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GINME > Week 7: Hypothyroidism > Flashcards

Week 7: Hypothyroidism Flashcards

1
Q

Describe thyroid histological features

A
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2
Q

Identify features of thyroid histology

A
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3
Q

Identify features of thyroid histology

A
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4
Q

Where does thyroid hormone synthesis occur?

A
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5
Q

Describe the synthesis of thyroid hormones

A

TSH from pituitary to TSH receptor and protein synthesis (thyroglobulin) Thyroglobuilin to the colloid and T3 and T4 are added and T3 and T4 are cleaved off and released to the body

Iodide is brought in via Na+-Iodide symporter

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6
Q

What happens to T3 and T4 in the target cell?

A
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7
Q

Describe Thyroid hormone metabolism

A
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8
Q

Describe the T4 metabolism to T3

A
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9
Q

Describe the Wolff-Chaikoff effect

A

excess iodine causes shut down of thyroid hormone production but after awhile can escape this effect and production will resume

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10
Q

TSH structure

A
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11
Q

Describe thyroid hormone structures

A
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12
Q

Production rate of T4

A

80-100 mcg/day

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13
Q

Where is T4 produced

A

Thyroid

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14
Q

T4 storage

A

extrathyroidal pool of about 800-1000 mcg

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15
Q

T4 rate of degradation

A

10% per day

80% is deiodinated

  • 40% converted to T3
  • 40% converted to reverse T3 (rT3)
  • 20% is conjugated with glucuronide and sulfate, deaminated and decarboxylated form tetraiodothryoacetic acid (tetrac), or cleaved between the two rings
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16
Q

Pathways of thyroid hormone metabolism

A
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17
Q

T3 production rate

A

30-40 mcg/day

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18
Q

T3 storage

A

extrathyroidal T3 pool of about 50 mcg which is intracellular

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19
Q

Where is T3 produced?

A

only about 20% is produced in the thyroid

80% is produced extrathyroidal deiodination of T4 by 5’-deiodinase

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20
Q

T3 rate of degradation

A

mostly by deiodination about 75% per day

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21
Q

How are thyroid hormones stored

A

essentially circulating in the blood bound to protein

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22
Q

What are plasma thyroid hormones bound to?

4 listed

A
  • Thyroxine-binding globulin (TBG)
  • Transthyretin
  • Albumin
  • Lipoproteins
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23
Q

What is TBG?

A

Thyroxine-binding globulin

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24
Q

Liver failure effects on TBG

A

Increased TBG due to hyper estrogenic state that occurs in cirrhosis

Elevated estrogen leads to increased TBG production in the liver

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25
Q

TBG levels

A

TBG increase in pregnancy or OCP use (estrogen TBG), cirrhosis due to hyperestrogenic state, also OCP

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26
Q

T4 binding globulins

A
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27
Q

T3 binding globulins

A

TTR = Transthyretin

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28
Q

Regulation of thyroid function

A
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29
Q

TSH secretion properties

A

75 -150 mU/day (15-30 mcg/day)

TSH secretion is pulsatile

TSH concentrations are 50 - 100% higher in the late evening than during the day

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30
Q

Cellular effects of thyroid hormone

A
  • T4 is converted to T3 (which is the active thyroid hormone)
  • DNA synthesis of various proteins
  • bone growth
  • CNS maturation
  • Increased O2 consumption (increase Na+K+ATPase and metabolic enzymes)
  • Increase β1 activity in the heart increasing heart rate and contractility
  • increase glycogenolysis
  • increase in CO2 and ventilation
  • Increase renal function
  • Decreased muscle mass
  • Decreased adipose from freeing up substrate
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31
Q

What is hypothyroidism

A

deficiency of thyroid hormone

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32
Q

What is primary hypothyroidism?

A

An issue within the thyroid

(High TSH levels)

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33
Q

What is secondary hypothyroidism?

A

(Low TSH)

Issue with the pituitary

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34
Q

What is tertiary hypothyroidism?

A

(Low TRH, low TSH)

hypothalamic disease

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35
Q

Thyroid hormone resistance

A

Rare

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36
Q

Primary hypothyroidism prevalence

A

95% of all hypothyroidism

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37
Q

Prevalence of hypothyroidism

A
  • 2% of adult women
  • 0.2% of adult men
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38
Q

Clinical features of hypothyroidism

A

Constitutional symptoms

  • Cold intolerance
  • Fatigue
  • lethargy
  • weakness
  • hoarseness

Integument

  • Thickened/yellowed, dry, non-pitting edema (“Myxedema”) of hands/feet/periorbital region
  • dry, cool skin
  • Alopecia
  • Hair- brittle and dry
  • brittle nails

Cardiovascular

  • reduced contractility
  • reduced rate
  • reduced cardiac output
  • pericardial/pleural effusions
  • increased peripheral vascular resistance
    • CHF-rare

Gastrointestinal

  • decreased appetite
  • constipation
  • weight gain (5-10% increase)

Gynecologic

  • menorrhagia
  • menstrual irregularities

Musculoskeletal

  • Myalgias
  • arthralgias
  • hypothyroid myopathy
    • proximal muscle weakness
    • CK elevation

Hematologic

  • anemia
    • normocytic, normochromic anemia

Neurologic

  • delayed relaxation phase of DTRs
  • difficulty concentrating
  • poor memory
  • somnolence
  • depression
  • headache
  • paresthesias
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39
Q

Constitutional symptoms of hypothyroidism

A
  • Cold intolerance
  • Fatigue
  • lethargy
  • weakness
  • hoarseness
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40
Q

Integument symptoms of hypothyroidism

A
  • Thickened/yellowed, dry, non-pitting edema (“Myxedema”) of hands/feet/periorbital region
  • dry, cool skin
  • Alopecia
  • Hair- brittle and dry
  • brittle nails
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41
Q

Cardiovascular symptoms of hypothyroidism

A
  • reduced contractility
  • reduced rate
  • reduced cardiac output
  • pericardial/pleural effusions
  • increased peripheral vascular resistance
  • CHF-rare
42
Q

What is this depicting?

A

Severe hypothyroidism

periorbital edema

43
Q

What is this depicting?

A
  • Severe hypothyroidism
  • periorbital swelling
  • loss of the outer third of eyebrows
44
Q
A
45
Q

Gastrointestinal symptoms of hypothyroidism

A
  • decreased appetite
  • constipation
  • weight gain (5-10% increase)
46
Q

Gynecologic symptoms of hypothyroidism

A
  • menorrhagia
  • menstrual irregularities
47
Q

Musculoskeletal symptoms of hypothyroidism

A
  • Myalgias
  • arthralgias
  • hypothyroid myopathy
    • proximal muscle weakness
    • CK elevation
48
Q

Hematologic symptoms of hypothyroidism

A
  • anemia
    • normocytic, normochromic anemia
49
Q

Neurologic symptoms of hypothyroidism

A
  • delayed relaxation phase of DTRs
  • difficulty concentrating
  • poor memory
  • somnolence
  • depression
  • headache
  • paresthesias
50
Q

Hypothyroid myopathy

A
  • proximal muscle weakness
  • CK elevation
51
Q

Type of anemia seen with hypothyroidism

A

normocytic normochromic anemia

52
Q

Causes of primary hypothyroidism

A

Iodine deficiency (undeveloped world from iodine salt in developed)

Iatrogenic

  • surgery
  • radioablation
  • external radiation therapy

Autoimmune thyroid destruction

Drugs interfering with hormone synthesis (lithium (bipolar), amiodarone, interferon alpha, tyrosine kinase inhibitors)

Infiltrative diseases

Congenital thyroid agenesis or defects in hormone synthesis

53
Q

Drugs that can interfere with thyroid hormone synthesis

4 listed

A
  • Lithium (bipolar)
  • amiodarone
  • interferon-alpha
  • tyrosine kinase inhibitors
54
Q

Infiltrative disease that can cause primary hypothyroidism

7 listed

A
  • fibrous thyroiditis (Riedel’s thyroiditis)
  • Hemochromatosis
  • Sarcoidosis
  • amyloidosis
  • scleroderma
  • leukemia
  • cystinosis
55
Q

What is the most common type of thyroid disease in developed regions?

A

Autoimmune (Hashimoto’s) Thyroiditis

56
Q

Autoimmune (Hashimoto’s) Thyroiditis epidemiology

A
  • most common type of thyroid disease in iodine-sufficient regions
  • mainly in females
  • aged 30-50
  • also common in children
  • Can be associated with polyglandular autoimmune disease (celiac, pernicious anemia, adrenal insufficiency)
57
Q

Hashimoto’s Thyroiditis can be associated with?

5 listed

A
  • Can be associated with polyglandular autoimmune disease (celiac, pernicious anemia, adrenal insufficiency)
  • Turner Syndrome
  • Down syndrome
  • HLA-DR5
  • Increased risk of non-Hodgkin Lymphoma (typically of B-cell origin)
58
Q

Serological tests for Hashimoto’s Thyroiditis

A

Autoantibodies

  • Thyroglobulin
  • Thyroid peroxidase
  • Thyroid Na/I transporter (not measurable)
59
Q

Histological features of Hashimoto’s Thyroiditis

A
60
Q

Histology of Hashimoto’s Thyroiditis

A

germinal centers forming

lymphocytic infiltrate Hurthle cells or oncocytic cells are hallmark of Hashimoto’s Thyroiditis

61
Q

Hashimoto’s Thyroiditis Clinical presentation

A

Hashitoxicosis

  • hyperthyroid early in course due to release of T4/T3 from ruptured thyroid follicles
  • then become hypothyroidic

Chronic inflammation over years leads to hypothyroidism

May present with moderately nontender thyroid

Later thyroid becomes atrophic and fibrotic

62
Q

What is postpartum thyroiditis?

A
  • Destructive thyroiditis induced by an autoimmune mechanism within one year of parturition
  • Can also occur after spontaneous or induced abortion
    *
63
Q

How is postpartum thyroiditis different from other types

A
  • hyperthyroid phase from thyroid follicle destruction with low TSH
  • may have brief euthyroid phase (normal level)
  • becomes hypothyroidic
  • High TSH and high 24-hour RAI uptake (which is a test for hyperthyroidism)
  • 20-30% have hyper followed by transient hypothyroidism
  • 40-50% have only transient hypothyroidism
  • hypothyroidism lasts several weeks r up to 6 months
  • 20-40% have only the hyperthyroidism
64
Q

How long does postpartum thyroiditis last?

A

postpartum hypothyroidism lasts several weeks up to 6 months

65
Q

Postpartum thyroiditis clinical presentation

A
  • Mildly enlarged, diffuse, nontender thyroid gland
66
Q

Postpartum thyroiditis associations

A
  • Consider in women
  • Type 1 DM
  • Hx of postpartum thyroiditis after a previous pregnancy
  • Hx of high serum antithyroid peroxidase antibody concentrations prior to pregnancy
  • Clinical manifestations of postpartum thyroiditis
  • Postpartum depression
67
Q

Treatment of Postpartum thyroiditis

A

Treat with T4 if symptomatic but is transient so just wait

68
Q

What is Riedel Thyroiditis?

A

Thyroid replaced by fibrous tissue with inflammatory infiltrate

fibrosis may extend to local structures (eg trachea, esophagus), mimicking anaplastic carcinoma

69
Q

Riedel Thyroiditis clinical presentation

A

fixed, hard (rock-like) painless goiter

1/3 of patients become hypothyroidic

70
Q

Riedel Thyroiditis histological features

A
71
Q

Riedel Thyroiditis associations

A

Considered a manifestation of IgG4-related systemic disease (eg, autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis)

72
Q

What is congenital hypothyroidism

A

1:2000 to 1:4000 newborns

One of the most common preventable causes of intellectual disability

73
Q

Congenital hypothyroidism cause

A

85% are sporadic

15% hereditary (autosomal recessive)

74
Q

Congenital Central hypothyroidism

A

defects in the production of TSH due to either hypothalamic or pituitary dysfunction

1:16,404 newborns

75
Q

Congenital hypothyroidism clinical manifestations during pregnancy and at birth

A

More than 95% of infants with congenital hypothyroidism have few if any clinical manifestations of hypothyroidism at birth

Some maternal T4 crosses the placenta so pregnant women with hypothyroidism are mainly treated with T4

76
Q

Congenital hypothyroidism clinical manifestations of infants who did not undergo screening

A

6 Ps

  • Pot-bellied
  • Pale
  • Puffy-faced child
  • protruding umbilicus
  • protuberant tongue
  • poor brain development

lethargy

hoarse cry

feeding problems (needing to be awakened to nurse)

Constipation

Macroglossia

umbilical hernia

large fotnanels

hypotpponia

dry skin

hypothermia

prolonged jaundice

77
Q

What is cretinism?

A

untreated maternal hypothyroidism due to severe iodine deficiency

78
Q

Types of cretinism

A
  • Myxedematous cretinism
  • Neurologic cretinism
79
Q

Myxedematous cretinism

A

intellectual disability

short stature

hypothyroidism

iodine deficiency

thyroid injury predominantly late in pregnancy and continuing after birth

80
Q

Neurologic cretinism

A

Intellectual disability

deaf mutism

gait disturbances

spasticity

But not hypothyroidism

Hypothyroidism in the mother during early pregnancy but a euthyroid state postnatally due to adequate iodine intake in the newborn

81
Q

Thyroid hormone and development

A

Thyroid hormone is essential for normal maturation of the central nervous system

82
Q

What is consumptive hypothyroidism

A
  • very rare form of hypothyroidism
  • excessive degradation of thyroid hormone due to ectopic production of the type 3 deiodinase
    • Metabolized T4 to reverse T3 and T3 to T2
    • Vascular and fibrotic tumors and in patients with gastrointestianl stromal tumors (GISTs)
83
Q

Causes of secondary hypothyroidism

A
84
Q

Causes of tertiary hypothyroidism

A
85
Q

How to Diagnose hypothyroidism and type

A
86
Q

Lab findings in subclinical hypothyroidism

A
87
Q

Lab findings in overt hypothyroidism

A
88
Q

Lab findings in primary hypothyroidism

A
89
Q

Lab findings in secondary hypothyroidism

A
90
Q

Treatment for hypothyroidism

A
91
Q

What is Myxedema coma?

A
92
Q

Signs and symptoms of Myxedema coma

A
93
Q

Evaluation of myxedema coma

A

History and physical exam

Check TSH, Free T4, cortisol

94
Q

Treatment of myxedema coma

A
95
Q

Nontthyroidal illness AKA

A

Euthyroidal sick Syndrome

96
Q

What is Euthyroidal sick syndrome

A
97
Q

Euthyroid sick syndrome problem with low T3

A
98
Q

T4 levels in nonthyroidal illness

A
99
Q

Recommended labs for hypothyroidism

A
100
Q

Treatment in critically ill patients

A

GINME (63 decks)

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