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Endocrine and Reproduction Systems > Adrenal > Flashcards

Adrenal Flashcards

1
Q

Where are the adrenal glands located? What is special about these glands, anatomically speaking?

A

Hat that sit on top of the kidneys. Part of neuroendocrine system (so regulated by hypothalamus and pituitary gland). They are the only hormonal tissue that has 2 distinct kinds of tissue.

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2
Q

Where are steroid hormones secreted from? Embryonically, where did it come from?

A

Adrenal cortex (mesoderm tissue). Cortex is made of zona glomerulosa, fasciculata, and reticularis…GFR. Secretes (glucocorticoids) cortisol.

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3
Q

Where are catecholamine hormones (epi and norepi) secreted from? Embryonically, where did it come from? When these hormones are released, where do they go?

A

Adrenal medulla…considered a post symp gang. Came from neuroectodermal tissue (hence the catecholamines). Epi and norepi are released into bloodstream (NOT a neuronal synapse)

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4
Q

What triggers release of hormones from adrenal cortex or medulla

A

Stress, which could be ANYTHING. even physiologically based, such as changes in water balance

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5
Q

Which is quicker? Releases of hormones from adrenal medulla or cortex?

A

Medulla catecholamine is dumb quick (seconds), while steroids from cortext take hours or days. Catecholamines use cascade responses (can’t get into the cell), which just so happens to be faster than doing it directly like steroid operate.

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6
Q

Describe catecholamine biosynth. Where are chatecholamines stored? What is another name for an adrenal medulla cell? Why do chatecholamines have the name they do?

A
  1. Starts with tyrosine.
  2. A bunch of conversion enzymes
  3. Finished and stored in in CHROMAFFIN GRANULE. Note that adrenal medulla cells = Chromaffin Cells. Also note that chatecholamines are made of a phenol ring with 2 hydroxyl groups and an amine group added to the end.
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7
Q

Describe the contact between the adrenal cortex and medulla?

A

Cortisol attacks medulla, which upregulates the enzyme that converts norepi to epi (WHEN CORTISOL IS TriGGERED, EPI IS FAVORED!!! Otherwise, norepi is favored). Epi = heart and bronchial stuff. Norepi = vasoconstrict stuff

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8
Q

Describe path of bloodflow to adrenal gland

A

Cortex to medulla to bloodstream

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9
Q

How does sympathetic innervation affect catecholamine production?

A
  1. DIRECTLY causes release of catecholamines from chromaffin cells. norepi is also released from symp gang.
  2. Stimulates conversion of tyrosine to norepi and epi
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10
Q

Why would one release catecholamines?

A
  1. Fight-or-flight response.
  2. Anxiety
  3. Pain
  4. Trauma
  5. HYPOvolemia
  6. HYPOglycemia
  7. HYPOthermia
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11
Q

What is the difference between adrenal gland and sympathetic ganglion?

A

Symp gang synapses are target cell while adrenal gland catecholamines are released into blood stream

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12
Q

What is the binding preference for the catecholamine hormones? What do they do in fight or flight response?

A

Alpha: Norepi
Beta: Epi

Beta: Glycogenolysis, gluconeogenesis, lypolysis, glucose utilization, cardiac contractility, and heart rate all increase. Arterial dilation also increases, which lowers BP affecting skeletal muscle and bronchioles. Rmemerb that thyroid hormones also causes the upregulation of beta receptors so that cardiac contractility and HR increases.

Alpha: Increases glycogenolysis, gluconeogenesis, arteriole vasoconstriction, and subsequently BP affecting visceral organs (such as spleen, stomach, liver, and GI), renal, cutaneous, and genital.

Note that the overall effect is to shunt blood from the visceral organs and towards the active skeletal muscle, bronchioles, and brain.

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13
Q

What are typical agonist sand antagonists that take advantage of alpha and beta receptors?

A

Agonists: Amphetamines, anything used for bronchial dilation and nasal dilation
Antagonists: Beta blockers, anything used to lower bp and treat arrhythmias or anxiety

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14
Q

What is the largest part of the adrenal gland? Which one exclusively makes mineralcorticoids? Which one makes glucocortioids?

A

Adrenal cortex: zona glomerulosa, fasciculata, and reticularis…GFR. zona glomerulosa exclusively makes mineralcorticoids (aldosterone). GLucocorticoids are made from fasciculata

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15
Q

Where does steroidogenesis take place? Where do the adrenal glands get cholesterol from?

A

Only occurs in gonads and adrenal cortex. All of them derive cortisol from cholesterol. Cholesterol can be made in the body from acetly CoA.. It is more predominantly obtained from diet and liver. It is found in the blood stream, bound to LDL’s, which binds to an LDL receptor and shuttles the cholesterol into the adrenal cortex cells.

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16
Q

Upon cholesterol entering the adrenal gland, describe the steroidogenesis process. Can steroid be stored? Why or why not?

A
  1. Cholesterol is stored in cholesterol esters
  2. Upon need, the esterized cholesterol is hydrolyzed and sent to the outer and then inner membrane of mitochondria.
  3. Cholesterole is converted to pregenolone with enzyme on INNER mitochondrial membrane
  4. Pregenelone is transported by mitochondria to ER, which it further goes enzymatic mods
  5. Modded steroid is sent back to mitochondria for another round of modification.
    Note that steroids cannot be stored because they are hydrophobic like the membranes, so they will literally just diffuse out. As a result, the adrenal cortex DOES NOT store hormone. SO, steroid hormone biosynth and secretion occur concomitantly.
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17
Q

Which step in steroidogenesis is the rate limiting step? Where does it take place?

A

The conversion of cholesterol to prenenelone. So drugs that work to upregulate steroid genesis do so by accelerating this step. Remember that it takes place on the inner mitochondrial membrane and is done by cholesterol-side chain cleavage complex (CYP11A aka P-450)

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18
Q

What does cholesterol-side chain cleavage complex (CYP11A) do?

A

Removes signature side chain of cholesterol and attaches an acetly group in its place.

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19
Q

WHat enzyme does the zona glomerulosa lack?

A

CYP17, which is why it’s pathway can only makes aldosterone (down pathway from pregnenelone). Also note that aldosterone synthase is only found in the zona glomerulosa.

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20
Q

Which two layers express CYP 17? WHy is this important?

A

Zona fasiculata and reticulosa. This makes it so that pregenelone and progesterone mainly become cortisol androgenic precursor (DHEA or androstedione).

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21
Q

Which is most potent mineralcoirticoid and glucocorticoid, upon activation?

A

Aldosterone and cortisol

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22
Q

What activates DHEA and androseridione? What is the active form?

A

17B-HSD is the enzyme, responsible for turning the precursors into testosterone.

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23
Q

Is the adrenal cortex a significant source of androgen in an adult?

A

Female: Yes. For muscle growth and normal female pattern of body hair growth, labido and such.
Male: No. That’s what the testes are for. This is where testosterone is made. Note that the testes make a crap ton of it.

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24
Q

How is steroid hormone released?

A

Adrenalcorticotropic hormone (ACTH), released from the pituitary. Note that is acts on the rate limiting step converting cholesterole to pregenelone in zona reticularis and faciculata.

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25
Q

Which more strongly stimulates aldosterone production? AII or ACTH?

A

AII.

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26
Q

What hormone causes release of ACTH?

A

Corticotropin releasing hormone (CRH), which is released by the hypothalamus, which still operates through stress (emotional, physical, etc).

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27
Q

What happens if there is a buildup of cortisol in the bloodstream?

A

Cortisol cuts off pit (ACTH) and hypothalamus (CRH) (negative feedback)

28
Q

Term for ACTH, CRH, Cortisol releasing setup.

A

Hypothalmic-pituitary-adrenocortical axis

29
Q

What predominates? The stress response or the negative feedback?

A

STRESS RESPONSE! Chronic stress will lead to chronically elevated levels of cortisol.

30
Q

Describe the pathway that leads to the release of ACTH

A

ACTH binds to ACTH g protein coupled receptor on adrenal cortical cell. This activated adenylate cyclase. This increases cAMP, which activates PKA and PKC. ACUTE ACTH stimulation increases cholesterole production and promotes conversion of cholesterol to pregenenlone. This is done by either (1) use of CYP11A or (2) catalyze the series of enzymes which hydrolyzes cholesterol ester into cholesterol and then transfers the cholesterol to the mitochondria. CHRONIC stimulation of ACTH upregulates LDL receptors and upregulates CYP17, which upregulates cortisal more so than other steroid hormones.

31
Q

What would cause constituent release of ACTH to release relentless amounts of cortisol?

A
  1. Stress
32
Q

When is cortisol release at its highest? Lowest? How much is released upon waking up? What alters cricadian cortisol release pattern?

A

Highest: Just before or after waking (like, 8am for instance). Usually about 50% of the daily dose of cortisol is released at this particular moment.
Lowest: After falling asleep.
Note that this entire process is altered if you are nocturnal (person working on night shift) or are blind.

33
Q

Why does the circadian release of cortisal make sense?

A

Cortisol mobilizes blood glucose, which we use when we are active in the morning. It also increases appetite, which correlates its higher amounts around meal times. In other words, cortisol is released regularly in normal physiologic instances.

34
Q

How does cortisol travel in the blood?

A

90% of circulating cortisol binds to cortisolsteroid-binding globulin (CBG) because it is hydrophobic and would otherwise be excreted. CBG = mobile reservoir for cortisol and it protects cortisol from being rapidly degraded in liver…it extends cortisol’s halflife.

35
Q

Why does aldosterone have a much lower halflife than cortisol?

A

It doesn’t have a carrier.

36
Q

How do you switch between cortisol and cortisone (inactive form of cortisol)? Where are these enzymes expressed? Which hormone, cortisole or cortisone, is used as a drug? Why?

A

To get cortisol FROM cortisone, use Type 1 11-HSD. To get Cortisone from cortisol, use Type 2 of the same enzyme.
Type 1: expressed throughout entire body. Uses NADPH.
Type 2: ONLY expressed in kidney and other aldosterone target tissues. Uses NAD.

Cortisone is dug worthy because it’s expressed in way more tissues (pit, liver, bone, muscle, gonads, adipose) and it can be rapidly metabolized into the active form with the type 1 enzyme.

37
Q

Where are cortisone and cortisol metabolized in the body?

A

Liver, with the bulk of them becoming glucurionic acid and excreted. 70% of these glucurionic acid compounds contain urinary 17-OH-corticoid group (can only be found on glucocorticoids found on the adrenal cortex). You could use this to track the amount of cortisol you body is making.

38
Q

Where does AII bind to stimulate aldosterone production? What acts as negative feedback to kill aldosterone production?

A
  1. Binds at zona glomerulosa.
  2. AII stimulates the rate limiting conversion of cholesterol into pregenelone.
  3. Increased blood volume cuts off macula densa, so that bp is normalized again.
39
Q

What do high K levels do to the adrenal zone glomerulosa?

A

Triggers th eneed to excrete K (so aldosterone is produced). Also causes depol of Ca channels, which lets Ca act as a secondary messenger, which acts directly for the increase in aldosterone production.

40
Q

What are nuclear hormone receptors? Describe properties of cortisol.

A

Ligand activated transcription factors. Note that cortisol is hydrophobic (so, carried around in blood by CBG). Once released, it passively runs through membrane of glucocorticoid target cell. It runs all the way to the nucleus, regulating gene expression through Hormone Response Elements on the DNA. Note that cortisol binds to mineralcorticoid receptor, stimulating its effects in the nucleus.

41
Q

What is the major metabolic action of cortisol? How does it operate in the liver? In muscle? In fat?

A

Elevates blood glucose by upregulating gluconeogenesis (production of glucose from non-carb sources like AA or lactic acid). in the liver. Cortisol also prevents insulin secretion, keeping blood in the blood. In skeletal muscle, cortisol is catabolic, upregulating enzymes which inhibit protein synthesis and break down protein, releasing AA’s into the bloodstream so that it can get to the liver and be used for gluconeogenesis. In CERTAIN adipose stores, cortisol stimulates lipolysis, which releases glycerol and FAA into bloodstream. Glycerol can then be used for gluconeogenesis. The FFAs can be oxidized to make ATP.

42
Q

How does cortisol effect appetite?

A

It stimulates an increase in appetite (very powerful at doing this). Increased intake in calories can lead to cortisol promoting selective lipogenesis (abdomen, trunk, neck, and face). The goal in stimulating appetite and building fat is so that the body has the energy and blood sugar to continue handling your stress. This is why people eat more when they are stressed out.

43
Q

What are the end results of chronic cortisol release?

A

Anabolic: Fat buildup (increased appetite) so that you can keep breaking down fat to make FFA’s (for atp) and glycerol (for gluconeogenesis)
Catabolic: Wrecks skeletal muscle for their proteins to be used in gluconeogenesis

44
Q

Job of insulin

A
  1. Inhibits glucose production in the liver

2. Increases glucose uptake into fat and muscle.

45
Q

Job of cortisol

A

Antagonize insulin, just like GH. It maximizes glucose production and minimizing glucose uptake. It legitimately shifts graph to the right.

46
Q

Describe cortisol’s actions in acute vs chronic conditions.

A

Acute: send glucose to brain and skeletal muscle. Increases liver gluconeogenesis.
Chronic: Break down muscle (so no more glucose is sent to muscle), send to brain still tho.

47
Q

Why does cortisol trump insulin’s blood sugar lowering actions?

A

To ensure that in times of stress there is plenty of glucose available to the skeletal muscles and brain. The brain needs it it cannot burn fat. Glucose is the only thing that can cross BBB. Brain and neuro system will die otherwise. Also note that cortisol is dumb slow. Regardless of the situation, acute or dire, brain gets a share of glucose. If dire, skeletal muscles will take that L.

48
Q

How does cortisol effect bone? Skin/connective tissue? Kidneys? Act as an Anti-inflammatory? Act as an immunosuppressive?

A

Bone: Inhibitory actions on bone, including killing bone formation by decreasing blood Ca by inhibiting osteoblast collagen synth and stimulating resorption by calling upon the osteoclasts. Also inhibits Ca reabsorption from kidneys. Note that the decrease in Ca would stimulate PTH, which will summon osteoclasts again…cycle.
Skin/connective tissue: inhibits collagen formation and inhibits fibroblast growth. Patients develop very thin skin and bruise tissue. Cortisol leads to this because collagen and skin account for 30% of the body’s protein…and cortisol kills protein to make glucose.
Kidneys: mineralcorticoid receptor agonist (cortisol will literally act like aldosterone by binding to aldosterone receptors. end result is the same as aldosterone. They have very similar structures.)
Anti-inflammatory: cortisol is a strong antiinflammatory.

49
Q

What kicks in during starvation periods?

A

cortisol

50
Q

What compounds are involved in inflammatory system during an injury, and how are they derived?

A

It causes local dilation of capillaries and increased capillary permeability what allows cells of the immune system to be trapped in the affected site to fight off a given infection. Compounds used are prostaglandins, thromboxanes, and leukotrienes. They’re derived from phosphatidyl choline in the cell membrane.

51
Q

How does cortisol act as an antiinflammatory?

A

It blocked phospholipiase and cyclooxygenase (the usual pharmacological target…cortisol is best at attacking this), cutting production of prostaglandins, thromboxanes, and leukotrienes and killing inflammatory pathway.
Cortisol also stabilizes damaged lysozomed cells that would otherwise release vasoactive substances that would augment local inflammation.

52
Q

How does cortisol act as an immunosuppressor, decreasing the number/activity of circulating T cells? (note its use for tissue transplant)

A

Note that normally antigens (outside jerks) are engulfed by macrophages, and the macrophages secrete interleukin-1 (which causes fevers) which leads to the summoning of T helpter cells, which summon interleukin 2 and 6, which summon even more T helper cells. Cortisol wrecks this by preventing macrophage’s ability to summon interleukin 1, 2, 6, and actually promotes cell death.

53
Q

What is the purpose of cortisol inhibiting the T cells and killing immune response?

A

By suppressing an immune response, cortisol is killing obsessive functions that the body was spending energy on, and directing that energy on more glucose production for the brain and skeletal muscle. It is essentially a co regulator.

54
Q

Describe the path of aldosterone at lumen of cortical collecting duct.

A

Passes directly into the cell, binding at a minercorticoid receptor on nucleus, which ultimately leads to increases in Na channels to allow Na into the cell (creating an electronegative condition promoting passage of K out of the cell.). Na/K atpases area also upregulated, which pumps Na out of the cell so that Na can get to the interstitium. Mitochondrial enzymes are also upregulated. THis is all upregulated in the gi and sweat glands, so K is now found in sweat and feces.

55
Q

What holds cortisol in check? How does this protect the kidneys?

A

TYPE 2 11-HSD. it converts cortisol to inactive form…cortisone. It is almost exclusively expressed in the kidneys. This allows the kidneys to shield themselves from the diverse effects of cortisol.

56
Q

What happens if someone inhertits a defective Type 2 11-HSD? What is a more common form of this potential issue? WHat about pharmacetucially speaking?

A

Have inherited hypertension and are more susceptible to diabetes. However, it is more common for this to manifest as a hyperadrenal disorder, pathologically high levels of cortisol can still flood the kidneys and negatively affect them just the same. This is seen in Cushing’s disease. These patients will also more than likely (80% chance) have hypertension. Of course, pharmaceutically speaking, prescribing a high dose of cortisol would also still have the same negative effect.

57
Q

What is Addison’s disease?

A

HYPOfunction of adrenal cortex. Suffers from

  1. Cortisol deficiency: loss of appetite, fatigue, nausea and vomiting, diarrhea, hypoglycemic, impaired gluconeogenesis, increased insulin sensitivity, HYPERPIGMENTATION (primary disease…as in the version caused by the auto immune destruction of adrenal cortex). Occurs in areas exposed to sunlight.
  2. Aldosterone deficiency: Decreased exctracellular fluid, hypotension, HYPERkalma, weight loss, excessive renin production
  3. Androgen deficiency: In females, reduction in pubic and axillary hair
58
Q

What is Cushing’s SYNDROME (where syndrom = collection of symptomes that point to a hyperactiv adrenal cortex)?

A

HYPERfunction of adrenal cortex.
Note: Negative feedback is wrecked.
1. Cortisol excess: Obesity in face and neck and abdomen, hyperglycemia, muscle atrophy, insulin resistance (30% have DM2), poor wound healing, suseptibility to infection, thin skin that’s easily bruised, osteoporosis, hypogonadalism in males, HYPERTENSION
2. Androgen excess: increased extracellular fluid volume, hypertension (which could also be triggered by too much cortisol…80% of these guys are hypertensive), hypokalemia
3. Androgen excess (females): Increased body/facial hair, oligomenorrhea, acne, deepening voice, regression of breast tissue, increased muscularity

59
Q

What could lead to addison’s disease aka adrenal insufficiency?

A
  1. Auto immune destruction/infection of adrenal cortex
  2. Pit timor (HYPO ACTH)
  3. Hypothalm tumor (HYPO CRH)
    Was originally made aware by newfound TB
60
Q

What could lead to cushing’s disease/syndrome

A
  1. Most commonly pit tumor (HYER ACTH) (TRUE Cushing’s Disease)
  2. Non-pit tumor (Ectopic ACTH Syndrome…note buffalo hump and moon face in females)
  3. Adrenal cortical pit tumor (hyper secreting)
61
Q

What risk is higher in patients with cushing’s disease/syndrome?

A

Bone fracture or osteoporosis.

62
Q

How would one treat a cushing’s disease/syndrome patient?

A
  1. Reduce Na, high Ca, high Vit D diet
  2. Thiazide, or other K sparing diuretic diuretic (Ameloride) because the crap ton of aldosterone likely excreted a ton of K. Need to replenish that. You could also use a mineralacoid ANTAGONIST (spiranolactone/EPLERENONE).
    You would also need ANDROGEN receptor antagonist (Bicalutamide) and Glucocorticoid receptor antagonists (Mifepristone). You could even use steroid hormone biosynth inhibitors (meytapone, ketoconazole….beware of hypogonadalism in males, as well as screwed up reproductive health in females.). Last resort = surgery.
63
Q

Why are melanocites affected in addison’s disease (version caused by auto immune destruction of adrenal gland)

A

In primary Addison’s disease, there is no negative feedback for cortisol because not enough cortisol is being produced. Leads to an ACTH enhanced production. ACTH expression in adrenal cortex is near a large pre-prohormone called POMC. This is processed into several hormones, including melanocyte stimulating hormone. Loss of pit gland amplifies both ACTH and melanocyte stimulating hormone.

64
Q

What would happen if someone develops a hypothalmic tumor that blocked CRH production, and they developed 2ndary Addison’s disease?

A

They would NOT have increased melanocyte stimulating hormone production. It is only in the primary disease.

65
Q

What would you give to a patient with an inflammatory disorder that minimizes side effects int he kidneys?

A
  1. Prednisone

2. 9a-Fluorocortisol (for those deficient in cortisol and aldosterone)

Endocrine and Reproduction Systems (8 decks)

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