Term
| What are the layers of the adrenal cortex, from superficial to deep? |
|
Definition
| zona glomerulosa, zona fasiculata, zona reticularis |
|
|
Term
| Where are the mineralocorticoids made? (be as specific as possible) |
|
Definition
| in the zona glomerulosa of the adrenal cortex |
|
|
Term
| Where are the glucocorticoids made? (be as specific as possible) |
|
Definition
| Mostly in the zona fasiculata and somewhat in the zona reticularis |
|
|
Term
| Where are the adrenal adrogens made? (be as specific as possible) |
|
Definition
| Mostly in the zona reticularis and somewhat in the zona fasiculata |
|
|
Term
| What is the most powerful glucocorticoid? |
|
Definition
|
|
Term
| What is the most powerful mineralocorticoid? |
|
Definition
|
|
Term
| What are the steps of mineralocorticoid synthesis once the cholesterol is already in the mitochondria? |
|
Definition
| cholesterol is converted into pregnenolone via cytochrome p450 (cholesterol desmolase) scc; pregnenolone can be converted into many different molecules; second messengers G-proteins, IP3, and PKC activate calcium channels; calcium activates CAM kinase II, which regulates cholesterol intake, and calcium stimulates the conversion of 11-deoxycorticosterone (a possible product of pregnenolone modification) into aldosterone |
|
|
Term
| How does cholesterol taken up to the place of adrenocorticoid synthesis? |
|
Definition
| cholesterol (mainly from LDL) is transported by attaching to the receptors in coated pits on the cell surface; the receptors are endocytosed, a lysosome fuses with the vesicle to digest the proteins and release the cholesterol, then the cholesterol is transported to the mitochondria |
|
|
Term
| What is the rate-limiting step for adrenocorticoid synthesis? |
|
Definition
| the conversion of cholesterol into pregnenolone |
|
|
Term
| What class of hormones is aldosterone? Steroid, peptide, gas, eicosanoid, or amine derivative? |
|
Definition
|
|
Term
| What is the function of aldosterone? |
|
Definition
| aldosterone regulates the reabsorption of sodium (and consequently water) and the secretion of potassium in the renal tubule epithelial cells of the kidneys (especially the principal cells of the collecting tubules) and the secretion of H+ in the intercalated cells of the cortical collecting tubules; aldosterone also regulates sodium (and water) reabsorption on the sweat glands, salivary glands, and the intestines |
|
|
Term
| What secondary effects does the reabsorption of sodium and water by aldosterone have? |
|
Definition
| reabsorption of sodium and water causes increased blood volume and, consequently, increased blood pressure; increased blood pressure will cause a decrease in heart rate to preserve a fairly constant cardiac output |
|
|
Term
| What is the mechanism of action for aldosterone? |
|
Definition
| being lipid soluble, aldosterone diffuses through the membrane of the tubular epithelial cells and binds to the mineralocorticoid receptor (MR) protein; this complex diffuses into the nucleus and encourages transcription of certain proteins related to potassium secretion and sodium reabsorption, such as the Na-K-ATP pump and the epithelial sodium channel (which works on the luminal side); after transcription, it diffuses out of the nucleus to encourage translation of the proteins |
|
|
Term
| What regulates the secretion or synthesis of aldosterone? |
|
Definition
| angiotensin II, ACTH, potassium levels, sodium levels |
|
|
Term
| How does angiotensin II regulate aldosteron? |
|
Definition
| angiotensin II regulates the conversion of cholesterol to pregnenolone; an increase in angiotensin II causes a large increase in aldosterone |
|
|
Term
| How does ACTH regulate aldosterone? |
|
Definition
| ACTH is necessary to regulate the number of LDL receptors, which help the intake of cholesterol; ACTH does not significantly affect the secretion of aldosterone |
|
|
Term
| How does potassium regulate the secretion of aldosterone? |
|
Definition
| When potassium levels are high, it stimulates aldosterone synthase to increase conversion of 11-deoxycorticosterone to aldosterone |
|
|
Term
| How do sodium levels regulate the secretion of aldosterone? |
|
Definition
| low sodium levels cause an increase in rennin secretion, which increases conversion into angiotensin II, which causes an increase in aldosterone secretion |
|
|
Term
| How is aldosterone cleared from the blood? |
|
Definition
| it is degraded in the liver and either excreted in the bile or converted into a highly soluble conjugate that is filtered by the kidneys |
|
|
Term
| What is the average blood concentration of aldosterone? |
|
Definition
|
|
Term
| How is aldosterone transported? |
|
Definition
| about 60% of aldosterone is bound to transcortin and about 40% is free in the plasma |
|
|
Term
| What is the half-life of aldosterone? |
|
Definition
|
|
Term
| What are some other mineralocorticoids? How significant is their activity? |
|
Definition
| 11-deoxycorticosterone, cortisone, corticosterone, and cortisol; each of the first 3 have slight activity and cortisol has very slight activity, but cortisol has a huge concentration compared to aldosterone, making it the second most powerful mineralocorticoid |
|
|
Term
| What effect does aldosterone have on principal cells in the kidney? |
|
Definition
| it promotes potassium secretion and sodium reabsorption; sodium concentration does not increase significantly because an appropriate amount of water follows, but blood volume does increase |
|
|
Term
| What effect does aldosterone have on intercalated cells in the kidney? |
|
Definition
| aldosterone stimulate the secretion of H+, raising pH; excess aldosterone can lead to alkalosis |
|
|
Term
| What is primary aldosteronism? |
|
Definition
| (Conn's syndrome) - a tumor in the zona glomerulosa, causing an excessive secretion of aldosterone |
|
|
Term
| What symptoms does Conn's syndrome cause? |
|
Definition
| hypokalemia, which raises the potassium gradient toward the outside of the cell, meaning potassium may flow out of the cell faster, yielding unintended depolarization, which leads to muscle weakness or paralysis; excess aldosteron also causes low rennin levels and excessive excretion of H+, which can cause metabolic alkalosis |
|
|
Term
| Is Conn's syndrome more common in men or women? |
|
Definition
| it is twice as common in women |
|
|
Term
| How is Conn's syndrome diagnosed? |
|
Definition
| low rennin levels (and combined with high aldosterone levels) |
|
|
Term
| How is Conn's syndrome treated? |
|
Definition
| surgical removal of the tumor in the zona glomerulosa, partial or total removal of the adrenal gland, or administration of an antagonist to the mineralocorticoid receptor, such as spironolactone or eplerenone |
|
|
Term
| What symptoms for mineralocorticoid deficiency cause? |
|
Definition
| that causes a deficiency in aldosterone; without aldosterone, there would be a loss of sodium, water, and chloride and reduced sodium absorption, causing diarrhea; it would also cause reduced H+ excretion, leading to acidosis, which would make ATP synthesis more difficult (because H+ concentrations are usually higher inside the cell, but reduced pH would reduce the gradient); aldosterone deficiency would also cause hyperkalemia, hyperpolarizing the membrane of cells, making it more difficult for them to depolarize; since aldosterone would not be preserving sodium and water, both would be lost, causing an increasing loss of blood volume, making the blood sluggish and thick, eventually causing hypovolumic shock |
|
|
Term
| What will happen if blood volume is maintained to prevent hypovolumic shock during mineralocorticoid deficiency? |
|
Definition
| the increasing concentration of potassium will still decrease heart constractility and eventually cause heart failure |
|
|
Term
|
Definition
| apparent mineralocorticoid excess syndrome |
|
|
Term
| What causes AME syndrome? What are its symptoms? |
|
Definition
| a genetic deficiency of 11-beta-hydroxysteroid dehydrogenase type 2, which converts cortisol into cortisone, the latter of which has less mineralocorticoid activity; this causes the body to react the same way as having excess aldosterone (hypokalemia, high blood volume, etc), but aldosterone levels will be low |
|
|
Term
| What chemical, if ingested in large enough quantities, can cause AME syndrome symptoms? How might one ingest this chemical? |
|
Definition
| glycerzic acid can causes a block of 11-beta-hydroxysteroid dehydrogenase type 2, which will cause AME syndrome symptoms; this chemical can be found in licorice |
|
|
Term
| What is secondary aldosteronism? What causes it? |
|
Definition
| Secondary aldosteronism is an excess of aldosterone triggered by a reduction in renal blood flow (possibly due to renal artery atherosclerosis); the reduction in renal blood flow increases the secretion of renin, which increases the conversion of angiotensin II, which causes an increased production of aldosterone; increased aldosterone causes increased blood volume, eventual hypernatremia, hypertension, possible muscle paralysis, and hypokalemia |
|
|
Term
| How is secondary aldosteronism treated? |
|
Definition
| with A-II receptor blockers or ACE inhibitors |
|
|
Term
| How is cortisol synthesized? |
|
Definition
| cholesterol in the form of LDL via receptors in coated pits, which are endocytosed; the resulting vesicle fuses with a lysosome to release the cholesterol, which is then transported to the mitochondria, which it is converted into pregnenolone by cytochrome 450 (cholesterol desmolase) scc |
|
|
Term
| What effects does cortisol have on blood glucose levels? Gluconeogenesis? Amino acid metabolism? |
|
Definition
| increase, increase, increase |
|
|
Term
| What effects does cortisol have on protein catabolism, amino acid influx, and glycolysis? |
|
Definition
| increase, decrease, decrease |
|
|
Term
| What effects does cortisol have on glycogen storage, FFA levels, and beta oxidation? |
|
Definition
| increase, increase, increase |
|
|
Term
| What effects does cortisol have on insulin levels and insulin resistance? |
|
Definition
|
|
Term
| What effects does cortisol have on protein anabolism and fat deposition? |
|
Definition
| decrease (except in the liver and plasma), and increased in certain areas (face, shoulders, and torso) |
|
|
Term
| What effects does cortisol have in the GI system? |
|
Definition
| increased gastric acid and increased proliferation of mucosa cells |
|
|
Term
| What effects does cortisol have in the cardiovascular system? |
|
Definition
| increased vasoconstrictor sensitivity |
|
|
Term
| What effects does cortisol have in the CNS? |
|
Definition
|
|
Term
| What is the mechanism of action for cortisol? |
|
Definition
| cortisol diffuses through the membrane and affects transcription at the glucocorticoid response elements with the help of transcription factors |
|
|
Term
| How does cortisol secretion change with obesity? |
|
Definition
| the body views obesity as a stressful state and, since cortisol is one of the hormones the body releases in response to stress, cortisol release is increased with obesity; increased cortisol can have diabetogenic effects |
|
|
Term
| What are the possible stimulations for cortisol secretion? |
|
Definition
| trauma, infection, intense heat or cold, injection of sympathomimetic drugs, surgery, injection of necrotizing substances, restraint (also stressful), most debilitating diseases |
|
|
Term
| What is the mechanism of stimulation of cortisol secretion? |
|
Definition
| various stimuli send nerve signals to stimulate the hypothalamus, which increases CRH, which stimulates the anterior pituitary to release ACTH, which activates G-proteins are the target tissues, which activates cAMP, which activates PKA, which activates transcription of StAR (steroidogenic acute regulatory protein), which increases cholesterol influx into the mitochondria, where it is converted by cholesterol demolase into pregnenolone, then it is converted into 11-deoxycortisol, then into cortisol; PKA also increases LDL receptors and enzymes to increase cholesterol influx and modification |
|
|
Term
| What is the rate-limiting step for cortisol synthesis? |
|
Definition
| the conversion of cholesterol into pregnenolone |
|
|
Term
| What are the mechanisms of CRH's stimulation of ACTH secretion? |
|
Definition
| 1. CRH activates adenylyl cyclase, which activates cAMP, which activates PKA, which inhibits potassium channels, which causes depolarization, which (with PKA) activates calcium channels, and calcium increases ACTH secretion; 2. adenylyl cyclase also activates PKA to activates CREB (cAMP response element binding), which stimulates activators protein 1 (AP-1), which activates transcription of the POMC gene, which results in the synthesis of ACTH |
|
|
Term
| What are the mechanisms of vasopressin's stimulation of ACTH secretion? |
|
Definition
| 1. vasopressin activates PLC, which makes DAG, which activates PKC, which activates adenylyl cyclase, which, through several second messengers, stimulates ACTH secretion; 2. vasopressin also activates PLC, which makes IP3, which releases calcium stores, which causes ACTH secretion; 3. adenylyl cyclase also activates PKA to activates CREB (cAMP response element binding), which stimulates activators protein 1 (AP-1), which activates transcription of the POMC gene, which results in the synthesis of ACTH |
|
|
Term
| How does cortisol affect ACTH secretion? |
|
Definition
| cortisol blocks the transcription of the POMC gene (from which ACTH is made), it activates potassium channels (preventing calcium channel activation by depolarization), and blocks calcium channels |
|
|
Term
| What is the mechanism of negative feedback for cortisol? |
|
Definition
| 1. cortisol secretion causes anti-inflammation, gluconeogenesis, etc, which can cause removal of the initial stimulus, preventing stimulated secretion; 2. cortisol also inhibits ACTH secretion by blocking second messenger systems involved in its releases and transcription; 3. cortisol also inhibits the section of CRH |
|
|
Term
| How does cortisol secretion vary throughout the day? |
|
Definition
| cortisol secretion varies based on various stresses and also is much higher shortly after waking up compared to shortly before going to sleep |
|
|
Term
| How is cortisol cleared from the body? |
|
Definition
| Cortisol is degraded in the liver and either excreted into the bile or converted into a highly soluble conjugate which is then excreted into the urine |
|
|
Term
| What is the average concentration of cortisol in the blood? What is the average daily secretion? |
|
Definition
| 12 micrograms/100 mL; 15-20 mg per day, depending on the person and the activities of the day |
|
|
Term
| How is cortisol transported in the blood? |
|
Definition
| almost all of cortisol is bound to plasma proteins such as transcortin, albumin, and cortisone-binding protein |
|
|
Term
| What is the half-life of cortisol? |
|
Definition
|
|
Term
| What are significant other glucocorticoids? How do their potencies compare to cortisol? |
|
Definition
| corticosterone (much weaker), cortisone (almost = to cortisol), prednisone (4X cortisol), methylprednisone (5X cortisol), and dexamethasone (30X cortisol) |
|
|
Term
| What is the first main stage of inflammation? |
|
Definition
| when the tissue gets damaged, the cells often release substances that activate inflammation |
|
|
Term
| What are the chemicals that cells often release to activate inflammation? |
|
Definition
| histamine, bradykinan, proteolytic enzymes, prostaglandins, and leukotrienes |
|
|
Term
What is a common chemical that macrophages produce to initiate inflammatory response in many tissues?
Hint: it has a huge variation in response depending on the tissue |
|
Definition
|
|
Term
| What effect does IL-1 have in the CNS? In endothelial tissues? On fibroblasts? |
|
Definition
| fever and sleep; the production of prostaglandins and leukotrienes; collagenase release and mitosis |
|
|
Term
| What effect does IL-1 have on muscles? On neutrophils? |
|
Definition
| the production of prostaglandins, which causes the release of lysosomes, which causes protein degradation; encourages chemotaxis |
|
|
Term
| What effect does IL-1 have on bones and cartilage? On T-lymphocytes? |
|
Definition
| the production of prostaglandins, which causes the release of lysosomes, which causes protein degradation; causes the production of IL-2, which causes mitosis |
|
|
Term
| What is the mechanism for interleukin 1 and tumor necrosis factor α for producing prostaglandins, thromboxanes, and leukotrienes? |
|
Definition
| IL-1, TNFα, and tissue insult → I-κB kinase → I-NF-κB → I-κB-PO4 and NF-κB; NF-κB → ↑ transcription of IL-1, TNFα, other cytokines, PLA2, COX 2, iNOS → NO; PLA2 and COX2 → prostaglandins, thromboxanes, leukotrienes |
|
|
Term
| What is the second main stage in inflammation? |
|
Definition
| increase blood flow in the inflamed area cause by some of the released products, referred to as erythema |
|
|
Term
| What is the third main stage in inflammation? |
|
Definition
| leakage of large quantities of almost pure plasma out of the capillaries into the damaged areas because of increased capillary permeability, following by clotting of the tissue fluid, causing a non-pitting edema |
|
|
Term
| What is the fourth main stage in inflammation? |
|
Definition
| infiltration of the area by leukocytes |
|
|
Term
| What is the fifth main stage in inflammation? |
|
Definition
| after days or weeks, ingrowth of fibrous tissue that often helps in the healing process |
|
|
Term
| What is cortisol's mechanism of action on the early stages of inflammation? |
|
Definition
| 1. cortisol attaches to the glucocorticoid receptor, which then blocks the transcription of PLA2, COX 2, iNOS, IL-1, TNFα, and other cytokines; 2. cortisol also binds to the glucocorticoid receptor, which blocks transcription of I-κB, which causes suppression of I-NF-κB; 3. the resulting effect is a rabid resolution of inflammation and increased healing |
|
|
Term
| What are the mechanisms of cortisol's prevention of inflammation? What are the mechanisms of resolution of inflammation? |
|
Definition
| it stabilizes lysosomal membranes, reducing exocytosis of granulocytes; it decreases permeability of the capillaries; it decreases migration of WBCs into the inflamed area and the phagocytosis of damaged cells (probably due to the reduction of PG and LT that would otherwise case vasodilation, capillary permeability, and motility of WBCs); it suppresses the immune system, which decreases lymphocyte reproduction; it reduces fever by decreases the release of IL-1, which also decreases vasodilation; 2. for resolution, the mechanisms are the same, but it reverses the actions, instead of reducing or preventing them |
|
|
Term
| What is cortisol's effect on allergic reactions? On white blood cells? On red blood cell count? |
|
Definition
| It blocks the inflammatory response in allergic reactions; it reduces immune response to WBCs; it increases RBC cell count |
|
|
Term
| What is cortisol's effect on liver proteins? Plasma proteins? Muscle proteins? Lymphoid proteins? |
|
Definition
| it is believed it enhances liver enzymes involves in liver and plasma protein production; it is believed it inhibits RNA formation in muscles and lymphoid cells |
|
|
Term
| How does cortisol affect glucose utilization? |
|
Definition
| It reduces glucose utilization, possibly by inhibition of the oxidation of NADH |
|
|
Term
|
Definition
| proopiomelanocortin; it is a large peptide from which other important peptides can be made |
|
|
Term
| What peptides can be made from POMC using only PC 1? |
|
Definition
|
|
Term
| What are the enzymes that split POMC into its active peptide parts? Which is used in the anterior pituitary? |
|
Definition
| prohormone convertase 1 and 2 (PC1 and 2); only PC 1 is used in the anterior pituitary |
|
|
Term
| What peptides can be made from POMC using PC 1 and PC 2? |
|
Definition
| ACTH, β-lipotropin, γ-lipotropin, β-endophin, α-melanocyte-stimulating hormone (α-MSH), β-MSH, γ-MSH, and corticotrophin-like intermediate peptide (CLIP) |
|
|
Term
| Where can POMC be processed? |
|
Definition
| the dermic cells, the hypothalamus, the anterior pituitary, and the lymphoid tissue |
|
|
Term
| If multiple hormones can be synthesized from the precursor molecule to ACTH, why do their effects rarely show up, except in cases of excessive ACTH production? |
|
Definition
| molecules besides ACTH are made in small enough amounts that they usually don't have an effect, and only ACTH and β-lipotropin are synthesized in the anterior pituitary (where most of the stimulus for POMC processing usually occurs) |
|
|
Term
| What important androgens are released from the zona reticularis? What important estrogens? |
|
Definition
| dehydroepiandrosterone (DHEA) and androstenedione; progesterone and estrogen |
|
|
Term
| What effects do adrenal androgens have on males? Females? |
|
Definition
| They may account for some pre-puberty development in males and cause pubic and axillary hair growth in females |
|
|
Term
| What kind of hormone are adrenal androgens? Peptide, steroid, gas, eicosanoid, or amine derivative? |
|
Definition
|
|
Term
| What kind of hormone is cortisol? Peptide, steroid, gas, eicosanoid, or amine derivative? |
|
Definition
|
|
Term
| What is adrenogenital syndrome? |
|
Definition
| occasionally, an adrenocortical tumor develops and secretes excessive amounts of androgens, resulting in a masculinizing effect or, in rare cases, the tumor will secrete excessive amounts of adrenal estrogens, resulting in a feminizing effect |
|
|
Term
| What are the symptoms of adrenogenital syndrome in women? |
|
Definition
| in women, is may cause the growth of facial hair, baldness (if she has the gene for baldness as well), male distribution of hair, a deeper voice, the growth of the clitoris to resemble a penis, and a more muscular build |
|
|
Term
| What are the symptoms of adrenogenital syndrome in prepubescent males? |
|
Definition
| the growth of facial hair, early growth of male distribution of hair, a deeper voice, a more muscular build, and rapid development of the male sexual organs |
|
|
Term
| What are the symptoms of adrenogenital syndrome in post-pubescent males? |
|
Definition
| symptoms are often obscured by normal virilizing characteristics of testosterone |
|
|
Term
| What could be a non-tumor cause of adrenogenital syndrome? What is the mechanism of the androgen production thereby? |
|
Definition
| a deficiency of a certain enzyme involved in cortisol production; when no cortisol is produced, the hypothalamus will be stimulated, releasing ACTH, which stimulates the adrenocortical cells, which causes an increase in androgens and no cortisol, which will cause the loop to repeat; eventually, excess androgens will be produced, which will inhibit the activity of the gonadotropes, causing a lack of FSH and LH; this last result means there will be no sex hormone production in the gonads and there will be no gamete production either |
|
|
Term
| How is adrenogenital syndrome diagnosed? |
|
Definition
| in addition to the symptoms, urinary excretion will include very high levels of 17-ketosteroids |
|
|
Term
|
Definition
| atrophy of or injury to the adrenal cortices, resulting in an inability of the cortices to produce sufficient adrenocortical hormones |
|
|
Term
| What causes primary hypoadrenalism? |
|
Definition
| addison's disease - the usual cause is the atrophy causes by a developed autoimmunity against the cortices; another possible cause would be tuberculous destruction of the glands or invasion by cancer |
|
|
Term
| What causes secondary hypoadrenalism? |
|
Definition
| atrophy due to impaired function of the pituitary gland and its ability to make ACTH, reducing the stimulation to the adrenal cortex, resulting in atrophy |
|
|
Term
| Which is more common: primary or secondary hypoadrenalism? |
|
Definition
|
|
Term
| What are the symptoms of Addison's disease? |
|
Definition
| deficiency of mineralocorticoids and glucocorticoids and blotchy melanin pigmentation |
|
|
Term
| What are the consequences of the mineralocorticoid deficiency in Addison's disease? |
|
Definition
| lack of aldosterone leads to a loss of renal tubular sodium reabsorption and H+ excretion, leading to an increase in excretion of sodium and chloride ions and water and a decrease in pH, which reduces blood volume and leads to hyponatremia, hyperkalemia, and acidosis; the former leads to a drop in blood pressure and an increase in blood viscosity and a drop in cardiac output, leading to hypovolumic shock |
|
|
Term
| What are the consequences of the glucocorticoid deficiency in Addison's disease? |
|
Definition
| a drop in cortisol leads to a loss of glucose maintenance between meals and reduced mobilization of fats and proteins, which leads to a loss of metabolic function; a loss of cortisol also reduces the ability to cope with physiological stress, which means even a mild infection could cause death |
|
|
Term
| What symptoms of primary hypoadrenalism will not occur in secondary hypoadrenalism? Why not? |
|
Definition
| mineralocorticoid deficiency (and all its associated symptoms) will probably not occur in secondary hypoadrenalism, because angiotensin II and potassium levels will still maintain mineralocorticoid levels even with a loss of ACTH (which is the cause of secondary hypoadrenalism) |
|
|
Term
| What causes the blotchy melanin pigmentation in Addison's disease? |
|
Definition
| loss of cortisol stimulates corticotropes to produce ACTH, which is made from POMC; POMC can also be processed by non-pituitary tissues into other hormones, such as melanocyte-stimulating hormone; increased MSH levels in some tissues results in increased melanin production in those tissues without an increase in cortisol (which starts the cycle again); pigmentation sometimes appears in blotches and darker pigmentation most notably shows up in the lips and nipples |
|
|
Term
| How is hypoadrenalism treated? |
|
Definition
| Primary hypoadrenalism can be treated with mineralocorticoid and glucocorticoid supplementation, though secondary hypoadrenalism only requires glucocorticoid supplementation |
|
|
Term
| Define Addisonian crisis. |
|
Definition
| Addisonian crisis is an issue that arises in hypoadrenalism because the body's cortisol level fluctuates regularly (especially in times of stress); various stresses on the body, especially with surgery, will require huge amounts of cortisol, in addition to what the patient would normally need, in order for patients to survive |
|
|
Term
|
Definition
| hypersecretion by the adrenal cortex |
|
|
Term
| What is the cause of primary hyperadrenalism? |
|
Definition
| adenomas in the adrenal cortex, resulting in increased cortisol and androgens |
|
|
Term
| What is another name for primary hyperadrenalism? |
|
Definition
|
|
Term
| What is another name for secondary hyperadrenalism? |
|
Definition
|
|
Term
| What is the cause of secondary hyperadrenalism? |
|
Definition
| There are 3 possible causes: 1. adenomas of the anterior pituitary, causing increased ACTH, which stimulates adrenal cortex hypertrophy, which causes increased cortisol and increased androgens; 2. abnormal function of the hypothalamus, causing increased CRH, which stimulates the anterior pituitary to secrete more ACTH which stimulates the adrenal cortex to increased cortisol and androgen secretion; 3. ectopic secretion of ACTH by a tumor elsewhere in the body (such as an abdominal carcinoma), stimulating the adrenal cortex to secrete more cortisol and androgens |
|
|
Term
| Which hormones are increased in secondary hyperadrenalism? |
|
Definition
|
|
Term
| What is a possible non-tumor cause of Cushing's syndrome? |
|
Definition
| long-term treatment of inflammation with steroids, such as in cases of rheumatoid arthritis, IBS, etc |
|
|
Term
| How is hyperadrenalism diagnosed? |
|
Definition
| hyperadrenalism will always have high cortisol secretion; a large dose of dexamethasone will help determine if it is ACTH dependent or independent; ACTH independent Cushing's would have little to no detectable ACTH with such high cortisol, but abnormal functions of the hypothalamus and pituitary would have large amounts of ACTH regardless |
|
|
Term
| What are the symptoms of hyperadrenalism? |
|
Definition
| a "moon"-shaped face, redistribution of fat to the face, shoulders, and torso instead of the thighs and buttocks, probable hypertension (due to the mineralocorticoid effects of cortisol), hyperglycemia, increased protein catabolism resulting in muscle weakness, osteoporosis, purplish striiae (due to breakdown of subcutaneous proteins), and lymphoid tissue breakdown resulting in immune system compromise; situations that involve an increase in androgens as well may result in an increase in facial hair and acne |
|
|
Term
| How is hyperadrenalism treated? |
|
Definition
| removal of tumor, when there is a tumor present and the removal is feasible; administration of steroidogenesis-blocking drugs, such as ketoconazole, metyrapone, and aminoglutethimide, or ACTH secretion inhibitors, such as serotonin antagonists, GABA-transaminase inhibitors, may be used if the removal of a tumor is not feasible; if ACTH levels cannot be satisfactorily decreased, an alternative is a partial or total bilateral adrenalectomy followed by the administration of adrenal steroids to compensate for possible insufficiency |
|
|
Term
| What is the stimulus for cortisol secretion in response to inflammation? |
|
Definition
| IL-1 and TNF-α, which are released during inflammation, can stimulate the release of CRH from PVN, stimulate the release of ACTH from anterior pituitary, and stimulate the release of cortisol from adrenal cortex; this leads to the release of cortisol to inhibits IL-1 and TNF-α |
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|
