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PHARMACOLOGY (2nd year) > DR. LEAL - THYROID & ANTITHYROID DRIGS > Flashcards

DR. LEAL - THYROID & ANTITHYROID DRIGS Flashcards

1
Q

Function: normalize growth and development, body
temperature, and energy levels.

A

THYROID HORMONES
○ Triiodothyronine (T3)
○ Tetraiodothyronine (T4, Thyroxine)

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2
Q

second type of thyroid hormone, is
important in the regulation of calcium metabolism.

A

CALCITONIN

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3
Q

Recommended Daily Adult Iodide (I−) Intake:

A

○ 150 mcg
○ 200 mcg during pregnancy and lactation
○ 250 mcg for children

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4
Q

absorbed best in the duodenum and ileum.

A

THYROXINE

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5
Q

THYROXINE ABSORPTION MODIFIED BY

A

food, drugs, gastric
acidity, and intestinal flora.

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6
Q

_ & _
IMPAIRED IN SEVERE MYXEDEMA WITH ILEUS

A

T3 AND T4 ABSORPTION

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7
Q

METABOLIC CLEARANCES OF T3 & T4 ARE INCREASED

A

HYPERTHYROIDISM

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8
Q

Drugs that induce hepatic microsomal enzymes increase the metabolism of both T4 and T3

A

Rifampin
phenobarbital
Carbamazepine
Phenytoin
Tyrosine kinase inhibitors
HIV protease inhibitors.

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9
Q

responsible for optimal growth, development, function, and maintenance of all body tissues.

A

T3 AND T4

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10
Q

EXCESS T3 AND T4 (THYROID HORMONES)

A

HYPERTHYROIDISM

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11
Q

INADEQUATE T3AND T4

A

HYPOTHYROIDISM

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12
Q

T OR F
Thyroid hormones are not effective and can be detrimental in the management of obesity, abnormal vaginal bleeding, or depression if thyroid hormone levels are normal.

A

TRUE

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13
Q

SYNTHETIC THYROID HORMONES

A

Levothyroxine
Liothyronine
Liotrix

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14
Q

CHOICE FOR THYROID REPLACEMENT & SUPPRESSION THERAPY

A

LEVOTHYROXINE (T4)

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15
Q

Long half-life (7 days), which permits once-daily to weekly administration

A

LEVOTHYROXINE (T4)

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16
Q

● 3-4x more potent than Levothyroxine
● Best reserved for short-term TSH suppression.
● Not recommended for routine replacement therapy

A

LIOTHYRONINE

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17
Q

AVOIDED IN PTS WITH CARDIAC DSE
GREATER RISK OF CARDIOTOXICITY

A

LIOTHYRONINE

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18
Q

○ Agents that interfere with the production
of thyroid hormones
○ Agents that modify the tissue response to
thyroid hormones
○ Glandular destruction with radiation or
surgery

A

ANTITHYROID AGENTS

Reduction of thyroid activity and hormone effects

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19
Q

Agents that suppress secretion of T3 and T4 to subnormal levels and thereby increase TSH, which in turn produces glandular enlargement (goiter).

A

GOITROGENS

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20
Q

Antithyroid compounds:

A

○ Thioamides
○ Iodides
○ Radioactive iodine

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21
Q

TXFOR THYROTOXICOSIS

A

THIOAMIDES
Methimazole, Carbimazole and Propylthiouracil
(PTU)

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22
Q

PREVENT PROTEIN SYNTHESIS

A

THIOAMIDES
Methimazole, Carbimazole and Propylthiouracil
(PTU)

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23
Q

ADVERSE EFFECT OF THIOAMIDES
Methimazole, Carbimazole and Propylthiouracil
(PTU)

A

MACULOPAPULAR RASH

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24
Q

MOST DANGEROUS COMPLICATION
THIOAMIDES
Methimazole, Carbimazole and Propylthiouracil
(PTU)

A

AGRANULOCYTOSIS

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25
Q

CROSS THE PLACENTAL BARRIER

Secreted in low concentrations in breast milk but are
considered safe for the nursing infant.

A

THIOAMIDES
(MCP)

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26
Q

● 10x more potent than Propylthiouracil.
● Drug of choice in adults and children.
● Readily accumulated by the thyroid gland.

A

METHIMAZOLE

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27
Q

● Single daily dose is effective in the management of
mild to severe hyperthyroidism.
● Associated with congenital malformations
● Cholestatic jaundice is more common.

A

METHIMAZOLE

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28
Q

USED FOR
1ST TRIMESTER OF PREGNANCY
THYROID STORM
ADVERSE RXNS TO METHIMAZOLE

A

PROPYLTHIOURACIL (PTU)

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29
Q

more strongly protein-bound and crosses the
placenta less readily.

A

PROPYLTHIOURACIL (PTU)

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30
Q

Black box warning:
severe hepatitis,
resulting in death.

A

PROPYLTHIOURACIL (PTU)

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31
Q

Perchlorate (ClO4)
Pertechnetate (TcO4−)
Thiocyanate (SCN-)

A

ANION INHIBITORS

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32
Q

Inhibits the first step of iodine synthesis; block uptake of iodide by the gland through competitive inhibition of the iodide transport mechanism.

A

ANION INHIBITORS

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33
Q

Block thyroidal reuptake of I− in patients with iodine-induced hyperthyroidism

A

POTASSIUM PERCHLORATE

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34
Q

ASSOCIATED WITH APLASTIC ANEMIA

A

POTASSIUM PERCHLORATE

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35
Q

● Major antithyroid agents prior to the introduction of the Thioamides in the 1940s.
● Rarely used as sole therapy today.

A

IODIDES

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36
Q

In susceptible individuals, ____ can induce hyperthyroidism (Jod-Basedow Phenomenon) or
precipitate hypothyroidism.

A

IODIDES

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37
Q

Disadvantages of iodide therapy

A

INITIATED AFTER ONSET OF THIOAMIDE THERAPY
AVOIDED IF TX WITH RADIOACTIVE IODINE SEEMS LIKELY
NOT SHOULD BE USED ALONE
CHRONIC USE IN PREGNANCY SHOULD BE AVOIDED

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38
Q

uncommon and in most cases reversible upon discontinuance.

A

IODISM

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39
Q

● The only isotope used for treatment of thyrotoxicosis.
● Administered orally in solution as sodium 1311.

A

RADIOACTIVEIODINE131

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40
Q

Advantages: easy administration, effectiveness, low
expense, and absence of pain.

A

RADIOACTIVEIODINE131

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41
Q

should not be administered to pregnant women or nursing mothers, since it crosses the placenta to destroy the fetal thyroid gland and it is excreted in breast milk.

A

RADIOACTIVE IODINE

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42
Q

● Beta blockers without intrinsic sympathomimetic activity are effective therapeutic adjuncts in the management of thyrotoxicosis since many of these symptoms mimic those associated with sympathetic stimulation.
● Beta blockers cause clinical improvement of hyperthyroid symptoms but do not typically alter thyroid hormone levels.

A

ADRENOCEPTOR-BLOCKINGAGENTS
PROPANOLOL

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43
Q

● Most widely studied and used in the therapy of
thyrotoxicosis.
● by inhibiting the peripheral conversion of T4 to T3.

A

PROPRANOLOL

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44
Q

DECREASE T3 AND T4
INCREASE TSH

A

HYPOTHYROIDISM

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45
Q

DEVELOP DWARFISM AND IRREVERSIBLE MENTAL RETARDATION
CAN OCCUR WITH OR WITHOUT THYROID ENLARGEMENT

A

HYPOTHYROIDISM

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46
Q

AUTOMIMUNE DESTRUCTION OF THYROID

A

HASHIMOTOS THYROIDITIS

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47
Q

IMPAIRED SYNTHESIS OF T4 DUE TO ENZYME DEFICIENCY

A

DYSHORMONOGENESIS

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48
Q

MANAGEMENT OF HYPOTHYROIDISM
MOST SATISFACTORY PREP

A

LEVOTHYROXINE

49
Q

T OR F
Higher thyroxine requirements in patients with Celiac Disease and H. pylori gastritis

A

TRUE

50
Q

CAN TYROSINE BE ADMINISTERED IN AN EMPTY STOMACH?

A

YES

51
Q

THYROXINE DOSAGE
YOUNG
OLD

A

YOUNG- FULL REPLACEMENT THERAPY
OLD - 50mcg/d

52
Q

in thyroxine usage
in cardiac patients
stop if?

A

THERE IS ANGINA PECTORIS OR CARDIAC ARRYTHMIA

53
Q

● End state of untreated hypothyroidism, a medical
emergency.

A

MYXEDEMA COMA

54
Q

TREATMENT FOR MYXEDEMA COMA

A

LEVOTHYROXINE

55
Q

IN MYXEDEMA COMA
____ IS indicated if the patient has associated adrenal or pituitary insufficiency.

A

IV HYDROCORTISONE

56
Q

HIGH OR LOW
____levels of circulating thyroid hormone actually protect the heart against increasing demands that could result in angina pectoris, atrial fibrillation, or
myocardial infarction.

A

LOW

57
Q

T OR F
CORRECTION OF MYXEDEMA
coronary artery surgery is indicated, it should be
done first, prior to correction of the myxedema by thyroxine administration.

A

TRUE

58
Q

HYPOTHYROID WOMEN
OVULATORY OR ANOVULATORY

A

ANOVULATORY

59
Q

HYPOTHYROID PTS
INCREASE OF ____ REQUIRED TO NORMALIZE SERUM TSH LEVEL IN PREGNANCY

A

25-30%

60
Q

Thyroxine should also be administered apart from prenatal vitamins and calcium by at least ____ HRS

A

FOUR HRS

61
Q

MAINTENANCE OF TSH FOR PREGNANT

A

○ First trimester: 0.1–2.5 mIU/L
○ Second trimester, 0.2–3.0 mIU/L
○ Third trimester: 0.3–3.0 mIU/L

62
Q

● An elevated TSH level and normal thyroid
hormone levels.

A

SUBCLINICAL HYPOTHYROIDISM

63
Q

Treating with levothyroxine should be individualized based on the risks and benefits of treatment.

A

SUBCLINICAL HYPOTHYROIDISM

64
Q

thyroid hormone therapy should be considered for patients with TSH levels greater than 10 mIU/L while close TSH monitoring is appropriate for those with lower TSH elevations.

A

SUBCLINICAL HYPOTHYROIDISM

65
Q

Also termed as thyrotoxicosis.
● Clinical syndrome that results when tissues are
exposed to high levels of thyroid hormone.

A

HYPERTHYROIDISM

66
Q

● Also known as diffuse toxic goiter.
● Most common form of hyperthyroidism.

A

GRAVES DSE

67
Q

● An autoimmune disorder in which a defect in
suppressor T lymphocytes stimulates B lymphocytes to synthesize TSH receptor–stimulating antibody (TSH-R Ab [stim]) to thyroidal antigens.

A

GRAVES DSE

68
Q

INCREASED T3 AND T4
DECREASE TSH

A

GRAVES DSE

69
Q

MANAGEMENT OF GRAVES

A

Antithyroid Drug Therapy
○ Methimazole and Propylthiouracil.

70
Q

○ Most useful in young patients with small
glands and mild disease.
○ The only therapy that leaves an intact
thyroid gland.
○ Require a long period of treatment and
observation (12-18 months).

A

Antithyroid Drug Therapy
○ Methimazole and Propylthiouracil.

71
Q

○ Preferred than propylthiouracil.
○ Lower risk of serious liver injury.

A

METHIMAZOLE

72
Q

Mild to moderately severe thyrotoxicosis

A

METHIMAZOLE

73
Q

PREFERRED IN PREGNANCY AND THYROID STORM

A

Propylthiouracil (PTU)

74
Q

Inhibits iodine organification, and inhibits the conversion of T4 to T3,

A

Propylthiouracil (PTU)

75
Q

treatment
of choice for patients with very large glands
or multinodular goiters.
○ Patients are treated with antithyroid drugs
until euthyroid (about 6 weeks).

A

THYROIDECTOMY

76
Q

preferred treatment for most patients over 21 years of age.
○ Patients without heart disease

A

RADIOACTIVE IODINE (RAI)

77
Q

IN REGARDS TO RAI
Patients with underlying heart disease or severe thyrotoxicosis and in elderly patients:TREAT WITH

A

METHIMAZOLE

78
Q

_______ should be avoided to ensure maximal 131I uptake.

A

IODIDES

79
Q

occurs in about 80% of patients following RAI.

A

HYPOTHYROIDISM

80
Q

When hypothyroidism develops,
prompt replacement with ________, 50–150 mcg daily, should be instituted.

A

ORAL LEVOTHYROXINE

81
Q

LARGE GOITER
METHIMAZOLE THEN PTU FOLOWED BY
SUBTOTAK THYROIDECTOMY

A

TOXIC MULTINODULAR GOITER

82
Q

Destruction of thyroid parenchyma with transient release of stored thyroid hormones during the acute phase of a viral infection of the thyroid gland (similar state may occur in patients with Hashimoto’s thyroiditis).

A

SUBACUTE THYROIDITIS

83
Q

IN SUBACUTE THYROIDITIS
SUPPORTIVE THERAPY IS GIVEN IF NOT RESOLVED SPONTY

A

B BLOCKERS (PROPANOLOL)
ASPIRIN OR NSAIDS
CORTICOSTEROIDS

84
Q

KNOWN AS THROTOXIC CRISIS

A

THYROID STORM

85
Q

● Sudden acute exacerbation of all of the symptoms of
thyrotoxicosis, presenting as a life-threatening
syndrome.

A

THYROID STORM

86
Q

MEDS FOR THYROID STORM

A

PROPANOLOL

87
Q

IN THYROID STORM
WHAT MEDS GIVEN IF

control the severe
cardiovascular manifestations.

A

ESMOLOL

88
Q

IN THYROID STORM
WHAT MEDS GIVEN IF
ASTHMATIC PATIENT

A

DILTIAZEM

89
Q

Release of thyroid hormones from the gland is retarded by the administration of

A

POTASIUM IODIDE SATURATED SOLUTION

90
Q

IN THYROID STORM

Hormone synthesis is blocked by the administration OF

A

PROPYLTHIOURACIL

91
Q

IN THYROID STORM IS THERE RECTAL FORMULATION OF PROPYLTHIOURACIL?

A

YES

92
Q

IN THYROID STORM RECTAL EXAM

A

METHIMAZOLE

93
Q

IN THYROID STORM

protect the patient against shock and will block the conversion of T4 to T3, rapidly reducing the level of thyroactive material in the blood.

A

HYDROCORTISONE

94
Q

IN THYROID STORM

essential to control fever, heart failure, and any underlying disease process

A

SUPORTIVE THERAPY

95
Q

IN THYROID STORM

been used to lower the levels of circulating thyroxine.

A

oral bile acid sequestrants(eg,cholestyramine), plasmapheresis, or peritoneal dialysis

96
Q

Ideally, women in the childbearing period with severe disease should have definitive therapy with __ AND __ prior to pregnancy in order to avoid an acute exacerbation of the disease during pregnancy or following delivery

A

IODINE 131
SUBTOTAL THYROIDECTOMY

97
Q

If thyrotoxicosis does develop during pregnancy,
WHAT is contraindicated because it crosses the placenta and may injure the fetal thyroid.

A

RADIOACTIVE IODINE

98
Q

IN PREGNANCY DURING THYROTOXICOSIS
WHAT IS THE PREFERRED TX

A

PROPYLTHIOURACIL - FIRST TRIMESTER
METHIMAZOLE - REMAINDER PREGNANCY

99
Q

subtotal thyroidectomy can be safely performed during the

A

MID TRIMESTER OR
2ND TRIMESTER

100
Q

may occur in the newborn infant, due either to passage of maternal TSH-R Ab [stim] through the placenta, stimulating the thyroid gland of the neonate, or to genetic transmission of the trait to the fetus.

A

NEONATAL GRAVE’S DISEASE

101
Q

NEONATAL GRAVE’S DISEASE
INCR OR DEC
T3 AND T4
TSH

A

T3 AND T4 - INCREASED
TSH - DECREASED
——————NORMAL INFANT INCREASED TSH

102
Q

NEONATAL GRAVE’S DISEASE
THERAPTY OR MANAGEMENT

A

PROPYLTHIOURACIL
LUGOLS SOLUTION
PROPRANOLOL

103
Q

NEONATAL GRAVE’S DISEASE
IF INFANT IS VERY ILL GIVE

A

ORAL PREDNISONE

104
Q

Defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels.

A

SUBCLINICAL HYPERTHYROIDISM

105
Q

Approximately 3% of patients receiving Amiodarone will develop hyperthyroidism.

A

AMIODARONE-INDUCED THYROTOXICOSIS

106
Q

AMIODARONE-INDUCED THYROTOXICOSIS

  • Often occurs in persons with underlying thyroid disease (eg, multinodular goiter, Graves’ disease)
  • Treatment: therapy with
    thioamides (methimazole)
A

IODINE INDUCED - TYPE 1

107
Q

AMIODARONE-INDUCED THYROTOXICOSIS

  • Occurs in patients without thyroid disease due to leakage of thyroid hormone into the circulation.
  • Treatment: can give anti-inflammatory drugs, responds best to glucocorticoids.
A

INFLAMMATORY THYROIDITIS - TYPE 2

108
Q

IN AMIODARONE -INDUCED THYROTOXICOSIS
OFTEN ADMINISTERED TOGETHER

A

THIOAMIDES
GLUCOCORTICOIDS

109
Q

A syndrome of thyroid enlargement without excessive thyroid hormone production.

A

NONTOXIC GOITER

110
Q

● Enlargement is often due to TSH stimulation from inadequate thyroid hormone synthesis.

A

NONTOXIC GOITER

111
Q

Most common cause of nontoxic goiter worldwide is

A

IODIDE DEFICVIENCY

112
Q

Most common cause of nontoxic goiter IN US

A

HASHIMOTOS THYROIDITIS

113
Q

Managed by prophylactic administration of iodide.
● The optimal daily iodide intake is 150–200 mcg.
● Iodized salt and iodate used as preservatives in
flour and bread are excellent sources of iodine in the
diet.

A

GOITER DUE TO IODIDE DEFICIENCY

114
Q

● Managed by elimination of the goitrogen or by adding sufficient thyroxine to shut off TSH stimulation.

A

GOITER DUE TO INGESTION OF GOITROGENS IN THE DIET

115
Q

Adequate thyroxine therapy—_______—will suppress pituitary TSH and result in slow regression of the goiter as well as correction of hypothyroidism.

A

150–200 mcg/d orally

116
Q

NOT RECOMMENDED FOR BENIGN LESIONS OR ADENOMAS

A

LEVOTHYROXINE

117
Q

Requires a total thyroidectomy, postoperative
radioiodine therapy in selected instances

A

THYROID CARCINOMA

118
Q

lifetime replacement with levothyroxine

A

THYROID CARCINOMA

119
Q

can produce comparable TSH elevations without discontinuing thyroxine and avoiding hypothyroidism.

A

recombinant human TSH (Thyrogen) - IM

PHARMACOLOGY (2nd year) (18 decks)

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