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Block 3 Week 6 Meg > O'Driscoll: Adrenal Gland > Flashcards

O'Driscoll: Adrenal Gland Flashcards

1
Q

Adrenal glands contribute significantly to maintaining homeostasis through their roles in regulation of the body’s adaptive response to (blank), maintenance of body (blank x3), and control of (blank)

A

stress
water, Na+, K+
blood pressure

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2
Q

Main hormones produced by the adrenal glands belong to 2 different families. What are they?

A

Steroid hormones: glucocorticoids, mineralocorticoids, and androgens
Catecholamines: norepinephrine and epinephrine

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3
Q

90% of the adrenal gland is the outer adrenal (blank); 10% is the inner adrenal (blank)

A

cortex; medulla

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4
Q

The adrenal glands are required for life. Complete adrenal insufficiency can lead to lead within 2 weeks. What two things can cause death?

A 
circulatory collapse (shock) 
hypoglycemic coma
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5
Q

4 functional zones of the adrenal glands

A

zona glomerulosa
zona fasciculata
zona reticularis
medulla

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6
Q

Which zone produces MINERALOCORTICOIDS and is controlled by ECF conc of angiotensin II and K+, as well as the kidney?

A

zona glomerulosa

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7
Q

Which zone produces GLUCOCORTICOIDS and is controlled by the hypothalamic-pituitary axis via ACTH?

A

zona fasciculata

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8
Q

Which zone produces ANDROGENS and is controlled by hypothalamic-pituitary axis via ACTH?

A

zona reticularis

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9
Q

Which zone produces CATECHOLAMINES and is controlled by the sympathetic nervous system?

A

medulla

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10
Q

Chief secretory product of the glomerulosa?

The fasciculata? The reticularis?

A

aldosterone; cortisol; sex hormones and DHEA

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11
Q

Very potent - ~90% of all mineralocorticoid activity

A

aldosterone

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12
Q

Some adrenocortical hormones have both mineralocorticoid and glucocorticoid activites. This hormone is very potent- ~95% of all glucocorticoid activity. Slight mineralocorticoid activity but large quantity secreted.

A

cortisol

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13
Q

Adrenocortical hormones are transported in blood bount to (blank) and (blank)

A

corticosteroid binding globulin (CBG); albumin

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14
Q

90-95% bound
T1/2 = 60-90 mins
[blood] = 12microg/dL

A

cortisol

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15
Q

60% bound
T1/2 = 20mins
[blood] = 6microg/dL

A

aldosterone

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16
Q

What mineralocorticoid does this:
increases sodium retention
increases K+ excression
targets the kidney (principal cells in distal tubule and collecting duct, and intercalated cells in the collecting duct)

A

aldosterone

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17
Q

Mineralocorticoids elicit effects by producing changes in (blank). Effects are not (blank) - require 45-60 min for proteins to be synthesized

A

gene transcription; immediate

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18
Q

Aldosterone has genomic and non-genomic effects. What are its genomic effects? Non-genomic?

A

increased transcription of genes involved in ion transport: reabsorption of Na+, loss of K+
activation of second messenger system: H+/bicarb exchange

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19
Q

Aldosterone increases renal tubular absorption of (blank) and secretion of (blank). What occurs with a total lack of aldosterone secretion? What is aldosterone a key mediator of?

A

Na+; K+
transient loss of Na+ in the urine
blood pressure

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20
Q

Excess Aldosterone causes an increase in ECF Volume and Arterial Pressure but has Only a Small Effect on Plasma Na+ concentration. Why?

A

Na+ reabsorbed and water follows. So there is little change in CONCENTRATION. ECF volume increases almost as much as the retained Na+ but without much change in Na+ concentration.

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21
Q

When aldosterone has its effect and increases arterial pressure, what is the compensatory mechanism that maintains blood pressure within normal range?

A

Increased distal tubule Na+ delivery, so increased kidney excretion of both sodium and water – aldosterone escape

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22
Q

What happens to Na+ when aldosterone secretion becomes zero?

A

Large amounts of Na+ lost in the urine
Decreases ECF volume
Severe dehydration, low blood volume
CIRCULATORY SHOCK!!!

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23
Q

What happens when there is excess aldosterone?

A

Loss of K+ in urine, so K+ is transported from ECF into cells. HYPOKALEMIA and muscle weakness and cramping ensue. Increased secretion of H+ in exchange for Na+ in the intercalated cells of the collecting tubules can result in METABOLIC ALKALOSIS.

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24
Q

What happens when there is too little aldosterone?

A

ECF K+ rises way too high. HYPERKALEMIA, which can cause cardiac toxicity.

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25
Q

(blank) is much less potent than aldosterone, but has a [plasma] that is 2000 times greater. Cortisol can bind to mineralocorticoid receptors with (blank) affinity, but cortisone DOES NOT.

A

cortisol; high

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26
Q

Renal epithelial cells contain 11β-hydroxysteroid dehydrogenase type 2. What does this do?

A

converts cortisol to cortisone

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27
Q

Genetic deficiency of 11β-hydroxysteroid dehydrogenase type 2 activity
Can also be caused by ingestion of large amounts of licorice

A

AME: apparent mineralocorticoid excess syndrome

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28
Q

AME patient has similar symptoms as a patient with excess aldosterone secretion, except for one thing…

A

plasma aldosterone levels are low

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29
Q

Aldosterone secretion is primarily regulated in these two ways

A
  1. decreased blood volume or blood pressure

2. increased K+ in blood

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30
Q

(blank) appears to play a “permissive role” in the regulation of aldosterone secretion. If there is even a small amount of it secreted by the anterior pituitary it is usually enough to permit the adrenal glands to secrete whatever amount of aldosterone is required. However, total absence of it can significantly reduce aldosterone secretion.

A

ACTH

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31
Q

Discuss how plasma volume is regulated by the renin-angiotensin-aldosterone system

A 
decreased plasma volume
increased angiotensin II
increased aldosterone
increased vasoconstriction
increased reabsorption of Na+ in distal tubule
increased plasma volume
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32
Q

Cortisol is a very potent (blank). It makes up 95% of (blank). What is its hallmark effect?!

A

glucocorticoid; glucocorticoids; increase blood glucose

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33
Q

Main function of cortisol?

What is its target? What cells express glucocorticoid receptors?

A

Effects metabolism of carbs, proteins, fats

Important in resisting stress and inflammation; virtually every tissue; most cells express these receptors

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34
Q

Cortisol has a cellular mechanism of action. It binds to the cytoplasmic glucocorticoid receptor, forms a hormone-receptor complex with specific regulatory DNA sequences called (blank) and induces or represses gene trx. High [glucocorticoid] can also have more rapid nongenomic effects.

A

glucocorticoid response elements

35
Q

Carb metabolism: Cortisol stimulates (blank) and decreases (blank) utilization by cells, which increases storage of (blank) as glycogen in liver cells. Cortisol increased (blank) concentration, which in turn stimulates secretion of (blank). Excess secretion of glucocorticoids can lead to what?

A

gluconeogeneis; glucose; glucose; blood glucose; insulin; hyperglycemia

36
Q

Protein metabolism: Cortisol mobilizes (blank) from the nonhepatic tissues, diminishes the tissue stores of (blank) and at the same time it increases the (blank) required for the hepatic effects

A

amino acids; protein; liver enzymes

37
Q

Fat metabolism: Cortisol increases use/oxidation of (blank) from adipose tissue for metabolic energy. This is an important factor for long-term conservation of body (blank) and (blank)

A

fatty acids; glucose; glycogen

38
Q

Principal effects of cortisol: preservation of (blank) reserves and increased mobilization of high energy fuels, like (blank) and (blank)

A

carbohydrate; protein; fat

39
Q

Why is it beneficial that glucocorticoid secretion increases in stressful situations? Cortisol also has (blank) effects.

A

Rapid mobilization of amino acids and fats makes them available for energy and synthesis of other compounds needed for maintenance
anti-inflammatory

40
Q

Five main stages of inflammation

A
  1. damaged tissue cells release chemical substances
  2. increase in blood flow to inflamed area
  3. increased capillary permeability
  4. infiltration of the area by leukocytes
  5. ingrowth of fibrous tissue
41
Q

High levels of cortisol have two basic anti-inflammatory effects

A
  1. can block the early stages of the inflammation process before inflammation begins
  2. if inflammation has begun, it causes rapid resolution of the inflammation and increased rapidity of healing
42
Q

High levels of cortisol stabilize (blank) membranes, decrease the permeability of (blank), decrease migration of (blank), decrease phagocytosis, suppress the (blank), and decrease fever.

A

lysosomal; capillaries; white blood cells; immune system

43
Q

Cortisol has therapeutic utility in these three realms

A

allergies
autoimmune diseases
transplantation

44
Q

What is cortisol’s effect on blood cells and on immunity in infectious diseases? So what can hypercortisolemia cause?

A

decreases blood eosinophils and lymphocytes; lymphocytopenia and eosinopenia

45
Q

Cortisol also increases the production of RBCs. If there is too much cortisol, what does this lead to? If there is no cortisol secretion, what does this lead to?

A

polycythemia; anemia

46
Q

What effect do glucocorticoids have on the CNS?

A

decreased CRH

47
Q

What effect do glucocorticoids have on the liver?

A

increased gluconeogenesis

48
Q

What effect do glucocorticoids have on the pituitary?

A

decreased ACTH secretion and synthesis

49
Q

What effect do glucocorticoids have on muscle?

A

Increased protein catabolism, decreased glucose utilization, decreased insulin sensitivity, decreased protein synthesis

50
Q

What effect do glucocorticoids have on the immune system?

A

Decreased conc of eosinophils, basophils, and lymphocytes

Decreased cellular immunity

51
Q

Cortisol secretion is regulated by (blank) secretion from the anterior pituitary. What controls secretion at the level of the hypothalamus?

A

ACTH; ACTH secretion controlled by CRF (corticotropin releasing factor) from the hypothalamus

52
Q

Cortisol has negative feedback effects on the hypothalamus to decrease formation of (blank) and on the anterior pituitary to decrease formation of (blank). This decreases plasma cortisol levels at times when the body is not stressed.

A

CRF; ACTH

53
Q

Release of CRH, ACTH, and cortisol is high in the (blank) but low in the (blank). Release is (blank).

A

early morning; evening; pulsatile

54
Q

adrenal androgen

A

DHEA

55
Q

Failure of the adrenal cortices to produce sufficient adrenocortical hormones

A

hypoadrenalism - adrenal insufficiency

56
Q

Causes: destruction of the adrenal cortex by

  • Autoimmunity (80%) antibodies that react with several steroidogenic enzymes (most often 21-hydroxylase)
  • Tuberculosis
  • fungal infections
  • adrenal hemorrhage
A

Primary adrenal insufficiency (Addison’s disease)

57
Q

Much more common
Causes: Pituitary gland fails to produce sufficient ACTH. If ACTH output is too low, cortisol production drops. Eventually, the adrenal glands can shrink due to lack of ACTH stimulation

A

Secondary adrenal insufficiency

58
Q

With Addison’s disease, there can be a mineralocorticoid deficiency leading to (blank), a glucocorticoid deficiency leading to (blank x3), or pigmentation due to increased (blank) production

A

circulatory shock
weight loss, weakness, extreme sensitivity to stress
melanin

59
Q

ACTH is derived from the POMC gene. When the rate of secretion of ACTH is high, increases formation of some of the other (blank)

A

POMC-derived hormones, like MSH

60
Q

Causes: a critical deficiency of mineralocorticoids and glucocorticoids, that generally follows acute stress, sepsis, trauma, surgery, or omission of steroid therapy in patients who have Addison’s

A

Addisonian crisis

61
Q

Describes the signs and symptoms associated with prolonged exposure to inappropriately high levels of the hormonecortisol (excess secretion of androgens may also cause important effects)

A

Cushing’s syndrome (hyperadrenalism)

62
Q

Hypersecretion of CRH or ACTH (Cushing’s disease)
Adrenal cortex adenomas
Ectopic secretion of ACTH
Hypercortisolism

A

Causes of cushing’s syndrome or hyperadrenalism

63
Q

Symptoms of Cushing’s syndrome due to glucocorticoid excess

A

increased gluconeogenesis, hyperglycemia
buffalo torso
moon face
weakness, osteoporosis, strige on skin

64
Q

Symptoms of Cushing’s syndrome due to androgen excess

A

acne, hirsutism (excess facial hair)

65
Q

High cortisol leads to a peculiar type of obesity with excess fat being deposited in chest and head regions giving rise to these two symptoms

A

buffalo torso

moon face

66
Q

Causes:
small tumor of the zona glomerulosa cells that secretes large amounts of aldosterone
hyperplastic adrenal cortices secrete aldosterone rather than cortisol

A

Conn’s syndrome - Primary aldosteronism

67
Q

What can mineralocorticoid excess lead to in Conn’s syndrome?

A

hypokalemia–> muscle paralysis
hypervolemia–>hypertension
low plasma renin

68
Q

Adrenocortical tumor secreting excessive quantities of androgens

A

adrenogenital syndrome

69
Q

What can androgen excess cause in females? In males?

A

masculinization; rapid development of male sexual organs

70
Q

Cause: Autosomal recessive disorder – enzyme inefficiencies commonly leading to deficient production of cortisol and aldosterone together with excessive production of sex steroids
95% of cases due to 21 hydroxylase deficiency

A

congenital adrenal hyperplasia

71
Q

In response to sympathetic neuronal stimulation & the resulting release of acetylcholine → stimulates the production and release of catecholamines

A

adrenal medulla

72
Q

Principal cell type of adrenal medulla; modified postganglionic neurons

A

chromaffin cells

73
Q

Secretory products of the adrenal medulla

A

epinephrine: norepi (4:1)

74
Q

The adrenals are the sole source of (blank)

A

epinephrine

75
Q

T/F: The adrenal medulla is not essential for life as long as the sympathetic nervous system is intact

A

True!

76
Q

The medulla is richly innervated by preganglionic sympathetic fibers and is in essence, an extension of the (blank) nervous system

A

sympathetic

77
Q

Catecholamines are synthesized in (blank) and stored in electron dense (blank)

A

chromaffin cells; chromaffin granules

78
Q

What are catecholamines (dopamine–>norepi->epi) derived from? How many enzymatic reactions does it take to go from tyrosine to epinephrine?

A

tyrosine; 4 rxns

79
Q

Following secretion into the blood, most catecholamines circulate bound to (blank) with low affinity. What is the T1/2 of catecholamines?

A

albumin; VERY SHORT

80
Q

What is the major end product of epi and norepi metabolism?

A

vanillylmandelic acid

81
Q

What is the main function of the adrenal medullary hormones? In the longer term, actions are supported by glucocorticoids.

A

to make rapid, short-term adjustments to changes in the external or internal environment (fight or flight)

82
Q

What is the mechanism of action of catecholamines?

A

physiological effects mediated by binding to cell membrane G protein–coupled adrenergic receptors distributed widely throughout the body

83
Q

Chromaffin cell tumor that causes over secretion of catecholamines; elevated heart rate, hypertension, anxiety, sweating, hyperglycemis

A

pheochromocytoma

Block 3 Week 6 Meg (7 decks)

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