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Physiology 2 Test 2 > Chapter 77 > Flashcards

Chapter 77 Flashcards

0
Q

What vertebral level is the adrenal gland at?

A

T12.

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0
Q

What % of the supra renal gland is medulla and cortex?

A

Medulla- 20%, Cortex-80%

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0
Q

Corticosteroids are made from what?

A

Cholesterol.

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0
Q

What are the 3 zones of the supra renal cortex?

A
  1. Fasiculata. 2. Glomerulosa. 3. Reticularis.
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0
Q

What are the catecholamine hormones?

A

Epinephrine and norephinephrine

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0
Q

80% of Cholesterol used to make glucocorticoids, mineralcorticoids, and sex hormones comes from where?

A

plasma LDL.

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0
Q

Angiotenson II changes the conversion of cholesterol to what?

A

Pregnenolone.

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0
Q

Glucocorticoids got their name how?

A

Because of their role in glucose metabolism.

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0
Q

Glucocorticoids can bind to what?

A

Cortisol receptors and trigger similar effects.

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0
Q

What is the name of a synthetic glucocorticoid?

A

Exogenous or synthetic glucocorticoid.

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0
Q

Cortisol is as potent as what?

A

Cortisone

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0
Q

What is about 4 times as potent as cortisol?

A

Prednisone.

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0
Q

What is about 5 times as potent as cortisol?

A

methylprednisone.

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0
Q

What is about 30 times as potent as cortisol?

A

Dexamethasone.

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0
Q

What is the main corticosteroid hormone produced by the adrenal cortex?

A

Cortisol.

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0
Q

What is the most important human glucocorticoid?

A

Cortisol.

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0
Q

Cortisol is aka?

A

The stress hormone.

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0
Q

Where are corisol (glucocorticoid) receptors found at?

A

In cells of almost all vertebrate tissues.

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0
Q

What is CRH and where will it come from and what will it do?

A

Corticotrophin releasing hormone. Released in response to stress from the hypothalamus, and it stimulates the release of ACTH from the Ant. Pituitary gland.

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0
Q

ACTH is released how from the ant. Pituitary gland?

A

As a preprohormone that contains melanocyte stimulating hormone (MSH), and beta-lipotropin and beta-endorhin.

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0
Q

High ACTH levels will cause what?

A

Secretion of MSH and cortisol and we may get hyperpigmentation, increased aldosterone secretion, and adverse pain/mood effects.

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0
Q

When will the diurinal variation of serum cortisol be present?

A

between 2 weeks and 9 months after birth.

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0
Q

Name a physical stressor that will cause variation in serum cortisol levels?

A

Hypoglycemia.

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0
Q

What happens with a total loss of cortisol?

A

Death in 3 days due to inability to cope with stressors.

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0
Q

What happens to the negative feedback loop where cortisol inhibits CRH and ACTH during chronic stress?

A

The normal feedbacks breakdown, and this creats a chronic cortisol exposure.

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0
Q

What % of cortisol is bound to a protein?

A

90-95 percent.

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0
Q

What will the binding protein do to cortisol?

A

It makes it slow to be eliminated and this creats a long half life of 60-90 minutes.

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0
Q

What type of cortisol is available to be used by receptors?

A

Free or the kind not bound to a protein.

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0
Q

What will excess cortisol do to the immune system?

A

Suppression of immune and inflammatory reactions.

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0
Q

What will excess cortisol do to CT, and bones?

A

Breaks them down.

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0
Q

Why will excess cortisol have a weak effect of mineralcorticoids control of electrolytes?

A

Because cortisol is similar to aldosterone.

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0
Q

Cortisol is a physiological anatagonist to what?

A

Insulin.

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0
Q

How is cortisol an anatagonist to insulin?

A

It increases gluconeogenesis, increases glycogen storage in liver, decreases glucose utilization of most cells.

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0
Q

Cortisol leads to what?

A

Increased circulation of glucose, and increased secretion of insulin.

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0
Q

Insulin works how with cortisol around?

A

Not as effective at increasing the plasma glucose uptake.

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0
Q

What else will inhibit the effects of insulin?

A

The increase in free fatty acid due to lipolysis of adipocytes.

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0
Q

Cortisol and excess growth hormone are what?

A

Diabetogenic.

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0
Q

When cortisol is metabloized it makes more Amino Acids available to the liver how?

A

Through protein catabolism.

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0
Q

Protein catabolism to increase the AA available to the liver can lead to what?

A

Muscle weakness.

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0
Q

What happens to all protein storages with cortisol?

A

All are reduced besides the liver.

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0
Q

Decreased proteins can lead to what?

A

Decreased immunity.

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0
Q

Cortisol metabolism shifts energy production from what to what during stress or starvation?

A

From utilization of glucose to utilization of fatty acids.

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0
Q

What 3 ways will cortisol weaken the immune system?

A
  1. Decreases the number of eospinophils and lymphocytes. 2. atrophy of lymphoid tissues. 3. Decreased output of T cells and antibodies.
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1
Q

Excess cortisol does what to the appetite?

A

Increases it, and can cause obesity.

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2
Q

What reason would you want to use cortisol to weaken the immune system?

A

To prevent the immunological rejection of transplanted organs/tissues.

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3
Q

What will cortisol do to inflammation?

A

It is a potent anti-inflammatory agent.

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4
Q

How will cortisol be an anti-inflammatory agent?

A

Blocks the early inflammatory process, and causes a rapid resolution of inflammation once it has begun.

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5
Q

What will cortisol do to the healing process?

A

It rapidly speeds it up.

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6
Q

Cortisol stabalizes what to help with the anti-inflammatory process?

A

Lysosomal membranes.

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7
Q

How will cortisol inhibit tissue destruction?

A

Decreases proteolytic enzyme release.

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8
Q

How will cortisol decrease swelling?

A

By decreasing capillary permeability, and decreases vasodilation.

9
Q

Increased cortisol does what to fevers?

A

Attenuates (weaken or reduce) them.

10
Q

Cortisol inhibits the production of prostaglandin and leukotrienes and result in what?

A

Decreased WBC migration, vasodilation, and suppresses cyclooxygenase potentiating the effect.

11
Q

Mineralcorticoid receptors bind what normally?

A

Aldosternone.

12
Q

Since cortisol is similar to aldosterone it can bind to mineralcorticoid receptors, but what has a larger binding affinity cortisol or aldosterone to mineralcorticoid receptors?

A

Aldosternone.

13
Q

For Cortisol to bind to mineralcorticoid receptors large amounts must be present in the body and once cortisol binds to mineralcorticoid receptors what happens?

A

Increased reabsorption of sodium and water which leads to increased blood volume and therefore increased blood pressure.

14
Q

How will short term amounts of cortisol effect memory?

A

It will help create memories when exposure is short term and is a proposed mechanism for storage of “flash bulb” memories at times of good/bad stress.

15
Q

How will long term amounts of cortisol effect memory?

A

Leads to cellular damage in the hippocampus resulting in impaired learning.

16
Q

Pharmacologic glucocorticoids are absorbed well where and are given how?

A

Given primarily by mouth, but can be injection and topically. They are absorbed well through the intestines.

17
Q

When would hydrocortisone be used via injection?

A

Severe allergic reactions resulting in anaphylaxis and angioedema. Also can be injected in inflammed joints for gout, rheumatoid arthristis and osteoarthritis.

18
Q

What could happen with chronic use of hydrocortisone?

A

Adrenal insufficiency.

19
Q

Chronic use of hydrocortisone can do what to blood sugar?

A

Cause hyperglycemia.

20
Q

What will chronic use of hydrocortisone do to skin?

A

Increase fragility and easy brusing.

21
Q

What will chronic use of hydrocortisone do to the CNS?

A

Excitatory effect.

22
Q

Chronic use of hydrocortisone can impair what processes?

A

Anabolic.

23
Q

What will chronic hydrocortisone do to the hands?

A

Cause expansion of malaar fat pads and dilation of small vessels in the skin.

24
Q

What will chronic hydrocortisone do to the menstural periods?

A

Anovulation or other irregularities.

25
Q

What will chronic hydrocortisone do to growth?

A

Growth failure, and pubertal delay.

26
Q

What is a combination of effects produced by prolonged, excess glucocorticoids, synthetic or endogenous called?

A

Cushing’s syndrome.

27
Q

Visceral fat has high concentration of what type of receptors?

A

Cortisol.

28
Q

Visceral fat promotes what?

A

Fat cell differentiation.

29
Q

When will sex hormones released by the supra renal gland play an important role?

A

During fetal development and puberty. Only a weak effect in adults.

30
Q

Where will the conversion of DHEA and Androstenedione to testoterone take place at?

A

Outside the adrenal gland.

31
Q

What is hypercortisolism aka and what is it?

A

AKA cushing’s syndrome. It is excessive levels of cortisol in blood.

32
Q

What is hypocortisolism aka and what is it?

A

AKA addison’s disease and it is decreased levels of cortisol in blood.

33
Q

JFK had addison’s disease and it stopped his body from being able to do what?

A

Deal with stress.

34
Q

What is a primary hypercortisolism?

A

Cushing’s syndrome aka hypercortisolism aka hyperadrenalism aka hyperadrenocortiscism.

35
Q

What are 5 causes of cushing’s syndrome?

A
  1. Abnormal function of hypothalamus and excess secretion of CRH. 2. Adenomas of anterior pituitary with excess ACTH. 3. Ectopic secretion of ACTH from abdominal carcinoma. 4. Adenoma of adrenal cortex. 5. Exogenous corticosteroid administration.
36
Q

What will a person with cushings syndrome look like?

A

Buffalo-like torso from mobilization of fat from lower body to thoracic and upper adbominal regions. They have edematous face (moon-like). Acne and hirsuitism (excess hair).

37
Q

What is purple striae and what can cause it?

A

Stretch marks can be caused by cushings syndrome.

38
Q

How is cushing’s syndrome diagnosed?

A

Dexamthasone challenge and by measuring ACTH levels and cortisol.

39
Q

What is primary and secondary hypercortisolism?

A

Primary- Increased cortisol and decreased ACTH. Secondary- Increased cortisol and ACTH.

40
Q

What are 2 treatments for cushing’s syndrome or hypercortisolism?

A
  1. Removal of a tumor. 2. Medications to block steroidogenesis or inhibit ACTH.
41
Q

The adrenal glands fail to do what with addison’s disease?

A

To produce mineralcorticoids and glucocorticoids.

42
Q

Addison’s disease causes what?

A

Autoimmune mediated atropy (80%), TB, cancer.

43
Q

what are the proteolytic products of ACTH?

A

1) increased visual attn
2) alters mood to reduce social interaction
3) increases anxiety

44
Q

What is adrenocortocoid derived from?

A

Cholesterol.

45
Q

Low aldosterone levels lead to what?

A

Decreased fluid, acidosis, low plasma volumes and high RBC concentration.

46
Q

Low plasma volume and high RBC concentration leads to what?

A

Decreased cardiac output, and death.

47
Q

What are the treatments for addison’s disease aka hypoadrenalism?

A

Small quantities of mineral- and glucocorticoids daily.

48
Q

What is the function of aldosterone?

A

Volume regulation sodium retention and K+ loss.

49
Q

What cells are capable of producing aldosterone?

A

Just those in the zona glomerulosa cells.

50
Q

What type of hormone is aldosterone?

A

Steroid.

51
Q

How much aldosterone is secreted per day?

A

0.15 mg.

52
Q

Aldosterone is an acute _______ hormone.

A

Lifesaving.

53
Q

Aldosterone leads to na retention and K excreting in what part of the kindey?

A

Collecting ducts and distal tubules.

54
Q

Since water follows Na with aldosterone when na is retained what happens?

A

Water is retained and this leads to increased thirst, and increased water intake.

55
Q

What is ACTH’s role in aldosterone secretion?

A

It stimulates the synthesis of aldosterone from cholesterol, but ACTH wont increase secretion.

56
Q

Total loss of Mineralcorticoids leads to what?

A

Death in 3-14 days.

57
Q

What is hyperkalemia?

A

High levels of K+.

58
Q

A mineralcorticoid or aldosterone deficiency does what to sodium levels?

A

Decreases them and this leads to decreased blood volume

59
Q

Hyperkalemia leads to what?

A

Cardiac toxicity, weak contractions, arrhythmia, and death.

60
Q

Mineralcorticoid or aldosteron deficiency does what to the GI tract?

A

Decreased water absorption and causes diarrhea.

61
Q

What is the cause of excess aldosteron or mineralcorticoids?

A

Adrenal tumor.

62
Q

How will mineralcorticoid excess lead to alkalosis?

A

With increased sodium H+ will exchanges for sodium

63
Q

What are the symptoms of alkalosis?

A

Confusion, muscle twitching, nausea, numbness, light headedness.

64
Q

What is primary aldosteronism?

A

A tumor of the zona glomerulosa that leads to excess aldosterone secretion.

65
Q

Primary aldosteronism is aka?

A

Conn’s syndrome.

66
Q

What type of growths may cause excess aldosterone not cortisol?

A

Hyperplastic growth of the adrenals.

67
Q

What are the 2 most important effects of primary aldosteronism aka conn’s syndrome?

A
  1. Hypokalemia leading to muscle weakness and possible paralysis. 2. Increase extracellular volume leadign to hypertension.
68
Q

What are the cardiovascular effects from epi and norepinephrine?

A

Redistribution of blood flow from Skin, GI, kidney.

69
Q

What are the pulmonary effects of epi and norepinephrine?

A

Increased rate and depth of breathing.

70
Q

What other 3 effects will epi and norepinephrine have?

A

Diaphoresis (sweating), anxiety, increased overall metabolism.

71
Q

What is pheochromocytoma?

A

A rare tumor of the chromaffin cells from the medulla of the adrenal glands.

72
Q

Besides the adrenal medulla where are chromaffin cells found at?

A

other nervous tissue.

73
Q

Can pheochromocytomas be found outside of the adrenal glands?

A

Yes.

74
Q

Where are the common locations for pheocromocytoma?

A

Heart, neck, bladder.

75
Q

What is an indicator of a pheochromocytoma?

A

Overproduction of the catecholamines (epi and norepinephron).

76
Q

Pheochromocytoma can develop at any age, but it is most commonly developed at what age?

A

30-60 years.

77
Q

Will pheochromocytomas be benign or malignant?

A

Benign.

78
Q

What is the treatment given for pheochromocytomas?

A

Normalizing blood pressure.

79
Q

What is von hippel-lindau disease?

A

Rare multisystem disorder at high risk of developing a pheochromocytoma.

80
Q

With pheochromocytoma what will a blood test show?

A

Elevated epi and norepinephrine, and breakdown products (metanephrines).

81
Q

What type of imaging should be done to test for a pheochromocytoma?

A

Abdominal CT scan/MRI

82
Q

A sudden release of catecholamines (epi and norepinephrine) can cause what?

A

Hypertension as high as 250/150.

83
Q

Chronic excessive catecholamine exposure increases the risk of what?

A

Diabetes.

84
Q

What is the treatment for pheochromocytoma?

A

Alpha/beta blockers (adrenergic antagonists), Surgery, radiation, chemotherapy, artery ablation (block off blood supply to tumor).

Physiology 2 Test 2 (4 decks)

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