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ClinMed exam III > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What are the two parts of the adrenal gland

A
  • superficial adrenal cortex

- inner adrenal medulla

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2
Q

What portion of the adrenal gland is the true endocrine gland

A

adrenal cortex

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3
Q

What does the adrenal cortex produce

A

corticosteriods, synthesized from cholesterol

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4
Q

Where are glucocorticoids produced

A

zona fasciculata

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5
Q

Most common glucocorticoid released by the body

A

cortisol

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6
Q

What does cortisol do

A
  • increases glucose metabolism and glycogen formation, especially in the liver
  • mobilization of fat, protein and carbohydrates
  • suppress the immune system through anti-inflammatory properties
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7
Q

What regulates the release of cortisol

A

anterior pituitary and ACTH via a negative feedback look

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8
Q

Where are mineralocorticoids produced

A

zona glomerulosa

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9
Q

What is the most common mineralocorticoid

A

aldosterone

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10
Q

What does aldosterone do

A

Na+ retention into serum with h20 and K secretion into the renal tubule (controls blood pressure)

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11
Q

Where are androgens produced

A

zona reticularis

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12
Q

What are the most common androgens produced

A

DHEA, androstenedione

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13
Q

What factors reduce cortisol levels

A
  • music therapy
  • massage therapy
  • omega 3 fatty acids
  • magnesium supplementation w/aerobic exercise
  • dancing
  • high dose vitamin C
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14
Q

What factors increase cortisole leverls

A
  • caffeine
  • sleep deprivation
  • intense or prolonged aerobic exercise
  • trauma or stressful event
  • subcutaneous adipose
  • anorexia
  • excessive alcohol intake
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15
Q

What is released by the adrenal medulla

A

epi, norepi, dopamine

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16
Q

What are chromaffin cells

A

modifiedpost ganglionic neurons w/ direct connection to sympathetic division of ANS

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17
Q

Where are the medullary cells and chromaffin cells located? why?

A

clustered around large vessels so there can be a direct and rapid release of catecholamines

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18
Q

What is the flight or flight response

A

physiological reaction that occurs in response to a perceived harmful event

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19
Q

Why do catecholamies get released during fight or flight response

A
  • increase blood flow to the muscles
  • increase blood pressure, heart rate and ventilatory rate
  • increase blood sugar and fats in order to supply the body with extra energy
  • pupils dialter to see better
  • increased perspiration to prevent over heating due to increased metabolic rate
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20
Q

What is a pheochromocytoma

A

rare adrenal medulla tumor that produces, store and secretes catecholamines

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21
Q

What is the most common clinical feature of a pheochromocytoma

A

hypertention, usually sustained

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22
Q

What are other common symptoms of a pheochromocytoma

A

headache, diaphoresis, palpatations

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23
Q

What lab tests are done to diagnose a pheo

A

24 hour urine collection to check metanephrine, VMA, total catecholamies, creatinine

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24
Q

Imagine done to diagnose pheo

A

abdominal CT or MRI

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25
Q

What is the treatment for a pheo

A

surgical resection

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26
Q

What must be done prior to a surgical resection of a pheo? why?

A

alpha adrenergic blockade 10-14 days before surgery and beta adrenergic blockade 2 days prior

prevent intraoperative HTN crisis

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27
Q

What are the medications usually given before a surgical resection of a pheo

A

phenoxybenzamine HCl

propranalol or nadolol

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28
Q

What happen to the plasma renin in primary hyperaldosteronism

A

low plasma renin

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29
Q

What happens to the plasma renin in secondary hyperaldosteronism

A

high plasma renin

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30
Q

What is another name for primary hyperaldosteronism

A

Conn’s syndrome

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31
Q

Most common causes of primary hyperaldosteronism

A
  • adrenal adenoma

- bilateral cortical nodular hyperplasia (idiopathic)

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32
Q

What are the classic findings in primary hyperaldosteronism

A
  • diastolic HTN
  • hypokalemia
  • metabolic alkalosis
  • low plasma renin
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33
Q

What happens with hypersecretion of aldosterone

A

increase in renal distal tubular exchange of Na+ which leads to K+ and H+ secretion

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34
Q

Lab findings for primary hyperaldosterone

A
  • hypokalemia
  • hypernatremia
  • low plasma renin
  • metabolic alkalosis
35
Q

EKG findings for primary hyperaldosteronism

A
  • u waves, ectopic beats
  • ST depression
  • prominent P wave, prolonged PRI
  • LVH criteria
36
Q

What do you find on a chest xray with a patient with primary hyperaldosteronism? urine?

A
  • cardiomegaly on chest xray

- proteinuria

37
Q

Cycle of primary hyperaldosteronism

A

increase aldosterone–>increased sodium–>increased volume–>decreased renin

38
Q

Diagnostic testing for primary hyperaldosteronism

A
  • renin hyposecretion w/ volume depletion
  • failed aldosterone suppression w/ volume expansion
  • abd/pelvis CT or MRI
39
Q

Treatment of primary hyperaldosteronism

A
  • surgical excision for adenomas
  • diet w/ sodium restriction
  • aldosterone antagonist (spironolactone)
40
Q

Criteria for diagnosis for primary hyperaldosteronism

A
  • diastolic HTN without edema
  • decreased secretion of renin when stimulated
  • increased secretion of aldosterone that cannot be suppressed
  • no diuretic use
41
Q

Causes of secondary hyperaldosterism

A
  • edema state (nephrotic syndrom, ascites, CHF)

- HTN (renin overproduction)

42
Q

Cycle of secondary hyperaldosteronism

A

increased sodium–>decreased volume–>increased renin–>increased aldosterone

43
Q

What causes Cushing’s syndrome

A

prolonged exposure to glucocorticoids either endogenous or exogenous

44
Q

Does endogenous or exogenous steroids cause Cushing’s more often

A

exogenous exposure

45
Q

What causes endogenous overproduction of glucocorticoids?

A
  • hypersecretions of cortisol from adrenal cortex

- most common pituitary overproduction of ACTH

46
Q

History of a pt with Cushing’s

A
  • weight gain
  • dermis changes
  • proximal muscle weakness
  • sexual dysfunction
  • psychiatric changes
  • tumor symptoms
  • increase infections/poor wound healing
  • pathologic fractures
47
Q

What would a physical exam of a patient with Cushing’s show

A
  • adipose deposition
  • dermis changes
  • cardiovascular/renal (HTN,edema)
  • peptic ulcer disease
  • galactorrhea, hypothyroid sx
48
Q

Diagnosis of Cushing’s

A
  • 24 hr urine cortisol
  • dexamethasone suppression test
  • CHR/Dex suppression test if above incolclusive
49
Q

What is considered diagnostic for a urine cortisol? normal?

A

> 300mcg/dL is diagnostic

<90 is normal

50
Q

What is a dex suppression test?

A

1mg of dexmethasone given at 11p then the cortisol is measured at 8am

51
Q

What is considered diagnosic in a CRH/dex suppression test

A

cortisol >50

52
Q

When should ACTH levels be low

A

in the early afternoon around 4p

53
Q

Surgical management of Cushing’s

A
  • remove tumor on pituitary

- consider radiation if failed

54
Q

Medical management of Cushing’s

A

only if surgical resection failed or contraindicated

  • ketoconazole
  • metyrapone
55
Q

What causes adrenocortical insufficiency

A

dysfunction or destruction of the adrenal cortex

56
Q

What is the primary cause of adrenocortical deficiency

A

Addison’s disease

57
Q

Eitology of primary adrenocortical deficiency

A
  • idiopathic autoimmune
  • TB
  • hematologic malignancy
  • AIDS
  • drugs
  • abdominal radiation therapy
  • congenital adrenal hyperplasia
58
Q

Clinical presentation of primary adrenocortical deficiency

A

slow insidious presentation

  • weakness/fatigue
  • hypotension/orthostasis/dehydration
  • weight loss/ anorexia
  • nausea/vomiting
59
Q

What is the tool of choice for diagnosis of primary adrenocortical deficiency

A

cortrosyn stimulation test

60
Q

What does the cortrosyn stimulation test do

A

tests functional ability of adrenal cortex to synthesize cortisol

61
Q

CMP in primary adrenocortical deficiency

A
  • decreased sodium
  • increased potassium
  • increased uring sodium
  • increased BUN/creatine
62
Q

EKG finding for a pt with primary adrenocorticol deificnecy

A

hyperkalemia findings

63
Q

Will TSH be elevated or decreased in a patient with primary adrenocortical deficiency

A

elevated

64
Q

Primary adrenal insufficiency

A

anatomic destruction or metabolic failure of the adrenal cortex

65
Q

Secondary adrenal insufficiency

A

suppress or disease of hypothalamic pituitary axis (ACTH deficiency)

66
Q

What distinguishes primary adrenal insufficiency from secondary

A

low ACTH

67
Q

Treatment of adrenal insurriciency

A
  • hydrocortisone
  • fludrocortisone

treat other sx

68
Q

What usually causes an adrenal crisis

A

exacerbation of chronic adrenal insufficiency

stress, sudden withdrawal of chronic steroids

69
Q

What is the less common cause of an adrenal crisis? What can cause it?

A

acute hemorrhagic destruction of bilateral adrenal glands

caused by Waterhourse-Frederichen syndrome, anticoagulation, pregnancy complication

70
Q

Stressors for an adrenal crisis

A
  • infection
  • trauma
  • surger
  • vomitin,diarrhea
  • emotional turmoil
71
Q

Symptoms of an adrenal crisi

A
  • hypotension
  • N/V/ abd pain
  • hyperpyrexia
  • mental status change
  • hypoglycemia, hyponatremia, hyperkalemia, metabolic acidosis
72
Q

Treatment of an adrenal crisis

A
  • IV fluid resuscitation
  • stress hydrocortisone or dexamethasone
  • ? vasopressors
  • ? abx
73
Q

What does the MEN1 gene cause

A

hyperparathyroid
pancreatic iselts
pituitary

74
Q

What cancer is the most common manifestation for MEN1

A

hyperparathyroid

75
Q

Neoplasm of hyperparathyroid

A

hyperplasia or adenoma

-sx of hypercalcemia

76
Q

Neoplasm of pancreatic islets

A

hyperplasia, ademona, carcinoma

  • occurs with hyperparathyroid
  • increased production in pancreatic islet cell hormones
77
Q

Neoplasm of the pituitary gland releases what

A
  • prolactin
  • growth hormone
  • ACTH
78
Q

Neoplasms of the pancreatic islet cells releases what

A
  • gastrin
  • insulin
  • glucagon
  • vasoactive intestinal peptide
  • somatostatin
79
Q

Diagnosis of MEN1

A
  • hormone/electrolyte assays
  • provocative testing
  • radiologic testing
80
Q

Therapy for MEN1

A
  • surgical resection

- medical management

81
Q

What does MEN2 cause

A

medullary thyroid carcinoma and pheochromocytoma

82
Q

Most common subtype of MEN2

A

MEN2a

83
Q

MEN2 treatment

A 
MTC= total thyroidectomy
Pheo= unilateral/bilateral resection
-hyperparathyroid= exision with partial remaining

ClinMed exam III (7 decks)

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