Adrenal Gland Flashcards

1
Q

Stress eating

A

Result from stress eating is that cortisol can then provide energy for cells through gluconeogenesis.
However, excessive food intake and excessive gluconeogenesis will result in hypertension.

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2
Q

Adrenal Gland Anatomy

A

two distinct structures
ADRENAL CORTEX: Outer 80%
Stimulated by ACTH and renin-angiontensin
Produces glucocorticoids, mineralcorticoids, and androgens

ADRENAL MEDULLA: Central 20%
Stimulated by sympathetic nervous system
Produces catecholamines (epinephrine and norepinephrine)
Very granular

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3
Q

Layer of adrenal cortex

A

synthesizes corticosteroid hormones from cholesterol

Zona glomerulosa 15%
Aldosterone production (help maintain BP/BV for proper renal filtration)
stimulated by angiontensin II and potassium
(somewhat regulated by the hypothalamic-pituitary as well)

Zona fasciculata 75%
Cortisol (glucose raising hormone) and some androgens
Stimulated by ACTH (in turn stimulated by the hypothalamus)

Zona reticularis 10%
Androgens (sex hormone precursors), estradiol, testosterone
Helps guide secondary sex characteristics

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4
Q

Adrenal Medulla

A

central core of the organ
Chromaffin cells: main source of catecholamine hormone epinephrine and norepinephrine
Sympathetic nervous system may activate chromaffin cells and release catecholamines onto the blood

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5
Q

Epinephrine and norepinephrine

A

Water-soluble hormones from tyrosine

fight flight response

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6
Q

HPA overview

A

Is a stress received from sympathetic nervous system
Stimulates the parvicellular region of the hypothalamus
Releases CRH (activates anterior pituitary corticotorpes)
ACTH is activated and activates the adrenal cortex (Zona Fasciculata) to activate cortisol

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7
Q

Negative Feedback of Cortisol

A

Can entirely inhibit Anterior Pituitary gland and thereby inhibit ACTH
Secondary inhibition of hypothalamus CRH, however, this will only lower amplitude not frequency.

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8
Q

Action of Cortisol

A

In the periphery is to conserve glucose
Release protein stores from all non-hepatic tissue
Encourages GNG in liver
Encourages lipolysis tofeednonhepaticcells fat

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9
Q

CRH Regulation

A

synthesized in the dorsomedial parvicellular region of the paraventricular nucleus
STIM: Circadian rhythm, any kind of physiological or psychological stress (norepinephrine delivered to paraventricular nucleus)

Under circadian rhythm: higher in the morning than in the evening

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10
Q

CRH actions

A

ENDOCRINE: classic hypothalamus releasing hormone
CRH binds to CRH receptors on the PM of corticotropes to stimulate ACTH production

IMMUNE: Inhibits immune cells function and inflammation (indirectly through cortisol)
Can directly stimulate pro-inflammatory cytokines in the periphery. CRH receptors on keratinocytes can stimulate proliferation
(Atopic Dermatits and Psoriasis)

REPRODUCTIVE: CRH directly inhibits leydig cell function. Lowers testoserone and libido

GI: Stimulate bowel emptying, inhibit gastric emptying, inhibit appetite.
inhibits apatite (stimulate satiety)

AUTONOMIC: Activate sympathetic, increase epinephrine (positive feedback loop)

BEHAVIORAL: Increase fear response

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11
Q

Prednisone and hydrocortisone

A

Cortisol analogs and they are able to inhibit CRH

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12
Q

Synthesis of ACTH

A

CRH stimulates the production of ACTH
Synthesized by corticotropesas a preprohormone called POMC that ALSO contains Melanocyte Stimulating Hormone, beta-lipotropin, and beta-endorphin

May release any of the cleavage products of POMC

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13
Q

beta-lipotropin and beta-endorphin

A

Natural pain relievers cleaved from POMC alongside ACTH

Released from corticotropes and pain tolerance may indicate a tumor in the corticotropes

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14
Q

Melanocyte Stimulating Hormone

A

Released alongside ACTH from POMC

Excess will result in hyperpigmentation

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15
Q

Loss of negative feedback of cortisol to corticotrope

A

Results in high levels of POMC proteolysis products and ACTH

Hyperpigmentation, pain resistance, mood effects, satiety stimulated by MSH,

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16
Q

ACTH actions (hormones)

A

Adrenal cortex hormones are dervied from cholesterol
(80% cholesterol is provided by plasma LDL = dietary cholesterol)

ACTH activates the adrenal cortex via adenyl cyclase and cAMP
Increases receptors for LDL on adrenocortical cells
Increases production of enzymes to liberate cholesterol from LDL
ACTH activates desmolase to convert convert cholesterol to pregnenolone (in mitochondria), precursor to cortisol, aldosterone, and sex homrones

17
Q

ACTH actions (nervous)

A

Increases protein synthesis of NT and increases membrane excitability

ACTH can be further processed to create NT that:
Increase visual attention
Alters mood to reduce social interaction
increases anxiety

18
Q

Hypothalamic pituitary regulation

A

Any physiologic or psychologic stress can stimulate parvicellular neurons
Also:
Insulin induced hypoglycemia (extreme) will stimulate ADH

19
Q

ADH and CRH

A

CRH released from parvicellular neurons and ADH released from the same during extreme stress will synergize to increase ACTH from corticotrope of anterior pituitary

Cortisol stimulate from ACTH will then restore glucose serum levels from hypoglycemia

20
Q

Oxytocin

A

Oxytocin bids alone to receptors on the placenta. Placenta produces CRH and ACTH.
CRH (from placenta) will increase sensitivity to oxytocin. Oxy and CRH will stimulate ACTH release form placenta.
ACTH will circle back for help with labor AND stimulate mom’s cortisol

When oxytocin acts alone on the parvicellular nucleus it reduces anxiety by inhibiting CRH production. Oxytocin can also inhibit ACTH from corticotropes. process reduces cortisol.

21
Q

Estrogen on HPA (ACTH, Cortisol)

A

Estrogen increases sensitivity of adrenal ACTH receptor expression

Also increases cortisol receptors in all tissues. Responsiveness to negative feedback in hypothalamus and anterior pituitary is increased. Can restore homeostasis from stress faster in women over men.

During follicular phase estradiol is at its peak and cortisol effects are maxed out. can recover from hypoglycemia faster.

22
Q

Serotonin on HPA

A

Serotonin increases CRH by binding serotonin receptors on parvicellular neurons.
Estradiol will lower the serotonin receptor and lower CRH output

23
Q

Glucocorticoids

A

Role on glucose metabolism
specific structure, receptors, and target cell interactions
Steroid hormone that binds receptors to form dimers that initiate transcription. bind glucocorticoid response elements

Most notable is Cortisol
Cortisol can also bindG-protein receptors and activate cAMP for non-genomic effects. May also pass through plasma membrane to activate adenyl cyclase or G subunit alone.

24
Q

Types of glucocorticoids

A

ENDOGENOUS
Cortisol: 95% of all GC activity
Cortisone (inactive cortisol) around 4% total GC activity

SYNTHETIC
Hyrdocortisone = 80% of cortisol
Cortisone = potency of cortisol
Prednisone = 4X as potent as cortisol
FLcortisone 15X as potent, 150x aldosterone
Methylprednison 15X as potent (medrol)
Dexamethasone 30 x as potent
*CPF also have effect of aldosterone
treat inflammation, autoimmune, lupus
25
Q

Cortisol

A

Widespread actions to restore homeostasis after stress
Glucose sparing effect

Highest levels early morning and lowest levels at midnight 3-5 hours after sleep

Lipid soluble hormone that must be transported in the blood by CBR (transcortin) and albumin
when bound:
Slows elimination - 60-90 minutes
transcortin creastes a reservoir to reduce rapid fluctuations in free hormone concentration
inactive when bound

26
Q

Diurnal variation of cortisol

A

Variation in cortisol levels is seen in:
Psychological stress and clinical depression
Physiological stressors - hypoglycemia, illness, fear, physical exertion
Abnormal ACTH levels, released in pulsatile fashiondue to CRH stimulation
Chronic stresscan override normal negative feedback and receptors may then be desensitized

27
Q

Cortisone

A

Cortisol is metabolized in the liver to form cortisone is inactive (by a hydroxylase)
25% excreted in bile
75% filtered by the kidney and liver
serum cortisol is severely affected by kidney and liver disease

28
Q

Cortisol actions

A

Essential for stress response
Allows CV system to respond to exercise
Mineralocorticoid effect so that the kidney can respond to wateroad or dehydration
Suppresses immune and inflammatory reactions
Allows breakdown of Ct, bone, muscle and non-hepatic tissue to supply liver with amino acids for GNG
Hyperglycemic effect may contibute to DM
Will anatgonize insulin receptor
Stimulate release of FFA from adipocyte (supplies a source of oxidation for non-hepatic tissue)
Stimulate PEPCK to allow liver to do more GNG

29
Q

Cortisol as an antagonist

A

antagonist to insulin

Increases GNG
Marked increase in glycogen storage in liver
with increased GNG cortisol activates glycogen synthase beta that will create glycogen

Decrease glucose uptake

Release of FFA from adipocytes via lipolysis further decreases insulin actions

30
Q

Cortisol weakens immune system

A

by inhibiting protein synthesis and breaking down proteins
decreases the number of eosinophils and lymphocytes. significant atrophy of lymphoid tissue. decrease output of T-cells and antibodies
Prevents excessive T cells and B cell production which enhances cytokines adn prevents aggregation of antibodies

31
Q

Cortisol: Anti-inflammatory effects

A

Directly reduce the release of arachidonic acid by inhibiting phospholipase A2
If arachidonic acid is still released then cortisol can inhibit cyclooxygenases and leukotrienes
Can specifically eliminate Il-1B (which causes fevers) and indirectly stop antibody production

Stabilizes lysomosomal membranes: decreases function

Decreases capillary permeability

Decreases ability to initiate fever

32
Q

Mineralocorticoid activity of cortisol

A

Cortisol and aldosterone bind with equal affinity to aldosterone receptor in the kidney
Can cause hypertension and hypokalemia via increased transcriptin of NA/K ATPase (absorb Na and H2O and excrete K)

Normally cortisol is converted to cortisone by a hydroxysteroid dehydrogenase
liquorice inhibits the conversion of cortisol to cortisone and links candy to hypertension