Hypothyroidism Hypothyroidism N Buttar

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					Hypothyroidism
      N. Buttar MD
Hypothyroidism

   1.8% of total population.
   Second only to DM as most common endocrine disorder.
   Incidence increases with age.
   More common in females.
   2-3% of older women.
      Etiology
PRIMARY HYPOTHYROIDISM
 Hoshimoto’s thyroiditis-most common
 Idiopathic hypothyroidism-probably old Hoshimoto’s
 Irradiation of thyroid
 Surgical removal
 Late stage invasive fibrous thyroiditis
 Iodine deficiency
 Drug therapy (Lithium, Interferon)
 Infiltrative Diseases:
  Sarcoidosis, Amyloidosis
  Scleroderma, Hemochromatosis
SECONDARY HYPOTHYROIDISM
 5% of cases.

 Pituitary or hypothalmic neoplasm.

 Congenital hypopituitarism.

 Pituitary necrosis (Sheehan’s syndrome)
Signs and Symptoms

   Non-specific.
   May be confused with other conditions especially in
    postpartum depression and elderly.
   Maintain high index of suspicion.
   In older patients, hypothyroidism may be confused with
    Alzheimer’s and depression.
   Patient may end up getting treated for depression.
Common signs and symptoms
S/S                         % pt’s affected
Weakness                           99
Skin changes                       97
Slow speech                        91
Eyelid edema                       90
Cold sensation                     89
Decreased sweating                 89
Cold skin                          83
Thick tongue                       82
Facial edema                       79
Coarse hair                        76
Skin pallor                        67
Forgetfulness                      66
Constipation                       61
Diagnosis

In Primary Hypothyroidism
 TSH is high.

 Free thyroid hormone are depressed.



In Secondary Hypothyroidism
 Both TSH and free thyroid hormones are low.
Anti bodies in hypothyroidism

Anti bodies:
 Anti thyroid peroxidase [ anti microsomal] antibodies

 Anti thyroglobulin antibodies.

 Anti bodies against T3 and T4 in auto immune
  hypothyroid disease.
 In primary hypothyroidism;

       - up to 12 % pt do have anti gastric parietal cell
         antibodies.
      - these pts. Can develop pernicious anemia.
Generally…

   Once diagnosis of primary hypothyroidism is made,
    additional imaging or serologic testing is unnecessary
    if gland is normal on exam.
   In secondary hypothyroidism, further testing with pituitary
    provocative testing and imaging to rule out
    microadenoma. In general, evidence of decreased
    levels of more than one pituitary hormone is indicative of
    a panhypopituitary problem.
      Lab Values

TSH level       Free T4 level     Free T3 level       Likely Diagnosis
High          Low                 Low       Primary Hypothyroidism

High (>10 U/mL Normal            Normal     Subclinical hypothyroidism with
[{10mU/L]}                                  high risk for future development
                                            of overt hypothyroidism
High (6-1uU/mL Normal            Normal    Subclinical hypothyroidism
{6-10mU/L])                                with low risk for future development
                                           of overt hypothyroidism

High          High              Low        Congenital absence of T4-T3
                                           converting enzyme; amiodarone
                                          Cordarone) effect on T4-T3
                                          conversion
High         High               High      Peripheral thyroid hormone
                                          resistance
Low          Low                Low       Pituitary thyroid deficiency
                                          or recent withdrawal of
                                          thyroxine after excessive
                                          replacement therapy
Thyroid Hormone Replacement

   Levothyroxine can cause increases in resting heart rate
    and blood pressure
   So replacement should start at low doses in older and
    patients at risk for cardiovascular compromise
Hormones


 In past…
 Thyroid preparations were prepared from dessicated
  samples of ground cow or pig thyroids.
 Standards based on iodine contents rather than T3 or T4
  content.
 Actual content of thyroid hormone varies considerably
  from manufacturer to manufacturer and even within
  product.
Generic or Brand Name

   Study of four products, two brands and two generic
    preparations showed bioequivalent.
   Patients switched from one product to another showed
    insignificance variations in thyroid function
   Only Synthroid produces more rapid and higher rise in
    T3 level after administration. However, not statistically
    significant.
Preparations Available

    Armour thyroid          15 mg(1/4 gr) ,30 mg(1/2 gr)
                             60 mg(1 gr),90 mg(1.5 gr)
                             120 mg(2 gr),180 mg(3gr)
                             300 mg(5 gr)
    50-100 mcg of Levothyroxine =60 mg of Armour Thyroid

    Synthroid (T4)         25,50,75,88,100,112
     Levothroid (T4)        125,137,150,175,200
     Levoxyl (T4)           300 mcg.
     Levothyroxine Sodium
Preparations Available


   Unithroid (T4)        25, 50, 75, 88,100,112
                         125,150,175, 200, 300 mcg.

50 mcg tabs. of Synthyroid, Levoxyl,and Unithroid is dye free.

    Cytomel(T3)          5,25, 50 micrograms
    ( Liothyronine Na)
Preparations Available

   Thyrolar:
Tabs in                Content(mcg)
Grain           T3                    T4
¼               3.1                   12.5
½               6.25                  25
1               12.5                  50
2               25                    100
3               37.5                  150
Preparations Available

   Injectables
        -Levothyroxine Sodium
        -Synthroid
     Available in 200 mcg and 500 mcg per 10 mL vials
    T3 as compare to T4
       - 4 times more potent.
       - Short duration of activity.
       - Rapid onset of action.
Initiating Treatment

   Most healthy adults-1.7 ugm/kg/day
   Elderly, falls down to – 1.0 ugm/kg/day
   Levothyroixine needed – 0.1-0.15 mg/day
   For full replacement children may need up to 4
    ugm /kg/day
Treatment

   Younger patients can be started at target dose usually
    0.075 mg/day
   Start low and go slow in elderly and high risk patients,
    usually 0.025 mg/day
   Increase in increments of 0.025 mg q four weeks until
    TSH returns to normal.
What if……?

 What if the patient still has impaired
 mood and memory and cold intolerance
 in spite of stable thyroid function?
In one study:
In study of 33 middle aged patients with
stable hypothyroid, on levothyroixine, adding
12.5 mcg/ day of triiodothyronine and
decrease of 50 mcg/ day of levothyroxine helped
impaired symptoms.
Long term effects not known.
Monitoring thyroid function
   Most patients can be followed by serial TSH
    measurements.
   Changes in TSH levels lag behind serum thyroid levels.
   So TSH should not be checked sooner than four weeks
    after adjusting of doses.
   Full effect of replacement on TSH may not become
    apparent until eight weeks.
   Patients with pituitary insufficiency, T3 and T4 can be
    followed.
   Goal is to keep thyroid hormone level in middle to upper
    range of normal.
Frequency

   TSH or Free T4 monitored yearly.
   No data supports the practice.
   Usually once stable dosage is established, it remains
    stable until 60-70 years.
   In elderly serum albumin levels may decrease, so
    dosage may have to be decreased by 20%.
   Less frequent monitoring in young patients and annually
    in elderly.
Treatment of Hypothyroidism
                        Need for replacement

              Patients >50 or high risk of Cardiac Disease


             YES                                       NO
  Start Levrothyroxine at                  Start at 0.075 mg/day
  0.025 mg/day



-Monitor TSH- Primary hyperthyroidism or
Free T4-Secondary hypothyroidism, every 6-8 Weeks and adjust doses
         Does patient still have lethargy or memory loss

           Yes                                       No
  Consider adding Triiodothyronine
  12.5 mcg/day and decrease            Continue therapy and annual
  Levothyroxine by 20%                 measurement of TSH or a free T4
Sub clinical Hypothyroidism

   High TSH with normal Free T4
   Commonest cause is chronic autoimmune thyroiditis
    (Hoshimoto’s disease)
   Associated with increased titer of antithyroid antibodies:
    - Anti thyroglobulin autobodies
    - Antimicrosomal (Antiperoxidase) antibodies
   Suspected with thyroid enlargement but may be
    associated with atrophy
Prognosis

   May stay sub clinical
   May progress to clinical,
    5% per year with positive antibodies
   In elderly risk is 20%/ year
     Normal T4, High TSH, Two readings, six weeks apart



                                                      TSH between 5-10 mU/L
TSH >10 mU/L

Check Thyroid antibodies
                            Antibodies or symptoms present     Antibodies negative
                                                               or no symptoms

Positive         Negative

                                   Consider therapy
               Symptoms                                       Observe, test
Therapy
               positive           No symptoms                 every six months




               Therapy
A patient with bipolar disorder is being treated with lithium.
Of the following, which one is the most likely side effect of
his therapy?

A)   Hypoparathyriodism
B)   Hypoaldosteronism
C)   Hypothyroidism
D)   Diabetes inspidus
Answer: C
Lithium is used as a mood stabilizer in bipolar
disease and can be used as monotherapy, especially
when the depression is mild. A well-recognized side
effect of lithium of hypothyroidism. It is
recommended that TSH be monitored in patients
treated with lithium. Hyperparathyroidism, but not
hypoparathyroidism, has been reported, but it is not
as common as hypothyroidism. Nephrogenic
diabetes insipidus has been reported only rarely.
Hypoaldosteronism is not a side effect of lithium
therapy.
Which of the following is a cause of thyrotoxicosis
characterized by decreased radioactive iodine uptake?

A)   Grave’s disease
B)   Subacute thyroiditis
C)   Toxic multinodular goiter
D)   Solitary toxic thyroid nodule
Answer: B
Thyrotoxicosis with high 24-hour radioactive
iodine uptake (RAIU) is caused by Graves’ disease,
toxic multinodular goiter, a solitary hot nodule, a
TSH-secreting pituitary tumor, molar pregnancy, and
choriocarcinoma. Thyrotoxicosis with a low 24-
hour RAIU may be the result of subacute thyroiditis,
sporadic silent thyroiditis, postpartum lymphocytic
thyroiditis, radiation-induced thyroiditis, iodine
induced thyroiditis, thyrotoxicosis factitia, metastatic
follicular thyroid cancer, and struma ovarii.
Which one of the following is associated with
galactorrhea?

A)   Hypothyroidism
B)   Breast cancer
C)   Fibrocystic breast disease
D)   Adrenal insufficiency
E)   Graves’ disease
Answer: A
Galactorrhea, or inappropriate lactation, is a
relatively common problem with multiple causes.
Systemic disease is one cause, the most common
being hypothyroidism. Low levels of thyroid
hormone result in increased levels of thyrotopin-
releasing hormone, which increases prolactin
secretion. Galactorrhea and symptoms of
hypothyroidism abate with thyroid hormone
replacement therapy. This condition is not
associated with breast cancer or fibrocystic disease
of the breast. Cushing’s disease, rather than adrenal
insufficiency, is associated with galactorrhea.
 Your 57-year-old white male patient has been seen in the ICU for the past
 ten days recovering from an exploratory laparotomy performed for a
 perforated duodenal ulcer. Postoperatively he developed acute renal
 failure and sepsis. When the patient became hypothermic three days ago,
 the resident on duty ordered a thyroid function panel and obtained the
 following results:
 T4 RIA………………….4 ug/dL (N5-12)
 T3 RIA……………..…60 ng/dL (N70-90)
 TSH…….………..2.0 uU/mL (N 0.5-5.0)
The patient has no previous history of thyroid disease. His gland is
normal in size. His condition today is critical but stable. The most
appropriate treatment at this time is to:

A)   Continue present management
B)   Order a TRH stimulation test
C)   Begin parenteral thyroixine immediately
D)   Begin parenteral thyroixine and hydrocortisone immediately
Answer: A
This patient in all probability has the euthyroid-sick
  syndrome, also known as nonthyroid illness
  syndrome (NTI)-the association of severe nonthyroid
  illness with biochemical parameters indicative of
  thyroid hypo function. Low T3 with normal T4 and
  low T3 with low T4 are the most common variants of
  this syndrome. TSH is usually normal but may be
  high or low. A TSH level >20 uU/mL would be
  inconsistent with NTI and indicates hypothyroidism.
  Replacement of T4 does not influence the outcome.
A 68-year-old African-American female with primary hypothyroidism is
taking L-thyroxine (Synthroid) 125 ug/day. Her thyroid-stimulating hormone
(TSH) level is 0.2 uU/mL (N0.5-5.0). She has no symptoms of either
hypothyroidism or hyperthyroidism. Which one of the following is true
regarding her management?

  A)    The L-thyroxine dosage should not be changed
  B)    The L-thyroxine dosage should be increased
  C)    The L-thyroxine dosage should be decreased
  D)    The L-thyroixine should be discontinued
  E)    A free thyroxine index (FTI) is needed to determine
        her thyroid hormone status more accurately
Answer: C
Because of the precise relationship between circulating
  thyroid hormone and pituitary TSH secretion,
  measurement of serum TSH is essential in the
  management of patients receiving L-thyroxine therapy.
  Immunoassays can reliably distinguish between normal
  and suppressed concentrations of TSH. In a patient
  receiving L-thyroxine, a low TSH level usually indicates
  over replacement. If this occurs, the dosage should be
  reduced slightly and the TSH level repeated in 2-3
  months time. There is no need to discontinue therapy in
  this situation, and repeating the TSH level in two weeks
  would not be helpful. A free thyroxine index would also
  be unnecessary, since it is not as sensitive as a TSH
  level for detecting mild states of excess thyroid hormone.
In a patient with symptoms of thyrotoxicosis and elevated
free thyroxine (T4), the presence of thyroid TSH receptor
site antibodies (TRAbs) would indicate which one of the
following?
A)   Toxic multinoduler goiter
B)   Graves’ disease
C)   Hashimoto’s (lymphadenoid) thyroiditis
D)   Toxic adenoma
E)   Subacute (giant cell) thyroiditis
Answer: B
When there is a question about the etiology of goiter
  and thyrotoxicosis, the presence of thyroid TSH
  receptor immunoglobulins would indicate the
  presence of Grave’s disease, which is considered an
  autoimmune disease. The prevalence of specific
  forms of TSH receptor site antibodies can distinguish
  Grave’s disease from Hashimoto’s disease. Both are
  autoimmune diseases, but in Graves’ disease there is
  a predominance of TSH receptor antibodies. TSH
  receptor-blocking antibodies are seen in Hashimoto’s
  disease. These immunoglobulins tend to disappear
  during therapy.
Chronic therapy with which one of the following
commonly used drugs is most likely to increase the
risk for osteoporosis?

A)   Antihypertensives
B)   Oral hypoglycemics
C)   NSAIDs
D)   Thyroid hormone
Answer: D
Thyroid hormone stimulates osteoclasts, and recent
  research shows decreased bone density in patients
  receiving standard replacement doses of thyroid
  hormone. This appears to occur even in patients
  who have never had thyrotoxicosis, a known cause of
  secondary osteoporosis. In patients taking thyroid
  hormone replacement for bona fide hypothyroidism, it
  is important, therefore, to use no more than the
  minimum dosage necessary to make the patient
  euthyroid. Also, it is wise to discontinue any thyroid
  replacement that is not really necessary. The other
  drugs listed are not associated with increased
  osteoporosis risk.
A 32-year-old think, white G2 P1 comes to your office for her initial
prenatal visit at 20 weeks gestation. On examination, you note slight
exopthalmos, a heart rate of 110 beats/min., and a tender, palpable thyroid.
She admits she has gained no weight during the pregnancy, but says she
is always hungry. Her serum TSH level is 0.01uU/L (N 0.5-5.0) and her free
T4 level is 22.5 pmol/L (N7.7-15.6).
The most appropriate initial management of this patient would be:

A)    Close observation, with repeat thyroid levels every
      two weeks throughout the pregnancy
B)    Propylthiouracil
C)    Iodine therapy
D)    Surgical referral for subtotal thyroidectomy
Answer: B
Prompt Dx and Tx of hyperthyroidism during pregnancy is
  extremely important to prevent maternal and fetal
  morbidity and mortality. Anti thyroid therapy with
  propylthiouracil is the therapy of choice in pregnant
  women. Iodine freely crosses the placental barrier and is
  contraindicated in pregnancy, since it may cause fetal
  goiter and hypothyroidism. Surgery may be performed
  during pregnancy, but should be reserved for severe
  cases unresponsive to antithyroid therapy. It carries a
  significant risk of spontaneous abortion and premature
  delivery.
A 52-year-old white male is being considered for
pharmacologic treatment of hyperlipidemia because of an
LDL cholesterol level of 180 mg/dL. Before beginning
medication for his hyperlipidemia, he should be screened
for:
A)   Hyperthyroidism
B)   Hypothyroidism
C)   Addison’s disease
D)   Cushing’s disease
E)   Pernicious anemia
Answer: B
According to the Summary of the National Cholesterol
  Education Program Adult Treatment Panel III Report
  of 2001, any person with elevated LDL cholesterol or
  any other form of hyperlipidemia should undergo
  clinical or laboratory assessment to rule out
  secondary dyslipidemia before initiation of lipid-
  lowering therapy. Causes of secondary dyslipidemia
  include diabetes mellitus, hypothyroidism, obstructive
  liver disease, chronic renal failure, and some
  medications.
A 56-year-old female presents for routine visit. An
otherwise normal adult physical exam reveals a 2 cm right-
sided thyroid nodule. Her TSH levels are normal. She has
no history of neck irradiation, and there is no family history
of thyroid cancer.
You Recommend:

 A)   A fine-needle aspiration biopsy
 B)   Suppression of the nodule with levothyroxine
      (Synthroid)
 C)   Removal of the nodule
 D)   A serum calcitonin level
 E)   A radioactive iodine uptake test and thyroid scan
Answer: A
In the absence of risk factors for cancer, a patient with a
   normal TSH level who is found to have a thyroid nodule on
   physical examination should have a fine-needle aspiration
   biopsy. Independent of morphology, fine-needle
   aspiration provides the most direct and specific
   information about a thyroid nodule.