Catos Exam 3 Hormones-2 Dr.cool

Front 1

What is the function of Nitric oxide?

Back 1

It acts in paracrine mode to vasodilate vascular smooth muscle, increasing cGMP synthesis and causing smooth muscle relaxation.

Front 2

What causes the release of nitric oxide?

Back 2

ACh and Nitric Oxide snythase cause L-arginine to be converted to L-citulline, thus releasing NO

Front 3

5 Stages to NO synthesis
Synthesis

Back 3

L-arginine is converted L-citrulline releasing NO

Front 4

5 Stages to NO synthesis
Packaging

Back 4

No packaging is required bc it is a gas and will diffuse out to the cells nearby

Front 5

5 Stages to NO synthesis
Processing

Back 5

N/A

Front 6

5 Stages to NO synthesis
Secretion

Back 6

N/A it is paracrine and autocrine

Front 7

5 Stages to NO synthesis
Degradation

Back 7

It is broken down by superoxide dismutase and H2O2. It can then diffuse out of the cell where it acts.

Front 8

What is the effect of chemical inhibitors of NOS

Back 8

Markedly decrease NO production, increase blood pressure, decreases production of cGMP, thus inhibiting platelet aggregation

Front 9

Cytokines are positive or negative effectors of NOS?

Back 9

Positive

Front 10

Glucocorticoids are positive or negative effectors of NOS?

Back 10

Negative

Front 11

Nitrovasodilators can increase or decrease cGMP directly?

Back 11

Increase

Front 12

What would be the effect of inhibitors of cGMP phosphodiesterase?
ex: sildenafil

Back 12

Increase nitric oxide activity

Front 13

How is NO involved in erections?

Back 13

The parasymp nervous system causes the release of NO in the corpus cavernosum of the penis leading to vasodilation.

Front 14

What is the function of eicosanoids?

Back 14

Plays a central role in the inflammatory response, paracrine signaling via G proteins.

Front 15

What are the four types of eicosanoids?

Back 15

Thromboxanes
Prostacyclin (PG12)
Leukotrienes
Prostaglandins

Front 16

What are the effects of thromboxanes?

Back 16

vasoconstrictor, induces platelet aggregation during clotting.

Front 17

Prostacyclins are agtagonistic with

Back 17

Thromboxanes

Front 18

What are the effects of prostacyclins?

Back 18

PG12's are vasodilators that inhibit platelet aggregation by inhibiting the ability of COX enzymes to synthesize the precursor of thromboxanse w/in platelets

Front 19

Where is thromboxane produced, and by what?

Back 19

It is produced in platelets by thromboxane-A synthase via the COX enzyme from arahidonic acid.

Front 20

How are prostacyclins related to COX inhibitors and PGH2.

Back 20

Cause the conversion of arachidonic acid to PGH2, the precursor of prostaglandins rather than thromboxanes

Front 21

What is the function of Leukotrienes?

Back 21

Important agents in the inflammatory response due chemotactic effect on neutrophils, can cause vasoconstriction and increase vascular permeability

Front 22

What are two effects of prostaglandins and how do they act?

Back 22

Cause vascular smooth muscle cells to constrict
Cause calcium movement, ie pain in spinal neurons (1003)
Can act via paracrine or autocrine

Front 23

5 Stages to Eicosanoid Synthesis
Synthesis

Back 23

Phospholipids are converted to arachidonic acid w/in granules of mast cells, bc they have a large pool of phospholipids

Front 24

5 Stages to Eicosanoid Synthesis
Packaging

Back 24

Stored inside secrectory vesicles inside mast cells and other immune cells

Front 25

5 Stages to Eicosanoid Synthesis
Processing

Back 25

They are already packaged w/ all the needed enzymes

Front 26

5 Stages to Eicosanoid Synthesis
Secretion

Back 26

Eicosanoids are stored along with other immune factors such as histamine in granules until released by mast cells and basophils.

Front 27

5 Stages to Eicosanoid Synthesis
Degradation

Back 27

Inactivated rapidly due to their own instability

Front 28

Cyclooxygenase and peroxygenase convert _____________ to into PGH2, the precursor to other prostaglandins and thromboxanse

Back 28

arachindonic acid

Front 29

Common Eicosanoid diseases

Back 29

Inflammation
Allergic Rxn
Chemotaxis

Front 30

Inhibition of lipoxygenase and leukotriene receptors:

Back 30

Zileuton
Montelukast & Zafirlukast

Front 31

Inhibition of Prostaglandin Endoperoxide Synthase (PES)
Aspirin binds to:
Ibuprofen binds to:
Naproxen binds to:

Back 31

Aspirin binds to: Cox I
Ibuprofen binds to: Cox II
Naproxen binds to: Cox I&II

Front 32

Lipocortins
(also called PLA2 inhibitory proteins)

Back 32

Inhibit the release of the prescursor molecule arachidonic acid

Front 33

Overview:Effects
Glucocorticoids
Mineralocorticoids
Androgens (DHEA)

Back 33

Glucocorticoids: Intermediary Metabolism
Mineralocorticoids: Salt-retaining activity
Androgens (DHEA): Sex hormones

Front 34

5 Stages of Steroid hormone synthesis:
Synthesis

Back 34

From cholesterol
ER of cells in adrenal cortex

Front 35

5 Stages of Steroid hormone synthesis:
Packaging

Back 35

Little packaging bc they readily diffuse out as they are made

Front 36

5 Stages of Steroid hormone synthesis:
Processing

Back 36

Several steps, involves P450 and other isomerases

Front 37

5 Stages of Steroid hormone synthesis:
Release

Back 37

N/A

Front 38

5 Stages of Steroid hormone synthesis:
Degradation

Back 38

Long 1/2 lives, hrs to days
Excreted in the urine

Front 39

Two types of Glucocorticoid Steroids (Zona Fasciculata)

Back 39

Cortisol
Corticosterone

Front 40

Functions (4) of Glucocorticoid Steroids, primarily through cortisol

Back 40

Alter metabolism by increasing gluconeogenesis and protein degradation
Inhibit glucose transport into unitlization by muscle and adipose cells
Increase blood pressure
Alter host defense mechanism, suppress immune respons

Front 41

Weak seroids and steroid precursors:

Back 41

Androgens

Front 42

DHEA is:
It is produced where:

Back 42

The precursor to natural estrogens
Steroid hormone produced from cholesterol in the adrenal cortex

Front 43

DHEA
DHEA-S
Androsetnedione
Testosterone

Back 43

Are all adrenal androgens

Front 44

Generic term for any natural os synthetic compound, usually a steroid hormone

Back 44

Androgens

Front 45

Usually stim or control the dev and maintenance of masculine characterisitics

Back 45

Androgens

Front 46

synthesized from cholesterol via delta5-pregnenolone in the mitochondria, or in the ER of cells in the adrenal cortex

Back 46

Glucocorticoids:
Cortisol and Corticosterone

Front 47

Steroids have a relatively long or short half life?

Back 47

Long

Front 48

Cortisol and Corticosterone circulate in the bound or free form?

Back 48

Both!
Associated in serum with high affinity carrier proteins

Front 49

Upon delivery of ACTH to the adrenal cortex, what is synthesized and secreted w/in minutes?

Back 49

Glucocorticoids

Front 50

Main regulator of cortisol and androgen production by the adrenal cortex?

Back 50

Glucocorticoids

Front 51

Cortisol inhibits CRH release fromt the:

Back 51

Hypothalamus

Front 52

Main regulator of cortisol and androgen production

Back 52

adrenal cortex

Front 53

Three main mechanisms of neuroendocrine control:

Back 53

1. Episodic secretion and circadian rhythm of ACTH
2. Stress responsiveness
3. Feedback inhibition by cortisol of ACTH secretions

Front 54

Produced by the zona fasciculata:

Back 54

Glucocorticoids: Cortisol and Corticosteone

Front 55

Produced by the zona glomerulosa:

Back 55

Mineralocorticoids: Aldosterone

Front 56

Produced by the zona reticularis:

Back 56

Androstenedione: Androgens

Front 57

Have potent anti-inflammatory and immunosuppressive properties.
Promoting maturation of the lung and production of the surfactant necessary for extrauterine lung function.

Back 57

Glucocorticoids

Front 58

The amount of ______ present in the serum undergoes diurnal variation, with the highest levels present in the early morning, and the lowest levels present around midnight, 3-5 hours after the onset of sleep.

Back 58

Cortisol

Front 59

There is long and short feedback inhibition of:

Back 59

Glucocorticoids
So, in the pituitary and the hypothalamus

Front 60

Feedback inhibition is:

Back 60

Product inhibition,
NOT Neg Feedback

Front 61

Fast feedback inhibition of glucocorticoids depends on the:

Back 61

Rate of increase, not the dose administered.

Front 62

When and how does slow feedback inhibition occur in regards to glucocorticoids?

Back 62

It happens after the transient rate-dependent effects (fast) by further supression of CRH and ACTH
(ACTH eventually becomes unresponsive to futher inhibition)

Front 63

What will result from ACTH deficiency?

Back 63

Atrophy of the zona reticularis and fasciculata

Front 64

Effects of prolonged glucocorticoid administration:

Back 64

Supression of CRH and ACTH release
Atrophy of zona fas and ret
Supressed HPA-axis
Delayed feedback acts via classic GC receptor

Front 65

The following are symptoms of:
ACTH and cortisol increase w/in minutes
Abolish circadian periodicity if stress is prolonged
High GC admin abolishes stress responsiveness

Back 65

Glucocorticoid diseases

Front 66

The principal mineralocorticoid steroid is:

Back 66

aldosterone

Front 67

Where is aldosterone produced?

Back 67

In the zona glomerulosa

Front 68

What are the primary functions of mineralocorticoids?

Back 68

Controlled by the renin-angiotensin system, they act in salt balance and hypertension by regulating plasma K and Na levels along w/ electrolyte regulation

Front 69

What is considered one of the key modulators of blood volume/pressure, cardiac and vascular function

Back 69

Renin-angiotensin system (RAS)

Front 70

The RAS pathway is a cascade that begins with the production of angiotensinogen in the:

Back 70

Liver

Front 71

Angiotensin I is cleaved to Angiotensin II, primarily in the lungs, by:

Back 71

Angiotensin Converting Enzyme
(ACE)

Front 72

AT II is a strong:
It turns on _______, decreases _______ and increases _________

Back 72

vascoconstrictor
It turns on aldosterone production, decreases urine (via Na resorption from distal tubules) and increases blood pressure

Front 73

Mineralcorticoids, especially via angiotensin II and thus aldosterone, cause an increase in blood pressure. This can cause:

Back 73

Hypertension

Front 74

angiotensin II has several important functions:

Back 74

Constricts resistance vessels
Releases aldosterone
Stimulate thirst
Stimulates release of vasopressin (ADH)
Enhances symp adrenergic fx
Stim cardiac hypertrophy and vascular hypertrophy

Front 75

Release of aldosterone causes

Back 75

kidney's to increase sodium and fluid retention