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Clin Med Exam 3 > Adrenal Gland - Young > Flashcards

Adrenal Gland - Young Flashcards

1
Q

what does the adrenal gland secrete?

A

hormones due to stress

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2
Q

how many parts is the adrenal gland divide into?

A

2

-a superficial adrenal cortex and an inner adrenal medulla

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3
Q

what’s the difference b/w adrenal cortex and medulla?

A

difference in how they are activated

-Cortex is regulated by negative feedback loops

-Adrenal Medulla is directly innervated by sympathetic nervous system between T5-T11
(The cells are converted post ganglionic neurons (chromaffin cells) that make and store catecholamines)

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4
Q

what hormones does the adrenal cortex produce?

A

corticosteroids (glucocorticoids, mineralocorticoids, androgens)

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5
Q

where are glucocorticoids produced in the adrenal cortex?

A

in the zone fasciculata

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6
Q

what is a glucocorticoid?

A

cortisol

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7
Q

at what rate is cortisol released from the adrenal cortex?

A

Cortisol released at diurnal basal rate with bursts d/t stress response regulated by anterior pituitary & ACTH via negative feedback loop (hydrocortisone is rx of cortisol)

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8
Q

what are the functions of glucocorticoids? (HINT: 4)

A
  • stimulates gluconeogenesis
  • mobilization of fat (fatty acids and amino acids)
  • suppresses immune system through anti-inflammatory pathways (inhibits edema, swelling, fluid mobility)
  • inhibits the effects of insulin
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9
Q

how do glucocorticoids suppress immune system through anti-inflammatory pathways?

A
  • maintenance of normal vascular response to vasoconstrictors
  • opposition to increases in capillary permeability (prevents edema and swelling)
  • stimulation of polymorphonuclear neutrophil (PMN) leukocytosis
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10
Q

when glucocorticoids stimulate PMN, what will you see for the patient in terms of WBC’s?

A

If patient is on prednisone chronically, then will see increased WBC’s, but it’s not due to an infection, it’s to the to the prednisone

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11
Q

where are mineralocorticoids produced in the adrenal cortex?

A

in the zone glomerulosa

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12
Q

what is a mineralocorticoid that the adrenal cortex releases?

A

aldosterone

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13
Q

function of aldosterone?

A

Na+ retention into serum with H2O & K+ secretion into renal tubule
(maintains blood pressure)

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14
Q

where are androgens produced in the adrenal cortex? examples?

A

zona reticularis

e.g., DHEA, androstenedione (precursor to testosterone)

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15
Q

factors that reduce cortisol levels?

A
  • music
  • massage
  • omega-3 fatty acids
  • Mg supplement w/aerobic exercise
  • dancing
  • high dose vit C
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16
Q

factors that increase cortisol levels?

A
  • caffeine
  • sleep deprivation
  • intense or prolonged aerobic exercise
  • trauma/stressful event
  • anorexia
  • excessive alcohol intake
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17
Q

what does the adrenal medulla produce & release?

A

catecholamines

-epi (80%), norepinephrine (20%), dopamine

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18
Q

what are chromaffin cells?

A

Cells CNS origin without dendrite/axons = modified post-ganglionic neurons with direct connection to sympathetic division of ANS

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19
Q

what type of response do medullarycells/chromaffin cells cause?

A

Direct rapid release of catecholamine targeting receptors throughout body

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20
Q

what is pheochromocytoma?

A

Massive pathologic release of catecholamines

caused by rare catecholamine-secreting adrenal medulla tumor (that produces, stores, & secretes catecholamines)

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21
Q

what syndrome pheochromocytoma associated with?

A

MEN 2a/2b
(multiple endocrine neoplasia disorders type 2’s)
(5% association)

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22
Q

clinical features of pheochromocytoma

A

malignant HTN (mc) (sustained - 60%, or labile)

sudden onset lasting min, hrs, longer of:
-PHE - palpitations, HA, excessive sweating (diaphoresis)
(also chest pain, abd pain, feeling of impending doom)

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23
Q

dx of pheochromocytoma

A

increased 24hr urinary collection of catecholamine metabolites (increased metanephrine & increased VMA)

  • also collecting total catecholamines & creatinine
    imaging: MRI or CT of abdomen to visualize adrenal tumor
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24
Q

when is the best way to collect urine sample for dx of pheochromocytoma?

A

when they are having an episode of symptoms

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25
Q

txt of pheochromocytoma

A

surgical resection

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26
Q

what medications do you give a pt before surgery for pheochromocytoma?

A

Alpha-adrenergic blockade 10-14 days and Beta-adrenergic blockade 2 days prior to surgical resection to prevent intra-operative HTN crisis

  • Phenoxybenzamine HCl -> alpha-blocker
  • propranolol or nadolol -> non-selective beta-blockers
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27
Q

why give beta-blocker 2 days prior to surgical resection and not earlier (like alpha-blockers) in pheochromocytoma

A

to prevent unopposed alpha constriction during catecholamine release triggered by surgery or spontaneously (can lead to life threatening HTN)

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28
Q

when do laparoscopic surgical resection?

A

Laparoscopic if <8cm preferred

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29
Q

what should be a differential diagnosis when working someone up for HTN?

A

hyperaldosteronism

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30
Q

types of hyperaldosteronism

A

primary (too much release of aldosterone) - renin independent

secondary (appropriate release of aldosterone) - due to increased renin secondary to increase in aldosterone via RAAS

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31
Q

what are causes of primary hyperaldosteronism?

A

idiopathic bilateral adrenal hyperplasia (mc in women)

conn’s syndrome (adrenal aldosteronoma)

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32
Q

what is the plasma renin level like for primary hyperaldosteronism?

A

plasma renin is LOW

Increased production of aldosterone -> increased flow through kidney (JGA) -> renin drops (suppresses renin)

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33
Q

what are causes of secondary hyperaldosteronism?

A

usually with someone in edematous state (e.g., chronic CHF, ascites, nephrotic syndrome)
-all due to decreased renal perfusion

-also associated with HTN (renin overproduction - decreased in renal blood flow, renin producing tumor)

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34
Q

what is the plasma renin level like for secondary hyperaldosteronism?

A

plasma renin HIGH

Appropriate release of aldosterone low flow through kidney (JGA) renin is high all the time aldosterone is always high all the time

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35
Q

classic primary hyperaldosteronism findings

A
  • diastolic HTN -> HA’s
  • hypokalemia -> muscle weakness & fatigue
  • metabolic alkalosis -> excess H+ secretion = HCO3 elevated
  • low plasma renin
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36
Q

labs & ekg & CXR findings for primary hyperaldosteronism

A
  • hypokalemia
  • hypernatremia
  • metabolic alkalosis
  • low plasma renin
  • proteinuria -> sign of nephropathy

EKG: U waves (b/c hypokalemia)

CXR: cardiomegaly - pt most likely has chronic HTN

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37
Q

diagnostic tests for primary hyperaldosteronism

A
  • renin hypo secretion test with volume depletion
  • failed aldosterone suppression test with volume expansion
  • abd/pelvis CT or MRI (done if 1st 2 tests are positive)
38
Q

therapy for primary hyperaldosteronism

A
  • adenoma (surgical excision)

- diet w/Na+ restriction & aldosterone

39
Q

criteria for dx of primary hyperaldosteronism

A
  • Diastolic HTN without edema
  • Decreased secretion of renin when stimulated
  • Increased secretion of aldosterone that can’t be suppressed
  • No diuretic use!!!
40
Q

why can’t you the pt use diuretics if primary hyperaldosteronism?

A

falsely decrease K and mess up electrolytes because that will make tests incorrect; take them off their diuretics for a few weeks

41
Q

what is cushing’s syndrome?

A

Prolonged exposure to glucocorticoids endogenous or exogenous

42
Q

what is the most common cause of exogenous exposure to glucocorticoids?

A

long-term high dose corticosteroid therapy

E.g., prednisone, decahedron, hydrocortisone

43
Q

what happens to the HPA axis when taking chronic prednisone?

A

suppression of the HPA axis b/c have exogenous cortisol, so don’t need endogenous cortisol from the adrenal cortex

44
Q

what is cushing’s disease?

A

hyper secretion of cortisol from adrenal cortex due to pituitary overproduction of ACTH
-overproduction of ACTH b/c of tumor in anterior pituitary gland

45
Q

what can occur if the anterior pituitary gland adenoma in cushing’s disease is large?

A

bi-temporal hemianopsia/optic chiasm compression

46
Q

clinical manifestations of cushing’s

A
  • weight gain in face, upper back (buffalo hump), torso (central adiposity)
  • purple/red striae, thin skin, easy bruising
  • proximal muscle weakness/wasting
  • sexual dysfunction (decreased libido, virilization female, fem male - adrenal mass suggested)
  • depression, emotional lability, cog dysfunction
  • increased infections, poor wound healing, osteoporosis and fractures
  • tumor symptoms for Cushing’s Disease
47
Q

Cushing’s Disease tumor symptoms

A

HA, vision changes

polyuria, nocturne - if gets big

48
Q

why is glucose high in Cushing’s Disease?

A

b/c cortisol stimulates glucose secretion

49
Q

diagnosis for cushing’s

A
  • 24hr urine cortisol (>300)
  • Dexamethasone suppression test
  • CRH/dex suppression test if urine and def test inconclusive
50
Q

how is the dexamethasone suppression test for cushings done?

A

give dexamethasone at 11pm then cortisol is measured at 8pm
-high amount of dexamethasone should tell body to reduce ACTH and cortisol, but doesn’t occur b/c have mass that is making a lot of ACTH or cortisol on its own

51
Q

how is CRH/Dex suppression test for cushing’s done?

A
  • CRH is produced by hypothalamus, precursor to ACTH, give a lot of dex and a little bit of CRH, cortisol should only increase a little bit but if it increases a lot then that’s diagnostic
  • Cortisol >50 = diagnostic
52
Q

if ACTH levels are high in the early afternoon (4pm), what does that mean?

A
  • ACTH level (should be low normally in early afternoon 4pm)

- If high, then usually from pituitary mass (brain tumor)

53
Q

if ACTH is high, what tests do you run?

A

cranial MRI & high dose dec-suppression test

54
Q

treatment of cushing’s

A

surgical transphenoidal resection of pituitary mass

55
Q

if surgical resection for cushing’s txt fails, what can you do?

A

radiation of pituitary tumor (localized)

56
Q

when do you perform an adrenalectomy?

A

Adrenalectomy with failed pituitary resection, adrenal mass, ectopic ACTH from another mass unable to resect (LAST LINE)

57
Q

when do you use medical management for cushing’s?

A

if surgical resection failure or C/I
-used ketoconazole which decreases cortisol production @ P450 enzymes of liver

-or use Metyrapone (blocks final step of cortisol synthesis) - used with ketoconazole should it fail to be fully effective

58
Q

what is the main medical management of cushing’s?

A

ketoconazole

59
Q

what is the main treatment for cushing’s?

A

surgical resection of tumor via transphenoidal

60
Q

what is Addison’s disease?

A

Adrenocortical insufficiency due to destruction or dysfunction of the adrenal cortex

-Insufficiency when >90% adrenals involved (not just glucocorticoids, includes mineralocorticoids, androgens)

61
Q

main causes of Addison’s disease (HINT: 2)

A

idiopathic autoimmune (80%) - causes adrenal atrophy

Tb (chronic granulomatous disease)

62
Q

clinical presentation of Addison’s disease

A

Slow insidious presentation:

  • Weakness/Fatigue (initially asthenia)
  • HypoTN/Orthostasis/Dehydration
  • Weight loss/Anorexia
  • +/- Hyperpigmentation (skin, mucosa)
63
Q

why do pts present with hyper pigmentation in Addison’s disease?

A

b/c adrenal glands aren’t making cortisol, so hypothalamus makes a lot of CRH (to make the cortisol) and also makes melanocyte stimulating hormone, so people become tan on sun exposed areas

64
Q

main diagnostic test for Addison’s disease

A

Cortrosyn Stimulatin Test (Cosyntropin)

  • ACTH stimulation test
  • test functional ability of adrenal cortex to synthesize cortisol (But adrenal gland can’t make cortisol)

-plasma cortisol measured before & after inject IV ACTH (measured at 30min and 60min post-injection, check plasma cortisol and aldosterone levels)

Dx: minimal to no change in cortisol & aldosterone levels

65
Q

CMP results in Addison’s disease?

A
  • decrease Na+
  • increased K+ (no aldosterone so have high K and less Na)
  • increased urine Na+
  • increased BUN/Cr
66
Q

EKG results in Addison’s disease?

A

hyperkalemia -> peaked T waves

67
Q

TSH in Addison’s disease?

A

elevated TSH

-Addison patients can make thyroid autoantibodies that cause the anterior pituitary to make more TSH

68
Q

why do CXR & PPD if suspect Addison’s?

A
  • b/c 10% of the time have Addison’s b/c of Tb
  • may have positive PPD
  • may have upper lobe consolidation (seen on CXR)
69
Q

what will you see on CT abdomen for Addison’s?

A

atrophic adrenals (most common) - idiopathic autoimmune

70
Q

what is secondary adrenal insufficiency? & most common cause?

A

suppression or disease of hypothalamic-pituitary axis (ACTH deficiency)

-most common cause is exogenous steroids

71
Q

symptoms of secondary adrenal insufficiency?

A

-similar to primary but NO hyper pigmentation

  • panhypopituitarism
  • physical findings of cushings
  • adrenal atrophy d/t HPA suppression

LOW ACTH

72
Q

what is the distinguishing feature of secondary adrenal insufficiency vs primary?

A

LOW ACTH
-b/c taking exogenous cortisol, so anterior pituitary doesn’t need to send signal of ACTH to increase cortisol secretion from adrenal cortex

73
Q

treatment of adrenal insufficiency

A

Glucocorticoid - hydrocortisone divided to stimulate diurnal adrenal rhythm (2/3am, 1/3pm)

Mineralocorticoid - fludrocortisone (aldosterone); sodium intake

Education & adequacy of therapy (BP titration, titrate meds for HTN/DM, electrolyte measurement (hypokalemia, hypernatremia) monitor, monitor weight

74
Q

adrenal crisis

A

rapid/severe adrenal collapse

  • if left untreated -> coma/death
  • d/t stressful event (bronchitis, GI bug), or sudden withdrawal/noncompliance of chronic steroid

rare cause: acute hemorrhagic destruction of bilateral adrenal glands (Waterhouse-Friederichsen syndrome - pseudomonas, meningococemia septicemia)

75
Q

stressors that cause adrenal crisis

A

infection, vomiting/diarrhea

76
Q

symptoms of adrenal crisis

A

-Shock, hypotension (refractory to any txt like fluids), hypovolemia

77
Q

treatment of adrenal crisis

A

IV fluids - to correct hypotension & hypovolemia (D5NS if hypoglycemic)

IV hydrocortisone q6hr or Dexamethasone (but hydrocortisone covers glucocorticoids and mineralocorticoids)

78
Q

what is MEN?

A
  • Multiple endocrine tumors clustered together that excessive produce hormones
  • Group of genetic disorders that have autosomal dominant inheritance of these oncogenes
79
Q

what’s MEN 1?

A

3 P’s
-hyperparathyroid (hyperplasia or adenoma), pancreatic islet tumors (Gastrin = Zollinger-Ellison), pituitary adenoma (prolactinoma)

80
Q

symptoms of hyperparathyroid in MEN 1?

A
  • Most common manifestation
  • Hyperplasia or adenoma (most common)

Symptoms:

  • hypercalcemia
  • Weak, N/V, constipated, polyuria

-Elevated ionized serum Ca++ and PTH normal

81
Q

what does a Zollinger-Ellison mass produce in pancreas?

A

mass that produces a lot of gastrin -> get recurrent ulcers (PUD)

82
Q

MEN 1 Dx

A
  • hormone/electrolyte assays
  • provocative testing (dx for Zollinger-Ellison)
  • radiologic testing (CT/MRI)
  • annual screening basal & post-prandial pancreatic polypeptides
83
Q

for MEN 1 dx, what hormones and electrolytes do you assay?

A
  • Gastrin level
  • Glucagon level
  • Ca++ and PTH levels
  • Hypokalemia, hypochloremia, metabolic acidosis
  • Growth hormone (for growth hormone adenoma)
  • Prolactin level
  • ACTH level
84
Q

what testing is diagnostic for Zollinger-Ellison and how is it performed?

A

Provocative testing

-Secretin stimulation test with gastrin levels

85
Q

what other provocative testing can you do for Men 1 dx?

A
  • Short or 72hr fast with serum insulin & C-peptide levels
  • Dexamethasone suppression test -> won’t be able to suppress cortisol levels b/c have Cushing’s disease
86
Q

MEN 1 surgical therapy

A

-Transphenoidal approach with pituitary tumors (often difficult b/c of multicentric)

Parathyroidectomy + thyroidectomy
(Do both because possibility of developing future malignant thyroid cancer)

Subtotal or total pancreatectomy
(For patients with insulinoma b/c insulinoma’s don’t respond well to medication)

87
Q

MEN 1 medical management

A 
Dopamine agonists (bromocroptine/cabergoline) for prolactinoma
-Dopamine inhibits prolactin release, reason to give dopamine agonist

H2 receptor antagonist, PPI for ZES
-Cimetidine, omeprazole

88
Q

what is MEN 2?

A

Medullary thyroid carcinoma & Pheochromocytoma

89
Q

what is MEN 2a?

A

MTC (medullary thyroid carcinoma), Pheo (50%), Hyperparathyroidism (15-20%)

Most common manifestation is MTC

MTC typically develops in childhood and >1cm tumor associated with local and distant metastasis

90
Q

what is MEN2b?

A

MTC, Pheo (>50%), mucosal neuromas, marfanoid body habitus

Childhood marfanoid morphology (really long arms/legs) and mucosal neuromas most distinctive

MTC develops earlier and is more aggressive than 2a

91
Q

Txt of MEN 2?

A

do thyroidectomy ASAP to prevent mortality

-genetic testing for oncogene mutations (if found do total thyroidectomy prophylactically)

Clin Med Exam 3 (6 decks)

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