adrenocortical hormones

Question 1

adrenal medulla and cortex secretions

Answer 1

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

Question 2

2 major adrenocortical hormones

Answer 2

mineral corticoid and glucocorticoid

Question 3

sex hormones released by adrenocortical hormones

Answer 3

androgenic

Question 4

The mineralocorticoids?

The glucocorticoids?

Answer 4

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

Question 5

example of mineral and glucocorticoid

Answer 5

aldosterone- mineral

cortisol- glucca

Question 6

3 layers of adrenal cortex

Answer 6

zona glomerulosa
zona fasciculata
zona reticularis

Question 7

zona glomerulosa

Answer 7

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

Question 8

zona fasciculata

Answer 8

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).

Question 9

The zona reticularis

Answer 9

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.

Question 10

mineralcorticoids

Answer 10

aldosterone 
deoxycorticosterone
corticosterone
cortisol
cortisone 
9a- fluorocortisol

Question 11

glucacorticoids

Answer 11

cortisone
cortisone
cortisol 
methylprednisone 
dexmethasone

Question 12

Adrenocortical Hormones Are Bound to Plasma

Proteins.

Answer 12

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.

Question 13

mineralocorticoid deficiency causes

Answer 13

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

Question 14

mineralocorticoid deficiency fixed

Answer 14

administration of aldosterone in the patient

Question 15

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

Answer 15

. 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.

Question 16

increase in blood volume causes an increase in

Answer 16

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

Question 17

aldosterone escape

Answer 17

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

Question 18

low aldosterone level leads to

Answer 18

circulatory shock due to low cardiac output and low blood volume

Question 19

excess and low aldosterone causes

Answer 19

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

Question 20

what else excess aldosterone causes

Answer 20

alkalosis due to hydrogen loss

Question 21

cellular mechanism of aldosterone action

Answer 21

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

Question 22

regulation of aldosterone

Answer 22

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

Question 23

EFFECTS OF CORTISOL ON

CARBOHYDRATE METABOLISM

Answer 23

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

Question 24

cortisol decrease what utulization of cells for carbohydrate metabolism

Answer 24

glucose utillization by cells

Question 25

adrenal diabetes

Answer 25

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

Question 26

Reduction in Cellular Protein.

Answer 26

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

Question 27

cortisol increases proteins where and how

Answer 27

plasma and liver proteins as it transports amino acid to liver

Question 28

increase transportation of amino acids to liver cause

Answer 28

(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

Question 29

EFFECTS OF CORTISOL ON | FAT METABOLISM

Answer 29

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

Question 30

situation of stress releasing more cortisol

Answer 30

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

Question 31

five main stages of inflammation

Answer 31

(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

Question 32

Cortisol Prevents the Development of Inflammation | by Stabilizing Lysosomes and by Other Effects.

Answer 32

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

Question 33

in what diseases cortisol are administered to patients

Answer 33

rheumatoid arthritis, rheumatic fever, and acute | glomerulonephritis.

Question 34

diagnostic for lymphocytopenia and eosinopenia is

Answer 34

increase level of cortisol in the body by adrenal gland

Question 35

what stimulated cortisol secretion

Answer 35

acth

Question 36

acth releasing is controlled by

Answer 36

arf which is release by paraventricular nucleus | released into capillary plexus of hypophysial portal then into median emmince and transferred to anterior pituitary

Question 37

Addison’s Disease

Answer 37

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

Question 38

mieracorticoid defeciency

Answer 38

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

Question 39

Glucocorticoid Deficiency.

Answer 39

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

Question 40

causes of cushings disease

Answer 40

(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.

Question 41

specials characteristics of people with Cushing disease

Answer 41

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

Question 42

Effects on Carbohydrate and Protein Metabolism cushings disease

Answer 42

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

Question 43

diagnosis of andrigenetial syndrome

Answer 43

finding of 17- ketosteroids