Psl 535: Scribe #8 Effects Of Thyroid Hormone

Front 1

What nervous system does excess thyroid hormone activate?

Back 1

sympathetic nervous system bc thyroid hormones inc. beta adrenergic receptors

Front 2

Name some symptoms of excess thyroid

Back 2

1. Increased basal metabolic rate, irritability, and brisk deep tendon reflexes
2. Heat intolerance
3. hyperthermia
4. Tachycardia
5. Hyperdefecation
6. Hypomenorrhea
7. Muscle weakness
8. smooth moist skin
9. fine hair
10. weight loss
11. low cholesterol
12. osteoporosis

Front 3

Symptoms of hypothyroidism

Back 3

1. Decreased basal metabolic rate, sluggishness, delayed relaxation phase of deep tendon reflexes
2. Cold intolerance
3. Impaired myocardial contractility
4. Constipation
5. Menorrhagia
6. Muscle weakness
7. Thick, coarses dry skin, brittle nails, and hair
8. Mild weight gain
9. Hypercarotenemia: too much carotein in body

Front 4

Myxedema

Back 4

Severe hypothyrodism

Puffiness of tissues bc of accumulation of mucopolysaccharides which retain fluids.

Edema of eyelids, thick tongue, hoarseness of voice, joint swelling/stiffness, fluid accumulation in spaces, and carpal tunnel syndrome

Front 5

Primary hypothyroidism

Back 5

Due to thyroid defects, thyroid doesn't make sufficient amounts of thyroid hormones

Front 6

Secondary hypothyrodisim

Back 6

Due to pituitary failure

TSH secretion is decreased bc of dsyfunctional pituitary

Thyroid can still make hormone but not stimulated to do so.

Front 7

How can one distinguish between primary and secondary hypothyrodism?

Back 7

TSH is high in hypothyroidism (less negative feedback from T3/T4; pituitary sensitive to TRH and will exaggerate amts of TSH)

TSH low in secondary hypothyrodism.

Front 8

TRH is administered intravenously; a baseline measure of TSH is taken and then TSH levels are re-measured one hour following TRH administration.

Back 8

TRH Stimulation Test:

Front 9

TRH Stimulation Test in a healthy person.

Back 9

In healthy person-->baseline TSH measured and with extra TRH see boost of TSH.

Front 10

TRH Stimulation Test in a primary hypothyroidism

Back 10

In patients with primary hypothyroidism-->initial TSH levels elevated (less neg. feedback due to dec. T3/T4). Anterior Pituitary very sensitive to TRH so higher rise in TSH with administered TRH.

Front 11

TRH stimulation test with secondary hypothyrodism

Back 11

Initial TSH levels low and TSH response to administered TRH subnormal.

TSH is constant flat-line value.

Front 12

Is a goiter caused by primary or secondary hypothyroidism?

Back 12

Primary hypothyrodism

Excessive TSH production causes thyroid to enlarge

Front 13

How are goiters and other signs of hypothyroidism treated?

Back 13

Replacement thyroid hormones to improve signs and symptoms of hypothyroidism

Only T4 is necessary because it can be converted to T3.

Front 14

Disease in which the immune system makes antibodies (immunoglobulins) directed against the thyroid gland.

Back 14

Graves' Disease

Front 15

Explain what occurs in Graves' Disease

Back 15

Thyroid stimulating immunoglobulins (TSI) produce hyperthyroidism by binding to TSH receptors on the thyroid, thereby simulating effects of TSH.

This results in goiter and inc. in thyroid hormones.

Excess thyroid hormones exert neg. feedback on pituitary and supress TSH secretion. so circulating TSH concentrations low and cannot be stimulated by TRH.

Hyperthyrodism is ALMOST NEVER caused by excessive pituitary TSH secretion.

Front 16

What happens to a person with Graves' disease after TRH stimulation test?

Back 16

No rise in TSH levels following TRH administration. TSH is shut down due to neg. feedback.

Front 17

Some people with Graves' Disease also suffer from autoimmune attack of the back of eye

Back 17

Exophthaolomos: a protrusion of the eyeball because there is too much swelling in the back of eye.

Not dependent on thyroid hormone levels

Front 18

Propylthiouracil (PTU)

Back 18

Drug that stops thyroid hormone synthesis.

Inhibits thyroid peroxidase, an enzyme on the apical membrane of thyrofollicular cells responsible for thyroid hormone synthesis.

This drug takes a few weeks to lower thyroid hormones in bloodstream because hormones already stored in colloid so those must be used up first.

Front 19

Beta adrenergic antagonists

Back 19

Relieve some symptoms of hyperthyroidism, like rapid heart rate, nervousness, shakiness, but does not reduce thyroid hormone synthesis and secretion levels.

Front 20

Radioactive Iodine

Back 20

Used to treat hyperthyroidism

A large dose is given and taken up by thyroid cells which will burn up the thyroid cells and destroy enough to normalize thyroid hormone levels in the bloodstream.

Front 21

Surgery

Back 21

Treatment for hyperthyroidism

Part of the thyroid is removed to reduce thyroid hormone output.

Front 22

What does a goiter tell us?

Back 22

Cannot tel us if person is hyper/hypothyroid or if hormones are normal.

Front 23

thyroid growth allows greater synthesis and secretion of thyroid hormones, but insufficient to return thyroid hormones to normal. TSH hormones remain elevated since less thyroid hormone provides less negative feedback.

Back 23

Goitrous Hypothyroid

Front 24

TSH dependent goiter, caused by congenital defects in thyroid hormone synthesis.

TSH mediated compensatory thyroid enlargement restores thyroid hormone secretion to normal. By the time patient is examined, T3/4 and TSH have returned to normal range.

Patient with hypothyroidism that gets a goiter, but once the thyroid enlarges, cells may be able to secrete more thyroid hormone so hormone levels may be back to normal

Back 24

Euthyroid goiter

Front 25

What are the types of goiters associated with hyperthyroidism?

Back 25

1. Graves' disease

2. Toxic multinodular goiter- one or more areas of thyroid become enlarged and hypersecrete thyroid hormones. Aka: thyrotoxicosis

Front 26

The Hypothalamic-Pituitary-Adenocortical Axis

Regulation of Adrenal glands

Back 26

1. Cortisol secreted in response to stress.

2. Stress perceived by CNS which activates hypothalamus

3. Hypothalamus secretes CRH

4. CRH stimulates the pituitary to secrete ACTH

4. ACTH stimulates adrenal cortex to secrete cortisol (the major glucocorticoid)

Front 27

Negative feedback of cortisol

Back 27

Cortisol negatively feedbacks on pituitary and hypothalamus to reduce CRH and ACTH secretion.

Front 28

What would happen if both adrenal glands were removed?

Back 28

No cortisol would be released, no negative feeback so both CRH and ACTH would increase.

Front 29

What would happen if one adrenal gland was removed?

Back 29

Cortisol released would be reduced, CRH and ACTH would increase causing adrenal gland to hypertrophy and inc. it's cortisol production to meet body's needs.

Front 30

What would happen if the pituitary stalk was removed (hypophysectomy)

Back 30

No direct route to pituitary so CRH would reach the pituitary via circulation which would dilute CRH. Thus ACTH release would decrease. There may not be enough ACTH to stimulate the adrenal glands to secrete cortisol

Front 31

What happens if the pituitary glands are removed (hypophysectomy)?

Back 31

CRH wasted, adrenal glands atrophy and do not secrete as much cortisol

Front 32

How is ACTH secreted?

Back 32

Noctural secretion

In early morning hours before waking, diurnal rhythm in a pulsatile manner.

Front 33

How is ACTH synthesized?

Back 33

As part of a larger protein known as pro-opiomelanocortin (POMC).

POMC contains everal peptides that are secreted simultaneously including MSH, endorphin, and LPH along w/ ACTH.

Front 34

What are the regulators of ACTH secretion?

Back 34

1. cortisol decrease (by taking out adrenal gland or taking drugs)

2. Stress

3. Psychiatric disturbances

Front 35

What causes cortisol inhibition?

Back 35

1. cortisol increase

2. glucocorticoid administration (dexamethasone-mimics cortisol so inhibits ACTH secretion through negative feedback)

Front 36

A synthetic glucocorticoid that can cause negative feedback on ACTH and CRH. It decreases cortisol secretion

Back 36

Dexamethasone

Front 37

KNOW TABLE

Back 37

SCRIBE #8, PAGE 7