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CMT-dos > Hypothyroid/thyroiditis > Flashcards

Hypothyroid/thyroiditis Flashcards

1
Q

Thyroid Gland

general

A

Largest endocrine gland

It is located below the larynx and wraps around the anterior and lateral sides of the trachea

Consists of two large lobes connected by a narrow anterior isthmus

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2
Q

thyroid

Thyroid follicles

A

Filled with colloid
Lined by follicular cells
Secrete 2 thyroid hormones
Thyroxine (T4)
Triiodothyronine (T3)

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3
Q

Thyroid

Parafollicular cells or C cells

A

Located between the follicular cells
Secrete calcitonin which lowers blood calcium levels

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4
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A
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5
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6
Q

Thyroid Hormones

T4 and T3

A

Include T4 and T3
Thyroid hormones are produced when the thyroid gland is stimulated by TSH (thyrotropin) from the anterior pituitary (80% is T4 and 20% is T3)
T3 is the primary active thyroid hormone
200-300x more active than T4

T4 circulates through the body and is converted (on demand) by your cells into the active T3 thyroid hormone

Stored thyroid hormones in the follicular lumen are bound to a protein called thyroglobulin (TG)
Bound hormones cannot diffuse into cells

Unbound or “free” hormone can bind thyroid receptors and exert effects (metabolic rate and temperature regulation)

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7
Q

Inhibition of the conversion of T4→T3

A

Aging
Fasting/Calorie restriction
Any type of inflammation
Lack of sleep
Stress
Acute & chronic conditions (kidney and liver)
Intestinal problems (IBD)
Obesity
Medications: amiodarone, propranolol, propylthiouracil
Alcohol

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8
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A
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9
Q

Functions of Thyroid Hormones

Increased metabolism

A

Increased transcription of cell membrane Na+/K+ adenosinetriphosphatase (ATPase) → oxygen consumption
Enhanced fatty acid oxidation andheatgeneration
Gluconeogenesis,glycolysis,lipolysis

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10
Q

Functions of Thyroid Hormones

Growth and development

A

Protein synthesis
Regulates cholesterol and triglyceride metabolism
Affectsbrain, reproductive system, and bone development and growth

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11
Q

Factors that increase the conversion of T4 to T3

A

are zinc, selenium, Vitamin A, and Vitamin E

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12
Q

Functions of Thyroid Hormones

Interrelated actions with catecholamines

A

Thyroid hormones enhance responsiveness to catecholamines (“fight or flight response”)
What are the 3 catecholamines?
↑ Expression of catecholaminereceptors

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13
Q

Functions of Thyroid Hormones

Regulates pituitary hormone synthesis(feedback loop)

A

:)

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14
Q

Hypothyroidism

general

A

Failure of the thyroid gland to produce sufficient thyroid hormones to meet metabolic demands

Common clinical disorder
Affecting 1 in 300 persons in the United States - 85% are women

Incidence increases with age
5% of individuals over age 60 are affected

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15
Q

hypothyroid

types
(4 meds can induce)

A

Types:
Primary gland failure (primary hypothyroidism)
Congenital abnormalities, autoimmune destruction, iodine deficiency, and infiltrative diseases
Iatrogenic forms
Thyroid surgery, radioiodine therapy, and neck irradiation
Medication-induced
Amiodarone, lithium, propylthiouracil,methimazole

Insufficient thyroid gland stimulation by the pituitary gland (secondary hypothyroidism or “central hypothyroidism”) or the hypothalamus (tertiary hypothyroidism)

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16
Q

Congenital hypothyroidism

Clinical Presentation

6 P’s

A

Pale
Puffy face
Protuberant tongue
Poor brain development
Pot-bellied
Protruding umbilicus

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17
Q

hypothyroid

Sx

A

Arthralgias/myalgias
Cold intolerance
Constipation
Depression
Difficulty concentrating/mental slowness
Dry skin
Fatigue
Hair thinning/hair loss
Menstrual irregularities/infertility
Weight gain (despite loss of appetite)

slow, low metabolism

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18
Q

hypothyroid

PE findings

A

Signs:
Bradycardia
Cognitive impairment
Delayed deep tendon reflexes
Thin or brittle hair
Goiter (often with Hashimoto thyroiditis)
Lateral eyebrow thinning
Macroglossia
Periorbital and/or peripheral edema

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19
Q

Thyroid Screening

A

Evaluate for thyroid dysfunction in all patients with symptoms of hypothyroidism
Asymptomatic patients with risk factors for hypothyroidism may be screened

The American Thyroid Association recommends measuring thyroid function in all adults beginning at age 35 years and every 5 years thereafter; more frequent screening may be appropriate in high-risk or symptomatic individuals

The American Academy of Family Practice does not recommend screening for hypothyroidism in asymptomatic adults

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20
Q

Thyroid

Risk Factors

A

History of autoimmune disease
History of head or neck irradiation
Previous radioactive iodine therapy
Presence of a goiter
Family history of thyroid disease
Treatment with drugs known to influence thyroid function

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21
Q

Primary Hypothyroidism

labs for Dx

A

Inability of the thyroid gland to produce adequate amounts of thyroid hormone

Subclinical:
Elevated TSH
Normal T3/T4

Overt:
Elevated TSH
Low T4/low-normal T3

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22
Q

primary hypothyroidism

Antibody testing

A

Includes thyroid peroxidase (TPOs) and thyroglobulin (TBGs) antibodies

Helps in subclinical hypothyroidism orgoiter and if there is active thyroiditis
Presence of antibodies → autoimmune hypothyroidism (Hashimoto thyroiditis)

23
Q

Secondary hypothyroid

Dx

A

Secondary Hypothyroidism
Insufficient thyroid gland stimulation by the pituitary gland
Present in only 5% of cases

Decreased TSH
↓ FT3/FT4levels

24
Q

hypothyroid

Tx with dosing and what to avoid

A

Most patients require lifelong thyroid hormone therapy
Levothyroxine – biologically equivalent to thyroxine (T4)
Initial dose 1.6 mcg/kg PO daily

Taken in the morning, 30 minutes before eating or bedtime dosing

Check TSH level every 4-6 weeks and titrate dose appropriately

Goal: TSH level of 1-2
Calcium and iron supplements should not be taken within 4 hours of taking levothyroxine

Maintain either brand-name or generic products, but do not switch back and forth

Poor adherence to therapy is the most common cause of persistently elevated TSH levels

25
Q

hypothyroid Tx

Persistent symptoms despite TSH level in the lower normal range

A

Combination T3/T4 therapy may be used in select patients
Armour thyroid
Levothyroxine plus liothyronine (Cytomel)

26
Q

Myxedema coma

general

A

Rare, but life-threatening condition
Most severe manifestation of hypothyroidism
Occurs when the body’s compensatory responses to hypothyroidism are overwhelmed by a precipitating factor
Infection, medications, surgery, trauma, hypoglycemia, failure to reinstate thyroid replacement therapy

27
Q

Myxedema coma

Clin man

A

Myxedematous face: generalized puffiness, macroglossia, ptosis, periorbital edema
Nonpitting edema of the lower extremities
Deterioration of mental status – confusion, psychosis, and rarely coma
Hypothermia < 35.5°C (95.9°F)

Admission to the ICU
Ventilatory, electrolyte, and hemodynamic support, thyroid replacement

The patient does not need to be comatose to be diagnosed with myxedema coma

28
Q
A
29
Q
A
30
Q

Thyroiditis

general

A

General term that refers to “inflammation of the thyroid gland”

Encompasses several etiologies that present in different ways
Autoimmune thyroiditis (Hashimoto thyroiditis)
Painful subacute thyroiditis

Each etiology has a specific pathologic mechanism

31
Q

Hashimoto Thyroiditis

general

A

Also known as chronic lymphocytic thyroiditis
Most common form of thyroiditis
Autoimmune thyroid disease resulting in the destruction and failure of the thyroid gland

Epidemiology:
Age of onset is usually between 30-50 years
More common in ♀>♂

Exact trigger is unknown, although genetic and environmental factors play a role
Hashimoto Thyroiditis

32
Q

hashimotos

etiology
Genetics

A

Genetic risk factors:
Associated with mutations in HLA-DR3 and DR5 genes
Disease clusters found in families suggest genetic susceptibility
↑Incidenceinpatientswith Down’s syndrome and Turner’s syndrome

33
Q

hashimotos

patho

A

Autoimmune destruction is initiated; progressive depletion ofthyroid epithelial cells

Thyroidcell destruction mediated by:
CD8+cytotoxic cells
Local production ofcytokines
Antibodiesmade tothyroglobulin (Tg) and thyroid peroxidase (TPO)- only need one not both antibodies

34
Q

hashimotos

Lymphocytic infiltration and fibrosisofthyroid cells → follicles are disrupted and releaseof stored thyroid hormones:

A

Transient ↑ ofthyroxine(T4) andtriiodothyronine (T3)
Compensatory ↓thyroid-stimulating hormone (TSH) follows →T3/T4stores gradually decline
End result: ↑ TSH +hypothyroidism (often permanent)

35
Q

hashimotos

Risks

A

Increased risk of:
Developing other autoimmune diseases
B-cell lymphoma of the thyroid gland due to chronic inflammation
Typically presents with a triphasic clinical course

36
Q

hashimotos

3 phases

A

Phases:
1. “Hashitoxicosis” - initial transient hyperthyroidism
2. Subclinical hypothyroidism
3. Overt hypothyroidism

37
Q

hashimotos

Hypothyroidism signs

A

+/-Goiter *
Dry, coarseskin;alopecia; cool extremities
Puffy face, hands, and feet (nonpittingedema/myxedema)
Bradycardia

38
Q

hashimotos

Hypothyroidism common symptoms

A

Fatigue, cold intolerance, weight gain
Dryskin, hair loss
Difficulty concentrating and poormemory
Hoarse voice, impaired hearing
Constipation
Menstrual irregularities (menorrhagia, thenoligomenorrhea oramenorrhea)
Paresthesia

39
Q
A
40
Q

hashimotos

Labs during 3 phases

A

Thyroid hormone levels will differ in each phase:
Hashitoxicosis: ↓ TSH + ↑ freeT3/T4
Subclinical hypothyroidism: ↑ TSH + normal freeT3/T4
Overt hypothyroidism: ↑ TSH + ↓ freeT3/T4

↑ Thyroid peroxidase antibody level (TPO Ab) – 90% of cases
High levels of TPO Ab predicts progression to symptomatic hypothyroidism
↑ Thyroglobulin antibodies (Tg Ab) – 40% of cases

41
Q

thyroiditis

Thyroid ultrasound

A

Differentiate between thyroiditis form multinodular goiter, thyroid nodules, or malignancy

42
Q

thyroiditis

Radioactive iodine uptake (RAIU)

A

low uptake → cold thyroid

checking for malignancy

43
Q

thyroiditis

Fineneedle aspiration

A

If there is a dominant nodule or suspicion ofmalignancy

44
Q

Thyroid uptake scans

A

Radiologic diagnostic tool used to determine thethyroidfunction and pathology
Uses radioactive iodine (I-123 or I-131)

Thyroiditis versus other thyroid diseases):
A: normal
B: Graves’ disease: diffuse increased uptake in both thyroid lobes
C: toxic multinodular goiter: “hot” and “cold” areas of uneven uptake
D: toxic adenoma: increased uptake in a single nodule with suppression of the surrounding thyroid
E: thyroiditis: decreased or absent uptake

45
Q

thyroiditis

Hashitoxicosis
Tx

A

Antithyroid medication should not be used
Nonspecific beta-blockers to block peripheral conversion of T4 → T3

46
Q

Overt hypothyroidism
Tx for young healthy pts and elderly
Adjust by how much?
Goal TSH

A

Levothyroxine - synthetic form ofT4 that is peripherally converted toT3
1.6 mcg/kg PO daily for young and healthy patients
25 mcg per day in the elderly
Adjust dose by 12.5 or 25 mcg every 4-6 weeks until clinically euthyroid; may also reduce goiter size
Goal: TSH level of 1-2
Absorptionreduced by antacids,iron,calcium

47
Q

Elevated TPO antibody levels and subclinical hypothyroidism
Tx

A

Levothyroxine 25-50 mcg PO daily
Adjust dose by 12.5 or 25 mcg every 4-6 weeks until clinically euthyroid

48
Q

Painful Subacute Thyroiditis

general

A

Transient thyrotoxic state characterized by anterior neck pain

Often follows an upper respiratory viral infection → triggers an inflammatory destruction of thyroid follicles

Most recover, but 1/3 evolve into overt hypothyroidism over a 10-year period
♀>♂

49
Q

Painful Subacute Thyroiditis

Initial Clinical Presentation

A

Neck pain in the area of the thyroid (cardinal feature) that may radiate to the jaw
Diffuse thyroid enlargement (goiter)
Dysphagia
Increased sweating
Tremor
Weight loss
Fever
Tachycardia

50
Q

Painful Subacute Thyroiditis

Labs during Thyrotoxic phase
Iodine uptake?

A

Lasts 4-8 weeks
↓ TSH
Initially ↑ free T4 and T3 (T4>T3 -transient hyperthyroidism is due to passive release of stored thyroid hormone)
↑ ESR and CRP
Thyroid scan with radioactive iodine uptake
Low uptake of iodine

51
Q

Painful Subacute Thyroiditis

Labs during Hypothyroid phase

A

Variable length
↑ TSH
↓ free T4 and T3

52
Q

Painful Subacute Thyroiditis

Tx

A

The thyroid gland spontaneously resumes normal thyroid hormone production after several months in most cases

Beta blockers may be used for patients with significant hyperthyroid symptoms

Thyroid hormone supplementation is only needed for patients who are symptomatic or have clear signs of hypothyroidism (levothyroxine)

53
Q

Painful Subacute Thyroiditis

Relief of thyroid pain

A

First-line therapy options:
Aspirin (acetylsalicylic acid) 2,600 mg/day in divided doses
Ibuprofen 3,200 mg/day in divided doses

If no improvement of neck pain after 4 days or patient has severe neck pain

Corticosteroids 40 mg/day x 5-7 days, then slowly tapered over 30 days

CMT-dos (95 decks)

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