Transcript Thyroid Disordersx

Thyroid Disorders
T₃: Triiodothyronine
T₄: Thyroxine
I. Hyperthyroidism (Thyrotoxicosis)
• Characterized by hypermetabolism of all body
systems & increased serum levels of free
thyroid hormones.
• More common in women.
• Rare in children
• Less common than hypothyroidism
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Thyroid Storm:
Exaggerated form of hypertoxicosis.
Medical emergency Prompt treatment
May be precipitated by : -Infection
-Trauma
- Surgery
-Embolism
-Diabetic ketoacidosis
-Others…
• Subclinical Hyperthyroidism:
• Suppressed TSH level w/ NL thyroid hormone
levels.
• Symptoms are NOT always present esp. in
elderly.
• Pathophysiology: See p. 987-990
• Treatment Goals of Hyperthyroidism:
1) Reverse S/S, normalize thyroid hormone
levels, min. deleterious S/Es of T₄ on organ
systems, prevent thyroid storm, & improve
overall functional capacity.
2) Reverse hyperthyroid complaints.
3) Reverse hyperthyroid physical findings.
4) Normalize free T₄, T₃, & TSH levels.
5) Reduce goiter size.
6) Improve cardiac function & prevent systemic
embolism.
7) Preserve bone density& prevent osteoporosis.
8) Improve emotional well being& quality of life.
9) Support placenta development & maintenance
of pregnancy.
10) Promote normal growth, & physical &
mental development.
• Causes of Hyperthyroidism: (table38.3 p.993)
1) Graves disease: -Autoimmune
-May occur w/ other
autoimmune disorders.
-Most common cause
-Charact. by hyperthyroid. &
one or more of the
following: * Goiter
* Exophthalmos
* Dermopathy
2) Toxic Nodules: -Single & multinodular
-Autonomous: independent of
TSH control.
-May be caused by:
*Iodine deficiency
*Genetic abnormality
*Immune System
3) Subacute Thyroiditis:
- Inflammatory thyroiditis,
i.e.Postpartum(PPT), viral (i.e. de Quervain).
- Hyperthyroid. from leakage of thyroid
hormones into circulation due to inflamed
gland & NOT increased synthesis.
-Hypothyroidism may follow.
4) Drug Induced:
-Iodides (Jod-Basedow), Amiodarone, Lithium,
Cytokines
5) Neonatal thyrotoxicosis (Graves):
-Transplacental passage of TRab causing the
infant to be extremely ill w/in delivery hrs.
-Self-limiting.
6) Hashitoxicosis:
-Hyperthyroid phase of Hashimoto thyroiditis
7) T₃ toxicosis:
-Preferential secretion of T₃, often precedes
T₄ toxicosis.
8) Tumors:
-Secretion of thyroid stimulating substances.
9) Factitious:
-Self-administration of levothyroxine
• Clinical Presentation & Diagnosis:
- Characteristics of Graves Dz. p.997 Table 38.6
-SxS of Hyperthyroidism & Hypothyroidism
p.995 Table 38.4
- Thyroid Function Tests (TFTs) p.987-988
• Diagnosis of Hyperthyroidism :
1) Confirmed w/ abnormally high levels of FT₄
or TT₃ & undetectable TSH.
2) +Antibodies, opthalmopathy, or dermopathy
confirms the diagnosis of Graves.
3) RAIU in Graves but is NOT cost-effective
4) TT₃ & + TRab are essential for atypical
presentation, i.e. in elderly.
5) Subacute Thyroiditis (PPT,…), Diagnosis is
confirmed by:
*Low or undetectable RAIU.
* TH levels.
*Suppressed or undetectable TSH level.
* ESR
* No Thyroid Ab.
* Leukocytosis, gland tenderness, &
S/S of hyper or hypothyroidism.
• Therapeutic Plan: (table 38.7, p.998-999)
• Major Modalities for Management of
Hyperthyroidism, include:
1) Thioamides
2) RAI
3) Surgery
** Treatment must be individualized, each has
advantages & limitations
**Effective Treatment Selection p.1000, Fig.38.3
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Treatment Adjuncts:
Iodides
Iodinated Contrast Media
K Perchlorate
Adrenergic Antagonists
Corticosteroids
Cholestyramine
Rarely Li
• In U.S., RAI is most commonly used except in
younger pts. for whom Thioamides are used.
• In Europe & Japan, Thioamides are the TOC.
• Surgery is the last choice unless there is:
*Obstructive symptoms
or* Malignancy
• Treatment is individualized a/c to:
1. Etiology
2. Pt. age
3. Goiter size
4. Thyroid & Medical complications
5. Social & Economic issues
1. Graves: All 3 methods are effective but pt. or Dr. may
prefer meds. over RAI or surgery.
2. TMG: RAI or surgery > effective than meds.,
but factors as medical condition or pt.
or Dr. may prefer RAI use over surgery.
3.Transient Treatment : may be used when the
disease is self-limited, i.e.:
* Subacute Thyroiditis (PPT,…)
*Neonatal Graves
*Drug-Induced Hyperthroidism
• In Uncomplicated Graves esp. in children,
Thioamides are preferred until remission.
• Thioamides: - Do NOT destroy the gland
- Control the disease
- Chronic thyroid replacement
may not be necessary (not like
w/ RAI or Surg.), however,
hypothyroid. may still develop
eventually.
• If RAI or Surgery is selected, most older pts. &
all severely ill thyrotoxic pts. should be
pretreated w/ Thioamides.
• Pretreatment:
1) Depletes gland of stored hormones.
2) Hypermetabolic rate.
3) Prevents leakage of hormone from gland
after RAI or during surgery preventing thyroid
storm.
• Optimal Tx of hyperthyroidism in Graves opthalmopathy is
unresolved.
• Some prefer RAI or surgery (<desirable) to remove the antigen
source (gland) & > effective than thioamides to prevent
progressive opthalmopathy.
• Prophylactic systemic corticosteroid (e.g., Prednisone 3040mg daily starting within a few days of RAI & cont. for
~2-3 wks. to prevent further progression of opthalmopathy in
pts. w/ re-existing cases.
• Hypothyroidism can aggravate preexisting eye complaints.
• Hyperthyroidism control & hypothyroidism prevention are
essential to prevent progression of opthalmopathy.
• Single or Toxic multinodular Dz.:
• Best managed with definitive Tx, i.e. RAI or
surgery, because spontaneous remission is
unlikely.
• Hyperthyroid Children:
The usual Tx choices are Thioamides & subtotal
thyroidectomy, although all 3 methods have been
used.
• In Pregnancy:
• Hyperthyroidism is difficult to manage.
• Spontaneous remission may occur because of the
decrease in TRab.
• Antithyroid meds. are often NOT necessary.
• If untreated, complications may occur.
• RAI & Iodides are Contraindicated in pregnancy.
• Surgery in 2nd trimester is an option.
• Neonatal Graves:
• Infants extremely ill w/in delivery hrs.
• Supportive measures, i.e. *sedation
*O₂
*Fluids/Electrolytes
• Short-term (temporary) thioamides, iodides, or
beta blockers since it is self-limiting.
• Symptoms disappear in 1-2 months, therefore,
withdraw antithyroids at this time.
• Subacute Thyroiditis:
• Self-limiting (common spontaneous recovery).
• Symptomatic treatment: *Heat
*Rest
*NSAIDs
*Beta-blockers
* Thioamides are NOT effective since it is due to
thyroid hormone leakage & NOT increase in TH
synthesis.
• Cont. Subacute Thyroiditis:
• Corticosteroids are indicated for severe
inflammation if NSAIDs are ineffective.
• In Hypothyroid phase: Transient thyroid
replacement is used to suppress further TSH
stimulation to damaged gland & treat
hypothyroid symptoms.
• Treatment: Fig.38.3 p.1000
• Pharmacotherapy:
1) Thioamides:
*Long-term 1⁰ therapy for Graves esp. in children
& adolescents.
*Transiently used to reduce TH levels before
definitive therapy w/ RAI or surgery.
*TOC for small goiters & mild dz. For whom a high
remission rate is likely.
• Advantages:
• Potential for remission without gland damage.
• Limitations:
1.Non-adherence
2.Strict parental & physician supervision in kids.
3.Low success rates.
4. Risk of ADRs.
• Thioamides:
1. Methimazole
2. Propylthiouracil (PTU)
a. They prevent TH synthesis.
b. PTU (Not Methimazole) inhibits peripheral
deiodination of T₄ to T₃.
c. They suppress TSH receptor Ab level by
unknown immunosuppressive MOA.
• Thioamides Selection:
• Pharmacologic Differences:
** Methimazole is preferred over PTU, because:
1. Single daily dose ( PTU Q6-8H)
2. More potent than PTU
3. Less toxic than PTU @ low doses.
4. Less costly.
** Both are equally effective @ equipotent
doses.
• PTU is preferred over methimazole in pts. w/
**Thyroid Storm
Or **Severe Hyperthyroidism
Because:
1. PTU blocks the conversion of T₄ to T₃ peripherally.
2. PTU may have faster OA.
*PTU is preferred in pregnancy because methimazole may be associated w/
congenital skin defect ( NOT sufficiently supported & has been used in
pregnancy without deleterious effects).
*Both can be used safely in pregnancy
*PTU is preferred in lactation because insignificant amounts are secreted in
the breast milk.
*Generally, Methimazole is the thioamide of choice EXCEPT in the
situations mentioned above where PTU is preferred , or if the patient
cannot tolerate methimazole.
• No IV preparations of thioamides.
• It usually takes 6-8wks before SxS subside & TH
normalize.
• Initial dose:
Methimazole 30-40 mg/d orally
or PTU 300-400mg/d in 3-4 divided doses.
**Tapering down dose only after SxS subside:
**Initial dose is reduced gradually by 1/3 each
month until daily M.D. of 5-15mg methimazole
or 50-150mg PTU is reached.
• Baseline FT₄ & WBC count w/ differ. should be done
before thioamides are started because
agranulocytosis can be induced by thioamides &
also hyperthyroidism is associated w/ relative
reduction of neutrophils.
• FT₄ or FT₄I & TSH should be monitored routinely @
4-8 wks after starting Tx & after any dose change.
• Once stable thioamide M.D. is reached, TFTs should
be monitored Q 2-4 or Q3-6 months.
• Recommended duration of Tx for Graves is emperic:
Generally 12-18 months.
• 12 months is the minimum Tx duration
recommended to maximize remission potential.
• Longer durations can be used if NO ADRs.
• Some pts. remain in remission & others relapse
????
• Toxic Reactions:
1) Pruritic Maculopapular Skin Rash:
Most common & treated w/ antihistamines.
2) Hepatatis:
*If LFTs normalize w/in 3 months of dose
reduction, NO need to discontinue PTU.
*If there is clinical evidence of hepatitis,
D/C PTU immediately.
* Routine monitoring of LFTs is required for:
1. Pts. w/ liver dz. history.
2. Hepatitis risk factors, i.e. alcoholism
3) Hypoprothrobinemia (w/ PTU):
* Rare
* Recovery may occur after D/C of PTU,
if not start steroids.
4) Agranulocytosis (PMNs<500):
*Most serious but rare.
* Likely to occur during the 1st 6 wks of Tx.
* Complete recovery is seen a few days to 3 wks
after D/C of thioamide.
* Granulocyte colony-stimulating factor &
corticosteroids may shorten the recovery period.
2) K Perchlorate:
MOA: Interferes w/ Iodine binding causing discharge of
non-organified iodide from the gland.
*Especially useful for the short-term management of
drug-induced hyperthyroidism because it is competitive
inhibitor of iodide, but its antithyroid effect can be
overcome by iodine administration.
*Short-term adm. (2-6wks) is well tolerated.
*Limited use of chronic Tx is due to:
1) Irreversible aplastic anemia
2) Nephrotic syndrome
3) Iodides:
*Clinical use superseded by thioamides & beta
blockers.
*MOA:
1)Inhibit iodide organification (Wolf-Chaikoff).
** 2)Inhibit TH release (Rapid Sx relief in 2-7d)
3)Decrease gland vascularity.
*Rapid effect is beneficial for:
1. Thyroid storm
2. Pts. awaiting thioamide onset
• Iodides are NOT to be given before RAI
because iodides block effective RAI retention
by the gland for several wks. after use.
• Iodides are given 10-14days before surgery
to:
1. Reduce vascularity
2. Increase firmness of hyperplastic gland
to facilitate surgical removal.
• Preoperatively:
Iodides+ Thioamides Comb. ( Preferred )
Iodides + Beta Blockers Comb.
All 3 of them could be used.
• Major S/Es of Iodides:
1. Hypersensitivity reactions
2. Hyperthyroidism ( from failure of Wolff-Chaikoff
block)
3. Hypothyroidism ( unable to escape from WolfChaikoff)
4. Chronic adm. in pregnancy
fetal goiter & asphyxation
• Advantages of Iodides:
1. Simplicity
2. Low cost
3. Low toxicity
4. No gland destruction
• Limitations:
1. Escape
2. Tx relapse
3. Allergy
4. Interference w/ subsequent RAI therapy
4) Adrenergic Blockers:
**Depletes or blocks the effects of TH on tissue
catecholamines Rapid symptomatic relief
before thioamides, RAI, or
surgery.
*Do NOT affect underlying dz.
*Are NOT used as primary therapy
*Propranolol  Standard & most widely used
(20-40mg TID or QID)
• Severe toxemia may need up to 480mg/day
• Symptoms relieved by beta-blockers include:
*palpitations
*tachcardia
*anxiety
*sweating
*tremor
*diarrhea
*Neuromuscular manifestations
• Symptoms NOT affected by beta-blockers include:
*circulating TH
*Wt. loss
*goiter
*O₂ consumption
*exophthalmos
• Beta-blockers are used as adjunct Tx w/ thioamides
or RAI for:
*Neonatal thyrotoxicosis
*Hyperthyroidism in pregnancy
*Thyroid storm
*Pre-operatively
• Only used for short term in pregnancy because
chronic use in pregnancy esp. 3rd trimester &
lactation should be avoided due to fetal
complications.
• Calcium Channel Blockers
esp. Diltiazem p.o. 120mg TID or 60mg QID
may be used as alternative to beta blockers
when contraindicated, i.e. asthma or DM1
5) RAI: Radioactive Iodine)
*Indicated for:
1. Post-adolescent hyperthyroid patients
2. Graves opthalmopathy
3. Hx of thyroid surgery
4. Poor surgical candidates
5. Who fail or experience thioamide toxicity
6. TOC for older patients w/ cardiac dz
or those w/ TMGs (Toxic Multinodular Goiter)
**I₁₃₁ isotope is the most commonly used
**Absolute contraindication in pregnancy: destroys the fetal
gland .
• RAI dosage is calculated using a certain formula.
• RAI pts. should be pretreated w/:
*thioamides to deplete the gland of the stored TH
Or*beta blockers or Ca channel blockers
before & after RAI to prevent exacerbations of
thyrotoxicosis w/in 10-14days after RAI due to leakage
of TH after RAI.
*Methimazole: *preferred as pretreatment over PTU
*showed > success as preTx.
*because PTU is associated w/poorer
RAI retention & higher RAI failure rates
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Resolution of hyperthyroidism is slow:
Sx improvement :by 3-6wks after RAI
Max. effect : 3-4 months after an ablative dose
Other therapies may be needed after RAI due to
delayed onset for symptomatic control.
• Major concerns: *Carcinogenesis
* Leukemia
* Genetic damage
which are unfounded.
• Advantages of RAI:
1) Effective
2) Quick
3) Painless
4) Nontoxic
Major Complications:
Hypothyroidism : Most common in the 1st year
& increases w/ time.
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Iodinated Contrast Media:(e.g. Ipodate)
Inhibits peripheral deiodination of T₄ to T₃.
Inhibits TH secretion.
Relatively non-toxic.
Useful adjuncts to thioamides in the management of:
Severe thyrotoxicosis
Thyroid storm
Amiodarone-induced thyrotoxicosis
Alternative for those allergic to thioamides
in the preoperative preparation
** Chronic use is not indicated because its effectiveness in
reducing TH is not sustained for more than 1 month in most
cases.
• Non-pharmacological Therapy:
• Surgery (Thyroidectomy):
• Treatment of Choice for:
1. Contraindications of RAI or Thioamides.
2. Large goiters causing:*cosmetic disfigurement
* resp. distress
* swallowing difficulties
3. Suspected Malignancies.
4. Selected children & pregnants.
• Euthyroidism produced by surgery is faster & is
assoc. w/ lower relapse rates than w/ RAI or
thioamides.
• Poor Surgical Candidates:
1. Severe cardiac, resp., or debilitating dz.
2. 3rd trimester pregnant (spontaneous labor)
**Risk of recurrent thyrotoxicosis is directly
proportional to amount of remnant left of the
gland.
**Subtotal Thyroidectomy is preferred
• Total thyroidectomy:
1. Increases the risk of hypothyroidism
2. Prevents recurrence of hyperthroidism
• Surgery pts. should be adequately prepared
w/standard combination of:
1. Thioamide
2. Iodides
or 3. Beta-blockers
• Major Surg. Complication:
*Hypothyroidism in the 1st 6mos-3yrsafter surg.
or as late as 10yrs. after surgery.
Advantages of Surgery:
1. Rapid recovery
2. Definitive surgical intervention
3. Lack of need for the rigid dosing schedule of the thioamides
Disadvantages of Surgery:
1. Expense
2. Need of hospitalization
3. Risk of anesthesia
4. Postoperative complications
5.Fear of surgery
• Special Treatment Issues:
1.Subclinical Hyperthyroidism:
• Tx is controversial
• Tx is considered for high risk pts.:
*>60y.o.
*Cardiac dz.
*Atrial Fibrillation
*Osteoporosis
* Without risk factors: Observe & Do routine
TSH monitoring
2. Exophthalmous & Ophthalmologic Complications:
*Ocular Tx: symptomatic till euthyroidism occurs
*Elevation of bed head for diuresis.
*Protective glasses
+
Methylcellulose (lubricant)
+
Hydrocortisone drops
*Avoid smoke & dust
*Tape eyes during sleep to prevent corneal scarring & drying.
*Systemic corticosteroids for progressive inflammatory exophthalmous & reduced
visual acuity: Prednisone 60-120mg/d in divided doses X 1-3 wks
then taper when sxs resolve over 2 wks
then Discontinue.
• External orbital radiation therapy for contraindications to corticosteroids.
• After euthyroidism & stable eye Sx  Lid or orbital surgery for cosmetic or visual
correction
3. Atrial Fibrillation & CHF:
*Hyperthyroidism or subclinical hyperthyroidism
can cause or worsen A. Fibrillation & CHF which
are difficult to control until euthyroid.
*Hyperthyroid pts. Resistant to Digoxin
*Hypothyroid pts.  Very sensitive to Digoxin
* Warfarin is recommended in pts. w/
hyperthyroidism-related A.Fib, valvular dz.,& CHF
due to high risk of systemic emboli
4. Thyroid Storm:
*Treatment:
1. Support vital signs w/:
*Sedation
*O₂
*Fluids/Electrolytes
*Antipyretics
*Treat infection
*Corticosteroids (Hydrocortisone 100-200mg I.V. Q6H)
2. Thioamides & Iodides in large doses:
*PTU 200-300mg Q6H
or
*Methimazole 30-40mg Q6H
*Iodides added 1hr after thioamides
3. Lithium used if iodides are contraindicated
4. Cholestyramines may also be recommended
• Thyroid Storm cont.:
4. Propranolol 20-80mg p.o. Q6H or 0.5-2mg IV or
comparable beta-blocker or Diltiazem 60-120mg p.o.
TID or QID to control HR.
5. Eliminating & correcting precipitating factors.
6. Removing circulating hormones by:
a. Plasmapheresis
b. Exchange transfusion
c. Dialysis
when routine measures fail.
TSH is the most sensitive for diagnosis.
Hypothyroidism
• Hypothyroidism:
• Caused by TH deficiency.
• Characterized by slowing down of all body systems.
• Myxedema:
• Exaggeration of SxS of severe prolonged hypothyroidism
preceding coma
• Myxedema Coma:
• End-stage of long-standing uncorrected hypothyroidism.
• Cretinism or Congenital Hypothyroidism;
• Hypothyroidism developing in the utero or in neonates
& can lead to mental & growth impairment.
• Subclinical Hypothyroidism:
• Increased TSH & Normal TH usually without
symptoms of hypothyroidism.
* Primary Hypothyroidism:
*Failure of thyroid gland to secrete sufficient TH
*Most common type
• Secondary Hypothyroidism:
• Rare
• Due to pituitary or hypothalamic injury.
• Treatment Goals: p.1007
• More common in females
• Risk Factors:
1.Family hx of thyroid or autoimmune disorder
2.Older age, esp. women
3.Medically treated thyroid dz.
Types of Hypothyroidism by cause:
1. Goitrous
2. Nongoitrous
1. Goitrous forms include:
*Hashimotos thyroiditis: *Most common in U.S.
*Autoimmune
*Drug-induced thyroiditis: *Iodides
*Lithium
*Cytokines
*Thiocyanate
*Dyshormogenesis: *Familial thyroid disorders from
abnormalities in synthesis, delivery,
or peripheral action of TH.
*Endemic thyroiditis: *Caused by Iodine deficiency during
growth years.
*Subacute Thyroiditis
*Multinodular Goiters (MNG)
2. Nongoitrous forms include:
*Cretinism
*Idiopathic atrophy (uncommon)
*Iatrogenic causes: *2nd most common
*by RAI or surgery
*Pituitary causes (uncommon)
• SxS: * Table 38.4
* Atypical in elderly
• SxS from naturally occurring hypothyroidism
(Hashimoto): insidious & unnoticed x mos-yrs
before terminal myxedema state.
• Iatrogenic Hypoth. (by RAI or Surgery):occur
rapidly.
• Hypothyroid. pts. : sensitive to meds. i.e.:
*Digoxin
*Anesthetics
*Narcotics
*Sedatives-hypnotics
• Medical Tx of concurrent diseases (DM,
Hyperlipidemia, Cardiac conditions):
Maybe influenced
• Diagnosis: May go unnoticed
• Recommended to measure TSH starting @ 35y.o. & every 5
yrs thereafter esp. in women.
• Adults:
* Low FT₄I or FT₄ (T₃ may be normal)
* Increased TSH
• Secondary Hypothyroid:
*Low FT₄
*Low TSH
*Other features of pituitary or hypothalamic dz.
• Hashimoto Thyroiditis:
*Antibodies present
* Low FT₄I or FT₄ (T₃ may be normal)
* Increased TSH
• Therapeutic Plan: Fig. 38.4 p.1011
• TH administration provides adequate replacement
therapy for Hypothyroidism & prevents progression
to myxedema coma.
• Average Dose=100-150 mcg L-thyroxine QD
(parallels normal TH production)
* 100-125 mcg QD in females
* 125-150 mcg QD in males
• Dosing requirements depend on:
age, weight, severity, cause, cardiac dz.,
hormone absorption.
• Treatment:
• Pharmacotherapy:
• L-thyroxine: Preparation of choice.
• Other commercial preparations (table 38.9)
• Young-healthy pt. w/ short duration dz.:
Administer L-thyroxine 100-150mcg QD
(1.6-1.7mcg/kg/d)
• Dose can be adjusted using SxS & lab values
@ steady-state (after 6-8 wks of Tx)
• Older pts.= 50-100 mcg QD
• Old w. Cardiovascular Dz.= 25 mcg QD
• Lower doses are sufficient for hypothyroidism
caused by RAI or surgery than with
spontaneous hypothyroidism.
• Pregnancy: Increase the pre-pregnancy dose
of L-thyroxine by 20-30% in 1st or
2nd trimester.
*Malabsorption by SBS or coadministration w/
several meds.(tab.38.10)Reduces thyroxine
absorption
*Improvement in typical SxS should be seen
after 3-4 wks of Tx.
*Wt., skin, hair, voice changes:
May NOT reverse for months despite normal TFTs.
*TSH & FT₄ : Should be evaluated @ SS
(after 2-3 mos. of daily dosing)
*Changes in TSH lag behind changes in TH.
Therefore, TSH & T₄ should be checked NOT earlier than 4 wks
after starting Tx.
*Once dose is established: Evaluate Tx @ yearly intervals
• Avoid over-replacement to avoid hyperthyroidism
which can increase the risk of: * osteoporosis
* Bone loss
* Cardiac arrhythmias
1. L-thyroxine (T₄) whose t⅟₂=7days: The most popular of
the 8 commercial preparations because of:
1. Potency
2. Cost-effectiveness
3. Lack of foreign protein antigenicity
4. Ease of dosing
2) T₃ (t ⅟₂=1.5d):
* May be used for short-term replacement.
*NOT recommended for routine Tx due to its:
1. Cardiotoxic effect
2. Multiple daily dosing
3. Greater difficulty in monitoring therapeutic
& toxic responses.
4. High cost
3) T₃+T₄ Combination:
• Needs to be further investigated
4) Dessicated Thyroid from Animals:
• Considered obsolete although inexpensive
due to allergic reactions & abnormal TFTs.
• Special Treatment Issues:
1. Congenital Hypothyroidism:
*The earlier the Tx begins, the better the
prognosis of mental & growth development.
*DOC: L-thyroxine
*Infants w/ long standing & severe myxedema:
Extremely sensitive to minute doses of TH
*Start w/ very small doses (tab.38.11) to prevent
toxicity.
* TSH should normalize after 3-4months of starting Tx.
2) Subclinical Hypothyroidism:
*Treatment: Debatable
*Not all cases progress to hypothyroidism:
Higher TSH elevation , greater risk
*Risk is greatest w/ TSH > 10mIU/L
*Decision to treat is based on:
1. Risk vs. benefit of Tx
2. Likelihood of overt hypothyroid (hx RAI or surgery)
3. Degree of TSH elevation
4. Hx of thyroid dz.
3) Myxedema Coma:
a. Hormone replacement
+
b. Supportive measures
+
c. Eliminate or correct precipitating factors
a. Hormone Replacement:
• L-thyroxine: Large IV dose (400-600mcg)
then M.D. 50-100 mcg IV QD
until p.o. is possible.
• Hydrcortisone: 50-100mg IV Q6H:
To prevent adrenal crisis in case of undetected
hypopituitarism exists.
b. Supportive Measures:
1. Assisted ventilation
2. Glucose infusion for hypoglycemia
3. Fluid restriction due to hyponatremia
4. Plasma expanders for shock & circulatory
collapse
**Heating blankets:
NOT recommended because it can aggrevate shock
by vasodilation.
c. Eliminate or Correct Precipitating Factors
** If properly treated, Recovery can occur w/in 24 hrs.