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Endocrinology > Adrenal disorders > Flashcards

Adrenal disorders Flashcards

1
Q

Is the adrenal medulla necessary for life?

A
  • no, the nervous system can kick in to produce E and NE
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2
Q

How long can you live without adrenal function?

A
  • 4-14 days
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3
Q

GFR

A

Glomerulosa:mineralocorticoids
Fasciculata: cortisol
reticularis: sex hormones (androgens)

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4
Q

What are adrenocorticoids?

A

steroid hormones secreted by adrenal cortex and classified by biological activity
- glucocorticoids, mineralocorticoids, and androgens
(acetate and cholesterol basis to all of these hormones)

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5
Q

What controls the secretion of the glucocorticoids?

A
  • ACTH which is secreted by anterior pituitary gland

- aldosterone is controlled by renin which is secreted by the kidneys

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6
Q

What are glucocorticoids?

A

general classification of adrenal cortical steroid hormones that are primarily active in protecting against stress and in affecting protein and carbohydrate metabolism (cortisol)

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7
Q

hypothalamus control over the adrenocroticoids?

A
  • regulated by negative feedback by HPA system

- hypothalamus releases: CRH -> anterior pituitary -> releases ACTH -> adrenal glands -> cortisol and androgens

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8
Q

When does coritol peak?

A
  • in the morning, declines as the day progresses due to CNS and rhythmic cycle
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9
Q

What are mineralocorticoids?

A
  • steroid hormone regulating the retention and excretion of fluids and electrolytes (especially Na and K) by the kidneys (aldosterone)
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10
Q

What are 2 different meanings of corticosteroids?

A
  • can refer to any of the steroid hormones secreted by the adrenal cortex or steroid hormones manufactured synthetically for use as a drug
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11
Q

What is the purpose of the adrenal sex hormones?

A
  • exert little effect on sexual function
  • DHEA (dehydroepiandrosterone)
  • pubertal growth of body hair
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12
Q

What is made in the adrenal medulla?

A
  • epi and NE
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13
Q

What are the 3 parts of the adrenal cortex?

A
  • zona glomerulosa: mineralocorticoid- aldosterone
  • zona fasciculata: glucocorticoids- cortisol, corticosterone
  • zona reticularis: androgens- DHEA, androstendione
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14
Q

Adrenal medulla physiology?

A

core of the adrenal gland

  • made of chromaffin cells (named because of their brown staining with chromic acid salts) -main source of catecholamines, epi, and NE)- hormones underlying the fight or flight response
  • receives input from SNS through preganglionic fibers originating in the thoracic spinal segments 5-11.
  • cortisol produced in the adrenal cortex reaches the medulla in high levels causing up regulation increasing production of epi
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15
Q

NE and E have longer or shorter effects when released from adrenals compared to nervous system?

A
  • 5x longer effects when released from adrenals

- just short term response from SNS: won’t last as long, pupils will dilate

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16
Q

Main functions of the SNS?

A
  • “fight or flight”
  • mobilize energy stores of the body
  • increase blood flow to skeletal muscles and heart while diverting flow from skin and internal organs
  • dilation of bronchioles
  • dilation of pupils
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17
Q

Where are Epi and NE released from?

A
  • from adrenal medulla

- interact with both alpha and beta receptors

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18
Q

What are the actions of Epi and NE?

A
  • cardiovascular: strengthens teh contractility of myocardium (beta 1 action, inotropic action)
    increases rate of contraction (beta 1 action, chronotropic action)
    constricts arterioles in the skin (alpha 1 action)
    dilates vessels to liver and skeletal muscle (Beta 2 action)
  • respiratory: powerful bronchodilation: by acting directly on bronchial smooth muscle (beta 2 action) this is impt to understand because it relieves all known allergic or histamine induced bronchoconstriction and can be life saving in the case of anaphylactic shock
  • hyperglycemia: increased release of glucagon, increased glycogenolysis (conversion of glycogen to glucose)
  • lipolysis
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19
Q

What is a pheochromocytoma?

A
  • a tumor derived from neural crest cells of the SNS that is responsible for about 0.1-2% of all cases of hypertension
  • the tumor relesases catecholamines, which cause episodic or sustained signs and sxs, such as palpitations, sweating, HAs, fainting spells, and hypertensive emergenices.
  • this is a surgically correctable form of HTN
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20
Q

What are the 2 main catecholamines?

A
  • NE and E
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21
Q

what is the relationship b/t adrenal medulla and ANS?

A

receives input from SNS through preganglionic fibers originating in the thoracic spinal cord segments 5-11 SNS -> fight or flight

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22
Q

How can we specifically explain sxs in a pt who has pheochromocytoma?

A
  • increased HR, pounding heart, cold hands and feet
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23
Q

What meds can be used to help lower BP in pt with pheochromocytoma?

A

Phenoxybenzamine (alpha blocker)

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24
Q

Where do the great majorit of pheochromocytomas present?

A
  • in adrenal medulla
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25
Q

Sxs of pheochromocytoma?

A

can be described by the effects that epi and NE have on the various organ systems:
- heart: catecholamines have 2 major effects, each mediated by Beta1 receptor
- blood vessels: vasoconstriction of cutaneous blood vessels via alpha 1 receptor
vasodilation of skeletal muscle blood vessels via Beta 2 receptor
-

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26
Q

If a pt had bad asthma, what would happen with their asthma sxs during an attack from the pheochromocytoma?

A
  • the asthma sxs would improve because of the increased release of epi and NE
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27
Q

What is the 90% tumor rule for pheochromocytoma?

A
  • 90% of time they arise from the adrenal medulla (with other 10% they can arise anywhere but the majority occur in the mediastinum or abdomen)
  • 90% of the time adrenal pheochromocytoma will be unilateral (otherwise it is bilateral and is likely to be a genetic syndrome)
  • 90% of time it isn’t malignant
  • 90% of time it occurs in adults
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28
Q

What are some keys to pheochromocytoma?

A

Hx is very impt: pt usually has episodes of HTN, HA, palpitation, and sweating

  • dx is made by demonstrating elevated urinary exretion of catecholamines or their metabolites (metanephrines and vanillylmandelic acid) during a period of HTN (24 hr urine test)
  • once a dx is made: have to hunt for a source: CT of abdomen with focus on adrenal gland or MRI
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29
Q

What is the function of aldosterone and where is it made?

A
  • made in the zona glomerulosa and is a mineralocorticoid
  • it increases Na and water reabsorption by the kidneys and increases the secretion of K, thereby indirectly regulating blood volume and blood pressure
  • this is the most impt sodium retaining hormone
  • it regulates water and salt balance
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30
Q

What controls aldosterone secretion?

A
  • secretion dictated minimally by adrenocorticotropic hormone by pituitary
  • *** secretion dictated to a much greater degree in association with changes in blood pressure
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31
Q

If more aldosterone is released via low blood pressure, then wahat do you think it helps to do?

A

Helps to retain volume, so increased Na reabsorption means increased water absorption and this will increase BP

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32
Q

What is the system that responds to lowering of the blood pressure?

A
  • the renin-angiotensin-aldosterone system controls blood pressure
  • lowering of blood pressure is sensed by the distal tubules of the kidneys and the system releases aldosterone
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33
Q

What can block the renin-angiotensin-aldosterone system?

A

diuretics -> flush out Na and water

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34
Q

Kidneys control of BP?

A

The kidneys provide a hormonal mechanism -> regulation of BP by managing blood volume - renin-angiotensin -aldosterone system of the kidneys regulates blood volume

  • decreasing blood pressure -> juxtaglomerular cells secrete renin and renin converts the plasma protein angiotensin II by the lungs
  • Angiotensin II activates 2 mechanisms that raise blood pressure. Angiotensin II constricts blood vessels throughout the body -> raising blood pressure. Constricted blood vessels reduce the amount of blood delivered to the kidneys, decreasing excretion of water (raising blood pressure by increasing blood volume)
  • angiotensin II stimulates the adrenal cortex to secrete aldosterone, reducing urine output by increasing retention of water by the kidneys (increasing bp by increasing blood volume)
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35
Q

What happens in the presence of increased aldosterone?

A
  • increased blood volume and blood pressure

- increased K excretion in the urine meaning the pt will be hypokalemic

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36
Q

What is hyperaldosterone associated with?

A
  • HTN, hypokalemia, and hypernatremia
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37
Q

Cause of hyperaldosterone?

A
  • 1 or both of adrenals are hyperactive

- adrenals are being overstimulated (secondary hyperaldosterone)

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38
Q

What happens with with decreased aldoseterone?

A
  • decreased blood volume and blood pressure

- decreased K excretion in the urine meaning hyperkalemia

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39
Q

What is the cause of primary aldosteronism?

A
  • occasionally a small tumor of the zona glomerulosa cells occurs and secretes large amounts of aldosterone
    (aldosterone causes an exchange transport of Na and K) so with primary aldosteronism we have Na conservation and K excretion
    hypernatremia -> increased volume -> hypertension
    hypokalemia -> if severe enough can cause muscle paralysis
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40
Q

Tx of primary aldosteronism?

A
  • usually surgical removal of adrenal tumor
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41
Q

What will your renin levels be in primary aldosteronism?

A
  • low because of negative feedback, have high aldosterone levels and this inhibits renin secretion.
42
Q

Hyperaldosteronism makes up what percentage of HTN cases?

A
  • 10%
43
Q

Dx of primary aldosteronism?

A
  • high aldosterone levels but low renin levels, HTN: >160/110, hypernatremic, hypokalemic
  • sliced CT of glomerulosa
44
Q

What is produced in the Zona Fasciculata?

A

glucocorticoids:
cortisol - cascade for release of cortisol initiated at level of hypothalamus in response to following: infection, pain, hypoglycemia, trauma, hemorrhage, sleep (all assoc with stress except for sleep)
- in response to stress -> perform necessary functions that are essential for survival, aid in regulating metabolic fuctions, essential for normal glomerular filtration
- also secretes corticosterone

45
Q

Negative feedback of cortisol?

A

HPA: will receive negative feedback when cortisol is increased.

HPA: releases CRH ->acts on pituitary -> releases ACTH this acts on fasciculata -> this releases cortisol

46
Q

Function of cortisol?

A
  • stimulates glucose production by the liver (gluconeogenesis) (raises blood sugars)
  • promotes protein breakdown
  • mobilization of fatty acids
  • immunologic and antiinflammatory effects: suppresses immune response by reducing humoral and cell-mediated immunity. With pharmacologic doses (as opposed to physiologic doses), blocks inflammation by decreasing capillary permeability and stabilizing lysosomal membranes so inflammatory mediators are not released
  • also blocks release of arachidonic acid which is precursos of prostaglandins and leukotreines

** stress stimulates cortisol

47
Q

Major adverse effects of excess glucocorticoid (cortisol)

A
  • elevated glucose levels (hyperglycemia)
  • suppresses the immune system
  • decreases bone density
  • CNS and mental status effects
  • elevation of blood pressure
  • stimulate gastric acid and pepsin production
  • muscle wasting, psychosis
48
Q

Where does negative feedback from cortisol occur?

A
  • on hypothalamus and the anterior pituitary gland
49
Q

What androgens are produced in the zona reticularis?

A
  • DHEA
  • androstendione
    ** normally have only weak effects, some conversion of these to testosterone in extra-adrenal tissues
    (body hair)
  • have more of an effect on women
50
Q

GFR gets sweeter towards center?

A
  • Glomerulosa = salt (mineralocorticoid)
  • Fasciculata = sugar (glucocorticoid)
  • reticularis = sex (androgens)
51
Q

Where sodium goes water….

A

water follows

52
Q

What would happen with the K level if there is an excessive amount of aldosterone in someone’s system?

A
  • hypokalemia and increased blood pressure because you are retaining more Na -> retaining more water -> increases blood pressure
53
Q

What causes inhibition of ACTH release from the anterior pituitary?

A

increased cortisol

54
Q

Signs of Cushing’s syndrome?

A
  • truncal obesity
  • peripheral wasting, muscle wasting
  • buffalo hump (intrascapular fat accumulation)
  • moon facies
  • dark purple striae
  • easy bruising
  • altered Ca
  • increased gastric acid secretion
  • increase in androgens: extra body hair, acne
  • decreased bone density
  • HTN
55
Q

Difference b/t Cushing’s syndrome and disease?

A
  • syndrome: too much cortisol, from any cause

- disease: specific ACTH secreting tumor: pituitary tumor

56
Q

What is an etopic form of cushing’s?

A
  • small cell carcinoma of lung that likes to secrete ACTH
57
Q

What labs would you see in Cushing’s disease?

A
  • low serum K
  • high fasting glucose
  • increased 24 hr free cortisol
  • serum ACTH will be elevated
58
Q

What is cushing’s syndrome?

A
  • the signs and sxs that result from prolonged exposure to excessive glucocorticoid hormones and can be caused by number of etiologies
59
Q

Endogenous ACTH dependent cushing’s syndrome? (pituitary)

A
  • Cushing’s disease: excessive production of ACTH from a pituitary gland tumor
60
Q

Endogenous ACTH independent Cushing’s?

A
  • adrenal adenomas, and adrenal carcinomas
61
Q

Exogenous cause of cushing’s syndrome?

A
  • excessive steroid administration (such as tx RA or SLE, or COPD)
  • most common cause of cushing’s syndrome
62
Q

What will 75% of pt’s with cushings also present with?

A
  • diabetes
63
Q

What does it mean if ACTH is elevated?

A
  • means that cause of Cushings is ACTH dependent, it has to involve the pituitary gland and elevated cortisol levels should inhibit the anterior pituitary gland from secreting more ACTH if it was a healthy pituitary gland
  • since it is ACTH dependent caused by problem with pituitary-> cushing’s disease
64
Q

What does an elevated 24 hr cortisol level mean?

A
  • confirms that it is at least cushings syndrome if not cushing’s disease
65
Q

Endogenous ACTH dependent ectopic source of ACTH?

A
  • usually from small cell lung cancer

- or from other malignant tissue

66
Q

Will the hypothalamus and the anterior pituitary be inhibited in ACTH independent Cushing’s syndrome if disease in adrenal cortex?

A
  • Yes, adrenal cortex is source of disease so it is producing excess cortisol which will greatly inhibit both the hypothalamus and the anterior pituitary gland.
  • ACTH will become undetectable because of inhibition
67
Q

Will an exogenous source of excess cortisol inhibit anterior pituitary and hypothalamus?

A
  • yes, both will be greatly inhibited

- ACTH will become undetectable

68
Q

Will there be detectable ACTH levels from an ectopic source?

A
  • yes even though both anterior pituitary and hypothalamus are inhibited the ectopic source is producing ACTH so there will be an increased amount of ACTH levels found -> which creates excess cortisol
69
Q

WHen is cushing’s syndrome most likely seen?

A
  • from exogenous administration of glucocorticoids
70
Q

What makes up most of endogenous causes of Cushing’s syndrome?

A
  • ACTH dependent account for 85% of cases
  • Cushing disease accounts for 80% of ACTH dependent Cushing’s syndrome
  • ectopic source of ACTH most commonly seen in pts with small cell lung carcinoma (pts usually older, hx of smoking, and present primarily with signs and sxs of lung cancer rather than Cushing sydrome)
71
Q

Female to male ratio for noncancerous forms of cushing’s syndrome?

A
  • 4:1
72
Q

What does a 24-hour urinary cortisol lab tell us?

- techniques?

A

it provides the most direct and reliable practical index of cortisol secretion (sensitivity and specificity both exceed 95-98%)

  • this should be performed in a nonstressful outpt setting (otherwise you may have false negative or false positive results)
  • 24 hour collection technique includes: urine creatine should be measured as well to confirm adequate 24 hour collection

** doing 24 hr collection b/c cortisol has diurnal variation (more in the morning)

73
Q

What should be done if there is an elevated urinary cortisol?

A
  • this just tells us that the pt has steroid excess.
  • may want to also get plasma ACTH (recommended measurement b/t midnight and 2 am)
  • also abdominal CT scan (adrenal masses?)
  • MRI of sella for pituitary tumor
74
Q

What is a dexamethasone suppression test?

A
  • give 1 mg of dexamethasone (a steroid) orally in evening
  • test serum cortisol at 8 next morning
  • this should suppress the HPA axis in normal physiology
  • but if cortisol is still elevated then this tells us that it is coming from ectopic source -> because it isn’t regulated like pituitary gland
75
Q

What are the 2 forms of adrenal insufficiency?

A
  • primary adrenal insufficiency (Addison’s disease) -> this results from destruction or dysfunction of the adrenal cortex
  • secondary adrenal insufficiency: results from inadequate stimulation of adrenal cortex by ACTH
  • tertiary: lack of CRH from hypothalamus
76
Q

Pathophysiology of adrenal insufficiency?

A
  • most commonly primary adrenal insufficiency results from autoimmune destruction of adrenal glands (addison’s disease)
  • both glucocorticoid and mmineralocorticoid secretion diminished in this condition
  • if untx may be fatal
  • adrenal medulla fxn usually spared
  • secondary adrenal insufficiency: usually occurs after discontinuation of exogenous steroids after prolonged suppression of HPA axis
77
Q

How much of the adrenals have to be dysfunctioning to have adrenal insufficiency?

A

90% of adrenals have to be gone before you notice insufficiency

78
Q

Clinical presentation of adrenal insufficiency?

A
  • hypotension
  • wt loss
  • increasing fatigue
  • vomiting
  • diarrhea
  • anorexia
  • muscle and joint pain
  • postural dizziness
79
Q

What are 2 interesting findings that are only seen in Addison’s disease?

A
  • hyperpigmentation and salt craving
80
Q

What causes the hyperpigmentation in Addison’s disease?

A
  • decreased levels of cortisol means less inhibition of HPA axis. This leads to increased proopiomelanocortin (POMC) synthesis which is precursor for ACTH. This POMC molecule contains melanocyte-stimulating hormone (MSH) fragments.
    Therefore, when POMC levels are increased, so are levels of MSH, which leads to pigmentation of the skin
81
Q

Why do people crave salt with addison’s?

A
  • because the disease is in the adrenal gland - we have low secretion of aldosterone which leads to hyponatremia and salt craving
82
Q

Mechanism of primary adrenal insufficiency?

A

disease is in the adrenal cortex so there is low cortisol secretion and low aldosterone. The low cortisol levels stimulate HPA axis to stimulate more CRH and ACTH but this has no effect on adrenal cortex because of disease
- so ACTH levels will be high
pt will be hypotensive, hyponatremic and hyperkalemic because of low aldosterone, no response to renin levels

83
Q

Mechanism of secondary adrenal insufficiency?

A
  • disease is in HPA axis, not the adrenal cortex so there will be low ACTH (means that there will be no hyper pigmentation), this doesn’t stimulate a lot of cortisol so this tries to stimulate HPA axis which doesn’t work because of diseaes
  • relatively normal aldosterone though becauase adrenal cortex should be functioning (means there is no salt craving)
84
Q

AM cortisol level meaning?

A
  • low plasma cortisol (20g/dL) strong evidence against dx of adrenal insufficiency
  • If in b/t numbers in pt with characteristic signs and sxs -> do a ACTH (cosyntropin) stimulation test, this will tell us if adrenals are responding or not to the ACTH
85
Q

ACTH (cosyntropin) test?

A
  • plasma cortisol measured
  • IV admin. of 250 ug of ACTH
  • in 30-60 minutes measure cortisol again
  • if ACTH is increased then it is an adrenal problem but if it is decreased than it is hypothalamus problem
86
Q

How to differentiate b/t primary and secondary adrenal insufficiency with ACTH (cosyntropin) test?

A
  • if plasma ACTH is increased this means its primary adrenal insufficiency
  • if plasma ACTH decreased: secondary adrenal insufficiency (most likely pituitary)
87
Q

Tx of Addison’s disease?

A
  • lifelong replacement of glucocorticoids and mineralocorticoids
  • tx with glucocorticoids should mimic physiology: doses should mimic diurnal surges with larger dose admin. first thing in AM and then smaller dose around 4 pm
  • main problem with tx is overtx of glucocorticoids and undertx of mineralocorticoids
  • tx with mineralocorticoids can be monitored by measuring plasma renin (aim for value of 1-3)
88
Q

Tx of acute adrenal insufficiency (Addisonian crisis)?

A
  • prompt recognition and admin of IV hydrocortisone is lifesaving
  • medical emergency
89
Q

Why would a pt with Cushing’s syndrome have elevated blood pressure?

A

volume retention

90
Q

Why is it impt to educate your patients carefully if they are taking daily steroids for chronic disease processes?

A
  • don’t want them to abruptly stop taking -> beacuse the pituitary won’t be able to produce ACTH, became dependent on exogenous steroids, takes awhile for body to get used to withdrawal of steroids so have to go through dosage reduction with steroids.
91
Q

What are 2 fundamentals of tx for addison’s?

A
  • steroids and aldosterone (be careful about HTN)
92
Q

Prescription corticosteroids: glucocorticoids?

A
  • hydrocortisone (DOC for adrenal insufficiency)
  • prednisone
  • methylprednisolone
  • dexamethasone
93
Q

Prescription corticosteroids: mineralocorticoids?

A
  • fludrocortisone (has potent Na retaining effect -> helps with hypotension but HTN is a SE)
94
Q

When should you up dosage of steroids for person with adrenal insufficiency?

A
  • when pt has infection, trauma, surgery (in stressful situations -> act like adrenal glands)
95
Q

Glucorticoid effects?

A
  • effects are essentially same as seen with endogenous cortisol
  • but antiinflammatory effects primarily come from pharmacologic doses (as opposed to physiologic doses): need high dose Rx for antiinflammatory response
96
Q

Therapeutic uses of glucocortiocoids?

A
  • relief of inflammatory sxs: such as RA, asthma, allergic rhinitis, allergic runs
  • replacement for adrenal insufficiency
  • acceleration of lung maturation
97
Q

Pharmacokinetics of glucocorticoids?

A
  • oral products readily absorbed in GI tract
  • metabolized by liver and products excreted by kidneys
  • several available IV, IM can be used intra-articularly
  • used in inhalation form all the time for asthma
98
Q

AE of glucocorticoids?

A
  • osteoporosis (most common
  • cushingoid appearance (redistribution of body fat, puffy face)
  • hyperglycemia
  • suppresses the immune system
  • CNS and mental status effects
  • elevation of BP
  • stimulate gastric acid and pepsin production
99
Q

What would you recommend to a pt who is on daily oral steroids?

A
  • Ca supplements

- Bisphosphates (Boniva, Fosomax)

100
Q

Mineralocorticoids: Fludrocortisone uses?

A
  • has both glucocorticoid and mineralocorticoid activity
  • most widely used mineralocorticoid
  • used for adrenal insufficiency
  • glucocorticoid amounts are too low to elicit antiinflammatory effects
101
Q

Dosing equivalency of corticosteroids?

A

hydrocortisone: 20
prednisone: 5
methylprednisolone: 4
dexamethasone: 0.75

Endocrinology (22 decks)

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