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22 spring: Physiology > Test 3: lecture 8 adrenal gland > Flashcards

Test 3: lecture 8 adrenal gland Flashcards

1
Q

layers of the adrenal cortex

A
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2
Q

___ are made by adrenal cortex

A

corticosteroids such as

mineralocorticoid – aldosterone (by zona glomerulosa)

glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

androgens (by zona fasciculata and zona reticularis)

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3
Q

___ are made in the zona glomerulosa

A

Corticosteroids by adrenal cortex

mineralocorticoid – aldosterone (by zona glomerulosa)

glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

androgens (by zona fasciculata and zona reticularis)

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4
Q

___ are made by the zona fasciculata

A

Corticosteroids by adrenal cortex

mineralocorticoid – aldosterone (by zona glomerulosa)

most of the glucocorticoids (by zona fasciculata and zona reticularis)

cortisol, corticosterone

some of the androgens (by zona fasciculata and zona reticularis)

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5
Q

___ are made in the zona reticularis

A

Corticosteroids by adrenal cortex

some of the glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

most of the androgens (by zona fasciculata and zona reticularis)

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6
Q

___ are made in the adrenal medulla

A

catecholamines

epinephrine

norepinephrine

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7
Q

___ are catecholamines made in the adrenal medulla

A

epinephrine

norepinephrine

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8
Q

cortisol and corticosterone are ___made where?

A

glucocorticoids (corticosteroids by the adrenal cortex) made in the zona reticularis and zona fasciculata

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9
Q

corticosteroids are made from ___ in the __

A

cholesterol

mitrochondria and ER

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10
Q

rate limiting step of synthesis of corticosteroids

A

cholesterol → pregnenolone

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11
Q

aldosterone formation does not use what enzyme

A

hydroxylase (this is used to make cortisol and androgen)

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12
Q

Cholesterol desmolase

A

also known as

P450scc CYP11A1

1st step and rate limiting step of cholesterol into catecholamines

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13
Q

17a-hydroxylase/17,20 lyase

A

also known as P450c17 CYP17

used to make cortisol and androgen

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14
Q

Aldosterone synthase

A

P450c11AS CYP11B2

used to make aldosterone

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15
Q

synthesis of corticosteroids occurs in

A

mitochondria and ER

results in release of cortisol

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16
Q

transport of cortisol hormone

A

75% bound to cortisol-binding globulin (transcortin)

15% to albumin,

10% free.

Half-life: 60-90 minutes

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17
Q

___: 50% bound to albumin. half life is 20 mins

A

aldosterone

50% bound to albumin,

10% to transcortin,

40% free.

Short half-life: 20 minutes

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18
Q

___ 75% is bound to transcortin with a 60-90 min half life

A

Cortisol

75% bound to cortisol-binding globulin (transcortin)

15% to albumin,

10% free.

Half-life: 60-90 minutes

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19
Q

why does aldosterone have a shorter half life then cortisol

A

40% of aldosterone is free (not bounded to protein)

can be broken down faster

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20
Q

___ is the most potent mineralcorticoid

A

aldosterone (90%)( made in the zona glomerulosa of the adrenal cortex)

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21
Q

what are some things other than aldosterone that can act as a mineralcorticoid?

A

Deoxycorticosterone (1/30 as potent, limited amount)

9a-fluorocortisol (synthetic, more potent)

Corticosterone (slight mineralocorticoid activity)- (type of glucocorticoid made mostly in the zona fasciculata)

Cortisol (slight, 10%)

Cortisone (synthetic, slight)

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22
Q

what is the major glucocorticoid

A

Cortisol (very potent, 95%)

Corticosterone (4%)

(type of glucocorticoid made mostly in the zona fasciculata, some made in the zona reticularis)

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23
Q

what are some synthetic glucocorticoids

A

Cortisone (as potent)

Prednisone (four times as potent)

Methylprednisone (five times as potent)

Dexamethasone (30 times as potent, specific)

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24
Q

what type of synthetic glucocorticoid does not have mineralocorticoid activity

A

Dexamethasone (30 times as potent, specific

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25
Q

aldosterone

A

mineralocorticoid – aldosterone (by zona glomerulosa)- adrenal cortex

responsible for Na+/K+ balance

sodium-retention hormone

stimulates excretion of K+ in the principal cells

stimulates excretion of H+ in the intercalated cells

most effect in the collecting tubules, less effect in the distal tubule and collecting duct

causes Na+ to be conserved and K+/H+ to be excreted

responsible for 90% of the mineralocorticoid effects

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26
Q

___ causes Na+ to be conserved and K+/H+ to be excreted

A

aldosterone

mineralocorticoid – aldosterone (by zona glomerulosa)- adrenal cortex

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27
Q

aldosterone stimulates the reabsorption of ___ in the ____

A

Na

kidneys, salivary and sweat glands

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28
Q

aldosterone stimulates the excretion of ___ in ___

A

K in the kidney, salivary and sweat glands

H in the kidney

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29
Q

mechanism of aldosterone

A

receptor in cytoplasm

leads to increase in Na/K ATPase (Na in/K out)

Na/H antiporters (Na in/H out)

sodium channels ( Na in)

30
Q

increased ___in extracellular fluid → increases aldosterone secretion

A

K+

31
Q

increased activity of the ____system → angiotensin II → increases aldosterone

A

renin-angiotensin

32
Q

breakdown of aldosterone

A

conjugated to form glucuronic acid and sulfates

excreted in bile (25%), feces and urine (75%)

present in nanogram (10-9) levels (1000 times less than cortisol) (present in very low levels- but very potent)

33
Q

Hypersecretion of aldosterone

A

Hypokalemia (low K+) –> muscle weakness

Alkalosis (more basic pH of blood, cause H are excreted)

Hypertension (increase in Na causes increased BP)

34
Q

Hyposecretion of aldosterone

A

Hyperkalemia (too much K)–> cardiac toxicity

Acidosis (pH decreases, more H in the blood)

hypovolemia (sodium loss→ low BP → shock) -> death

35
Q

____ is the stress hormone

A

cortisol

type of glucocorticoids (by zona fasciculata and zona reticularis) which is a corticosteroid made in the adrenal cortex)

36
Q

___ is necessary to resist stress and inflammation

A

cortisol

type of glucocorticoids (by zona fasciculata and zona reticularis) which is a corticosteroid made in the adrenal cortex)

37
Q

cortisol stimulates ___ by liver

A

gluconeogenesis

  • Cortisol mobilizes amino acids from the extrahepatic tissues mainly from muscle
  • Cortisol increases the enzymes required to convert amino acids into glucose in the liver
38
Q

•Cortisol mobilizes ____ from the extrahepatic tissues mainly from muscle

A

amino acids

39
Q

•Cortisol increases the enzymes required to convert amino acids into ___ in the liver

A

glucose

stimulation of gluconeogenesis by liver

40
Q

cortisol has anti-___ effects causing a decrease in the use of cellular glucose

A

insulin

41
Q

cortisol increases blood ___ and can lead to ____

A

glucose

adrenal diabetes

42
Q

cortisol will cause the increase of proteins___ and the reduction of proteins ___

A

in the liver

in the muscles

increased blood amino acids (aa), increased aa transport into hepatic cells, but decreased aa transport into extrahepatic tissues

reduction in cellular proteins in all tissues except liver

increased liver and plasma proteins

enhanced mobilization of fatty acids from adipose tissue and utilization of free fatty acids for energy

43
Q

cortisol enhanced mobilization of fatty acids from ___ and utilization of free fatty acids for energy

A

adipose tissue

44
Q

cortisol will increase blood ___

A

glucose, amino acids and fatty acids

45
Q

Inflammation Processes

____: release of chemical substances by damaged tissue.

•Red (erythema): increased blood flow.

____: leakage of capillaries.

•Fever

___ by leukocytes.

•Scar: ingrowth of fibrous tissue.

A

pain

  • Edema
  • Infiltration
46
Q

anti-inflammatory effect of cortisol

A
  • stabilizes lysosomal membranes- reduces tissue damage
  • decreases permeability of capillaries- reduces edema
  • decreases migration of white blood cells (WBCs) to inflamed areas
  • suppresses the immune system, especially T lymphocytes
  • lowers fever – reduces release of IL-1 from WBCs
  • also causes resolution of inflammation

keeps inflammatory process under control

47
Q

large doses of cortisol will have a ___ effect

A

immunosuppressive

  • decreases the number of lymphocytes
  • decreases the output of both T cells and antibodies
  • prevents rejection of transplanted organs
48
Q

why use large dose cortisol for transplanted organs

A

will suppress the immune system- suppress rejection

49
Q

receptor for cortisol is ___

A

in the plasma

50
Q

what is the DNA element that cortisol binds to

A

cortisol binds to receptor in the plasma, then the cortisol-receptor complex will go into nucleus and bind with the GRE (glucocorticoid response element)

51
Q

regulation of cortisol secretion is by ___

A

Adrenocorticotropic hormone (ACTH) made by the anterior pituitary gland

(peptide hormone)

also called corticotropin

52
Q

how does ACTH work

A

ACTH binds to melanocortin 2 receptor

activation of adenylyl cyclase

increased intracellular cAMP

conversion of free cholesterol to pregnenolone (1st step of coricosteroid production)

will eventually stimulate adrenal gland to make cortisol

53
Q

____ is the receptor for ACTH

A

melanocortin 2 receptor

54
Q

___ is the precursor to MSH and ACTH

A

POMC (proopiomelanocortin)

55
Q

increased ACTH also means there is more ___ which leads to ___

A

MSH

skin pigmentation

both ACTH and MSH come form POMC

56
Q

injection of angiotensin II will cause the expansion of ___

A

zona glomerulosa

57
Q

an injection of ACTH would cause the expansion of ___

A

zona fasciculata

zona reticularis

58
Q

HPA

A
59
Q

cortisol deficiency would result in

A

high ACTH and increase in skin pigmentation cause there is more MSH (from same precursor -POMC)

cortisol not there to inhibit the production of ACTH

60
Q

hyperadrenalism

A

cushing’s disease

  • Pituitary tumor-
  • Ectopic ACTH-secreting tumors- increased amount of ACTH

Adrenocortical tumors- decreased amount of cortisol

•Mitotane is used to treat adrenocortical tumors

61
Q

hypoadrenaliam

A

addison’s disease

Mineralocorticoid deficiency

Glucocorticoid deficiency

Causes

idiopathic: autoimunne destruction of adrenal cortex.

sponataneous: infections, tumors, trauma

iatrogenic:(adrenal suppressive therapeutic agents)→Cytotoxic (mitotane)•Ketoconazole (blocks ACTH actions)

62
Q

3 causes of addisons

A

hypoadrenalism

Causes

idiopathic: autoimunne destruction of adrenal cortex.

sponataneous: infections, tumors, trauma

iatrogenic:(adrenal suppressive therapeutic agents)→ •Cytotoxic (mitotane)•Ketoconazole (blocks ACTH actions)

mitotane is used to treat hyperadrenalsim- can go to far and cause hypo

63
Q

what are made in the adrenal medulla

A

catecholamines → norepinephrine and epinephrine

64
Q

catecholamines come from ___

A

tyrosine

65
Q

sympathetic nervous system produces what type of catecholamines?

A

norephinephrine

66
Q

why is the adrenal medulla redundant?

A

produces catecholamine- 80%epinephrine• 20% norepinephrine.

the sympathetic nervous system also creates norepinephrine, which can be used to make epinephrine

67
Q

physiological effect of epi and norepinephrine

A

regulate activities of visceral organs

cause excitatory effects in some organs but inhibitory effects in others

increase force and rate of the heart

increases glycolysis in the muscle and liver

increases mental alertness

increases rate of blood coagulation

increases metabolic rate

increase blood flow to active muscles and liver concurrent with decreased blood flow to most organs such as GI tract and kidneys

increases BP

68
Q

mechanism of epinephrine

A

binds to B and alpha receptors

very rapid response from G protein receptors

69
Q

adrenal medulla is stimulated by

A

special preganglionic nerve (special) does not synapse in the celiac ganglion like the other sympathetics, just passes through

70
Q

adrenal medulla cells originated from the same cells as ___ neurons.

A

post-ganglionic

sympathetic innervation causes immediate reaction in emergency situations (flight or fight)

71
Q

Hyperadrenalism (Cushing’s disease) results from excess secretion of glucocorticoids from the adrenal glands. What would some clinical signs be?

A

Symptoms:

Moon face in humans. Mobilization of fat from the lower part of the body, with concomitant extra deposition of fat in the thoracic and upper abdominal regions, giving rise to a buffalo torso.

Increased blood glucose concentration – adrenal diabetes.

Protein depletion in muscles, bone, and lymphatic tissues: muscle weakness, suppressed immune system (death of infection), osteoporosis.

72
Q

hypoadrenalism (Addison’s disease) results from hyposecretion of either glucocorticoids (glucocorticoid-deficient Addisonian) or glucocorticoids and mineralocorticoids (Addisonian). What would some clinical signs and clinicopathologic changes be? How would these two syndromes differ from each other?

A

Mineralocorticoid deficiency: hyperkalemia, acidosis, sodium loss → decreased blood volume → circulatory shock → death within a few days.

Glucocorticoid deficiency:

Failure to maintain blood glucose concentration, failure to mobilize fat and proteins, causing consuming weakness (lethargy).

Highly susceptible to the deleterious effects of stress. A mild infection can cause death.- immune system is suppressed

Increased melanin skin pigmentation, due to increased production of ACTH and MSH as a result of glucocorticoid deficiency.

22 spring: Physiology (34 decks)

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