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physiology > adrenocortical hormones > Flashcards

adrenocortical hormones Flashcards

1
Q

adrenal medulla and cortex secretions

A

medulla secretes epinephrine and norepinephrine which has sympathetic stimulations
adrenal cortex releases corticosteroids which are derived from steroid cholesterol

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2
Q

2 major adrenocortical hormones

A

mineral corticoid and glucocorticoid

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3
Q

sex hormones released by adrenocortical hormones

A

androgenic

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4
Q

The mineralocorticoids?

The glucocorticoids?

A 
especially affect the electrolytes (the “minerals”) of the extracellular fluids, especially sodium and potassium.
exhibit important effects that increase blood glucose concentration. They have additional effects on both protein
and fat metabolism that are equally as important to body
function as their effects on carbohydrate metabolism
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5
Q

example of mineral and glucocorticoid

A

aldosterone- mineral

cortisol- glucca

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6
Q

3 layers of adrenal cortex

A

zona glomerulosa
zona fasciculata
zona reticularis

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7
Q

zona glomerulosa

A

present beneath the capsule
compose 15% of adrenal cortex
mean secretory cells of aldosterone because aldosterone synthase
and secretion of aldosterone is controlled by ecf concentration of angiotensin II and potassium ions

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8
Q

zona fasciculata

A

the middle and widest zone,
constitutes about 75 percent of the adrenal cortex
and secretes the glucocorticoids cortisol and corticosterone, as well as small amounts of adrenal
androgens and estrogens. The secretion of these cells
is controlled in large part by the hypothalamic pituitary axis via adrenocorticotropic hormone
(ACTH).

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9
Q

The zona reticularis

A

inner zone of the cortex,
secretes the adrenal androgens dehydroepiandrosterone and androstenedione, as well as small
amounts of estrogens and some glucocorticoids.
ACTH also regulates secretion of these cells,
although other factors such as cortical androgenstimulating hormone, released from the pituitary,
may also be involved. The mechanisms for controlling adrenal androgen production, however, are not
nearly as well understood as those for glucocorticoids and mineralocorticoids.

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10
Q

mineralcorticoids

A 
aldosterone 
deoxycorticosterone
corticosterone
cortisol
cortisone 
9a- fluorocortisol
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11
Q

glucacorticoids

A 
cortisone
cortisone
cortisol 
methylprednisone 
dexmethasone
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12
Q

Adrenocortical Hormones Are Bound to Plasma

Proteins.

A

Approximately 90 to 95 percent of the cortisol in
the plasma binds to plasma proteins, especially a globulin
called cortisol-binding globulin or transcortin and, to a
lesser extent, to albumin. This high degree of binding to
plasma proteins slows the elimination of cortisol from the
plasma; therefore, cortisol has a relatively long half-life of 60 to 90 minutes. Only about 60 percent of circulating
aldosterone combines with the plasma proteins, so about
40 percent is in the free form; as a result, aldosterone has
a relatively short half-life of about 20 minutes. These hormones are transported throughout the extracellular fluid
compartment in both the combined and free forms.

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13
Q

mineralocorticoid deficiency causes

A

excess loss of na and cl and hyperkalemia
decreases ecf volume
blood volume
decrease cardiac output and shock like state

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14
Q

mineralocorticoid deficiency fixed

A

administration of aldosterone in the patient

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15
Q

Although
aldosterone has a potent effect to decrease the rate of
sodium excretion by the kidneys, the concentration of
sodium in the extracellular fluid often rises only a few
milliequivalents. why

A

. The reason for this is that when sodium
is reabsorbed by the tubules, simultaneous osmotic
absorption of almost equivalent amounts of water occurs.
Also, small increases in extracellular fluid sodium concentration stimulate thirst and increased water intake, if
water is available, and increase secretion of antidiuretic hormone, which enhances water reabsorption by the
distal and collecting tubules of the kidneys. Therefore, the
extracellular fluid volume increases almost as much as the
retained sodium, but without much change in sodium
concentration.

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16
Q

increase in blood volume causes an increase in

A

aterial presurre which causes in increase in pressure diuresis and pressure natriuresis
which causes excretion of water and na by the kidney to maintain the blood volume level back to normal

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17
Q

aldosterone escape

A

This return to normal of sodium and water excretion
by the kidneys as a result of pressure natriuresis and
diuresis is called aldosterone escape

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18
Q

low aldosterone level leads to

A

circulatory shock due to low cardiac output and low blood volume

19
Q

excess and low aldosterone causes

A

excess causes hypokalemia
which causes muscle weakness due to alteration of excitability of muscle and neurons and inability to conduct impulse for contraction
low causes hyperkalemia which cases arrhythmia, and consequently heart failure

20
Q

what else excess aldosterone causes

A

alkalosis due to hydrogen loss

21
Q

cellular mechanism of aldosterone action

A

as it is lipid soluble it crosses the renal tubular membrane easily into the cytoplasm of renal tubule cells
it joins with the mineralocorticoid receptor protein and the complex diffuses into nucles means mrna
mrna then diffuses into cytoplasm to form different proteins
enzymes like na-k atpase pump at basolateral part
and epithelial sodium channels and potassium

22
Q

regulation of aldosterone

A

The following four factors are known to play essential
roles in regulation of aldosterone:
1. Increased potassium ion concentration in the
extracellular fluid greatly increases aldosterone
secretion.
2. Increased angiotensin II concentration in the
extracellular fluid also greatly increases aldosterone
secretion.
3. Increased sodium ion concentration in the extracellular fluid very slightly decreases aldosterone
secretion.
4. ACTH from the anterior pituitary gland is necessary for aldosterone secretion but has little effect in
controlling the rate of

23
Q

EFFECTS OF CORTISOL ON

CARBOHYDRATE METABOLISM

A
  1. Cortisol increases the enzymes required to convert
    amino acids into glucose in liver cells. This results
    from the effect of glucocorticoids to activate DNA
    transcription in the liver cell nuclei in the same way
    that aldosterone functions in renal tubular cells,
    with formation of mRNAs that in turn lead to the
    array of enzymes required for gluconeogenesis.
  2. Cortisol causes mobilization of amino acids from the extrahepatic tissues, mainly from muscle. As a result, more amino acids become available in the plasma to enter into the gluconeogenesis process of the liver and thereby to promote the formation of glucose.
  3. Cortisol antagonizes insulin’s effects to inhibit gluconeogenesis in the liver. As discussed in Chapter 79,
    insulin stimulates glycogen synthesis in the liver and inhibits enzymes involved in glucose production by the liver. The net effect of cortisol is to
    increase glucose production by the liver
24
Q

cortisol decrease what utulization of cells for carbohydrate metabolism

A

glucose utillization by cells

25
Q

adrenal diabetes

A

high levels of glucocorticoid reduce the sensitivity of many tissues, especially
skeletal muscle and adipose tissue, to the stimulatory
effects of insulin on glucose uptake and utilization effect of glucocorticoids to mobilize lipids from fat depots, may
impair the actions of insulin on the tissues
The increase in blood glucose concentration is occasionally great enough (50 percent or more above normal)
that the condition is called adrenal diabetes

26
Q

Reduction in Cellular Protein.

A

reduction of the protein stores in essentially all cells of the
body except those of the liver. This reduction is caused by
both decreased protein synthesis and increased catabolism of protein already in the cells.
less amino acids in extrahepatic cells and less transcription of rna in extrahepatic cells to synthesize proteins
specially in muscles and lymphoid tissues

27
Q

cortisol increases proteins where and how

A

plasma and liver proteins as it transports amino acid to liver

28
Q

increase transportation of amino acids to liver cause

A

(1) increased rate of deamination of amino acids by
the liver, (2) increased protein synthesis in the liver, (3)
increased formation of plasma proteins by the liver, and
(4) increased conversion of amino acids to glucose—that
is, enhanced gluconeogenesis

29
Q

EFFECTS OF CORTISOL ON

FAT METABOLISM

A

mobilization of fatty acids inceasing free fatty acid in the bloood also increases the utilization of fatty acids for energy throigh oxidation
- excess cortisol causes obesity

30
Q

situation of stress releasing more cortisol

A
  1. Trauma
  2. Infection
  3. Intense heat or cold
  4. Injection of norepinephrine and other sympathomimetic drugs
  5. Surgery
  6. Injection of necrotizing substances beneath the skin
  7. Restraining an animal so it cannot move
  8. Debilitating disease
31
Q

five main stages of inflammation

A

(1) release
from the damaged tissue cells of chemicals such as histamine, bradykinin, proteolytic enzymes, prostaglandins,
and leukotrienes that activate the inflammation process;
(2) an increase in blood flow in the inflamed area caused
by some of the released products from the tissues, an
effect called erythema; (3) leakage of large quantities of
almost pure plasma out of the capillaries into the damaged
areas because of increased capillary permeability, followed by clotting of the tissue fluid, thus causing a nonpitting type of edema; (4) infiltration of the area by leukocytes;
and (5) after days or weeks, ingrowth of fibrous tissue that
often helps in the healing process

32
Q

Cortisol Prevents the Development of Inflammation

by Stabilizing Lysosomes and by Other Effects.

A
  1. Cortisol stabilizes lysosomal membranes.
  2. Cortisol decreases permeability of the capillaries,
  3. Cortisol decreases both migration of white blood
    cells into the inflamed area and phagocytosis of the
    damaged cells
  4. Cortisol suppresses the immune system, causing
    lymphocyte reproduction to decrease markedly
  5. Cortisol attenuates fever mainly because it reduces
    release of interleukin-1 from white blood cells
33
Q

in what diseases cortisol are administered to patients

A

rheumatoid arthritis, rheumatic fever, and acute

glomerulonephritis.

34
Q

diagnostic for lymphocytopenia and eosinopenia is

A

increase level of cortisol in the body by adrenal gland

35
Q

what stimulated cortisol secretion

A

acth

36
Q

acth releasing is controlled by

A

arf which is release by paraventricular nucleus

released into capillary plexus of hypophysial portal then into median emmince and transferred to anterior pituitary

37
Q

Addison’s Disease

A

Addison’s disease results from an inability of the adrenal
cortices to produce sufficient adrenocortical hormones,
and this in turn is most frequently caused by primary atrophy or injury of the adrenal cortices. In about 80
percent of the cases, the atrophy is caused by autoimmunity against the cortices. Adrenal gland hypofunction may
also be caused by tuberculous destruction of the adrenal
glands or invasion of the adrenal cortices by cancer.
In some cases, adrenal insufficiency is secondary to
impaired function of the pituitary gland, which fails to
produce sufficient ACTH

38
Q

mieracorticoid defeciency

A

Lack of aldosterone
secretion greatly decreases renal tubular sodium reabsorption and consequently allows sodium ions, chloride ions,
and water to be lost into urine in great profusion which casues decrease in ecf volume low cardiac output increase in rbc in plasma and shock
also causes hyperkalemia and hyponatremia

39
Q

Glucocorticoid Deficiency.

A

normal blood glucose concentration between
meals because he or she cannot synthesize significant
quantities of glucose by gluconeogenesis. Furthermore,
lack of cortisol reduces the mobilization of both proteins
and fats from the tissues, thereby depressing many other
metabolic functions of the body
the person’s muscles are weak, indicating that
glucocorticoids are necessary to maintain other metabolic
functions of the tissues in addition to energy metabolism

40
Q

causes of cushings disease

A

(1) adenomas of the anterior pituitary that secrete large
amounts of ACTH, which then causes adrenal hyperplasia
and excess cortisol secretion; (2) abnormal function of
the hypothalamus that causes high levels of corticotropinreleasing hormone, which stimulates excess ACTH release;
(3) “ectopic secretion” of ACTH by a tumor elsewhere
in the body, such as an abdominal carcinoma; and (4)
adenomas of the adrenal cortex.

41
Q

specials characteristics of people with Cushing disease

A

s 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-like torso. The
excess secretion of steroids also leads to an edematous
appearance of the face, and the androgenic potency of
some of the hormones sometimes causes acne and hirsutism (excess growth of facial hair). The appearance of the
face is frequently described as a “moon face,” and cause hypertension

42
Q

Effects on Carbohydrate and Protein Metabolism cushings disease

A

The abundance of cortisol secreted in Cushing’s syndrome
can increase blood glucose concentration, sometimes to
values as high as 200 mg/dl after meals
catabolism
are often profound in Cushing’s syndrome, causing greatly
decreased tissue proteins almost everywhere in the body
with the exception of the liver; the plasma proteins also
remain unaffected. The loss of protein from the muscles in
particular causes severe weakness. The loss of protein synthesis in the lymphoid tissues leads to a suppressed immune
system, and thus many of these patients die of infections.
Even the protein collagen fibers in the subcutaneous tissue
are diminished so that the subcutaneous tissues tear easily,
resulting in development of large purplish striae

43
Q

diagnosis of andrigenetial syndrome

A

finding of 17- ketosteroids

physiology (25 decks)

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