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Endocrine > Adrenal > Flashcards

Adrenal Flashcards

1
Q

What is another name for the adrenal glands?

A

The Suprarenal glands

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2
Q

What cells make catecholamines?

A

Chromaffin cells in the adrenal medulla

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3
Q

All catecholamines are derived from what substance?

A

Tyrosine

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4
Q

Name the four catecholamines?

A
  1. DOPA
  2. Dopamine
  3. Epinephrine
  4. Norepinephrine
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5
Q

T/F: Epinephrine is made only in the adrenal cortex?

A

False; made only in the adrenal medulla

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6
Q

How much epinephrine is made in comparison to norepinephrine?

A

80%=Epinephrine

20% =Norepinephrine

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7
Q

What causes the body to initiate fight or flight response?

A

Pain, fear, hemorrhage, cold, hypoglycemia, hypotension, heat, exercise, surgery

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8
Q

Which areas of the body have increased/decreased CO?

A

Increased CO to heart and skeletal muscle.

Decreased CO to kidneys, skin, and mucosa

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9
Q

Is respiration increased or decreased with fight/flight response?

A

increased

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10
Q

Epinephrine and norepinephrine both act on which adrenergic receptor to cause arterial vasoconstriction?

A

Alpha-1

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11
Q

Which has a stronger Beta-1 effect?

A

Epinephrine

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12
Q

What causes norepinephrine to convert to epinephrine?

A

Phenylethanolamine N-Methyltransferase (PNMT)

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13
Q

PNMT expression is regulated by what?

A

Glucocorticoids (which helps account for glucocorticoids role in affecting blood pressure.

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14
Q

Pheochromocytoma is a tumor typically caused by what to types of tissue?

A
  1. Adrenal medullary hyperplasia

2. Extra-adrenal chromaffin tissue

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15
Q

What are symptoms of pheochromocytoma?

A

Paroxysmal HTN, tachycardia, H/A, sweating, anxiety, tremor, glucose intolerance.

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16
Q

Which type of pheochromocytoma tumor is most common?

A

85-90% are solitary tumors localized to single adrenal gland (Usually right)
10% of tumors are extra-medullary (mostly in the abdomen).

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17
Q

How are pheochromocytomas diagnosed?

A

1st by symptoms, then 24hrs VMA levels, then imaging

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18
Q

What substance are both epinephrine and norepinephrine degraded into?

A

Urinary Vanillylmandelic acid

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19
Q

Patient with diagnosed pheochromocytoma must first be started on beta blockers to lower HR?

A

False; Alpha Adrengergic antagonists must be started 10-14 days prior to surgery to normalize BP, then beta blockade can be started.

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20
Q

What is the risk of beginning beta blockers before alpha blockers on pheochromocytoma patients?

A

Risk of unopposed alpha mediated vasoconstriction

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21
Q

What are intraoperative risks associated with poorly controlled pheochromocytoma?

A

Large BP fluctuations, MI, CHF, dysrrhythmias, and CVA

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22
Q

What medications should be avoided intraoperatively with pheochromocytomas

A

Histamine releasing agents, metoclopramide, and glucagon

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23
Q

What can be expected changes in VS after pheochromocytoma removal?

A

Hypotension

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24
Q

How long does it take for catecholamine levels to return to normal after removal of pheochromocytoma?

A

Several days after and 75% of patients are normotensive within 10 days postop

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25
Q

Why is adrenal medullary hyposecretion not a serious problem?

A

Because the SNS compensates for cardiovascular regulation and other regulatory hormones compensate for metabolic effects.

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26
Q

What are the three zones of the adrenal cortex?

A
  1. Zona Glomerulosa
  2. Zona Fasciculata
  3. Zona Reticularis
27
Q

Which zone of the adrenal cortex produces androgens?

A

Zona Reticularis

28
Q

Which zone of the adrenal cortex produces Glucocorticoids?

A

Zone Fasciculata

29
Q

Which zone of the adrenal cortex produces Mineralcorticoids?

A

Zone Glomerulosa

30
Q

What is the primary mineralcorticoid?

A

Aldosterone

31
Q

What is the primary Glucocorticoid?

A

Cortisol

32
Q

What is the primary androgen?

A

Androstenedione

33
Q

All of the steroid hormones from the adrenal medulla are synthesized from ______?

A

Cholestrol

34
Q

What are aldosterones major effects on the body?

A

Effects salt and water balance and thereby effects long term regulation of BP

35
Q

What part of the renal tubules are effected by aldosterone?

A

Distal convoluted tubules and collecting ducts

36
Q

Ultimately, excess aldosterone causes what changes in salt, water, potassium, and acid/base balance, VS changes?

A

Hypertension.
Extracellular fluid expansion
Hypokalemia
Metabolic alkalosis

37
Q

What does aldosterone cause metabolic alkalosis?

A

Your body excretes more H+

38
Q

What triggers the kidneys to secrete renin?

A

Hypovolemia

39
Q

Through the RAAS, what does renin trigger?

A

Through a series of steps it angiotensin II is produced which causes potent vasoconstriction and stimulates secretion of aldosterone.

40
Q

T/F: Adrenalcorticotropic Hormone (ACTH) exerts complete control over the release of aldosterone?

A

False; ACTH and Na+ levels do not exert much control; however, it is primarily controlled by the RAAs and K+ levels.

41
Q

What is the name of the disease/syndrome assoicated with hyperaldosteronism?

A

Conn’s Syndrome

42
Q

What causes Conn’s syndrome?

A

Aldosterone secreting tumors

43
Q

Effects of Conn’s Syndrome:

A

Hypertension
Increased ECF volume
K+ depletion
Metabolic alkalosis

44
Q

Patient with Conn’s syndrome have high or low renin levels?

A

Low renin d/t negative feedback from high aldosterone levels.

45
Q

What are the effects of hypoaldosteronism?

A

Na+ lost in urine
K+ retained
Plasma volume decrease
Hypotension

46
Q

What is another name of cortisol?

A

Hydrocortisone

47
Q

What are glucocorticoids effects on metabolism?

A

Stimulates gluconeogensis.
Decreases glucose utilization by cells
Elevates blood glucose concentration

48
Q

What is gluconeogenesis?

A

Formation of carbohydrate from protein by the liver

49
Q

What hormone stimulates release of cortisol?

A

ACTH from anterior pituitary gland

50
Q

What are 5 things that cause ACTH to be released by the anterior pituitary gland?

A
  1. Trauma
  2. Infection
  3. Heat/Cold
  4. Surgery
  5. Catecholamine injection
51
Q

T/F: High levels of cortisol have inflammatory effects?

A

False; Anti-inflammatory effects. Prevents development of inflammation by decreasing capillary permeability, decreasing migration of WBCs

52
Q

What stimulates ACTH release by the anterior pituitary gland?

A

Corticotropin-Releasing Factor (CRH) from the hypothalamus

53
Q

Does a high cortisol level cause inhibition or stimulation of ACTH and CRH release?

A

Inhibition; negative feedback loop

54
Q

What is the name of the disease that is identified by ACTH secreting tumor of the pituitary?

A

Cushing’s Disease

55
Q

What 4 things can cause Cushing’s Syndrome?

A
  1. ACTH secreting ectopic tumor
  2. Overactive Hypothalamic secretion of CRH
  3. Primary glucocorticoid secreting adrenal tumor
  4. Iatrogenic (chronic administration).
56
Q

What are the 9 physiologic changes that can be seen in Cushing’s Syndrome?

A
  1. Connective tissue: thin skin, bruising, poor healing
  2. Bone: Decreased bone formation and osteoporosis d/t decrease Ca++ and bone resorption
  3. Muscle: wasting, weakness, fatigue
  4. Fat: trucal obesity, moon face, buffalo hump
  5. Skin: hirsutism, acne
  6. Endocrine: impaired glucose tolerance
  7. Renal: salt/water retention, hypokalemia
  8. CV: HTN
  9. CNS: Euphoria, irritability, emotional lability, depression.
57
Q

What is failure to produce adrenocortical hormones (glucocorticoids and mineralocorticoids) called?

A

Addison’s Disease

58
Q

Primary Addison’s disease is mostly causes by what?

A

Adrenal nonfunction- mostly autoimmune

59
Q

Secondary Addison’s disease is mostly caused by waht?

A

(hypothalamic or pituitary nonfunction)
Metastatic tumor.
Tuberculosis
Acute withdrawal of glucocorticoid tx

60
Q

What are symptoms of glucocorticoid deficiency in Addison’s Disease?

A
  1. Hypoglycemia
  2. Fatigue
  3. Weight loss
  4. Hyperpigmentation
  5. Severe deterioration to stress
61
Q

How is Addisonian Crisis treated?

A

Cortisol

62
Q

What are symptoms of Mineralocorticoid deficiency in Addison’s disease?

A
  1. Dehydration
  2. Polyuria
  3. Hypotension
  4. Low Na+
  5. K+ retention
  6. Metabolic acidosis
63
Q

Which induction medication should be used sparingly in patients with septic shock and why?

A

Etomidate,

Profound suppression of cortisol for at least 24 hrs

64
Q

How should glucocorticoids be administered in the perioperative period for patients on chronic steroids?

A

50-100mg Hydrocortisone IV

Endocrine (6 decks)

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