result of ↑ adrenergic
activity. It is important to differentiate these ocular manifestations,
which occur in all forms of thyrotoxicosis, from those of infiltrative
orbitopathy, which are characteristic of hyperthyroid Graves’ disease.
These manifestations will often abate when the thyrotoxicosis is
relieved.
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Clinical features
8.SKIN and HAIR
- warm, moist, pink skin (← cutaneous vasodilatation and excessive sweating);
the patient blushes readily
The hair is fine and friable and hair loss may be excessive; the nails are often
soft and friable
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ASSOCIATED DISEASES
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DM Type 1
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CSR I
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vitilligo, celiac disease, myastenia gravis
Goiter
 Graves’ disease– the goiter is diffuse and usual symmetrical; the consistency
varies from soft to firm and rubbery; the surface is generally smooth; in severe
cases, a thrill may be felt, usually over the upper poles, and a thrill is always
accompanied by an audible bruit ( the thrills and bruits  ↑ blood flow and are
usually continuous but sometimes are present only in systole)
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Toxic adenoma ; a firm nodule on one side with little thyroid tissue on the other
side
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Toxic multinodular goiter – multinodular goiter that may be small or quite large
and may even extendly substernally; consistency: firm the surface:
inhomogeneous
Clinical features
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INFILTRATIVE ORBITOPATHY of GRAVES’DISEASE
precedes, follows or its onset is simultaneous with
thyrotoxic manifestations
 More frequently in women
 More severe in men
 bi/unilateral, symmetrical / asymmetrical
Clinic : irritation in the eyes, excessive tearing that is often
made worse by exposure to air or wind, exophtalmos,
periorbital edema, double vision, photophobia…
Pathogenesis: the extraocular muscle and adipose tissue are
swollen by the accumulation in the extracellular matrix of
GAG that are secreted by fibroblasts under the influence of
citokines from local Ly, sensitized to a common antigen
such as the TSH-Rec ( that is found in orbital fibroblasts,
orbital muscle and thyroid tissue) . This accumulation
disrupts and impairs the function of muscle  diplopia and
leads to proptosis; proinflammatory citokines also 
redness, congestion and conjunctival and periorbital
edema. As the disease runs its course and inflammation ↓,
the damaged muscle become fibrosed.
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Clinical features
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WERNER’S CLASSIFICATION OF EYE CHANGES IN GRAVE’S DISEASE
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class 0 (N) : no signs or symptoms
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class 1 (O) – only signs, no symptoms ( signs limited to upper lid retraction, stare, lid lag,
globe lag…)
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class 2 (S) :soft tissue involvement:periorbital edema, irritation in the eyes, excesive
tearing, conjunctival congestion or edema (chemosis), enlarged lacrimal glands ; proptosis
<22mm
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Class 3 (P): proptosis >=22mm
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Class 4 (E)– extraocular muscle involvement diplopia; ophtalmoplegia (especially of
upward gaze← affection of the inferior rectus); weakness of the extraocular muscles is
evident in the patient’s inability to achieve or maintain convergence.
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Class 5 (C) – corneal involvement (keratitis) due to inability to close the eyes completely
=lagophthalmos ( proptosis >32mm),
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Class 6 (S) – sight loss (optic nerve involvement) ← likely due to ischemia of the nerve
from compression of the surrounding enlarged extraocular muscles
Clinical features
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!Classes 2-6 represents true infiltrative disease involving orbital
muscle and orbital tissues and are specific to Graves’ disease.
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INFILTRATIVE DERMOPATHY (PRETIBIL MYXEDEMA)
Rare
Hyperpigmented, nonpitting induration of the skin of the legs,
commonly over the pretibial area
Laboratory findings
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1. HORMONAL ASSESSEMENT
 TSH/↓↓, T3, T4 (FT4) (FT4 =the unbound portion, is the active part)
 exception: TSH-secreting pituitary adenoma: ↑ TSH, FT4↑
2. IMAGISTIC INVESTIGATIONS
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Thyroid ultrasonography
 Graves’ disease – diffuse thyroid hypertrophya, homogenous aspect;
hipoechoic
 Toxic adenoma/toxic multinodular goiter– one nodule/ enlarged gland that is
diffusely inhomogeneous with multiple individual nodules
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RAIU
– ↑ values in thyrotoxicosis with hipertiroidism (2h-10-15%, 24h-45-50%)
↓ values in subacute thyroiditis or “ silent thyroiditis”, iodine-induced
hyperthyroidism
 131I
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THYROID SCINTHYGRAPHY ( RADIOIODINE SCAN)
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Graves’disease – enlarged gland that is usually rather symmetric with a
typically very homogenous distribution of tracer
Toxic adenoma – a “ hot “ nodule with ↓ or absent function of the contralateral
lobe
Toxic multinodular goiter – multiple functioning nodules in the gland or
occasionally an irregular, patchy distribution of radioactive iodine
Laboratory findings
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3. OTHERS
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glycemia normal, IGT, DM
  cholesterol
n/  AF
ECG – sinus tachycardia, AF, SVT, LVH
TRAbs(+) –are relatively specific to Graves’ disease; useful in
patients who presents with unilateral or bilateral exophtalmos
without obvious signs or laboratory manifestations of Graves’
disease; useful indicator of the degree of disease activity and the
level of TRAbs correlates with the severity of the eye disease
TPO Abs and TG Abs are usually present in both Graves’
disease and Hashimoto thyroiditis
ULTRASONOGRAPHY, CT and MRI scan of the orbita : reveal
extraocular muscle enlargement in most patients with Graveas’
disease
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Complications
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THYROTOXIC CRISIS (“ THYROID STORM”)
 = the acute exacerbation of all of the symptoms and signs of thyrotoxicosis; lifethreatening
 Fever (38-41ºC), cardiac arrhythmias , heart failure, diarrhea, vomiting, marked
agitation, delirium, coma
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THYROTOXIC CARDIAC INVOLVEMENT (CARDIOTHYREOSIS)
 cardiac arrhythymias– AF
 Heart failure
 Myocardial ischaemia
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THYROTOXIC MYOPATHY
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THYROTOXIC OSTEOPOROSIS
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DIABETES MELLITUS
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THYROTOXIC HEPATHOPATHY
 Hepatic dysfunction occurs particularly when thyrotoxicosis is severe – jaundice,
hepaomegaly, ↑ ALT
TREATMENT OF HYPERTHYROIDISM
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! Although autoimmune mechanisms are responsible for the syndrome
of Graves’ disease, managements has been largely directed toward
controlling the hyperthyroidism
Methods of treatment;
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1. Medical treatment- Antithyroid drug therapy
2. Surgery
3. Radioactive iodine therapy
TREATMENT OF HYPERTHYROIDISM
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Medical treatment
Anthithyroid drugs (ATS)
Mechanisms of action:
 ( - ) TPO-mediated iodination of Tg to form T4,T3 within the thyroid gland
 PTU (but not methimazole ) blocks peripheral T4  T3 conversion
 both drugs may have immunosuppressive effects that may be
responsible for the remission from the disease that some patients have
after 1-2 years of treatment
 THIONAMIDE CLASS
 I. THIOURACIL DERIVATES
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METYLTHIOURACIL (50 mg/tb)
PROPYLTHIOURACIL (PTU)(50 mg/tb)
II. IMIDAZOLE DERIVATES
TIAMAZOLE (THYROZOL) 5mg/tb
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CARBIMAZOLE 5mg/tb
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Initial dose - 6-12 tb/day ( 30-60 mg/ day of thyrozole)
Maintenance dose- 1-3 tb/day
SE : rash, agranulocytosis(= indication for discontinuing the
medication), cholestatic jaundice with tiamazole and hepatocellular
toxicity with PTU , drug-induced hypothyroidism with an ↑ of goiter(
← ↑ of TSH secretion)  adding T4 supplements to prevent the
patient from becoming hypothyroid
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TREATMENT OF HYPERTHYROIDISM
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Surgical treatment
Indications:
Postdrug relapse of Graves’ disease
Very large, compressive glands or multinodular goiters
Toxic adenoma in youth
Patients who are allergic to or noncompliant with ATS
 subtotal or total thyroidectomy
 The patient is prepared with ATS until euthyroid ( about 6 weeks);
in addition, starting 2 weeks before the day of operation,
saturated solution of potassium iodide (SSKI) or Lugol’s solution
(3* 3drops daily → 3* 15 drops/day ) is added  will diminish the
hyperplasia and hypervascularity of the gland (the gland usually
becomes firm) and simplify surgery
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Complications of surgery: hypothyroidism, hypoparathyroidism,
reccurent laryngeal nerve injury
TREATMENT OF HYPERTHYROIDISM
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Radioactive iodine therapy
Indications:
Toxic adenoma, toxic multinodular goiter
Allergy to or nonresponse to ATS
Contraindications to surgery
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3-10 mCi 131I
Following the administration of radioactive iodine (which typically is
giving orally as a single capsule) the gland will shrink and the patient will
usually become euthyroid over a period of 2-6 months
SE :
Hypothyroidism is the almost inevitable complication of radioactive iodine
therapy ( > 80%)
Severe Grave’s eye disease is a contraindication to radioiodine therapy;
several prospective studies have shown that that radioiodine can
exacerbate eye problems when they are severe at baseline; however,
potential worsening can be prevented by administration of prednisone
40-60mg/day for 1-2 months (gradually tapering the dose) following the
radioiodine treatment
Treatment of hyperthyroidism
Other medical measures
 Rest
 Beta-adrenergic blocking agents : propranolol
10-40mgevery 6 hours or longer acting beta-blockers :
metoprolol, atenolol control many adrenergic
symptoms, tachycardia, hypertension, FA
 Sedatives
 multivitamins
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Treatment of infiltrative orbitopathy
Symptomatic treatment : ( useful mainly in mild forms)
dark glasses ( for those with photophobia, sensitivity to
wind or cold air), artificial tears
 Glucocorticoids : prednisone 50-60mg/day, tapering
the dose 10mg every 2 weeks
intravenous methylprednisolone pulse
therapy 1g/day for 3 days- in severe cases ( the
advantage of fewer SE than high doses of prednisone)
External radiation to the retrobulbar area
- The dosage is usually: 1000 cGy/ orbit in 10 fractions
given over a period of 10 days
- → if corticosteroid therapy is not effective or
contraindicated
The best results are obtained by combining these 2
therapies ( glucocorticoids + external x-ray therapy)
Surgical orbital decompression can be used in very
severe cases when vision is threatened
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HYPOTHYROIDISM
Hypothyroidism
= a clinical syndrome resulting from a deficiency of
TH, which in turn results in a generalized slowing
down of metabolic processes
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Classification:
I – according to etiology;
a)
Primary (thyroid failure)-by far the most common
b)
Secondary (due to pituitary TSH deficiency)
c)
Tertiary (due to hypotalamic deficiency of TRH)
d)
Peripheral resistance to the action of TH
II – according to the presence of goiter
Hypothyroidism –with goiter
- without goiter
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Etiology of primary hypothyroidism
Primary hypothyroidism with goiter
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1. CONGENITAL
Inherited defects in hormone biosynthesis (thyroid dyshormonogenesis) (e.g.
Pendred sdr = a defect in iodine organification+ sensory nerve deafnes)
 Endemic cretinism
2. ACQUIRED
 Hashimoto’s thyroiditis=by far the most common cause
 Iodine deficiency (endemic goiter)
 Excessive iodide intake (radiocontrast dye, amiodarone)
 Cytokines: interferon alfa (used to treat hepatitis C)
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Primary hypothyroidism (atrophic)
1. CONGENITAL
 Thyroid agenesia
 Ectopic thyroid( lingual thyroid)-functions poorly ( absence of thyroid tissue or its
ectopic location can be ascertained by scintiscanning!)
2. ACQUIRED
 Hashimoto’s disease
 Postablative due to 131 I (radioactive iodine therapy), surgery
Transient (Post-thyroiditis ) hypothyroidism
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Subacute thyroiditis
Postpartum, silent thyroiditis
Hypothyroidism- pathogenesis
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TH deficit in infants and children results in marked
slowing of growth and development, with serious
permanent consequences, including mental retardation,
when it occurs in infancy. Hypothyrodism with onset in
adulthood a generalized ↓in metabolism, with slowed
heart rate, diminished oxygen consumption, and
deposition of GAG in intracellular spaces,
particularly in skin, heart muscle and striated
muscle, producing in extreme cases the clinical
picture of myxedema.
Clinical features
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Insidious onset
The common features of moderate- severe hypothyroidism include:
 fatigability
 Skin and appendages: cool, rough, dry, pale skin; cold sensitivity ;
puffy face, hands and feet( ←non-pitting edema)→ ”pale moonlike face” or “”toad-like face”; reduced conversion of carotene to
vit A may give the skin a yellowish color; macroglossia ;large lips
 head and body hair is dry and brittle and tends to fall out; hair
may be lost from the temporal aspects of the
eyebrows=Herthoge’s sign; the nails are brittle and grows sloly
 Digestive manifestations
 Constipation,
 ↓appetite,
 Modest gain in weight (generally <10-20pounds)
 Neuromuscular system: Numbness and tingling of the extremities,
muscle cramps, muscle weakness
 Central and peripheral NS :all intelectual functions, including
speech, are slowed; loss of initiative, memory deficits, lethargy
and somnolence are present; psychiatric disorders are common:
depression or even agitation (“myxedema madness”) ; slow
reflexes
Hearing loss
Thick, slurred speech, hoarseness
Clinical features
Reproductive function
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Excessive menstrual bleeding , menorrhagia , failure of ovulation,
↓fertility, galactorrhea
↓libido, impotence, oligospermia
Cardiovascular signs
→ impaired ventricular contraction, bradycardia, ↑peripheral
resistance resulting in ↓cardiac output, narrowing of pulse
pressure
convergent BP formula (TAd=90-100mm Hg ←↑ systemic vascular
resistance) ; heart sounds are diminished in intensity
Cardiac enlargement ← interstitial edema, left ventricular dilatation,
(nonhemodynamically significant) pericardial effusion
Pulmonary function
dyspnea
obstructive sleep apnea
Renal function
-is impaired , with ↓ glomerular filtration rate and impaired ability
to excrete a water load
Clinical features
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Hashimoto’s thyroiditis may associate other autoimmune disorders
 Endocrine
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CSRI (with adrenal autoantibodies), gonadal
insufficiency , DM type I (with islet cell antibodies0
Non-endocrine
vitiligo, pernicious anemia, alopecia
=Schmidt’s syndrome
These conditions are part of what has been termed
“autoimmune polyglandular syndrome”
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HYPOTHYROIDISM-Diagnosis
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1. Hormonal determinations
 Basal
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Dynamic tests – TRH test →in diagnosis of Central H for assessment
of TSH pituitary reserve ( give protirelin (TRH) 200-400 µg iv; blood
for determination of plasma TSH is obtained at 0’ and 60’)
normal response: ↑TSH > 2 * baseline value
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Primary H – the combination of TSH , T3, T4
(FT4)=diagnostic
Central H – TSH/low-normal, T3, T4(FT4)
anti-Tg antibodies, anti-TPO antibodies =↑ in Hashimoto’s
thyroiditis
In central H – no response/ subnormal response
In primary H – an exaggerate TSH response
2. Imagistic findings
 Thyroid ultrasonography – thyroid volume: normal, ↑, ↓; an
hypoechogen aspect in Hashimoto’s thyroiditis is usually present
 RAIU + Thyroid scintigraphy – usually employed for assessing inherited
defects in hormone biosynthesis or thyroid agenesia, ectopic thyroid
HYPOTHYROIDISM-Diagnosis
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Serum cholesterol and tryglicerides 
Anemia: usually –mild normocytic, normochromic anemia ← impaired
hemoglobin synthesis/ macrocytic anemia←folate deficiency from
impaired intestinal absorption of folic acid, pernicious anemia,
with vit B12-deficient megaloblastic anemia/ microcytic,
hypochromic anemia← increased iron loss with menorrhagia,
defective absorption of iron resulting from achlorhydria
Creatine phosphokinase (CPK), AST, LDH ← abnormal muscle
membranes (the source is skeletal muscle)
ECG
 Low-voltage of QRS complexes and P and Twaves (with
improvement in response to thearpy)
 Prolongation of the QT and PR intervals
 Sinus bradycardia; rarely complete heart block
 alterations of the ST segment and flattened or inverted Twaves
Thoracic X-ray
 Cardiac enlargement
Echocardiography
 Effusion into the pericardial sac
Complications
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1.Mixedema coma: the end stage of untreated hypothyroidism; it is characterized by
progressive weakness, stupor, hypothermia (T< 35 ºC), hypoglycemia, hyponatremia,
hypoventilation and it may ultimately result in shock and death
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2. Mixedema cardiomyopathy → congestive heart failure
 ECG – bradycardia, prolongation of the QT and PR intervals, AV block
 Echocardiography – cardiac hypertrophy, then ventricular enlargement with  EF
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3. Mixedema pericarditis ( pericardial effusion is rarely of sufficient magnitude to cause
tamponade)
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4. Coronary artery disease- likely related to ↑ levels of total cholesterol, LDLcholesterol
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5. Myopathy
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6. In newborn infants – impairment of linear growth results in dwarfism with the limbs
disproportionately short in relation to the trunk +retardation of mental and physical
development  ! The importance of routine screening of newborns for TSH or T4 because
early diagnosis can prevent permanent mental retardation ( a drop of blood obtained by
heel stick 24-48h after birth is placed on filter paper; a serum T4< 6µg ‘dl or a serum
TSH>25 mU/l is suggestive of neonatal hypothyroidism; the diagnosis can then be
confirmed by repeat testing and radiologic evidence of retarded bone age)
Treatment of Hypothyroidism
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= replacement treatment- with T4, which is available in pure forms, and is
stable and inexpensive
Drugs
 L-T4 (Levothyroxine, Euthyrox) 50-100(200)microg/day with a mean of
125 µg/day ( because T4 is converted to T3 in peripheral tissues, both
hormone become available even though only one is administered); the
T1/2 of T4 is about 7days, so it need be given only once daily; before
breakfast for an optimal absorption
 ( L-T4/T3 (NOVOTHYRAL) 100 LT4 + 20T3/tb)
Considerations:
 Usually for life, with the exception of transient hypothyroidism (e.g.
subacute thyroiditis);
 The initial dose of levothyroxine prescribed depends on the degree of
hypothyroidism, the age and general health of the patient
 in most patients (young or middle- aged and otherwise healthy with no
associated cardiovascular or other abnormalities ), one can begin
treatment with the full estimated dose requirement
 in older patients or patients with underlying heart disease, it is best to
start with a low dose of T4 (eg 25 µg/day) and increase the dose slowly(
at 1-2 week intervals) until the full dose required with careful clinical
and laboratory evaluation ; association of beta-adrenergic blocking
agents is helpful
Treatment of Hypothyroidism
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The goal in the patient with primary
hypothyroidism is to return serum TSH
concentrations to normal; the serum TSH should
be evaluated 6 weeks after a theoretically completed
replacement dose has been instituted
In patients with central hypothyroidism serum
TSH is not a reliable index of adequate
replacement and the serum FT4 should be
restored to a concentration in the upper half of the
normal range. !such patients should also be
evaluated and treated for glucocorticoid deficiency
before institution of thyroid replacement
Monitoring replacement therapy: initially at 68weeks, then 2*/year