Ex2 Glucocorticoids

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Elevated potassium
raises production of
___

Aldosterone

20.

GCRc is bound to ___

in cytoplasm, which
acts to ___

HSP (Heat shock Protein;

Chaperone), anchors GCRc to
cytoplasm

Aldosterone regulates
what transporters in
the distal convoluted
tubule?

Na/Cl symporter, Na/K ATPase

21.

Adrenal cortex
produces which
hormones?

cortisol, aldosterone, androgens

adrenal medula
produces ___

epinephrine, norepinephrine

Cl exites the
basolateral membrane
of the distal
convuluted tubule via
___

Cl Channel

zona reticularis
produces

androgens

steps to produce
aldosterone

cholesterol, pregnenolone,
progesterone, aldosterone

Aldosterone also helps

control ___, ___,
____

Sweat, GI tract, Salivary glands.

Electrolyte and water balance

steps to produce
cortisol

cholesterol, pregnenolone,
progesterone OR 17-OHpregnenolone, 17-OHprogesterone, cortisol

Aldosterone acts on a
____

nuclear receptor

aldosterone is a ___,
made in the ___

mineralcorticoid, zona
glomerulosa (outer section)

steps to make
androgens

cholesterol, pregnenolone, 17-OHprogesterone OR 17-OHpregnenolone, androgens

Aldosterone increases
___

Na resorption, K secretion, water

retension (BP)

In the kidney,
aldosterone ___, and
___

phosphorylates an amiloride
sensitive Na channel, and
upregulates Na/K/ATPase

In the collecting
tubule, aldosterone
actions are ___

More Na channels, Na/K/ATPase,

change in permability of tight
junctions

GC are also
stimulated by ADH
and CRH?

true????

AIP is ___

Aldosterone induced porteins

Aldosterone affects
channels by ___

more trancript/translate, and also

inserts them into the membrane

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ACTH is a ___

Growth Factor

Aldosterone also
affects the

mitochondria

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Excess ACTH causes

Adrenal Hyperplasia

Insufficient ACTH
causes

Atrophy of the inner cotex

body makes tons more

___ than ___

GC than MC

Cortisol circulates
___

protein bound

what is the name of

the enzyme that
converts cortisol to
cortisone?

11-Beta-Hydroxysteroid
dehydrogenase

When GC binds GCRc,

GCRc forms ___, and
recruites ____

dimer, activators or repressors

in the collecting ducts,

aldosterone ___

upregulates Na channels, Na/Cl

symporter, Na/K ATPase

34.

GCRc bindes to ___

after forming dimer

GRE

Cortisol is a ___,
made in the ____

glucocorticoid, zona fasciculata

35.

surfactant proteins
are ___ in lung by GC

upregulated

Cortisol causes ____

increased Blood Sugar, decreaed

immune system, increased fat,
protein, carb metabolism,
decreased bone formation

36.

GC-RC coactivators
are

CBP/TRB (activators, repressors)

Cortisol is converted
to cortisone in the ___

Gut, Kidney, Salivary, Sweat

glands. So MC rules here

can overide enzyme by

___

giving large doses of GC that also

have MC activity

GC Rc resides where
when empty

cytoplasm

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repression 1
steps

GCRc complex blocks other transcription

promoting factors from binding to their
promotor regions. In this scheme. GCGCRc
is bound to the "wrong" promotor, instead of
binding to a GRE like it is supposed to.

are K+
channels
upregulated
by
Aldoserone?

no

Na/K/ATPase
are found
where?

everywhere in the tubule. All of them are

upregeulated by Aldosterone, everywhere

repression II

GCGCRc travels to the nucleus but doesn't

dimerize. Instead it forms a complex by
binding with other transcription factors.
These factors can no longer bind to
promotor that it should have bound to

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GC are usually
used to
suppress ___

inflammation

in the liver, GC
will

increase gluconeogenesis (for needed

energy), and glycogen storage (for
conserving extra for later), increase protein
synthesis for these

In striated
muscle, GC
increases ___

protein catabolism for making glucose

In adipose
tissue, GC
increases ___

lipolysis for making glucose

in bone and
skin, GC will
__

decrease Ca uptake in the gut, inhibit

calcitonin, enhance oseoclastic activity,
inhibit osteoblastic activity, decrease protein
synthesis

which fat is
the most
active?

viceral

GC will make
you hyper or
hypocalcemic?

hyer, by inhibiting Vit D, decreases bone

density

under chronic
stress, GC will
make you

develop more fat, not full osteoporosis, more

blood glucose

Prolonged
doses of GC
does what to
the gland?
How to adjust
dose?

adrophies (Adrenal Cortex), taper the dose

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Cortisol
suppresses ___

CRH, ACTH, Immune System

(lymphocytes, Macrophages, Monocytes,
Neutrophils)

Which
inflammation
factors does GC
repress?

IL-1,2,6, TNF-alpha

which chemicals
stimulate the
hypothalamus to
secrete CRH?

Ach, 5-HT, NE

Which chemicals
suppress
Hypothalamus
CRH secretion?

NE, GABA

Which
inflammation
factorss increase
Cortisol?

IL-1,2,6, TNF-alpha

Cushings is a
result of

excess cortisol

High blood
pressure is a
result of

excess aldosterone

cardiac
remodeling is
caused by

aldosterone, high blood pressue, by

direct action

aldosterone
antagonists treat
___ and prevent
___

high BP, deleterious cardiac remodeling

How does GC
inhibit
Macrophages
and monocytes?

Phospholipase A2 is inhibited, limiting

the supply of arachadonic acid, which
suppresses COX enzymes.

When
Macrophages
and monocytes
are inhibited,
___

no prostoglandins or leukotriens are

produced; acute phase reactants,
including some compliment compontnes
are reduced. Turns down pain.

GC inhibits
endothelial cells
by ____

Reducing the expression of adhesion

molecules

reducing the
expression of
adhesion
molecules results
in

no homing or concentrating of
leukocytes at infection sites.

GC inhibits
Basophils by ___

inhibiting histamine production by

suppression of IGF dependant role

GC inhibits Lyphocytes by ___

inhibiting cytokine production, by limiting chemotaxis or the expansion of immune cells by IL-2,
IL-6

giving pregnant mom GC during

pregnancy will stimulate

fetal surfactant gene

addison's disease is a result of

___

cortisol or aldosteron deficiency

tumor in zona fisticulada will

cause ___

excess cortisol

vasoactive mediators are effected

by __, and makes ___

aldosterone excess, vaculature more sensetive to ANGII, and catecholamines (negative effect)

69.

Signs of Cushings Syndrome

Increased susceptibility to infection, fat redistribution, peripheral muscle wasting, Skin thinning,
Increased bruising, Hypertesnio, Bone loss, buffalo hump, moon face

70.

Symptoms of Addison's disease

Can't make MC or GC, volume contraction, don't retain sodium, Na is excreeting, hyponeutremic,
low volume

71.

primary addison's disease is

adrenal deffect, need surgical removal

Secondary and tertiary addison's

disease are

defect in pituitary (2ndary) or hypothalamus (tertiary)

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