Week 2 Flashcards

1
Q

THYROID + sole function

A

 is the biggest gland in the neck. It is
situated in the anterior (front) neck
below the skin and muscle layers.
 gland takes the shape of a butterfly with
the two wings being represented by the
left and right thyroid lobes which wrap
around the trachea.
 sole function of the thyroid is to make
thyroid hormone. The function of the
thyroid therefore is to regulate the
body’s metabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

function of the thyroid gland

A

 The function of the thyroid gland is to take
iodine, found in many foods, and convert it
into thyroid hormones: thyroxine (T4) and
triiodothyronine (T3).
 These cells combine iodine and the amino
acid tyrosine to make T3 and T4. T3 and
T4 are then released into the blood stream
and are transported throughout the body
where they control metabolism (conversion
of oxygen and calories to energy).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Metabolic Function (Thyroid)

A

 Energy metabolism – Oxygen/Heat
 Carbohydrate metabolism
 Protein metabolism
 Lipid Metabolism
 Cardiovascular- increases heart rate,
output, systolic volume and
contractility
 Beta adrenergic effects
 Bone growth
 GI tract motility
 Erythropoietin production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Receptors related to the Thyroid hormone

A

The thyrotropin (TSH) receptor
plays a preeminent role in thyroid
physiology.
 TSH, acting through the TSH
receptor, is the major stimulator of
thyroid cell growth, differentiation
and function.

Thyroid hormone receptors (TRs)
are members of the nuclear
receptor superfamily that exhibit a
dual role as activators or
repressors of gene transcription in
response to thyroid hormone (T3).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Receptor isoforms

A

Modulate various physiological
functions in many organ systems.
The TRα and TRβ isoforms and
TRα1 and TRβ1 isoforms.

Have genomic or non-genomic
effects
 Genomic signaling pathway
directly influences
gene transcription and translation
 Non-genomic pathway involves
more rapid, cellular changes,
some of which also regulate gene
expression through more indirect
signaling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the key players for
Thyroid hormone regulation?

A

Hypothalamus: Thyrotropin-
releasing hormone (TRH)
 control of thyroid stimulating
hormone (TSH)

Pituitary: Thyroid stimulating
hormone (TSH)
 controls production of the thyroid
hormones by binding to TSH
receptors located on cells in the
thyroid gland.

Thyroid: triiodothyronine (T3) and
thyroxine (T4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Binding proteins

A

The major serum thyroid hormone-
binding proteins are:
-Thyroxine-binding globulin [TBG
or thyropexin],
 binds thyroid hormones in
circulation

Transthyretin
 a transport protein in the
serum and cerebrospinal fluid
that carries the thyroid
hormone thyroxine (T4)

Albumin (HAS, human serum
albumin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CONTROL AND REGULATION

A

 Is under the control of the pituitary gland, a
small gland the size of a peanut at the base of
the brain.
 When the level of thyroid hormones (T3 & T4)
drops too low, the hypothalamus is part of the
brain and produces TSH Releasing Hormone
(TRH) which tells the pituitary gland to
stimulate the thyroid gland (release TSH).
 The pituitary gland produces Thyroid
Stimulating Hormone (TSH) which stimulates
the thyroid gland by binding to the TSH
receptors to produce more hormones.
 The pituitary senses this and responds by
decreasing its TSH production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Thyroid Autoantibodies

A

Thyroid peroxidase antibodies
(TPO). These antibodies can be a sign of:
 Hashimoto disease, also known as
Hashimoto thyroiditis.
 This is an autoimmune disease and
the most common cause
of hypothyroidism. Hypothyroidism is
a condition in which the thyroid
doesn’t make enough thyroid
hormones.
 Graves’ disease.
 This is also an autoimmune disease
and the most common cause
of hyperthyroidism. Hyperthyroidism
is a condition in which the thyroid
makes too much of certain thyroid
hormones.

Thyroglobulin antibodies (Tg).
 These antibodies can also be a sign of
Hashimoto disease. Most people with
Hashimoto disease have high levels of
both Tg and TPO antibodies.
Thyroid-stimulating hormone
(TSH) receptor.
 These antibodies can be a sign of
Grave’s disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Common Thyroid Problems

A
  1. Those concerning the production
    of hormone (too much, or too
    little),
  2. Those due to increased growth
    of the thyroid causing
    compression of important neck
    structures or simply appearing
    as a mass in the neck,
  3. The formation of nodules or
    lumps within the thyroid which
    are worrisome for the presence
    of thyroid cancer, and
  4. Those which are cancerous.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Laboratory Diagnosis

A

Measurement of serum thyroid-stimulating
hormone (TSH): Measuring serum TSH is
the best way to determine thyroid dysfunction

Direct measurement of free T4 and T3:
Since free thyroid hormones are
available to peripheral tissues, directly
measuring serum free hormones avoids
the pitfalls of interpreting total levels,
which are influenced by the level of the
binding proteins. Thus, serum free
levels more accurately diagnose true
thyroid function.

Measurement of thyroid
autoantibodies:
 Autoantibodies to thyroid
peroxidase and, less commonly, to
thyroglobulin are present in almost
all patient’s thyroid autoimmune
disease,
 Thyroid peroxidase autoantibodies
are usually detected in patients with
Graves’ disease.
 Both these antibodies are
commonly measured by enzyme
immunoassays

Measurement of thyroglobulin:
 The principle use of serum
thyroglobulin is mostly used as a
tumour marker test to help guide
thyroid cancer treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hypothyroidism types

A

There are 3 types of hypothyroidism:
 Primary hypothyroidism – when your
thyroid gland becomes diseased and
cannot produce sufficient hormones
 Subclinical hypothyroidism- early and mild
form of hypothyroidism
 Secondary hypothyroidism – when your
pituitary gland isn’t stimulating your
thyroid to produce enough hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Etiology PRIMARY HYPOTHYROIDISM

A

Hashimoto’s thyroiditis-most common (most common)

 Iodine deficiency
 Drug therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signs and Symptoms hypothyroidism

A

Non-specific.
May be confused with other
conditions especially in postpartum
depression and elderly.

 Fatigue.
 Increased sensitivity to cold.
 Constipation.
 Dry skin.
 Weight gain.
 Puffy face.
 Hoarseness.
 Muscle weakness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Auto antibodies in hypothyroidism

A

Autoantibodies:
Thyroid autoantibodies
are antibodies that develop when a
person’s immune system mistakenly
targets components of the thyroid gland
or thyroid proteins, leading
to chronic inflammation of the thyroid
 Anti thyroid peroxidase [anti
microsomal] antibodies
 Anti thyroglobulin antibodies.
 Anti bodies against T3 and T4 in
auto immune hypothyroid disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Primary Hypothyroidism -Hashimoto thyroiditis

A

Chronic autoimmune inflammation of
the thyroid with lymphocytic
infiltration.

Diagnosis involves demonstration of
high titers of thyroid peroxidase
antibodies.

 Diagnosis
 High TSH with low Free T4/T3
 High Thyroid autoantibodies

17
Q

Subclinical Hypothyroidism

A

 An early, mild form of hypothyroidism,
a condition in which the body doesn’t
produce enough thyroid hormones.
 It’s called subclinical because only the
serum level of thyroid-stimulating
hormone from the front of the pituitary
gland is a little bit above normal.

Diagnosis
 Elevated TSH and Normal T4/T3 level

18
Q

SECONDARY HYPOTHYROIDISM diagnosis

A

Diagnosis
 Low levels of T4/T3 with high
level of TRH

19
Q

HOFFMAN SYNDROME

A

Is a specific, rare form of hypothyroid myopathy, which
causes proximal weakness and pseudohypertrophy of
muscles.

20
Q

hypothyroidism diagnosis summary

A

Primary hypothyroidism (elevated TSH and low Free T4 level)

Subclinical hypothyroidism (elevated TSH and normal Free T4 level)

Secondary hypothyroidism (normal or low TSH and low Free T4 level)

21
Q

Thyroid Hormone Replacement

A

 Levothyroxine can cause increases
in resting heart rate and blood
pressure
 So replacement should start at low
doses in older and patients at risk for
cardiovascular compromise

22
Q

Treatment hypothyroidism

A

 Younger patients can be started at
target dose usually 0.075 mg/day
 Start low and go slow in elderly and
high-risk patients, usually 0.025
mg/day

23
Q

Hyperthyroidism meaning

A

“Hyperthyroidism” refers to
overactivity of the thyroid gland
leading to excessive synthesis of
thyroid hormones and
accelerated metabolism in the
peripheral tissues.

24
Q

Sign and Symptoms hyperthyroidism

A

 Unintentional weight loss, even when your appetite and food intake stay the same or increase
 Rapid heartbeat (tachycardia) — commonly more than 100 beats a minute
 Irregular heartbeat (arrhythmia)
 Pounding of your heart (palpitations)
 Increased appetite
 Nervousness, anxiety and irritability

25
Q

Etiology hyperthyroidism

A
  1. Grave’s disease
     Autoimmune disease caused by
    antibodies to TSH receptors
  2. Toxic multi-nodular goiter
     Active multinodular
    goiter associated with
    hyperthyroidism.
     Excess production of thyroid
    hormones from functionally
    autonomous thyroid nodules, which
    do not require stimulation from thyroid
    stimulating hormone (TSH).
  3. Toxic adenoma
  4. Thyroiditis subacute
     Abrupt onset due to leakage of
    hormones
     Follows viral infection
     Resolves within eight months
     Can re-occur
  5. Lymphatic and postpartum
26
Q

Grave’s Disease

A

Most common cause of hyperthyroidism, is characterized by
hyperthyroidism.

Caused by an autoantibody against the thyroid receptor for thyroid-
stimulating hormone (TSH)
 Unlike most autoantibodies, which are inhibitory, this autoantibody is stimulatory,
thus causing continuous synthesis and secretion of excess T4 and T3.

Infiltrative ophthalmopathy (responsible for the exophthalmos in Graves
disease) is poorly understood but may result from immunoglobulins
directed to the TSH receptors in the orbital fibroblasts and fat that result in
release of proinflammatory cytokines, inflammation, and accumulation of
glycosaminoglycans.

27
Q

Toxic solitary or multinodular
goiter (Plummer disease)

A

Results from TSH receptor gene mutations causing
continuous thyroid activation.

Patients with toxic nodular goiter have none of the
autoimmune manifestations or circulating antibodies
observed in patients with Graves disease.

28
Q

Inflammatory thyroid disease (thyroiditis)

A

Hyperthyroidism is more common in
subacute granulomatous thyroiditis R

Results from destructive changes in
the gland and release of stored
hormone, not from increased
synthesis.

Thyroid storm can occur
 is a life-threatening health condition
that is associated with untreated or
undertreated hyperthyroidism.

Hypothyroidism may follow.

29
Q

Diagnosis for Graves disease, Multinodular Goiter and Thyroiditis

A

All have increased Free T4 and T3 and decreased TSH

on RAIU-Thyroiditis has decreased uptake
on RAIU-Multinodular Goiter has areas of increased and decreased uptake
on RAIU-Graves disease has diffuse uptake