Adrenal Gland - Young Flashcards
1
Q
what does the adrenal gland secrete?
A
hormones due to stress
2
Q
how many parts is the adrenal gland divide into?
A
2
-a superficial adrenal cortex and an inner adrenal medulla
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)
4
Q
what hormones does the adrenal cortex produce?
A
corticosteroids (glucocorticoids, mineralocorticoids, androgens)
5
Q
where are glucocorticoids produced in the adrenal cortex?
A
in the zone fasciculata
6
Q
what is a glucocorticoid?
A
cortisol
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)
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
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
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
11
Q
where are mineralocorticoids produced in the adrenal cortex?
A
in the zone glomerulosa
12
Q
what is a mineralocorticoid that the adrenal cortex releases?
A
aldosterone
13
Q
function of aldosterone?
A
Na+ retention into serum with H2O & K+ secretion into renal tubule
(maintains blood pressure)
14
Q
where are androgens produced in the adrenal cortex? examples?
A
zona reticularis
e.g., DHEA, androstenedione (precursor to testosterone)
15
Q
factors that reduce cortisol levels?
A
- music
- massage
- omega-3 fatty acids
- Mg supplement w/aerobic exercise
- dancing
- high dose vit C
16
Q
factors that increase cortisol levels?
A
- caffeine
- sleep deprivation
- intense or prolonged aerobic exercise
- trauma/stressful event
- anorexia
- excessive alcohol intake
17
Q
what does the adrenal medulla produce & release?
A
catecholamines
-epi (80%), norepinephrine (20%), dopamine
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
19
Q
what type of response do medullarycells/chromaffin cells cause?
A
Direct rapid release of catecholamine targeting receptors throughout body
20
Q
what is pheochromocytoma?
A
Massive pathologic release of catecholamines
caused by rare catecholamine-secreting adrenal medulla tumor (that produces, stores, & secretes catecholamines)
21
Q
what syndrome pheochromocytoma associated with?
A
MEN 2a/2b
(multiple endocrine neoplasia disorders type 2’s)
(5% association)
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)
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
24
Q
when is the best way to collect urine sample for dx of pheochromocytoma?
A
when they are having an episode of symptoms
25
txt of pheochromocytoma
surgical resection
26
what medications do you give a pt before surgery for pheochromocytoma?
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
27
why give beta-blocker 2 days prior to surgical resection and not earlier (like alpha-blockers) in pheochromocytoma
to prevent unopposed alpha constriction during catecholamine release triggered by surgery or spontaneously (can lead to life threatening HTN)
28
when do laparoscopic surgical resection?
Laparoscopic if <8cm preferred
29
what should be a differential diagnosis when working someone up for HTN?
hyperaldosteronism
30
types of hyperaldosteronism
primary (too much release of aldosterone) - renin independent
secondary (appropriate release of aldosterone) - due to increased renin secondary to increase in aldosterone via RAAS
31
what are causes of primary hyperaldosteronism?
idiopathic bilateral adrenal hyperplasia (mc in women)
conn's syndrome (adrenal aldosteronoma)
32
what is the plasma renin level like for primary hyperaldosteronism?
plasma renin is LOW
Increased production of aldosterone -> increased flow through kidney (JGA) -> renin drops (suppresses renin)
33
what are causes of secondary hyperaldosteronism?
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)
34
what is the plasma renin level like for secondary hyperaldosteronism?
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
35
classic primary hyperaldosteronism findings
- diastolic HTN -> HA's
- hypokalemia -> muscle weakness & fatigue
- metabolic alkalosis -> excess H+ secretion = HCO3 elevated
- low plasma renin
36
labs & ekg & CXR findings for primary hyperaldosteronism
- 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
37
diagnostic tests for primary hyperaldosteronism
- 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
therapy for primary hyperaldosteronism
- adenoma (surgical excision)
| - diet w/Na+ restriction & aldosterone
39
criteria for dx of primary hyperaldosteronism
- Diastolic HTN without edema
- Decreased secretion of renin when stimulated
- Increased secretion of aldosterone that can’t be suppressed
- No diuretic use!!!
40
why can't you the pt use diuretics if primary hyperaldosteronism?
falsely decrease K and mess up electrolytes because that will make tests incorrect; take them off their diuretics for a few weeks
41
what is cushing's syndrome?
Prolonged exposure to glucocorticoids endogenous or exogenous
42
what is the most common cause of exogenous exposure to glucocorticoids?
long-term high dose corticosteroid therapy
| E.g., prednisone, decahedron, hydrocortisone
43
what happens to the HPA axis when taking chronic prednisone?
suppression of the HPA axis b/c have exogenous cortisol, so don't need endogenous cortisol from the adrenal cortex
44
what is cushing's disease?
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
what can occur if the anterior pituitary gland adenoma in cushing's disease is large?
bi-temporal hemianopsia/optic chiasm compression
46
clinical manifestations of cushing's
- 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
Cushing's Disease tumor symptoms
HA, vision changes
| polyuria, nocturne - if gets big
48
why is glucose high in Cushing's Disease?
b/c cortisol stimulates glucose secretion
49
diagnosis for cushing's
- 24hr urine cortisol (>300)
- Dexamethasone suppression test
- CRH/dex suppression test if urine and def test inconclusive
50
how is the dexamethasone suppression test for cushings done?
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
how is CRH/Dex suppression test for cushing's done?
- 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
if ACTH levels are high in the early afternoon (4pm), what does that mean?
- ACTH level (should be low normally in early afternoon 4pm)
| - If high, then usually from pituitary mass (brain tumor)
53
if ACTH is high, what tests do you run?
cranial MRI & high dose dec-suppression test
54
treatment of cushing's
surgical transphenoidal resection of pituitary mass
55
if surgical resection for cushing's txt fails, what can you do?
radiation of pituitary tumor (localized)
56
when do you perform an adrenalectomy?
Adrenalectomy with failed pituitary resection, adrenal mass, ectopic ACTH from another mass unable to resect (LAST LINE)
57
when do you use medical management for cushing's?
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
what is the main medical management of cushing's?
ketoconazole
59
what is the main treatment for cushing's?
surgical resection of tumor via transphenoidal
60
what is Addison's disease?
Adrenocortical insufficiency due to destruction or dysfunction of the adrenal cortex
-Insufficiency when >90% adrenals involved (not just glucocorticoids, includes mineralocorticoids, androgens)
61
main causes of Addison's disease (HINT: 2)
idiopathic autoimmune (80%) - causes adrenal atrophy
Tb (chronic granulomatous disease)
62
clinical presentation of Addison's disease
Slow insidious presentation:
- Weakness/Fatigue (initially asthenia)
- HypoTN/Orthostasis/Dehydration
- Weight loss/Anorexia
- +/- Hyperpigmentation (skin, mucosa)
63
why do pts present with hyper pigmentation in Addison's disease?
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
main diagnostic test for Addison's disease
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
CMP results in Addison's disease?
- decrease Na+
- increased K+ (no aldosterone so have high K and less Na)
- increased urine Na+
- increased BUN/Cr
66
EKG results in Addison's disease?
hyperkalemia -> peaked T waves
67
TSH in Addison's disease?
elevated TSH
| -Addison patients can make thyroid autoantibodies that cause the anterior pituitary to make more TSH
68
why do CXR & PPD if suspect Addison's?
- 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
what will you see on CT abdomen for Addison's?
atrophic adrenals (most common) - idiopathic autoimmune
70
what is secondary adrenal insufficiency? & most common cause?
suppression or disease of hypothalamic-pituitary axis (ACTH deficiency)
-most common cause is exogenous steroids
71
symptoms of secondary adrenal insufficiency?
-similar to primary but NO hyper pigmentation
- panhypopituitarism
- physical findings of cushings
- adrenal atrophy d/t HPA suppression
LOW ACTH
72
what is the distinguishing feature of secondary adrenal insufficiency vs primary?
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
treatment of adrenal insufficiency
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
adrenal crisis
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
stressors that cause adrenal crisis
infection, vomiting/diarrhea
76
symptoms of adrenal crisis
-Shock, hypotension (refractory to any txt like fluids), hypovolemia
77
treatment of adrenal crisis
IV fluids - to correct hypotension & hypovolemia (D5NS if hypoglycemic)
IV hydrocortisone q6hr or Dexamethasone (but hydrocortisone covers glucocorticoids and mineralocorticoids)
78
what is MEN?
- Multiple endocrine tumors clustered together that excessive produce hormones
- Group of genetic disorders that have autosomal dominant inheritance of these oncogenes
79
what's MEN 1?
3 P's
-hyperparathyroid (hyperplasia or adenoma), pancreatic islet tumors (Gastrin = Zollinger-Ellison), pituitary adenoma (prolactinoma)
80
symptoms of hyperparathyroid in MEN 1?
- Most common manifestation
- Hyperplasia or adenoma (most common)
Symptoms:
- hypercalcemia
- Weak, N/V, constipated, polyuria
-Elevated ionized serum Ca++ and PTH normal
81
what does a Zollinger-Ellison mass produce in pancreas?
mass that produces a lot of gastrin -> get recurrent ulcers (PUD)
82
MEN 1 Dx
- hormone/electrolyte assays
- provocative testing (dx for Zollinger-Ellison)
- radiologic testing (CT/MRI)
- annual screening basal & post-prandial pancreatic polypeptides
83
for MEN 1 dx, what hormones and electrolytes do you assay?
- Gastrin level
- Glucagon level
- Ca++ and PTH levels
- Hypokalemia, hypochloremia, metabolic acidosis
- Growth hormone (for growth hormone adenoma)
- Prolactin level
- ACTH level
84
what testing is diagnostic for Zollinger-Ellison and how is it performed?
Provocative testing
| -Secretin stimulation test with gastrin levels
85
what other provocative testing can you do for Men 1 dx?
- 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
MEN 1 surgical therapy
-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
MEN 1 medical management
```
Dopamine agonists (bromocroptine/cabergoline) for prolactinoma
-Dopamine inhibits prolactin release, reason to give dopamine agonist
```
H2 receptor antagonist, PPI for ZES
-Cimetidine, omeprazole
88
what is MEN 2?
Medullary thyroid carcinoma & Pheochromocytoma
89
what is MEN 2a?
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
what is MEN2b?
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
Txt of MEN 2?
do thyroidectomy ASAP to prevent mortality
-genetic testing for oncogene mutations (if found do total thyroidectomy prophylactically)
