ENDOC- HYPOTHYROID Flashcards
(89 cards)
1
Q
_____________ is caused by any structural or functional derangement that interferes with the
production of adequate levels of thyroid hormone.
A
Hypothyroidism
2
Q
Hypothyroidism is a fairly common disorder,
and by some estimates the population prevalence of overt hypothyroidism is 0.3%, while
subclinical hypothyroidism can be found in greater than 4%. [7]
The prevalence of
hypothyroidism increases with age, and it is nearly tenfold more common in____________
It can result from a defect anywhere in the hypothalamic-pituitary-thyroid axis.
As in the case of
hyperthyroidism, this disorder is divided into primary and secondary categories, depending on
whether the hypothyroidism arises from an intrinsic abnormality in the thyroid itself, or occurs as
a result of pituitary and hypothalamic disease ( Table 24-4 ).
A
women than in men.
3
Q
_____________ accounts
for the vast majority of cases of hypothyroidism, and can be accompanied by an enlargement in
the size of the thyroid gland (goiter).
A
Primary hypothyroidism
Note :Primary hypothyroidism can be congenital, acquired, or
autoimmune
4
Q
Causes of Hypothyroidism
A
- Primary
- secondary (central)
5
Q
Primary Hypothyroidism
A
- Developmental (thyroid dysgenesis: PAX8, FOXE1, TSH receptormutations)
- Thyroid hormone resistance syndrome (THRB mutations)
- Postablative
Surgery, radioiodine therapy, or external
irradiation - Autoimmune hypothyroidism
Hashimoto
thyroiditis [*] - Iodine deficiency [*]
- Drugs (lithium, iodides, p-aminosalicylic acid) [*]
- Congenital biosynthetic defect (dyshormonogenetic goiter)
6
Q
SECONDARY (CENTRAL)
A
- Pituitary failure
- Hypothalamic failure
- (rare)
7
Q
** ______________**account for the majority of cases of hypothyroidism in developed
countries.
A
Hashimoto thyroiditis and
postablative hypothyroidism
8
Q
Associated with enlargement of thyroid (“goitrous hypothyroidism”).
A
- thyroiditis [*]
- Iodine deficiency [*]
- Drugs (lithium, iodides, p-aminosalicylic acid) [*]
- Congenital biosynthetic defect (dyshormonogenetic goiter) [*]
9
Q
Worldwide, ______________is most often the result of endemic iodine deficiency in
the diet (see below).
A
**congenital hypothyroidism **
10
Q
Other less common forms of congenital hypothyroidism include , such as
A
- inborn errors of thyroid metabolism (dyshormonogenetic goiter),
- wherein any one of the multiple steps leading to thyroid hormone synthesis may be deficient
11
Q
What arthye the steps in thyroid hormone synthesis?
A
(1) iodide transport into
thyrocytes, (2) iodide “organification” (binding of iodide to tyrosine residues of the storage
protein, thyroglobulin), and (3) iodotyrosine coupling to form hormonally active T3 and T4.
12
Q
_______________ gene are the most common cause of
dyshormonogenetic goiter.
A
Mutations in the thyroid peroxidase (TPO)
13
Q
_____________, characterized by hypothyroidism and
sensorineural deafness
A
Pendred syndrome
14
Q
Pendred syndrome is due to:
A
, is caused by mutations in the SLC26A4 gene, whose product, **pendrin, **is an anion transporter expressed on the apical surface of thyrocytes and in the inner ear.
15
Q
In rare instances there may be complete absence of thyroid parenchyma (thyroid agenesis), or
the gland may be greatly reduced in size (thyroid hypoplasia).
Germline mutations in transcription factors that are expressed in the developing thyroid and regulate follicular differentiation, such as_______________________, have been reported in individuals with thyroid agenesis.
A
thyroid transcription factor-2 (TTF-2), also known as FOXE1, and
paired box-8 (PAX-8)
16
Q
What is the typical presentation of patients wit thryoid agenesis?
A
These patients
typically present with a constellation of extra-thyroidal malformations.
17
Q
Inactivating germline
mutations of the_____________ is a rare genetic cause of isolated hypothyroidism (note
that activating somatic mutations of TSHR are found in autonomous thyroid nodules, see
below).
A
TSH receptor (TSHR)
18
Q
__________ is a rare autosomal-dominant disorder caused
by inherited mutations in the thyroid hormone receptor, which abolish the ability of the receptor
to bind thyroid hormones.
Patients demonstrate a **generalized resistance to thyroid hormone, **despite high circulating levels of T3 and T4.
Since the pituitary is also resistant to feedback
from thyroid hormones, TSH levels tend to be high as well.
A
Thyroid hormone resistance syndrome
19
Q
Acquired hypothyroidism can be caused by____________ ablation of thyroid
parenchyma.
A
surgical or radiation-induced
20
Q
A large resection of the gland ___________ for the treatment of hyperthyroidism of a primary neoplasm can lead to hypothyroidism.
A
(total thyroidectomy)
21
Q
The gland may also be
ablated by radiation, whether in the form of radioiodine administered for the treatment of
hyperthyroidism, or exogenous irradiation, such as external radiation therapy to the neck.
A
22
Q
What are the Drugs given intentionally to decrease thyroid secretion_____________
can cause acquired hypothyroidism, as can agents used to treat nonthyroid conditions (e.g.,
lithium, p-aminosalicylic acid).
A
(e.g., methimazole and propylthiouracil)
23
Q
________________ is the most common cause of hypothyroidism in iodine-sufficient
areas of the world.
A
Autoimmune hypothyroidism
24
Q
The vast majority of cases of autoimmune hypothyroidism are due to
_____________.
A
Hashimoto thyroiditis
25
```
Circulating autoantibodies, including\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_,are found in this disorder, and the **thyroid is
typically enlarged (goitrous).**
```
anti-microsomal, anti-thyroid
peroxidase, and anti-thyroglobulin antibodies,
26
**Autoimmune hypothyroidism** can occur in **isolation or in
conjunction with \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**** (**see discussion in
“Adrenal Glands”).
autoimmune polyendocrine syndrome (APS), types 1 and 2
27
Secondary (or central) hypothyroidism is caused by\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
NOTE :Necrosis, trauma, and nonpituitary tumors), or of **hypothalamic damage**
**from tumors, trauma, radiation therapy, or infiltrative diseases can cause central
hypothyroidism**
deficiency of TSH, and far more
uncommonly, that of TRH.
28
Classic clinical manifestations of hypothyroidism include\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_.
cretinism and myxedema.
29
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ refers to hypothyroidism that **develops in infancy or early childhood.**
Cretinism
TRIVIA: The term **cretin**
was derived from the **French chrétien, meaning “Christian**” or **“Christlike,”** and was applied to
these **unfortunates because they were considered to be so mentally retarded as to be
incapable of sinning**.
In the past this disorder occurred fairly commonly in areas of the world where dietary iodine deficiency is endemic, such as the **Himalayas, inland China, Africa, and
other mountainous areas**.
It has become much less frequent in recent years, as a result of the
widespread supplementation of foods with iodine. On rare occasions**, cretinism may also result
from inborn errors in metabolism**that**interfere with the biosynthesis of normal levels of thyroid
hormone (**dyshormonogenetic goiter, see above)
30
What are the clinical features of Cretinism?
Clinical features of cretinism include:
* impaired development of the **skeletal system and central nervous system, manifested by:**
* **severe mental retardation,**
* **short stature,**
* **coarse facial features,**
* **a protruding tongue,**
* **and umbilical hernia. **
31
The severity of the mental impairment in cretinism
seems to be related to the\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_.
time at which thyroid deficiency occurs in utero
32
Normally, maternal
hormones, including **T3 and T4, cross the placenta** and are critical to fetal brain development.
If
**there is maternal thyroid deficien**c**y** before the development of the fetal thyroid gland, mental
retardation is severe. In contrast, reduction in maternal thyroid hormones later in pregnancy,after the fetal thyroid has developed, allows normal brain development.
33
The term\_\_\_\_\_\_\_\_\_\_\_\_ is applied to **hypothyroidism d**eveloping in the **older child or adult.**
myxedema
34
**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**was first linked with thyroid dysfunction in 1873 by Sir William Gull
in an article addressing the **development of a “cretinoid state” in adults**.
Myxedema, or Gull disease,
35
In myxedeme the clinical
manifestations vary with the **age of onset of the deficiency**.
The older child shows signs and
symptoms intermediate between those of the cretin and those of the adult with hypothyroidism.
In the adult the condition appears insidiously and may take years to reach the level of clinical
suspicion.
36
What aret the clinical features of myxedema
are characterized by a:
**slowing of physical and mental activity .**
* The initial symptoms include **generalized fatigue, apathy, and mental sluggishness,** which may **mimic depression in the early stages of the disease.**
* Speech and intellectual functions become slowed.
* Patients with myxedema are **listless, cold intolerant**, and **frequently overweight**.
* **Decreased sympathetic activity results in constipation** and **decreased sweating**.
* The skin of these patients is **cool and pale because of decreased blood flow.**
* Reduced cardiac output probably contributes to **shortness of breath and decreased exercise capacity, two frequent**
**complaints in individuals with hypothyroidism**.
37
**Thyroid hormones** regulate the transcription of
several **sarcolemmal genes**, such a**s calcium ATPases,** whose encoded products are critical in
maintaining efficient cardiac output.
In addition, **hypothyroidism promotes an atherogenic profile
—an \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**—probably
contributing toward the **adverse cardiovascular mortality rates in this disease.**
increase in total cholesterol and low-density lipoprotein (LDL) levels
38
Histologically,
there is an accumulation of matrix substances, such as **glycosaminoglycans and hyaluronic**
a**cid, in skin, subcutaneous tissue, and a number of visceral sites.** This results in \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
non-pitting
edema, a broadening and coarsening of facial features, enlargement of the tongue, and
deepening of the voice.
39
Laboratory evaluation plays a vital role in the diagnosis of suspected hypothyroidism because
of the **nonspecific nature of symptoms**.
Patients with **unexplained increase in body weight or
hypercholesterolemi**a should be assessed for potential hypothyroidism
. Measurement of the
serum \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_is the most sensitive screening test for this disorder.
TSH level
40
The TSH level is
**increased** in **\_\_\_\_\_\_\_\_\_\_\_\_\_\_-** as a result of a **loss of feedback inhibition of TRH and TSH**
production by the hypothalamus and pituitary, respectively.
**primary hypothyroidism**
41
The **TSH level** is **not increased in**
persons with **hypothyroidism** **due to** \_\_\_\_\_\_\_\_\_\_\_\_. T4 levels are
decreased in individuals with hypothyroidism of any origin.
primary hypothalamic or pituitary disease
42
\_\_\_\_\_\_\_\_\_\_\_\_\_, encompasses a **diverse group of disorders**
characterized by **some form of thyroid inflammation**.
These diseases include conditions that
**result in acute illness with severe thyroid pain (e.g., infectious thyroiditis, subacute
granulomatous thyroiditis) and disorders in which there is relatively little inflammation and the
illness is manifested primarily by thyroid dysfunction—subacute lymphocytic thyroiditis and
fibrous (Reidel) thyroiditis.**
Thyroiditis, or inflammation of the thyroid gland
43
Thyroiditis conditions include:
* result in acute illness with severe thyroid pain (e.g., infectious thyroiditis, subacute granulomatous thyroiditis)
* and disorders in which there is relatively little inflammation
* and the illness is manifested primarily by thyroid dysfunction—subacute lymphocytic thyroiditis and
* fibrous (Reidel) thyroiditis.
44
Infectious thyroiditis may be either\_\_\_\_\_\_\_\_\_\_\_ or \_\_\_\_\_\_\_\_\_\_
acute or chronic.
45
Acute infections can reach the thyroid by
**\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**such as through a fistula from
the piriform sinus adjacent to the larynx.
* hematogenous spread
* or through direct seeding of the gland,
46
Other infections of the thyroid, including\_\_\_\_\_\_\_\_\_\_\_\_\_,\_\_\_\_\_\_\_\_\_\_ and\_\_\_\_\_\_\_, are more chronic and frequently occur in
immunocompromised patients.
* mycobacterial,
* fungal,
* and Pneumocystis infections
47
In thyroiditis, whatever the cause, the inflammatory involvement may cause
* sudden onset of neck pain
* and tenderness in the area of the gland and is accompanied by fever, chills, and other signs of infection.
48
Infectious thyroiditis can be **self-limited** or can be
**controlled with appropriate therapy.**
**Thyroid function is usually *_not significantly affected_***, and
there are **few residual effects except for possible small foci of scarring.**
This section focuses on
the more common and clinically significant types of thyroiditis:
1) Hashimoto thyroiditis,
(2) granulomatous (de Quervain) thyroiditis,
(3) subacute lymphocytic thyroiditis.
49
\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is the **most common cause of hypothyroidism in areas of the world where
*_iodine levels are sufficient_*.**
Hashimoto thyroiditis
Note: The name Hashimoto thyroiditis is derived from the 1912 report by Hashimoto **describing patients with goiter and intense lymphocytic infiltration of the thyroid
(struma lymphomatosa).**
50
. [10]\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ and ______________ (see below) are the **two
most common immunologically mediated disorders**of the**thyroid.**
Hashimoto thyroiditis and Graves disease
51
Hashimoto thyroiditis is
characterized by\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
gradual thyroid failure because of autoimmune destruction of the thyroid
gland.
52
Hashimoto thyroiditis is most prevalent between\_\_\_\_\_\_\_\_\_\_\_\_\_
45 and 65 years of age
53
In what gender is Hashimoto Disease more common?
**women** than in men,
with a **female predominance** of **10 : 1** to **20 : 1.**
NOTE:
Although it is **primarily a
disease of older women**,**it can occur in children and is a major cause of nonendemic goiter in
the pediatric population.**
54
is a major cause of nonendemic goiter in
the pediatric population.
Hashimoto's disease
55
Akin to other autoimmune diseases, Hashimoto thyroiditis has a **strong genetic component.**
This
is supported by the concordance of disease in as many as 4**0% of monozygotic twins,** as well as
the **presence of circulating antithyroid antibodies** in approximately **50% of asymptomatic siblings**
of Hashimoto patients.
56
Increased susceptibility to Hashimoto thyroiditis is associated with
* *polymorphisms in multiple immune regulation**–associated **genes,** the **most significant of which is**
* *the linkage to \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_**. [11]
cytotoxic T lymphocyte–associated antigen-4 (CTLA4) polymorphisms
57
What does the gene CTLA4 function for?
It is a **negative regulator of T-cell responses**, and not surprisingly, polymorphisms of the
CTLA4 gene that result in reduced protein level or function are **associated with a predisposition
to autoimmune disease**.
Negative regulator meaning inhibits so kaya pagnasira predispose to autoimmune disease
58
Another recently described genetic determinant of susceptibility to
Hashimoto thyroiditis is a **functional\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** gene that **encodes a lymphoid tyrosine phosphatase**, which **is also thought to inhibit
T-cell function.**[12]
polymorphism in protein tyrosine phosphatase-22
| (PTPN22)
59
* *Susceptibility** to **other autoimmune diseases**, such as **type 1 diabetes** (see
below) , **has been associated** with **polymorphisms** i**n both** ______ and \_\_\_\_\_\_\_\_\_\_.
1. CTLA4
2. and PTPN22.
60
What is the Pathogenesis.of Hashimoto thyroiditis
is caused by a **breakdown in self-tolerance to thyroid auto-antigens**.
This is exemplified by the **presence of circulating autoantibodies against _thyroglobulin_ and _thyroid
peroxidase_**in the vast majority of Hashimoto patients. The inciting events leading to breakdown
in self-tolerance in Hashimoto patients have not been fully elucidated, but possibilities include
**abnormalities of regulatory T cells (Tregs**) [13] , **or exposure of normally sequestered thyroid
antigens** ( Chapter 6 ).
61
Induction of thyroid autoimmunity is accompanied by a **progressive depletion** of **thyrocytes** by **apoptosis and replacement of the thyroid parenchyma by**
**\_\_\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_\_\_\_.**
mononuclear cell infiltration and fibrosis.
62
Multiple immunologic mechanisms may contribute to
thyroid cell death, including
• **CD8+ cytotoxic T cell–mediated cell death**: CD8+ cytotoxic T cells may cause thyrocyte destruction.
• **Cytokine-mediated cell death**: Excessive T-cell activation leads to the production of TH1 inflammatory cytokines such as interferon-γ in the thyroid gland, with resultant
recruitment and activation of macrophages and damage to follicles.
• **Binding of anti-thyroid antibodies (anti-thyroglobulin, and anti-thyroid peroxidase **antibodies) followed by antibody-dependent cell-mediated cytotoxicity ( Chapter 6 ).
63
What is the gross morphology of Hashimoto's thyroiditis?
* The thyroid is often **diffusely enlarged, although more localized enlargement **may be seen in some cases.
* The _capsule_ is **intact, and the _gland is well demarcated_ from adjacent structures.**
* **The cut surface is *_pale, yellowtan, firm, and somewhat nodular._***
64
WHat is the mcroscopic examination of Hashimotos thyroiditis?
* reveals **extensive infiltration** of the **parenchyma by a mononuclear inflammatory infiltrate containing small lymphocytes, plasma cells,**
* and well-developed germinal centers ( Fig. 24-11 ).
* The **thyroid follicles are atrophic** and are **lined in many**
* **areas by epithelial cells** **distinguished by the presence of abundant eosinophilic, granular cytoplasm, termed *_Hürthle cells_*.**
65
The\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is** characteristic of Hashimoto thyroiditis**.
presence o**f Hürthle cells **in conjunction with a **heterogeneous population of lymphocytes**
66
What is the **metaplastic response** of the **normally low cuboidal
follicular epithelium to ongoing injury.**
* extensive infiltration of the parenchyma by a **mononuclear inflammatory infiltrate** containing small lymphocytes, plasma cells,
* and well-developed germinal centers ( Fig. 24-11 ).
* The thyroid follicles are atrophic and are lined in many areas by epithelial cells distinguished by the **presence of abundant eosinophilic, granular cytoplasm, termed Hürthle cells.**
67
What is Hürthle cells?
presence of **abundant eosinophilic, granular
cytoplasm in the epithelial cells that line the atrophic thyroid follicles ** seen in Hashimotos thyroiditis
"H for H"
**"H**ürthle cells for **H**ashimotos"
68
In **“classic” Hashimoto thyroiditis**,\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
* interstitial connective tissue is increased and may be abundant.
* A fibrous variant is characterized by severe thyroid follicular atrophy
* and **dense “keloid-like” fibrosis**,
* broad bands of **acellular collagen encompassing residual thyroid tissue. **
69
What is the difference in Hashimoto's disease and Reidel thyroiditis?
Unlike Reidel thyroiditis (see below), the **fibrosis does not extend beyond the capsule of the gland.**
The remnant thyroid parenchyma demonstrates features of chronic lymphocytic thyroiditis.
70
What is the clinical Course of Hashimoto thyroiditis ?
most often comes to clinical attention as :
* painless enlargement of the thyroid, usually associated **with some degree of hypothyroidism**, in a **middle-aged woman.**
* The enlargement of the gland is **usually symmetric** and **diffuse**, but in **some cases it may be sufficiently localized to raise a suspicion of neoplasm.**
* In the usual clinical course, hypothyroidism **develops gradually**.
*
71
In some cases in Hashimoto's Thyroiditis, however, it may be preceded by **transientthyrotoxicosis** which is caused by?
**disruption of thyroid follicles,** with** secondary release of thyroid hormones (“hashitoxicosis”).**
72
In Hashimoto's Disease thyrotoxicosis, what happens?
During this phase**,**
* **free T4 and T3 levels are elevated,**
* TSH is diminished,
* and radioactive iodine uptake is decreased.
* As hypothyroidism supervenes, T4 and T3 levels fall, accompanied by a **compensatory increase in TSH. **
73
Individuals with Hashimoto thyroiditis are at increased risk for :
* for developing other autoimmune diseases, both endocrine (type 1 diabetes, autoimmune adrenalitis) and nonendocrine (systemic lupus erythematosus, myasthenia gravis, and Sjögren syndrome; see Chapter 6 ).
* They are also at increased risk for the **development of B-cell non-Hodgkin lymphomas**, especially **marginal zone lymphomas of
mucosa-associated lymphoid tissues (MALT lymphomas; see Chapter 13 ).**
**** NOTE: The relationship between Hashimoto disease and thyroid epithelial cancers remains controversial, with some
morphologic and molecular studies suggesting **a predisposition to papillary carcinomas.**
74
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
thyroiditis, occurs much less frequently than does Hashimoto disease.
The disorder is most
common **between the ages of 40 and 50** and, like other forms of thyroiditis, **affects women
considerably more often than men (4 : 1).**
**Subacute thyroiditis**, which is also **referred to as granulomatous thyroiditis or De Quervain**
75
Subacute thyroiditis is believed to be triggered by a\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
viral infection
Note: . The **majority of patients** have
a **history of an upper respiratory infection just before the onset of thyroiditis**.
76
SUBACUTE (GRANULOMATOUS) THYROIDITIS has a
seasonal incidence, with occurrences **peaking** in the \_\_\_\_\_\_\_\_\_\_
summer, and clusters of cases have been
reported in association with coxsackievirus, mumps, measles, adenovirus, and other viral
illnesses.
77
What is the pathogenesis of subacute thyroiditis?
Although the pathogenesis of the disease is unclear, one model suggests that it
* *results from a viral infection** that **leads to exposure to a viral** or t**hyroid antigen,** which is
* *released secondary to virus-induced host tissue damage.**
This antigen stimulates cytotoxic T
lymphocytes, which then damage thyroid follicular cells. In contrast to autoimmune thyroid
disease, the immune response is virus-initiated and not self-perpetuating, so the process is
limited.
78
What is the morphological appearance of Subacute Thyroiditis?
* The gland may be **unilaterally or bilaterally enlarged**
* and firm, with an intact capsule
* It may b**e slightly adherent to surrounding structures.**
* On cut section, the **involved areas are firm and yellow-white** and **stand out from the more rubbery, normal brown thyroid substance.**
79
Histologically what is the appearance of subacute thyroiditis?
* the changes are **patchy and depend on the stage of the disease.**
* Early in the active inflammatory phase, **scattered follicles may be entirely disrupte**d
* and** replaced by neutrophils** forming microabscesses.
* Later, the more characteristic features appear in the form of **aggregates of lymphocytes, activated macrophages, and plasma cells about collapsed and damaged thyroid follicles.**
*
80
Why is subacute thyroiditis called granulomatous?
Multinucleate giant cells **enclose naked pools or fragments of colloid** ( Fig. 24-12 ), hence the designation granulomatous thyroiditis.
In later stages of the disease a chronic inflammatory infiltrate and fibrosis may replace the foci of injury.
**Different histologic stages are sometimes found in the same gland, suggesting waves of destruction over a period of time.**
81
What is the clinical course of Granulomatois or subacute thyroiditis?
* There is a variable enlargement of the thyroid.
* The thyroid inflammation and hyperthyroidism are transient, usually diminishing in 2 to 6 weeks, even if the patient is not treated.
* Nearly all patients have **high serum T4 and T3 levels** and **low serum TSH** levels during this phase.
* However, unlike in hyperthyroid states such as Graves disease, **radioactive iodine uptake is diminished.**
* After recovery, generally in 6 to 8 weeks, normal thyroid function returns.
82
\_\_\_\_\_\_\_\_\_\_\_\_ is the most common cause of thyroid pain.
Granulomatous (de Quervain) thyroiditis
83
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_, which is also referred to as **painless thyroiditis**, usually comes
to clinical attention **because of mild hyperthyroidism, goitrous enlargement of the gland, or both.**
Although it can **occur at any age**, **it is most often seen in middle-aged adults** and is more
**common in women**.
Subacute lymphocytic thyroiditis
84
A disease process resembling painless thyroiditis can occur during the
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_).
postpartum period in up to 5% of women (postpartum thyroiditis
85
\_\_\_\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_\_\_ are **variants of Hashimoto thyroiditis**, since the **majority of patients have circulating**
**anti-thyroid peroxidas**e antibodies or a family history of other autoimmune disorders.
As many
as a third of cases can evolve into overt hypothyroidism over time, and the thyroid histology is
also reminiscent of Hashimoto thyroiditis (see below).
Painless and postpartum
thyroiditides
86
What is the morphology of Subacute Lymphocytic ( Painless Thyroiditis)?
Morphology.
Except for possible **mild symmetric enlargement, the thyroid appears normal
on gross inspection.**
The _***most specific histologic features consist of lymphocytic infiltration with hyperplastic germinal centers within the thyroid parenchyma and patchy disruption and
collapse of thyroid follicles***_
**. Unlike in frank Hashimoto thyroiditis, however, fibrosis and
Hürthle cell metaplasia are not prominent features.**
87
What is the Clinical Course of Subacute Painless Thyroiditis?
* Individuals with painless thyroiditis can present with a painless goiter, transient overt hyperthyroidism, or both.
* Some patients **transition from a hyperthyroid state to hypothyroidism before recovery.**
* The vast majority (∼80%) of individuals with postpartum thyroiditis are euthyroid by 1 year.
* **Postpartum thyroiditi**s can **resemble Graves disease,** the incidence of which is also increased in the setting of pregnancy.
* Infiltrative ophthalmopathy and other manifestations of Graves disease (see below) are, however, **not present in the former**
* **.** As stated, as many as a third of affected individuals **eventually progress to overt hypothyroidism over a 10-year period.**
88
Other, less common forms of thyroiditis include**\_\_\_\_\_\_\_\_-**
* , a rare disorder of unknown etiology characterized by **extensive fibrosis involving the thyroid and contiguous neckstructures.**
* The presence of a hard and fixed thyroid mass clinically simulates a thyroid carcinoma.
* It may be associated with idiopathic fibrosis in other sites in the body, such as the retroperitoneum.
* The presence of circulating anti-thyroid antibodies in most patients suggests an autoimmune etiology.
** Riedel thyroiditis**
89
