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29 Cards in this Set

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cortisol and inflammation
COrtisol inhibts:
1. formation of arachidonic acid through action of lipocortin (induced) on on Phospholipase A2.
cortisol -------Neutrophil binding of leukotrienes
2. inhibits their infiltration and inhibts their phagocytic properties
same
3. cox 2
same
4. Platelet activation factor production (reduces neutrophil invasion)`
Same
inhibts production of NO, reduces vasodilation
The above were immediate responses
cortisol also inhibts imtermediate responses by stabilizing lysosomal membranes and reducing the release of proteolytic enzymes that contribute to tissue swelling. Also inhibts mast cell proliferation. Lowers local histamine levels.
Also has late response
cortisol inhibits fibroblast growth. preventing keloid and adhesion foramtion, also inhibts collagen formation and scar formation.
Immunosuppressive actions
1. inhibts IL-1 by macophages preventing T-cel stimulation
2. INhibts Il-2 production by T cells blocking t cell proliferation
3. inhibts interferon by t cells inhibtig macrophage activation
summary
cortisol stops the proliferation of circulating t cells and their function
T cells are blocked from
secreting IL2, y interferon, and other cytokines
WBC differential is altered by cortisol
lymphocytes are decreased, neutrophils are increased
eosoniphils and basophils are decreased.
You should know the roles of IL1 and IL 2 and interferon
pg. 70
immunofeedback loop
cortisol inhibts IL-1 and cytokines, but IL-1 and other cytokines stimulate CRH release from the hypothalamus. Thus an infection increases cortisol which inhibts the inflammation, but the cytokines releases increases cortisol release.Thus both are controlled by each other.
Diurnal Rythym
CRH and ACTH are secreted in pulses or bursts. Cortisol has the strong circadian rhythym you remember. With a peak at the time of wakening.
dexamethazone suppression test.
evaluates whether cortisol is subject to normal feedback. DEX is given at midnight and then an 8 am cortisol peak is measured. Used to test for ACTH secreting tumors.
metayrapone test
this test evaluates wheter ACTH synthesis is adequate. Metayrapone is an inhibitor of 11b-hydroxylase, and therefore inhibts cortisol synthesis. After metyrapone, ACTH should be stimulated; 11-dexoycortisol levels rise but do not exert negative feedback. ACTH is endpoint measured.
aldosterone and cortisol
both bind to the same receptor but glucs are in much higher concnetration, thus glucs need to be inactivated in aldosterone target cells so that aldosterone can exert its effects.
stimulation of aldosterone secretion.
angiotension through Gq stimulates the zonula glomerulosa.
K+ plasma up
increased K+---opens volatage gated Ca2+ channels on glomerulosa cells, stimulating aldosterone synthesis. Aldosterone then reacts to excrete K+, restroing the appropriate levels of K+.
ALSO ACTH
signals through Gs and cAMP, does increas ALDO--not important. Glomerulosa does not atrophy in absence of ACTH. Stress cause aldosterone secretion.
Metabolism of aldosterone and adrenal androgens
aldosterone has a half life of 20 minutes. but it is metablized in a similar fashion to cortisol . Adrenal androgens are weak and are met. to 17 keto steroids. most keto steroids in urine are of adrenal.
rememeber that thinks that have to with kalemia, blood pressure, sodium intake, and postural tension
only affect aldosterone and not cortisol. however, stress, and physical trauma and hemmorahgae affect cortisol.
ADdisions disease. - primary adrenal insufficiency
Onset is frequently slow and insiduous, often mistake for depression or tired housewife syndrome.
Addisonian crisis
hypovolemic shock and coma resulting in death if untreated
Addision Its symtpoms include;
hyponatremia , hyperpigmentation, hypotension, weakness due to hyperkalemia, weight loss.
Androgenital syndrome
blockade of 21 or 11 Ohase produce. 21 Ohase causes masculinization, slat loss and hypotension. 11-ohase is associated with hypertension due to accumulation of DOC.
17a hydroxylase defeciecny
have sexaul infantilism along with hypertension and hypokalemic alkalosis (excess mineralcorticoids)
See figure 12 for overview of above
pg. 76
Conn's syndrome
or primary aldosteronism is caused by an aldosterone secreting tumor. The effects of the excess aldosterone are increased ECF volume, hypertension, hypokalemia, and metabolic alkalosis.