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Medicine > Hyperthyroidism > Flashcards

Hyperthyroidism Flashcards

1
Q

State of thyroid hormone excess of ANY etiology

A

Thyrotoxicosis

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2
Q

State of thyroid hormone excess due specifically to excessive thyroid gland function

A

Hyperthyroidism

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3
Q

Primary thyroid disorder is a disorder that originates from the

A

thyroid gland

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4
Q

Secondary thyroid disorder is a disorder due to the stimulation of thyroid gland by excess

A

TSH

HCG

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5
Q

The most common cause of hyperthyroidism

A

Grave’s disease

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6
Q

Life-threatening exacerbation of hyperthyroidism

A

Thyroid storm

Throid crisis

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7
Q

Grave’s disease prevalence

Lifetime risk
Associated with increased intake of

Sex

Age

A

1%

Iodine intake

F>M 7-10:1

Rare before adolescence
Typical range: 20-50
May occur in elderly as “apathetic hyperthyroidism”

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8
Q

Most common etiology of thyrotoxicosis

A

Grave’s (60-80%)

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9
Q

Genetic risk factors for Grave’s

A

HLA DR
Cytotoxic T lymphocyte-associated antigen 4 variants
Protein tyrosine phosphatase-22 (PTPN22)

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10
Q

A cell regulatory gene

A

PTPN22

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11
Q

Monozygotic concordance of Grave’s

Dizygotic twin concordance of Grave’s

A

20-30%

<5%

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12
Q

Smoking in

Grave’s

Ophthalmopathy

A

Minor risk factor for Grave’s

Major risk factor for ophthalmopathy

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13
Q

Sudden increase in dietary iodine intake
Radiocontrast materials containing high iodine content
Medications (amiodarone)

A

Iodine intake

Grave’s

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14
Q

3 fold increase in Grave’s

A

Postpartum

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15
Q

Grave’s disease is caused by thyroid-stimulating

A

immunoglobulin against the thyrotropin TSH receptor

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16
Q

Antibodies against the thyrotropin TSH receptor in Grave’s cause

A

Autonomous growth of thyroid

Autonomous production of thyroid hormones

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17
Q

Intrathyroidal inflammatory cells in Grave’s produce cytokines:

A

IL-1
TNF a
IFN a

cytokines help sustain intrathyroidal autoimmune process

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18
Q

IL-1
TNFa
IFNa

induce expression of

A

adhesion
regulatory
HLA II

which in turn activate local inflammatory cells

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19
Q

Edema
Inflammation of EOM
Increase in orbital connective tissue and fat

A

Thyroid-associated ophthalmopathy

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20
Q

Edema in Grave’s ophthalmopathy is due to hydrophilic action of

secreted by

A

Glycosaminoglycans

Fibroblast

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21
Q

Inflammation in Grave’s ophthalmopathy is due to infiltration of EOMs and orbital connective tissue by

A

lymphocytes

macrophages

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22
Q

Thyroid associated opthalmopathy may result from immunoglobulins directed to specific antigens ie

A

thyrotropin TSH receptors on preadipocyte subpopulation of orbital FIBROBLASTS

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23
Q

Lymphocytic infiltration of dermis
Accumulation of glycosaminoglycans
Non-pitting edema

A

Dermopathy

Pretibial myxedema

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24
Q

Unusual disorder associated with

hyperthroidism
sporadic episodes of acute muscle weakness
hypokalemia

Asian men

Prodrome: muscle ache, stiffness, LE proximal muscle weakness progressing to flaccid quadriplegia

Serum K not always below normal

Subtle hyperthyroidism symptom

A

Thyrotoxic period paralysis

Tx: K supplement

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25
Q

Classic hyperthyroidism symptoms

A 
Unintentional weight loss with ravenous apetite
Heat intolerance and sweating
Palpitations
Hyperactivity/anxiety
Tremulousness
Fatigue and weakness
Insomnia
Irritability
Impaired concentration
Increased stool frequency with diarrhea and steatorrhea
Pruritus
Oligomenorrhea or amenorrhea
Erectile dysfunction
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26
Q

Unusual hyperthyroidism symptoms

A

Weight gain: 5% due to disproportionate increase in caloric intake
Gynecomastia
Urticaria

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27
Q

Diffusely enlarged goiter

Pantay ang laki ng lahat

A

Grave’s disease

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28
Q

Nodular

A

Toxic adenoma

Toxic multinodular goiter

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29
Q

Cardiovascular signs of Grave’s

A

Sinus tachycardia
Bounding pulse/widened pulse pressure
Aortic systolic murmur (Mitral regurg)
Atrial fibrillation >50 years of age

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30
Q

Neurologic Grave’s signs

A

Hyperreflexia
Muscle wasting
Proximal myopathy without fasciculation

Rare: chorea, hypokalemic periodic paralysis

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31
Q

Dermatologic Grave’s signs

A

Warm, moist skin
Palmar erythema
Onycholysis
Finer hair texture - diffuse alopecia up to 40% of patients

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32
Q

Opthalmologic Grave’s signs

A

Lid retraction or lag
Stare
Rarified blinking

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33
Q

A presentation of Grave’s in elderly the elderly
Paucity of classic symptoms

Fatigue
Weight loss
Atrial fibrillation

May be mistake for Depression

A

Apathetic hyperthyroidism

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34
Q

Life-threatening exacerbation of hyperthyroidism usually precipitated by surgery or acute illness

Fever
Delirium
Seizures
Coma
Vomiting
Diarrhea
Jaundice
A

Thyrotoxic crisis

Thyroid storm

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35
Q

Occurs in the absence of thyroid dysfunction in 10% of patients

Early symptom:
Grittiness
Eye discomfort
Excessive tearing

Late symptom:
Diplopia (5-10% due to eye muscle swelling and fibrosis)

Proptosis (1/3 often asymmetrical)
Periorbital edema
Conjunctival injection
Chemosis
Papilledema due to optic nerve compression
Peripheral field defects due to optic nerve compression
Unilateral in up to 10%

A

Grave’s ophthalmopathy

Thyroid-associated ophthalmopathy

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36
Q

Thyromegaly in Graves

A

Bilateral, symmetric enlargement
Firm
Accompanied by thrill or bruit due to increased vascularity of the gland and hyperdynamic circulation

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37
Q

Noninflamed, indurated plaque
Deep pink or purple color
Orange skin appearance

Anterior and lateral aspects of lower leg (pretibial myxedema) or in other sites after trauma

Nodular involvement, rarely can extend over the whole lower leg and foot mimicking elephantiasis

Accompanied with moderate to severe ophthalmopathy

A

Thyroid dermopathy (<5%)

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38
Q

Form of clubbing

Strongly associated with thyroid dermopathy

A

Thyroid acropachy (<1%)

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39
Q

Diagnostic test to reliably distinguish euthyroidism from mild hyperthyroidism

A

serum TSH with 3rd or 4th-generation immunoassay

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40
Q

When thyrotoxicosis is suspected on clinical grounds, order

A

serum TSH and free thyroxine T4

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41
Q

When serum TSH level is low, and free T4 level is within the normal range, order

A

free triiodothyronine T3

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42
Q

Accurate diagnosis of hyperthyroidism during pregnancy can be difficult because total thyroid hormone levels increase reflecting an increased

A

thyroid-binding globulin level

actions of HCG

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43
Q

Essential after biochemical diagnosis of thyrotoxicosis

A

Determine underlying cause

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44
Q

Supportive information that may be useful in identifying an underlying cause of thyrotoxicosis

A

Previous thyroid function test results
History of recent upper respiratory illness
Amiodarone
Pregnancy

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45
Q

Antibody that will support diagnosis of Grave’s

A

+ TPO Thyroid peroxidase antibodies

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46
Q

Features sufficient to confirm a diagnosis of Grave’s in a patient with biochemical hyperthyroidism WITHOUT NEED FOR FURTHER TESTING:

meaning Grave’s talaga

A

Diffuse goiter

Signs of ophthalmopathy or dermopathy

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47
Q

Features supporting Grave’s

A

Diffuse goiter
ophthalmopathy
Positive TPO antibodies
Personal/family history of autoimmune

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48
Q

Studies indicated to distinguish other causes of thyrotoxicosis in patients with biochemical thyrotoxicosis if lacking features of Diffuse goiter or opthalmopathy:

Meaning, mukang di grave’s

A

Radionuclide (99mtechnetium, 123iodine or 131iodine) uptake

Scan of thyroid

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49
Q

In select cases of Grave’s measurement of this antibody may be useful to establish diagnosis

A

serum TSH receptor antibodies

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50
Q

A diagnosis of secondary hyperthyroidism should be followed by further investigation

A

Elevated TSH
Elevated HCG

endocrinologic referral

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51
Q

Norma TSH

Normal free T4

A

exclude thyrotoxicosis

no further testing necessary

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52
Q

Primary thyrotoxicosis is indicated in the following 3 patterns:

A

Low TSH, high free T4
Low TSH, high free T4, high free T3
Low TSH, normal free T4, high free T3 (T3 toxicosis)

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53
Q

Subclinical thyrotoxicosis will show

A

Low TSH level
Normal free T4 and normal T3

Subclinical hyperthyroidism

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54
Q

TSH-secreting pituitary adenoma
Thyroid hormone resistance

will show

A

Normal or Increased TSH level
High free T4

Secondary hyperthyroidism

55
Q

Gestational thyrotoxicosis
Germ-line tumor

will show

A

Low TSH level
High Free T4

Secondary hyperthyroidism

56
Q

Other laboratory abnormalities associated with thyrotoxicosis

A

Elevated bilirubin and liver aminotransferase
Elevated ferritin level
Microcytic anemia
Thrombocytopenia

57
Q

Test for Grave’s

A

Antibody against thyrotropin TSH receptor

Second-generation assay

58
Q

Test With High sensitivity and specificity for Grave’s

Predict likelihood of remission in patients who have been treated with thionamides

A

Second generation

Antibody thyrotropin TSH

59
Q

Used in pregnancy or after iodine load where nuclear imaging cannot be performed

A

Thyrotropin TSH antibody with second generation assay

60
Q

Measurement of thyrotropin TSH antibody is recommended in pregnant women at

A

third trimester

to assess the likelihood of neonatal hyperthyroidism

61
Q

Test that helps distinguish hyperthyroidism from other causes of thyrotoxicosis

A

Radionucleotide UPTAKE

62
Q

Diseases that present with high radionucleotide uptake

A

Grave’s
Toxic adenoma
Toxic multinodular goiter
Trophoblastic disease and germ-cell tumors that produce HCG

63
Q

Diseases that present with Low radionucleotide uptake

A

Any form of thyroiditis (<1%)
Ectopic thyroid tissue (strums ovarii)
Functioning metastasic follicular thyroid carcinoma (rare)
Factitious thyrotoxicosis

64
Q

If radionucleotide uptake of the thyroid is HIGH, this will help distinguish among causes of high radionucleotide uptake:

A

Radionucleotide SCAN

65
Q

Enlarged gland

Homogenously increased uptake

A

Grave’s

66
Q

Focal area of increased uptake with supressed uptake in remainder of gland

A

Toxic adenoma

67
Q

Enlarged gland with multiple areas of increased and decreased uptake

A

Toxic multinodular goiter

68
Q

Orbital imaging for Grave’s opthalmopathy

A

Ultrasonography or CT of orbits

More sensitive for detecting opthalmopathy than is clinical examination

69
Q

Ultrasonography or CT of the orbits detect

A

Enlarged EOM muscles

70
Q

Indicated for the further evaluation of secondary hyperthyroidism to search for a TSH-secreting pituitary adenoma

A

Pituitary MRI

71
Q

Regardless of etiology, as sson as biochemical confirmation of thyrotoxicosis is made, patient must be started on

A

B adrenergic blockers

Atenolol 25-50 mg/d
Propranolol 20-40 mg; 4x daily

72
Q

The Grave’s goals of treatment are to

alleviate symptoms
reduce thyroid hormone synthesis

through

A

3 forms
Radioiodine (131iodine) treatment
Administration of thionamide (antithyroid)
Subtotal thyroidectomy

73
Q

Factors important to consider in choice of treatment for Grave’s

A

Pregnancy, breastfeeding, planning pregnancy
Presence of ophthalmopathy
Patient age

74
Q

Used as initial treatment or

for relapses after failed surgical or medical therapy

A

Radioiodine therapy

75
Q

Radioiodine is transported to thyroid cells and cause

A

progressive destruction

76
Q

Dose range of radioiodine therapy

A

5-15 mCi dependending on size and radioiodine uptake

77
Q

Small risk immediatelt after radioiodine therapy

minimized by

A

Thyrotoxic crisis

Pretreatment with thionamide 1 MONTH BEFORE treatment

78
Q

Pretreatment with thionamide is highly recommended for

A

elderly patients

cardiovascular disease

79
Q

High doses of radioiodine therapy are associated with high rate of cure but may cause

A

hypothyroidism

80
Q

Full effect of radioactive therapy requires

A

2-3 months

81
Q

If hyperthyroidism persists, patient can be treated with

A

second dose of radioiodine

6 months after first dose

82
Q

Side effect of Radioactive therapy

A

Mild pain occuring 1-2 weeks after

Radiation thyroiditis

83
Q

Carbimazole or Methimazole must be stopped at least how many days before radioiodine administration to achieve iodine uptake

A

3 days before

84
Q

PTU had prolonged radiolrotective effect and must be stopped how many days before radioiodine

A

Weeks before

Or larger dose of radioiodine necessary

Antithyroid and beta blockers may be resumed after administration until full effects of radioiodine are achieved

85
Q

Precaution after radioiodine therapy

A

Avoid close prolonged contact with children and pregnant during the first few days after treatment due to transmission of isotope and radiation from the gland

86
Q

Radioiodine should be used cautiously in

A

Children and adolescents
Iodine allergy
Concurrent severe ophthalmopathy in smokers

87
Q

Prevents exacerbation of opthalmopathy

A

Prednisone 40 mg/d at time of radioiodine treatment tapered over 3 months

88
Q

Absolute contraindication for radioiodine therapy

A

Pregnant - patient can conceive safely after 6 months of treatment
Breastfeeding

89
Q

Used as initial therapy to attain euthyroidism
Before radioiodine therapy or surgery
As prolonged course with goal of tapering

A

Thionamides

90
Q

Reduces oxidation and organification of iodine
Inhibiting the TPO enzyme and thyroid hormone synthesis

Possible immunomodulatory role to attenuate the autoimmune process

A

Thionamides

91
Q

As thyrotoxicosis improves, starting doses may be gradually reduced after

A

3-4 weeks

92
Q

Thionamides

A

PTU 100-200mg every 6-8h

Methimazole 10-20mg every 8-12h
Carbimazole 10-20mg every 8-12h
OD if euthyroid

93
Q

High doses of thionamide combined with
Levothyroxine

Avoid possibility of hypothyroidism
Does not provide index of treatment response
Exposes patients to higher doses

A

Alternative regimen

Block-replace regimen

94
Q

Euthyroidism with the use of thionamides canbe achieved in

A

4-6 weeks

95
Q

Treatment with thionamides is continued for

A

6 - 12 months

96
Q

Long term remission after cessation of thionamides is possible in

A

20%

97
Q

PTU is given to pregnants only until

A

1st trimester

98
Q

Rare but serious side effect that require discontinuation of thionamide

A

Agranulocytosis (<1%)
Sore throat, fever, mouth ulcers
CBC

Hepatitis
SLE

99
Q

Common side effects that resolve spontaneously after thionamide drug

A 
Rash
Urticaria
Fever
Mild leukopenia
Arthralgia (1-5% of patients)
100
Q

Should be given in higher doses when given concurrently with thionamides due to accelerated plasma clearance

A

Warfarin

101
Q

Needs increased dose during thyrotoxic state because of increased clearance

A

Digoxin

102
Q

In pregnancy this regimen should be employed to avoid feta hypothyroidism

A

Titration

103
Q

Preferred thionamide for pregnant because of greater safety profile

First line in pregnancy

A

PTU

104
Q

Spontaneous remission of hyperthyroidism occurs in this trimester permitting discontinuation of thionamides

A

third

105
Q

Breastfeeding is safe with low doses of

A

PTU <450 mg/day

106
Q

Use of carbimazole and methimazole in pregnancy is discouraged because of weak association with:

May be used if allergic

A

aplasia cutis

choanal atresia

107
Q

Subtotal thyroidectomy indications

A

Pregnant whose thyrotoxicosis is not controlled by thionamide
Relapse after thionamide drugs and decline treatment with radioiodine
Very large goiters with probability of effective treatment with radioiodine or thionamide is judged to be low
Risk for cancer

108
Q

Surgery prep to avoid thyrotoxic crisis

A 
Control of thyrotoxicosis with antithyroid drugs
Potassium iodide (3 drops of saturated solution PO TID)
109
Q

Possible surgical complications

A

Bleeding
Laryngeal edema
Hypoparathyroidism
Damage to recurrent laryngeal nerves

110
Q

Thyroid storm treatment

A

Large dose of PTU (600 mg loading dose and 200-300 mg every 6 hours)
PO, NGT, rectum

1 hour after first dose give stable iodine to block thyroid hormone synthesis

Saturated solution of potassium iodide, 5 drops every 6 hours

Ipodate or iopanoic acid (0.5 mg q12 PO)

Sodium iodide (0.25 g IV q6)

Propranolol 40-60mg q4 for tachycardia and other adrenergic manifestations

Dexamethasone 2mg q 6 to inhibit peripheral T4-T3 conversion and reduce thyroid hormone by supressing TSH secretion

111
Q

Supportive measures during thyroid storm

A

Antibiotics (if infection is present)
Cooling
Oxygen
Intravenous fluids
Intensive monitoring/supportive care
Identification and treatment of precipitating cause
Urgent reduction of thyroid hormone synthesis

112
Q

Mild/moderate ophthalmopatht treatment:

A

Meticulous Control of thyroid hormone levels
smoking cessation
Explanation on Natural history of ophthalmopathy
Occular discomfort: artifical tears (1% methycellulose) and dark glasses with frames

Periorbital edema may respond to more upright sleeping position or diuretic

Corneal exposure during sleep can be avoided by using patches or taping eyelids shut

Minor degrees of diplopia improve with prisms fitted to spectacles

113
Q

Optic nerve involvement

Chemosis with corneal damage

A 
Prednisone 40-80mg/d in 2/3 of patients
Taper by 5 mg every 1-2 weeks over 3 months
Pulse therapy with IV methylprednisone 
Orbital decompression surgery 
External beam radiotherapy
114
Q

Thyroid dermopathy treatment

A

Topical high potency glucocorticoid

Ocreotide

115
Q

Primary hyperthyroidism

Monitoring

A

on antithyroid drug:

Follow free T4 until TSH normalizes
Then use both TSH and FT4

116
Q

Anithyroid medication should be titrates on the basis of

A

FT4 until TSH normalizes

117
Q

Patients should be followed up closely for relapse until after discontinuation of antithyroid drug therapy

Then

A

First year after discontinuing antithyroid drug therapy

annually thereafter for life

118
Q

Patients treated with radioiodine especially higher doses are at particularly high risk for

A

hypothyroidism

119
Q

Patients who underwent radioiodine ablation should have close follow-up

A

for the first year after ablation followed by at least annual thyroid function test

120
Q

Should be monitored for the first several months following ablation rather than TSH levels

A

FT4

121
Q

Useful in third trimester to assess the risk of neonatal hyperthyroidism

A

TSH receptor antibodies

Monitor thyroid levels throughout pregnancy
Monitor thyroid function closely in postpartum

Fetal hyperthyroidism may develop even if the mother has previously been rendered euthyroid because TSH receptor antibodies can persist

122
Q

Develops in up to 15% of patients with Grave’s

A

Spontaneous immune HYPOTHYROIDISM

123
Q

Develops in 80% of patients treated with radioiodine

A

HYPOTHYROIDISM

124
Q

Thyrotoxic crisis may be precipitated by

A

Acute illness (stroke, infection, trauma, diabetic ketoacidosis)
Surgery (especially on thyroid)
Radioiodine treatment for partially treated or untreated hyperthyroidism

125
Q

Pregnancy complicated by uncontrolled hyperthyroidism is associated with increased risks of

A

Spontaneous abortion
Premature labor
Preeclampsia
Stillbirth

Postpartum period has risk for relapse of Grave’s

126
Q

Grave’s disease may fluctuate between hypo and hyperthyroidism due to changes in the

A

functional activity of TSH receptor antibodies

127
Q

Incomplete treatment with radioiodine ablation or early relapse is more common in

A

Men <40 years

128
Q

Predictors of persistent hyperthyroidism

A

Younger age
Larger thyroid gland
Higher serum T4 concentrations at diagnosis
Higher 24-hour 123 iodine thyroid uptake value

129
Q

Hyperthyroidism prognosis

A

Pretreatment with a thionamide before radioiodine is associated with a lower rate of successful treatment

Risk of hypothyroidism after RAI depends on dosage of at least 10-20% in first year, 5% per year after

Most patients progress to hypothyroidism over 5-10 years

130
Q

Predictors of remission

A 
Disappearance of TSH receptor antibodies
Smaller goiters
Mild hyperthyroidism
Age >40 years
Female sex

15% who achieve remission after use of antithyroid drugs develop hypothyroidism 10-15 years later

131
Q

Recurrent rates for subtotal thyroidectomy

A

<2%

132
Q

Ophthalmopathy prognosis

A

Clinical course does not parallel that of thyroid disease
Typically worsens over the initial 3-6 months, plateaus over the next 12-18 months, then gradually improves, particularly in the soft-tissue changes
Course is fulminant in 5% of patients, requiring intervention in the acute phase (for optic nerve compression or corneal ulceration)
Radioiodine treatment may WORSEN eye disease in smokers

133
Q

Appears 1-2 years after development of Graves

May improve spontaneously

A

Thyroid dermopathy

134
Q

In thyrotoxic crisis or thyroid storm, there is 30% risk of death even with treatment due to

A

Cardiac failure
Arrhythmia
Hyperthermia

Medicine (29 decks)

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