Jackson Lectures 4

Question 1

Actions of cortisol are essential under non-stress conditions, but they can become damaging when

Answer 1

cortisol is elevated for long periods of time and combined with chronic activation of the SNS

Question 2

• cortisol is highly catabolic on substrates used to produce needed

Answer 2

glucose;

tissue can be rebuilt when stress is over, but catabolism continues as long as stressor is present

Question 3

• cortisol has anti-inflammatory and anti-immune effects to inhibit

Answer 3

cytokines and phagocytosis, and block proliferation of white blood cells
- this conserves energy in the short term, but damaging with chronic stress

Question 4

• mobilization of metabolic fuels increases

Answer 4

lipids in the blood which, when combined with increased blood pressure (sympathetic response), can lead to development of atherosclerosis and hypertension

Question 5

So problems arise when a continued physical or psychological stressor turns a short-term response into

Answer 5

chronic activation of CRH (cortisolreleaseing hormone) neurons.

Question 6

Evidence for an interaction between immune function and activation of the stress response.

Answer 6

• HSV + psychiatric illness → increased recurrences and duration of outbreak
• influenza + family dysfunction → increased frequency and severity of illness
• hepatitis B + exams → delayed antibody response to vaccine

Question 7

Adrenal insufficiency or

Answer 7

Addison’s Disease

Question 8

Causes of primary adrenal insufficiency: disease

Answer 8

disease – tuberculosis destroys adrenal cortex

Question 9

Causes of primary adrenal insufficiency: congenital disorder

Answer 9

– improper development or mutation in enzyme

Question 10

Causes of primary adrenal insufficiency: autoimmune disorder

Answer 10

– affects all cortex cells,

Question 11

Causes of secondary adrenal insufficiency: pituitary problem

Answer 11

– aldosterone not typically affected, as aldosterone is stimulated by something else.

Question 12

Causes of secondary adrenal insufficiency: glucocorticoid therapy

Answer 12

– use of exogenous corticosteroids for a number of conditions has feedback effects on CRH and ACTH and can impair a normal stress response.

Question 13

Adrenal insufficiency: This is an important consideration for dental patients because

Answer 13

there may be complications with maintaining blood pressure during anesthesia, and diminished immune and inflammatory responses.

Question 14

Symptoms of adrenal insufficiency

Answer 14

• low cortisol and high ACTH
• weakness, lethargy, decreased appetite
• low blood pressure
• low glucose when fasting
• hyperpigmentation due to lack of negative feedback control of POMC production

Question 15

Adrenal insufficiency: Treat with

Answer 15

exogenous glucocorticoids and/or dietary control

Question 16

Hypercortisolinemia or

Answer 16

Cushing’s disease

Question 17

Hypercortisolinemia is typically due to a

Answer 17

pituitary tumor (or administering too much exogenous glucocorticoid), and can be treated by removing the tumor.

Question 18

Hypercortisolinemia Symptoms are related to =

Answer 18

elevated basal concentrations of cortisol
• excessive tissue catabolism, especially bone, skin, and muscle

• diabetes – like symptoms – increased appetite and circulating glucose, redistribution of fat stores
• impaired immune function
• threat of hypertension

Question 19

Hypercortisolinemia: In dental patients, the primary concern is

Answer 19

impairment of immune function after a procedure, but hypertension, osteoporosis, and increased bleeding are also problematic.

Question 20

The three major classes of sex steroids differ with respect to the

Answer 20

number of carbons they contain: or pregnanes (21 C), androgens or androstanes (19 C), and estrogens or estranes (18 C).

Question 21

start with progesterone, converted to

Answer 21

androgens, converted to estrogens.

Question 22

The primary male hormone is

Answer 22

testosterone (T) which is an androgen

Question 23

. T is more potent than

Answer 23

DHEA and androstenedione.

Question 24

T is converted to the most potent androgen, DHT, by the

Answer 24

enzyme 5α-reductase. All for 1 recepter = higher affinity.

Question 25

Conversion to DHT occurs in

Answer 25

target tissues.

Question 26

The primary female hormones are

Answer 26

progesterone (P) which is a progestin, and estradiol (E2) which is an estrogen (most common).

Question 27

Progesterone can serve a precursor for other

Answer 27

steroids.

Question 28

Estradiol is an estrogen produced from

Answer 28

testosterone by the enzyme aromatase.

Question 29

Synthesis (and secretion) of sex steroids are controlled by the

Answer 29

neuroendocrine system; the reproductive or HPG axis includes the hypothalamus, anterior pituitary gland and the gonads.

Question 30

GnRH secretion from the hypothalamus is

Answer 30

pulsatile due to the activity of pacemaker neurons (leaky to sodium – hypothalamic) that spontaneously produce action potentials resulting in secretory bursts of GnRH.

Question 31

An increase or decrease in the frequency of the pacemaker activity will

Answer 31

increase or decrease GnRH secretion.

Question 32

Secretion of the gonadotropic hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the anterior pituitary is pulsatile in response to bursts of

Answer 32

GnRH from the hypothalamus.

Question 33

Pulsatile secretion of LH and FSH stimulates

Answer 33

pulsatile secretion of gonadal steroids.

Question 34

The pulsatile nature of GnRH stimulation is necessary for

Answer 34

gonadotropin secretion.

Question 35

Continuous, nonpulsatile GnRH downregulates

Answer 35

GnRH receptors in the anterior pituitary and inhibits LH and FSH secretion.

Question 36

Both the GnRH neurons and gonadotropes are subject to the

Answer 36

feedback actions of gonadal hormones.

Question 37

Most of the time the gonadal steroids exert

Answer 37

negative feedback control of GnRH and LH secretion

Question 38

In females, E2 has

Answer 38

positive feedback actions on LH secretion prior to ovulation.

Question 39

Spermatic cells (gametes) include

Answer 39

mitotically active spermatogonia and meiotic spermatocytes.

Question 40

Spermatogenesis proceeds as the spermatic cells move through the

Answer 40

wall of the seminiferous tubules from the basal lamina towards the apical surface and lumen.

Question 41

2. Leydig cells or interstitial cells lie outside of the

Answer 41

seminiferous tubules.

Question 42

Leydig cells synthesize T in response to

Answer 42

LH.

Question 43

In the gonad, T regulates

Answer 43

spermatogenesis.

Question 44

In the brain, T regulates

Answer 44

sexual behavior (after being aromatized to E2).

Question 45

Elsewhere in the body, T regulates

Answer 45

secondary sex characteristics.

Question 46

3. Sertoli cells or sustentacular cells are the

Answer 46

epithelial cells lining the seminiferous tubules.

Question 47

In response to FSH, they regulate

Answer 47

spermatogenesis and produce the peptide hormone inhibin.

Question 48

Inhibin has negative feedback actions on

Answer 48

FSH secretion.

Question 49

Sertoli cells also produce an androgen binding protein that helps sequester

Answer 49

T in the testis so spermatogenesis is continuous.

Question 50

The Sertoli cells also secrete

Answer 50

tubular fluid to provide nutrient support for spermatozoa.