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EXCI 360 > Adrenocortical hormones > Flashcards

Adrenocortical hormones Flashcards

1
Q

what is the central part of the adrenal gland

A

adrenal medulla

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2
Q

adrenal medulla is regulated by

A

SNS

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3
Q

major secretion of adrenal medulla and minor secretion

A

major: epinephrine
minor: norepinephrine

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4
Q

what are the 3 zone of the adrenal cortex

A

zona reticular is: inner layer
zona fasciculatas: middle layer
zona glomerulosa: outer layer

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5
Q

adrenal cortex secrete what

A

corticosteroid

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6
Q

corticosteroid include how many type of hormones

A

30

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7
Q

what is the principal mineralocorticoid

A

aldosterone

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8
Q

aldosterone is secrete from

A

outer layer of adrenal cortex (zona glumerulosa)

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9
Q

mineralcorticoids affect what

A

electrolyte Na, K ions in extracellular fluid

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10
Q

does mineralocorticoid have weak or great glucocorticoid effect

A

weak

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11
Q

what is the principal glucocorticoid

A

cortisol

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12
Q

glucorticoid is secrete from

A

middle and inner layer of adrenal cortez

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13
Q

which corticosteroid mainly increase glucose concentration in blood

A

glucorticoid

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14
Q

abrogent play _ role as compared to estrogen and testosterone

A

minimal

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15
Q

androgen is secrete from

A

middle and inner layer

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16
Q

androgen as _ effect on body as testosterone

A

similar

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17
Q

adrenocortical hormone are what type of compound

A

steroid-based

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18
Q

adrenocortical hormones are mainly form from

A

cholesterol

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19
Q

which type of protein contain cholesterol in blood

A

LDL

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20
Q

LDL is absorbed from blood by

A

endocytosis through cell membrane

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21
Q

the cell membrane from adrenal cortex promote what

A

endocytosis

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22
Q

small amount of cholesterol is also synthesized where

A

in the cortical cell from acetyl-com

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23
Q

cholesterol become what

A

pregnenolome

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24
Q

T/F andrenocorticol hormone are hydrophobic

A

true which means they rely on carrier protein to get them around the circulation to the target tissue and get into ECF around cell

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25
Q

up _ % of cortisol bind with _ also know as _ or _

A

94 %, globulin, cortisol-binding globulin or transporting

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26
Q

about_ % is _ in blood

A

6, floating freely in blood

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27
Q

what does dynamic equilibrium means

A

cortisol is jumping on and off the carrier

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28
Q

up to _ of aldosterone binds with _

A

50, plasma protein

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29
Q

what is the effect of aldosterone on transport of Na and K

A

promote transport through renal tubular and in renal cortex and in renal collecting ducts

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30
Q

what are the cell responsible for the transport fo Na and k

A

principal cells

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31
Q

the transport of ions through renal tubular walls, cortex and collecting duct increase reabsorption of _ which means

A

Na, which means Na is conserved in ECF and decrease the loss of Na into urine

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32
Q

what happen when NA is reabsorbed

A

it increase K excretion into urine and caused water reabsorption by osmosis

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33
Q

what are the substances regulated by the kidney

A

Na, K, water, glucose, Cl, Ca and phosphate

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34
Q

explain the cellular mechanism of aldosterone action that increase sodium reabsorption

A

The lipid soluble aldosterone can diffuse readily into the principal epithelial cells,➔ binds with a receptor in the tubular cell, diffuses into the nucleus, ➔ Causes the formation Channel proteins and Na-K ATPase pump ➔now Na+ can be reabsorbed, K+
excreted.

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35
Q

where does channel protein inserted and what do they diffuse

A

nserted into luminal membrane of principal cell and result in rapid
diffusion of Na+ ions from lumen side, into cell cytoplasm

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36
Q

the lumen side is pointing where

A

inward where the kidney urine is located

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37
Q

where does Na and K are pump

A

at the basolateral membrane of renal principal cells

38
Q

what structure are working together to pump Na and K

A

Na-K ATPase enzyme and membrane transport protein

39
Q

where does the bas-lateral membrane face

A

outward to the interstitial fluid that is connected to the blood circulation

40
Q

explain the effect on ECF volume and partial pressure from aldosterone

A

Aldosterone causes Na ions to be conserved ➔ tendency of increasing concentration of sodium ➔ simultaneous osmotic absorption of water by principal cells ➔ keep the concentration of Na constant ( very little rise ) in extracellular fluid ➔ absorption of water increases the volume of extracellular fluid ➔ increase blood pressure cause great increase of excretion of both water and salt (sodium chloride) from kidney at
hypertension ( called pressure diuresis ).

41
Q

effect of aldosterone on sweat gland, salivary glad and intestinal absorption

A
  • Aldosterone increase reabsorption of NaCl and secretion of K ions by principal cells to conserve body salt when water is secreted by sweat gland and salivary gland.
  • Enhance NaCl absorption by intestine especially in the colon to prevent salt loss in the stools.
42
Q

what happen with lack of aldosterone

A

Lack of Aldosterone causes loss of salt (Na) in urine ➔ decrease sodium-chloride in extracellular fluid and the volume of fluid ➔ great reduction of total volume of extracellular fluid (dehydration) and diminished cardiac output ➔ low blood pressure ➔ circulatory shock ➔ cause death in few days.

43
Q

what happen if aldosterone is chronically low or defective due to a genetic mutation

A

the above sequence can be fatal. It can be prevented by providing medicine including aldosterone or other mineralocorticoids. It is an acute life-saver.

44
Q

what happen if aldosterone is not working

A

it can cause gradual increase of K+ concentration in extracellular fluid and blood that is far above the normal which causes serious cardiac toxicity

45
Q

what is hyperkalemia and what are the symptom

A

due to lack of aldosterone, when K concentration reaches to 60 to 100% above normal,weakness of heart contraction, arrhythmia (irregular heart beat).

46
Q

What happens if there is a chronic excess of aldosterone?

A

excess aldosterone causes massive retention of Na+ and water reabsorption, which increases blood pressure and may trigger pressure diaresis.
* It causes excessive loss of K+ from extracellular fluid which can lead to a serious decrease of K+ concentration in blood. This is called hypokalemia.
* When K+ concentration fall below 1/2 to 1/3 normal it prevents transmission of normal action potential in the nerve which develops severe muscle weakness.

47
Q

how can pressure dieresis can occurs

A

excess aldosterone causes massive retention of Na+ and water reabsorption, which increases blood pressure

48
Q

what is hypokalemia

A

due to excess aldosterone, It causes excessive loss of K+ from extracellular fluid which can lead to a serious decrease of K+ concentration in blood.

49
Q

how can muscle weakness can occurs if there is a problem with aldosterone regulation

A

du to chronic excess of aldosterone, When K+ concentration fall below 1/2 to 1/3 normal it prevents transmission of normal action potential in the nerve which develops severe muscle weakness.

50
Q

what are the 4 factors that regulated aldosterone secretion (order of importance)

A
  1. A small increase of K+ concentration in extracellular fluid will increase aldosterone secretion.
  2. An increase of activity of renin-angiotensin system will increase aldosterone secretion
    3a. An increase of Na+ concentration in extracellular fluid decreases aldosterone secretion.
    3b. A 10 to 20% decrease of Na ion concentration can double aldosterone secretion. When adrenocoticotropic hormone 4. (ACTH) is secreted from anterior pituitary it causes aldosterone secretion. This is the most minor factor, however, if there is a total absence of
    ACTH, like a genetic disease, it can significantly reduce aldosterone secretion.
51
Q

what is gluconeogenesis and it’s stimulate by what

A

Cortisol stimulates gluconeogenesis. This is the formation of glucose from amino acids and other substances by liver.

52
Q

rate of gluconeo can increase as munch as

A

6 to 10 fold

53
Q

what are the cascade of event by which cortisol increase gluconegenisis

A

Cortisol binds with receptor in the cytoplasm of hepatic cells ➔ diffuses into liver cell nucleus and activates DNA transcription ➔ formation of messenger RNA ➔ increase the enzymes needed to convert amino acids into glucose in hepatic (liver) cells.

54
Q

cortisol mobilize amino acids from where

A

muscle

55
Q

when the cortisol mobilize AA from muscle its what type of effect

A

catabolic

56
Q

where does the amino acids goes when they leave the muscle

A

goes in the plasma. They fo from plasma to enter into the liver for gluconeogenesis

57
Q

cortisol cause a _ in the utilization of glucose by cells

A

moderate decrease

58
Q

why does cortisol cause a moderate decrease utilization of glucose by cells

A

because cortisol antagonize insulin andIt also depresses the oxidation of nicotinamide-adenine dinucleotide (NADH) to form NAD+ and NADH. Those must be oxidized to allow the use of glucose by cells. This is why cells can not effectively use glucose for energy

59
Q

what is adrenal diabetes

A

If cortisol is in excess for long time, the glucose will accumulate in the blood and can be 50% more above normal.

60
Q

what happen if cortisol is in excess for long time

A

the glucose will accumulate in the blood and can be 50% more above normal. This is called adrenal diabetes.

61
Q

does cortisol allow the body to have carbs reserve

A

yes

62
Q

glucose reserve can be used if what is present

A

epinephrine or glucagon

63
Q

What is the effect of cortisol on protein metabolism?

A
  • Cortisol reduces the protein stores in all body cell due to catabolic effects.
  • Cortisol prevents amino acids from entering extra-hepatic cells (all the non-liver cells).
  • Except, protein will increase in the liver because cortisol promotes uptake of amino acids into liver for gluconeogeneis, thus, cortisol promotes large amounts of liver enzymes that
    are needed for gluconeogenesis.
  • In the end, most proteins in muscles and other tissues are decreased by cortisol except for
    liver proteins which are increased.
64
Q

What is the effect of cortisol on fat metabolism?

A

Cortisol promotes mobilization of fatty acids from adipose tissue.

65
Q

can excessive cortisol secretion make weight gain

A

Even though cortisol promotes ‘fat burning’, if there is excessive secretion of cortisol it may make a person hungry all the time and stimulate food intake. In this case weight gain may be observed if deposition of fat in tissues is greater than the rate of fat burning. Below, is a diagram summarizing the metabolic effect of cortisol.

66
Q

what are the stage of inflammation

A
  • Chemicals release from the damaged tissue cell and activate inflammation process. The chemicals include histamine, bradykinin, proteolytic enzyme, prostaglandins and leukotrienes.
  • Blood flow is increased in the inflamed area (called erythema).
  • Large amount of plasma leak out of the capillaries into damaged area because of the
    increased capillary permeability.
  • Leukocytes infiltrate through the area.
  • At the end of inflammation, there is growth of fibrous tissue for the healing process.
67
Q

what are the 2 basic anti-inflammatory effect of cortisol

A

It can block (attenuate) the early stage of inflammation or If inflammation has already begun, cortisol blocks most of factors that promote inflammation and causes rapid resolution of inflammation, and increases healing rate.

68
Q

explain how cortisol can block the early stage of inflammation

A

Most of the proteolytic enzymes that cause inflammation are stored in lysosomes in the tissue cell. Cortisol can make the membrane of lysosome cell much more difficult to be ruptured ➔ greatly decrease the release of proteolytic enzymes into the inflamed area.

(b) Cortisol decreases the permeability of capillaries because of the reduced release of proteolytic enzymes ➔ reduce loss of plasma into damaged tissue area.

(c) Cortisol decreases the mobility of white blood cell into inflamed area ➔ decrease phagocytosis of the damaged tissues.

(d) Reduce the release of interleukin-1 from white blood cell ➔ suppresses the hypothalamic temperature control system ➔ lower the fever.

69
Q

explain how cortisol can cause rapid resolution of inflammation and increase healing rate

A

a) Cortisol causes mobilization of amino acids and promote the use of them to repair damaged tissues, to increase glucose and fatty acids for cellular energy.
b) Plays an important role in combating rheumatoid arthritis, rheumatic fever, and acute glomerulonephritis.

70
Q

what are some other effect of cortisol

A

reduce allergic reaction by reducing inflammation and the release of inflammatory product

decrease rate of lymphocyte and antibodies from lymphoid tissue which suppressed immunity of body -> makes cortisol and other glucocorticoids to be the most useful drugs for preventing immunological rejection of transplanted heart, kidney and other tissues.

increase production of red blood cells and probing healing of tissue

71
Q

what can you do if you want to prevent immunological rejection of transplant tissue

A

use cortisol and other glucorticoids

72
Q

secretion of cortisol is regulated by what

A

regulated by ACTH ( corticotropin or adrenocorticotropin ) which is secreted by anterior pituitary gland in response to corticotropin releasing hormone

73
Q

how CRH is release

A

hypothalamus release corticotropin-releasing hormone (CRH) through hypophysial portal system in median eminence to anterior pituitary, which causes secretion of ACTH from anterior pituitary. ACTH acts on the adrenal cortex to synthesize adrenocortical hormones and cause them to be secreted.

74
Q

explain how cortisol can be release in response to physical stress or tissue damage

A

Cause release of CRH to hypophysial portal system ➔ release of ACTH from anterior pituitary into blood, ➔ ACTH to adrenal cortex, ➔ release of cortisol, ➔ increase concentration of cortisol,

75
Q

cortisol has a (negative/ positive) feedback effect on (hypothalamus/ ant. pituitary) to ( increase/decrease) formation of (CRH/ACTH)

A

Cortisol has a direct negative feedback effect on the hypothalamus to decrease formation of CRH.

76
Q

cortisol had _ direct (negative/positive) feedback on the (hypothalamus/pituitary gland) to (increase/decrease) the formation of (CRH/ACTH)

A

Cortisol also has a direct negative feedback on the anterior pituitary gland to decrease the formation of ACTH.

77
Q

what can cause immediate increase in ACTH secretion by anterior pituitary gland

A

stress: pain, trauma, infection, intense heat or cold, injection of norepinephrine, surgery, injection of necrotizing chemical beneath skin, debilitating disease, psychological

78
Q

if there is an increase in ACTH secretion due to stress there is a (increase/decrease) rate of secretion of cortisol by adrenal cortex

A

increase

79
Q

what is hypoadrenalism

A

primary adrenal insufficiency. It is primary because the adrenal gland does not make enough of the adrenal hormones. This could be due to atrophy (small size), loss, or injury to the adrenal glands. Can be caused most often by autoimmune disease, but also by infections like tuberculosis or cancer that destroys the glands. Can be a side effect of chemotherapy treatments.

80
Q

exemple of hypoadrenalism

A

addison’s disease

81
Q

what is secondary adrenal insufficiency

A

caused by a defective pituitary gland which doesn’t secrete enough ACTH. It is more common than Addison’s disease. Causes vary, could be genetic mutation, birth defect, infection of pituitary, or some problem with hypothalamus or CRH.

82
Q

what happen if the primary or secondary adrenal insufficiencies are chronic : lack of aldosterone

A

lack of mineralcorticoids such as aldosterone, the sodium ions are excreted into urine, which causes loss of water by osmosis. If its untreated blood pressure and dehydration can be fatal. Also, there is compensatory increase in potassium in the blood that can lead to hyperkalemia.

83
Q

what happen if the primary or secondary adrenal insufficiencies are chronic : lack of aldosterone: lack of cortisol

A

If there is a lack of glucocorticoids such as cortisol, then in between it is difficult to maintain blood glucose levels since gluconeogenesis is impaired. Stress of infection can be deadly because cortisol normally suppresses inflammation and promotes healing.

84
Q

what happen if the primary or secondary adrenal insufficiencies are chronic : lack of aldosterone: lack of catecholamine

A

If the medulla is defective, then the lack of catecholamines such as adrenaline will alter mood and make hypoglycemia more likely. Adrenaline is able to mobilize glucose in times of need, so lacking it is dangerous.

85
Q

what happen if melanin deposition increased

A

Melanin has various functions including skin pigmentation. Because cortisol is low, the pituitary over produces ACTH, which also provides more MSH (melanin stimulating hormone) which gets unevenly distributed in skin, creating a spotty appearance in the skin. This would not occur if the patient has an ACTH deficiency.

86
Q

what are the treatment for adrenal insufficiency

A
  • Daily supplement with synthetic mineralcorticoids and glucocorticoids
  • In cases of trauma, extra glucocorticoids must be given
  • Corticosteroids given to suppress the immune system if it is autoimmune in nature
  • allergic reactions may need more medication to control inflammation
87
Q

Addison disease is a primary or secondary adrenal insufiency

A

primary

88
Q

exemple of hyperadrenalism

A

Cushing’s syndrome or Conn’s syndrome

89
Q

what is hyperadrenalism

A

It is defined by hypersecretion of adrenal hormones. The cause may be adenoma tumor which produces adrenal hormones out of control. May be in glands or elsewhere in body. Or, an abnormal function of the hypothalamus-pituitary axis that makes more ACTH than needed.

90
Q

effect of excessive glucocorticoid (cortisol):

A

high blood sugar leading to pituitary diabetes, and loss of protein from muscle, and redistribution of fat into the torso

91
Q

effect of excessive androgen

A

over masculinizing effect

EXCI 360 (14 decks)

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