Phrx 308 Exam 1 2011 (P1) Outline 3

Front 1

Describe peptide hormones.

Back 1

Synthesis: In advance
Storage: secretory vesicles
release from parent cell: exocytosis
Transport in blood: dissolved in plasma
Half-life: short
Receptor location: cell surface
Receptor-ligand binding response: Channel and 2nd messenger enzyme activation.
General target response: modification of existing proteins and induction of new protein synthesis
Examples: Insulin, PTH

Front 2

Describe steroid hormones.

Back 2

Synthesis: on demand
release from parent cell: diffuse
Transport in blood: bound to carrier proteins
Half-life: long
Receptor location: cytoplasmic/ nucelar
Receptor-ligand binding response: gene expression.
General target response: induction of new protein synthesis
Examples: Estrogen, androgens, cortisol

Front 3

Explain catecholamines.

Back 3

Fight of flight hormones released by the adrenal glands in response to stress. part of the sympathetic nervous (epinephrine, norepinephrine, and dopamine.)

Front 4

Oxytocin

Back 4

milk ejection during breast feeding. Uterine contraction during labor.

Front 5

Vasopressin (ADH)

Back 5

regulation of water balance. Indirectly effects Na+. causes vasoconstriction at high levels. Water retention. Increased BP.

Front 6

Thyrotropin-releasing hormone (TRH) [prolactin releasing hormone]

Back 6

Stimulate thyroid-stimulating hormone (TSH) release from anterior pituitary (primarily).
Stimulate prolactin release from anterior pituitary

Front 7

Dopamine (PIH)
[Prolactin-inhibiting hormone]

Back 7

Inhibit prolactin release from anterior pituitary

Front 8

Growth hormone-releasing hormone (GHRH)

Back 8

Stimulate Growth hormone (GH) release from anterior pituitary

Front 9

Somatostatin (GHIH)
(growth hormone-inhibiting hormone)

Back 9

Inhibit Growth hormone (GH) release from anterior pituitary.
Inhibit thyroid-stimulating hormone (TSH) release from anterior pituitary.

Front 10

Gonadotropin-releasing hormone (GnRH)

Back 10

Stimulate follicle-stimulating hormone (FSH) release from anterior pituitary.
Stimulate luteinizing hormone (LH) release from anterior pituitary

Front 11

Corticotropin-releasing hormone (CRH)

Back 11

Stimulate adrenocorticotropic hormone (ACTH) release from anterior pituitary.

Front 12

What are the basic actions of hypothalamic pituitary hormones?

Back 12

secreted from the posterior pituitary and control the release of anterior pituitary hormones by releasing or inhibiting. (includes PRF, dopamines, TRH, CRH, GHRH, GnRH, and somatostatin)

Front 13

What are the basic actions of anterior pituitary hormones?

Back 13

regulated by hormones secreted by the hypothalamus. produces and secretes 6 trophic hormones which stimulate the release of other hormones. (includes prolactin, TSH, ACTH, GH, FSH, LH, Prolactin, B-endorphins) [mnemonic for hormones: FLATPEG]

Front 14

What are the basic actions of posterior pituitary hormones?

Back 14

synthesized by the hypothalamus. They are then stored and secreted by the posterior pituitary into the bloodstream. (includes ADH and oxytocin)

Front 15

What are the 3 types of hormone interactions?

Back 15

Synergistic, permissive, and antagonistic

Front 16

What is a synergistic effect?

Back 16

effect of interacting hormones is more than additive- causes an outcome that could not have occurred independently.

Front 17

What is a permissive effect?

Back 17

effect of 1 hormone allows another hormone to exert its full effect.

Front 18

What is an antagonistic effect?

Back 18

Hormones have an opposing effect.

Front 19

Primary endocrine disorder

Back 19

problem with the LAST endocrine gland in a reflux.

Front 20

Secondary endocrine disorder

Back 20

problem is NOT with the last endocrine gland in a reflux.

Front 21

Apparent endocrine disorder.

Back 21

problem with an abnormal receptor or 2nd messenger system.

Front 22

Melatonin

Back 22

Site of origin: pineal gland in the brain
Functions: sets body's natural clock, sleep
Uses as a natural product: impove circadian rhythm sleep disorders in the blind. improve sleep-wake cycle disturbances in children/ adolescents w/ autism, mental retardation, and other CNS disorders. mildly decreases sleep latency in insomnia. modestly impoves jet lag symptoms.

Front 23

What hormones are produced in the adrenal medulla?

Back 23

"fight or flight"
Epinephrine, Norepinephrine, Dopamine

Front 24

What hormones are produced in the adrenal cortex?

Back 24

"mediates stress response"
Glucocorticoids: [glucose metabolism; inflammation; asthma]
*Cortisol= hydrocortisone
*Methylprednisolone= medrol & prednisone
Mineralcorticoids: [Na+ balance]
*aldosterone
Weak androgens: can be converted into strong androgens/ estrogens in other tissues

Front 25

What are 2 androgenic hormones that are precursors to testosterone and dihydrotestosterone?

Back 25

DHEA and Androstenedione

Front 26

What is the role of aromatase in estrogen biosynthesis?

Back 26

Enzyme needed for estrogen sythesis; produces estrone from androstenedione or estradiol from testosterone.

Front 27

Describe the regulation of glucocorticoid secretion.

Back 27

1. Secretion is stimulated by ACTH/corticotropin from the anterior pituitary.
2. synthesis/ secretion can go up about 10x during stress.
3. mediator of long term stress
4. Cortisol is the major form

Front 28

Describe glucocorticoid actions in mediating a response to stress in view of blood glucose.

Back 28

1.Protect against HYPOglycemia by having permissive effects on glucagon and catecholamines.
2. promote gluconeogenesis and glycogen synthesis in the liver.
3. Makes insulin dependent tissues (muscle & fat) insensitive to insulin so they primarily use fatty acids as a fuel source (sparing glucose for obligate tissues)

Front 29

Describe glucocorticoid actions in mediating a response to stress in view of lipolysis (fat breakdown).

Back 29

1. Promote lipolysis to provide energy source for nonglucose obligate tissues such as muscle and fat
2. Provide glycerol for gluconeogensis

Front 30

Describe glucocorticoid actions in mediating a response to stress in view of the vasculature.

Back 30

1. enhance vascular reactivity to other vasoactive substances (angiotensin II & epinephrine)
2. Cortisol maintains vascular integrity by decreasing vascular permeability which leads to a decrease in edema associated w/ inflammation
3. Low BP can occur w/cortisol deficiency

Front 31

Describe glucocorticoid actions in mediating a response to stress in view of the immune system.

Back 31

1. stress leads to cytokine production and an immune response.
2. Some cytokines (ie IL-1, TNFa) activate HPA axis which increases cortisol (immune suppressing effects).

Front 32

In the Immune system glucocorticoids inhibit many factors involved in Inflammatory and immune responses, including:

Back 32

IL-1 (fever), TNFa, prostoglandins (pain), leukotrienes (asthma)

Front 33

In the Immune system glucocorticoids stabilize ____ ___and decrease ____.

Back 33

Lysosomal membranes (these decrease liberation of digestive enzymes); Lymphocytes

Front 34

Glucocorticoids do what to body calcium?

Back 34

decrease (decrease absorption in the gut, increase excretion in the kidney)

Front 35

Since glucocorticoids decrease body calcium this causes bone ___, which increases the risk of ___.

Back 35

Catabolism (breakdown); Osteoporosis

Front 36

How do glucocorticoid receptors inhibit gene expression?

Back 36

interact with (& inhibit) other transcription factors & thereby inhibit transcription (gene repression)
Ex. block production of many inflammatory cytokines

Front 37

How do glucocorticoid receptors induce gene expression?

Back 37

directly interact w/ DNA leading to an increase in gene expression (gene induction).

Front 38

What are the anti-inflammatory effects of glucocorticoids?

Back 38

1. Stabilize lysosomal membranes
2. Decrease capillary permeability → increase vascular integrity
3. Decrease migration of WBC to inflamed area
4. Suppress immune system
5. Decrease fever by decreasing IL-1 from WBC
6. Decrease inflammatory prostaglandins & leukotrienes

Front 39

What is the general adaptation syndrome?

Back 39

How the body reacts to a stressor.

Front 40

What is the role of the hypothalamus, anterior pituitary, adrenal medulla, and adrenal cortex in the general adaptation syndrome?

Back 40

1. Stressor
2. Hypothalamus secretes CRH and alerts the sympathetic nervous system
*The SNS in turn releases NE (leads to hyperglycemia and lipolysis) and activates the Adrenal Medulla, who secretes epinephrine (leads to vasoconstriction and increased heartrate)
*CRH stimulates the secretion of ACTH in the anterior pituitary, which releases B-endorphins (used as analgesic) and activates the adrenal cortex, who then releases cortisol (mobilizes energy stores).
3. Via negative feedback cortisol ultimately contributes to the termination of the response by acting on the hypothalamus and pituitary.

Front 41

What is Cushing's syndrome?

Back 41

Adrenal tumor that autonomously secretes cortisol.

Front 42

What is Cushing's disease?

Back 42

Pituitary tumor that autonomously secretes ACTH.

Front 43

What is Iatrogenic hypercortisolism?

Back 43

Hypercortisolism caused by treatment.
*High cortisol therapy can cause this

Front 44

Name signs and symptoms of hypercortisolism.

Back 44

1. muscle fatigue/ loss
2. immune suppression
3. increased central adiposity
4. hypertension
5. hyperglycemia
6. easy bruising

Front 45

What is Addison's disease?

Back 45

Hyposecretion of all adrenal steroids (usually autoimmune destruction of adrenal cortex)

Front 46

Hypocortisolism (adrenal insufficiency) can be caused by?

Back 46

1. genetic defects in enzymes needed for cortisol synthesis.
*sometimes shunts precursors to androgens
2. Iatrogenic effects- rapid cortisol withdrawal of glucocorticoid therapy.

Front 47

What are some signs/ symptoms of hypocortisolism?

Back 47

1. decreased BP (can lead to circulatory collapse)
2. dehydration
3. N/V
4. weakness
5. increased pigmentation
6. depression

Front 48

What are some major indications of glucocorticoid drug therapy?

Back 48

1. Replacement Therapy (~ 10 mg/d hydrocortisone equivalent)
2. Inflammatory Disorders
3. Asthma
4. Allergic Rxns
5. Rheumatoid Disorders
6. Dermatitis
7. Inflammatory Bowel Disorders
8. Certain Cancers
9. Immune Suppression (transplant patients)

Front 49

How does glucocorticoid's normal circadian secretion influence its administration?

Back 49

Natural cortisol secretion is highest between 6am- noon and lowest during the night time hours. Cortisol therapy is given in the morning.

Front 50

Why would you increase the dose of glucocorticoid given to a patient who has been on long term therapy during times of stress?

Back 50

The body needs cortisol during times of stress. High dose glucocorticoid treatments can lead to atrophy of the adrenal cortex. During times of stress the dose needs to be increased to give the patient the amounts they would have produced if the adrenal cortex was functioning properly.

Front 51

What is the biochemical relationship between POMC, ACTH, a-MSH, and B-endorphin?

Back 51

1.ACTH and B-endorphin are synthesized from POMC in the pituitary.
2. ACTH synthesizes a-MSH in the non- pituitary tissues that leads to Melanin synthesis, immune response, and decreases food intake

Front 52

Describe the regulation of GH.

Back 52

The hypothalamus regulates growth hormone secretion by using specific releasing and inhibiting hormones.
*GRH- releases
*GHIH (somatostatin)- inhibits

Front 53

GHRH and somatostatin are secreted from the ___.

Back 53

Hypothalamus

Front 54

Growth Hormone is secreted by the ___?

Back 54

Anterior pituitary

Front 55

Ghrelin is from the stomach and can have a major effect on the excretion of what?

Back 55

Growth Hormone

Front 56

Growth hormone enters the liver and other tissues and produces what?

Back 56

Insulin like growth factors (IGFs)

Front 57

What are the effects of IGFs?

Back 57

Stimultes the differentiaion/proliferation of:
1-condrocytes (cartilage cells) which leads to BONE GROWTH
2-myoblasts which leads to MUSCLE GROWTH
3. Stimulates amino acid uptake & protein synthesis in muscle & other tissue

Front 58

What are the effects of GHs?

Back 58

Direct: GH binds to receptor on target cells (metabolic)
Ex. lipolysis, insulin resistance (adipocytes), & hepatic gluconeogenesis
Indirect: mediated by somatomedins such as IGF-1 produced in liver (growth)
Ex. IGF-1 stimulates BONE GROWTH

Front 59

GH is thought to directly mediate most ___ effects.

Back 59

metabolic

Front 60

IGF-1 is thought to directly mediate most ___ effects.

Back 60

growth

Front 61

What is Dwarfism?

Back 61

Severe GH deficiency

Front 62

What is Giantism?

Back 62

Oversecretion of GH in children (from benign pituitary tumor)

Front 63

What is Acromegaly?

Back 63

Oversecretion of GH in adults (from benign pituitary tumor)
*Overgrowth of extremities & soft-tissue swelling (Ex. macroglossia- can cause sleep apnea)
*Frontal Bossing (Forehead growth)
*Abnormalities in jaw structure
*Cardiac Disease
*Metabolic derangements such as hyperglycemia

Front 64

What are the indications for GH therapy?

Back 64

1. Dwarfism
2. GH def. in adults
3. AIDS associated wasting
4. Children w/pathologically short stature
5. animal agriculture
-NOT for athletic performance

Front 65

What are the indications for somatostatin (GH inhibitory hormone) therapy?

Back 65

1. used to treat GH excess
2. severe diarrhea associated w/hormone secreting tumors of GI tract

Front 66

What are the signs and symptoms of hypocalcemia?

Back 66

Low serum calcium levels in the blood
*usually appears as a symptom of PTH deficiency/ malfunction or Vit. D deficiency.
Symptoms include: Petechia, Tetany, cardiac arrhythmias, and laryngospasms

Front 67

What are the signs and symptoms of hypercalcemia?

Back 67

Elevated calcium level in the blood.
90% of hypercalcemia causes are due to hyperparathyroidism (increased PTH).
Symptoms include:
1. decreased neural excitability
2. kidney stones
3. constipation
4. peptic ulcers
5. bone pain
6. deperession, lethargy, confusion

Front 68

What are the major roles of osteoblasts?

Back 68

produce osteoid (organic matrix) that becomes calcified by the
precipitation of hydroxyapatite calcium crystals.
*Matrix deposits on outer bone surface that makes diameter increase causing linear bone growth at epiphyseal plates. [BONE GROWTH]

Front 69

What are the major roles of osteoclasts?

Back 69

dissolve bone

Front 70

What is importance of bone remodeling?

Back 70

1. repair micro-damage within the skeleton to maintain strength
2. supply Ca++ from the skeleton to maintain serum calcium.

Front 71

Why is Calcium important?

Back 71

1. muscle contractions
2. signaling
3. neuron excitability
4. blood coagulation

Front 72

PTH is stimulated by low ___ or high ___.

Back 72

calcium; phosphate

Front 73

PTH increases serum ionized by ___.

Back 73

calcium

Front 74

What are the hormonal Influences on stimulation & inhibition of bone resorption?

Back 74

1. PTH binds to receptors on osteoblasts which increases production of RANKL
2. RANKL binds to receptors on preosteoclasts & osteoclasts (RANK) & increases their maturation & bone resorbing activity.
3. Hormones such as Estrogen cause osteoblast to produce a decoy receptor, osteoprotegerin (OPG) that bind RANKL & prevent its resorptive activity.

Front 75

Discuss the physiology of PTH in regards to bone health.

Back 75

increase blood calcium when it’s low (this increases bone resorption, renal retention of Ca++, excretion of phosphate, and renal formation of vitamin D) Indirectly Ca++ absorption

*When administered as a drug, has opposite effect meaning it builds new bone “anabolic” therapy (used for osteoporosis)

Front 76

Discuss the physiology of Vitamin D in regards to bone health.

Back 76

[Steroid hormone]
1. Mainly increases calcium GI absorption
* in lesser effects it can increase osteoclast recruitment to resorption sites & osteoblast production of cytokines related to bone resorption, & increase renal retention of Ca++

Front 77

Discuss the physiology of calcitonin in regards to bone health.

Back 77

1. release stimulated when serum Ca++ increases
2. inhibits osteoclast bone resorption "antiresorptive"
3. used for osteoporosis
4. From C cells in thyroid

Front 78

Discuss the physiology of estrogen in regards to bone health.

Back 78

1. Antiresorptive
2. 2nd line osteoporosis therapy
3. SERMS are related drugs