Why do you see these signs and symptoms with a
hypofunctioning thyroid?

A hypofunctioning thyroid gland may be clinically termed
“hypothyroidism.” By definition, hypothyroidism results
from the under production of thyroid hormone from the
thyroid gland (Alberta Clinical Guidelines, 1999;
McCance & Huether, 2006). Since the main purpose of
thyroid hormone is to “run the body’s metabolism”, it is
understandable that persons with hypothyroidism will
have symptoms associated with a “slow metabolism”, such
as weight gain, fatigue, cold intolerance, depression,
and lethargy (Endocrine Web, 2008; Toward Optimized
Practice, 2008).

Thyroid hormone (TH) is produced by the thyroid gland
and is regulated through a negative-feedback loop
involving the hypothalamus, anterior pituitary, and
thyroid gland (McCance & Huether, 2006). Thyroid hormone
levels are detected by the hypothalamus; here,
thyrotropin-releasing hormone (TRH) is synthesized,
stored, and released into the hypothalamic-pituitary
system where it travels to the anterior pituitary
(Endocrine Web, 2008; McCance & Huether). The TRH causes
the anterior pituitary to release thyroid-stimulating
hormone (TSH), thus stimulating the production of TH in
the thyroid gland (McCance & Huether). When TH levels
are low (as in the case of hypothyroidism), the
hypothalamus will try to correct this “problem” by
increasing the TRH released, thereby stimulating
increased release of TSH. However, in persons with
hypothyroidism, the thyroid gland is unable to increase
TH production when stimulated by the increased levels of
TSH. This is clinically significant as an elevated TSH
level is the key diagnostic indicator of hypothyroidism
(Endocrine Web; Ladenson et al., 2000; McCance &
Huether; Toward Optimized Practice, 2008). The severity
of symptoms associated with hypothyroidism is directly
related to the degree of TH deficiency, and the onset
may be slow and gradual over months to years (McCance &
Huether). 

What Causes Hyperthyroid?

Simply stated, hyperthyroidism results from the over
production of thyroid hormone (Alberta Clinical
Guidelines, 1999; McCance & Huether, 2006).
Hyperthyroidism is also known as ‘thyrotoxicosis’
(Endocrine Web, 2008; McCance & Huether). Although there
are several different causes of hyperthyroidism, most of
the symptoms experienced by patients are the same
regardless of the cause (Endocrine Web). These symptoms
are usually ‘opposite’ to those of hypothyroidism as
hyperthyroid causes and increase in metabolic rate.
Therefore, symptoms include weight-loss, heat
intolerance, nervousness, palpitations, and insomnia to
name a few (Endocrine Web; McCance and Huether).
According to McCance and Huether, goiter is almost
always present in hyperthyroidism. 

Identifying the cause of hyperthyroidism is important,
as the cause of the disease will determine the
treatment. Primary hyperthyroidism is the most common
form of hyperthyroidism, and results from the over
production of TH from the thyroid gland (McCance &
Huether, 2006). This can be caused by specific diseases
that include: Graves disease, toxic multi-nodular
goiter, solitary hyper-functioning nodules of the
thyroid gland, and thyroid cancer (Endocrine Web, 2008;
McCance & Huether; Toward Optimized Practice, 2008).
Secondary hyperthyroidism is less common and is caused
by a malfunctioning of the anterior pituitary gland,
whereby excessive amounts of TSH are released, thus
stimulating an increased production/release of TH from
the thyroid (Endocrine Web; McCance & Huether).

Due to the negative feedback loop of thyroid regulation,
virtually all types of primary hyperthyroidism
encountered in clinical practice are accompanied by a
suppressed serum TSH concentration (Ladenson et al.,
2000). Typically those patients with serum TSH levels
less than 0.2 mU/L and accompanying clinical
manifestations are suspected to be hyperthyroid (Toward
Optimized Practice, 2008). 


~Paige and Sarah

PS. The attached PDF is "patient friendly" information
on thyroid  dysfunction...NP student friendly too!


References:

Alberta Clinical Guidelines (1999). Important patient
information on thyroid dysfunction: Laboratory
investigation. Alberta Medical Association: Edmonton. 


Endocrine Web (2008). Retrieved June 2, 2008, from
www.endocrineweb.com/hyper1 and
www.endocrinebeb.com/hypo1. 


Ladenson, P. W. et al. (2000). American thyroid
association guidelines for detection of thyroid
dysfunction. Archives of Internal Medicine, 160,
1573-1575. 

McCance, K. L., & Huether, S. E. (2006).
Pathophysiology: the biologic basis for disease in
adults and children. Elsevier Mosby: Philadelphia. 


Toward Optimized Practice (2008). Clinical practice
guideline: Investigation and management of primary
thyroid dysfunction. Alberta Clinical Practice
Guidelines: Edmonton