Endocrine Diseases

Front 1

Diabetes Inspidus

Back 1

Hypofunction of Posterior Pituitary

ADH deficiency

Front 2

What are the two primary causes of Diabetes Inspidus.

Name two other causes.

Back 2

Nephrogenic and Drug induced

Neurogenic (trauma) and Psychogenic (rare)

Front 3

Syndrome of Inappropriate ADH secretion (SIADH)

Back 3

Hyperfunction of the Posterior Pituitary

caused by neoplams, surgery, psychiatric (due to antipyschotics), drug induced (due to anti depressants)

Front 4

In SIADH, what will increase

Back 4

blood pressure, blood volume; CV injury long term

Front 5

Hyponatremia or Hypernatremia in SIADH?

Back 5

Hyponatremia; ions in the blood will be diluted causing hyponatremia, causing lethargy and confusion

Front 6

what do the hypothalamic nuceli code for?

Back 6

the control of salts, water, serum osmolality, pH

Front 7

What major endocrine organ is the posterior pituitary responsible for?

Back 7

kidney

Front 8

Hypofunction of the anterior pituitary:
Hypopituitarism

Back 8

the lack of production of one type of hormone

Front 9

Hypofunction of the Anterior Pituitary:
Panhypopituitarism

Back 9

describes lack of all hormones of anterior and posterior pituitary

Front 10

Panhypopituitarism

Back 10

describes lack of all hormones of anterior and posterior pituitary

Front 11

Loss of Thyroid stimulating hormone (TSH)results in

Back 11

thyroid deficiency.

Front 12

Loss of Luteinizing hormone (LH) or Follicle-stimulating hormone (FSH)

Back 12

gonadal failure

Front 13

Etiology of Anterior Pituitary Dysfunction:

Back 13

Primarily, intrinsic pituitary disease due to ischemia, trauma, injury, infections, tumors (rare)

Front 14

Functional etiology of anterior pituitary hypofunction

Back 14

anorexia, chronic starvation because you do not receive energy or building blocks to make hormones

Front 15

Can you live with a dysfcn anterior pituitary? If so, how much of the cell subtypesdo you have to lose?

Back 15

yes, you can lose 70-80%. But certain hormones are essential--ACTH.

Front 16

Role of ACTH (essential hormone)

Back 16

helps maintain blood volume, blood pressure, electrolyte balance, use of carbohydrates, anabolic and catabolic function

Front 17

Hypopitutary Dwarfism

Back 17

GH deficiency.

Limbs are symmertrical; there is no abnormal growth.

Front 18

Hypopituitarism Characteristics

Back 18

-short stature, abnormal deposition of fat, lack of muscle mass in extremities, lack of maturation of sexual characteristics

Front 19

Hyperfunction of the Anterior Pituitary is caused by what?

Back 19

Pituitary adenoma (rare)

Front 20

Acromegaly

and its manifestations

Back 20

Hyperfunction of Ant. Pituitary

GH released in higher amounts

Term applied to adults, gigantism in adolesence.

Prognathism (large chin), kyphosis (hunched back), cardiomegaly, rheumatoid-like pains

Front 21

T4 and T3 lipid soluble or water soluble?

Back 21

lipid soluble

Front 22

T4 versus T3

Back 22

T4 is the major project but is converted into T3, which is the most potent increaser of metabolism

Front 23

Calcitonin

Back 23

C-type cells in thyroid; promotes deposition of calcium in the bones (less Ca in circulation)

Front 24

What kind of release does GH have?

Back 24

Pulsatile release in morning and at night.

In acromegaly, GH doesn't turn off; its a continuous secretion

Front 25

What organ does the thyroid lie over?

Back 25

trachea

Front 26

Goiter

Back 26

enlargement of the thyroid caused by hyperthyorid, euthryroid, hypothyroid

Front 27

How would hypothyroid result in goiter?

Back 27

goiter because when the body senses decreased levels of T3 and 4, it releases TSH to try to increase thyroid function. This results in hypertrophy.

Front 28

Manifestations of Graves disease, the most common cause of endogenous hyperthroidism:

Back 28

-thyroid enlargment
-protopsis (exophthalmia)
-pretibial edema of legs

Front 29

Why does exopthalmia (protopsis) occur in Graves disease?

Back 29

increased T3,4 causes production of polysaccharides as byproduct of increased metabolism which will deposit in the fat pads of the eyes causing increased pressure

Front 30

Etiology of Graves disease

Back 30

auto-immune etiology – B-cells are over-proliferating and producing thyroid receptor antibodies

When they bind, they act as 2nd messengers increasing production of T3,4

Front 31

Toxic diffuse Goiter

Back 31

irreversible change to thyroid follicular cells after periods of increased thyroid production.

no feedback control, thyroid insensitive to TSH and T3,4.

o The area in which the follicular cells are changed may hypertrophy, but the rest may atrophy causing involution of the remaining gland. This is because that part IS sensitive to feedback control and responds to the overproduction of T3, 4 by the hypertrophic cells.

Front 32

Treatment of Toxic Diffuse Goiter

Back 32

PTU-propoylthiouracil
surgery
radioactive iodine

Front 33

Thyrotoxic crisis

Back 33

• if hyperthyroidism is untreated…
• An acute stressor like a death in family or job loss can lead to significant T3, 4 effects.
o Hyperthermia
o Tachycardia
o Heart failure
o Delirium
o Nausea/Vomiting/Diarrhea

Front 34

Hashimoto’s Thyroiditis

Back 34

• Painless swelling may occur, but it may be transient and difficult to catch
• Occurs primarily in middle aged females (45-65)
• Female:male ratio >10:1
• Caused by TSH-receptor auto-antibodies
o Blocking of TSH receptors because auto-antibodies bind but do not activate them
• Results in gradual onset of hypothyroidism

Front 35

Lymphocytic Thyroiditis

Back 35

Hypothyroidism
have an immune attack of the thyroid gland in which there can be loss of mass and function.

Front 36

Hypothyroidism--Primary

Back 36

• Significant female:male ratio
• Primary
• Loss of thyroid tissue due to autoimmunity
o The immune system sends out antibodies, cytokines to attack thyroid.
o Inflammatory
o Chronic lymphocytic thyroiditis or Hashimoto disease

Front 37

Hypothyroidism--Secondary

Back 37

• Pituitary or hypothalamus disease
• Peripheral resistance to T3/T4 by receptors

Front 38

Hypothyroidism

Back 38

• Demographic is people in 50s – 60s, overwhelmingly female
• usually diagnosed 4-10 years after the loss of thyroid hormones occurs
o it is not critical to life and even a low amount can sustain its effects
o the clinical effects are slow to develop
 over time the patient gains weight
• loss of control of metabolism
 myxedema – skin disorder, boggy/moonish face, puffy eyes
 lack of thyroid hormone also results in deposition of polysaccharides
• (slide 49) central obesity
• (slide 50) it can have a very normal manifestation and frequently does