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Cushings/adrenal insufficiency Flashcards

1
Q

know the top two zones and their hormones.

A
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2
Q

Hypothalamic-pituitary-adrenal (HPA)axis

A

Hypothalamussecretes CRH →releaseof ACTH from the anteriorpituitary gland

ACTH release:
Like CRH, therelease of ACTH follows the circadian rhythm
Increased in the early morning hours (before awakening), with peak levels in the morning (~8:00 a.m.) and ↓ in the evening

Adrenal gland (cortex):
ACTH mainly stimulates thezona fasciculata (cortisol) andzona reticularis (androgens)
Zona glomerulosa (aldosterone) is primarily regulated by the renin-angiotensin system andpotassium levels

peaks in the morning, peaks off during day

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3
Q

Cushing Syndrome

general

A

umbrella term

Constellation of clinical abnormalities caused by chronic high blood levels of cortisol

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4
Q

cushing syndrome

Primary hypercortisolism

A

↑Production of glucocorticoids by adrenal glands (tumor - adrenal adenoma or adrenal carcinoma)

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5
Q

Cushing syndrome

Secondary hypercortisolism

A

Cushing’s disease – a subtype of Cushing Syndrome
↑Pituitary ACTH production leading to adrenal glandhyperplasia (most likely due to a pituitary adenoma)

Ectopic ACTH syndrome
↑ ACTH production outside the pituitary andadrenal glands (paraneoplastic syndromes – small cell lung cancer)

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6
Q

Exogenous Cushing syndrome

general

A

Most common form of hypercortisolism

Medical use ofglucocorticoids
Exogenous cortisol causes negative feedback at the level of the hypothalamus and anterior pituitary → (decreased CRH and ACTH)

Long-term exogenous glucocorticoid use
Cortisol will not be released by the body
Atrophy of the zona fasciculata

Abrupt discontinuation of exogenous glucocorticoid use
Body cannot produce enough cortisol and adrenal insufficiency will occur → adrenal crisis

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7
Q
A

ACTH-dependent means the body makes too much ACTH which in turn increases the production of cortisol
ACTH-independent means the adrenal glands produce cortisol without stimulation from ACTH

ACTH-dependent causes account for 80% of cases
ACTH-independent causes account for 20% of cases

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8
Q
A
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9
Q

cushings syndrome

clin man

A

Moon face
Truncal (central) obesity
Prominent supraclavicular and dorsal cervical fat pads (buffalo hump)
Thin distal extremities and fingers
Proximal muscle wasting
Weakness
Osteopenia/osteoporosis
Glucose intolerance or diabetes mellitus
Hypertension
Recurrent opportunistic or bacterial infections
Cryptococcus neoformans, Candida species
Easy bruising
Thin and atrophic skin
Facial acne
Poor wound healing
Violaceous striae wider than 1 cm (abdomen)

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10
Q
A
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11
Q

cushings syndrome

24 hour urine

A

Exclude use of exogenous glucocorticoids
24-hour urine for free cortisol level (> 4 times the upper limit of normal)

Serum or saliva cortisol measurement at midnight to assess the normal fall

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12
Q

cushings syndrom

Dexamethasone suppression test

A

1-2 mg of dexamethasone is given orally at 11 p.m. (normally should ↓ ACTH) and serum cortisol is measured at 8 a.m. the next morning (normally should ↓ serum cortisol)
↑ cortisol levels = positive test and further testing is needed

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13
Q

cushings syndrome

Plasma ACTH levels will tell us
Hi

A

Measured to determine the cause of Cushing syndrome
High levels → secondary pituitary (Cushing disease) or ectopic source
Low levels → primary adrenal cause (adenoma, carcinoma, exogenous glucocorticoids)

might need additinal imaging for tumors

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14
Q

cushings syndrome

CRH Stimulation Test

A

For secondary

Patient is given synthetic CRH
No ↑ in ACTH and cortisol – ectopic ACTH secretion → order a CT scan of the chest, abdomen, and pelvis
↑ in ACTH and cortisol – Cushing disease → order an MRI of the brain with contrast

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15
Q

cushings syndrome

Tx

A

Stop exogenous glucocorticoids – gradual withdrawal

Pituitary, adrenal, or ectopic ACTH-producing tumors
Surgical removal
Radiation therapy

Adrenalectomy
Patients will require glucocorticoid replacement therapy

Nonresectable tumors
Glucocorticoid-receptor antagonists
Mifepristone - blocks the effects of cortisol in tissues
Adrenal enzyme inhibitors
Ketoconazole and metopirone - decrease cortisol production
Dopamine agonists
Inhibit ACTH secretion

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16
Q

Pheochromocytoma

general (location ) and Tx

A

Catecholamine-secreting tumor that mimics over-activity of the sympathetic nervous system
Majority of tumors originate in the adrenal medulla (90%)

Treatment:
Surgical resection

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17
Q

Pheochromocytoma

Clin Man

A

Clinical Presentation:
Headache
Sweating
Tachycardia/Palpitations
Hypertension (sustained or paroxysmal) – most common symptom
Elevated metabolic rate
Hyperglycemia
Nervousness

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18
Q
A
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19
Q
A
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20
Q

Adrenal Glands

general

A

Sit at the superior poles of the kidneys

Consists of:
Adrenal medulla and cortex

21
Q

adrenal medulla

A

inner portion
Responds to sympathetic stimulation by secreting catecholamines (epinephrine and norepinephrine)

22
Q

adrenal glands

Adrenal cortex

A

Thicker outer portion
Synthesizes 25 steroid hormones that are collectively known as corticosteroids
Consisting of 3 layers
Zona glomerulosa (outer)
Zona fasciculata (middle)
Zona reticularis (inner)

23
Q

adrenal glands

mineralcorticoids

A

Mineralocorticoids
Secreted by the zona glomerulosa
Control electrolyte balance by acting on the kidneys
Main mineralocorticoid is aldosterone

24
Q

adrenal glands

Glucocorticoids

A

Secreted by the zona fasciculata
Stimulate fat and protein catabolism
Gluconeogenesis (the synthesis of glucose from non-carbohydrate sources) in the liver
Release of fatty acids and glucose into the blood
Help the body adapt to stress
Main glucocorticoid is cortisol

25
Q

adrenal glands

sex hormones

A

Sex steroids
Secreted by the zona reticularis
Androgens and estrogens
Main androgen is dehydroepiandrosterone (DHEA)

26
Q
A
27
Q

adrenals

aldosterone
Wren is it secreted

A

Part of a hormone family with renin and angiotensin
Secreted directly in response to hyperkalemia and via the RAA system in response to low blood volume/low blood pressure

28
Q

Actions of Aldosterone

A

aldosterone acts on collecting ducts and DCTs

29
Q

Adrenal Insufficiency (AI)

general

A

Inadequate production of adrenocortical hormones: glucocorticoids (cortisol), mineralocorticoids (aldosterone), and adrenal androgens

Types of adrenal insufficiency
Primary
Secondary
Tertiary

30
Q

AI

Primary

A

(Addison’s disease)
Dysfunction or destruction of theadrenal cortex

31
Q

AI

secondary

A

Conditions that cause deficiency inpituitary adrenocorticotropic hormone (ACTH)secretion
Most common form

32
Q

AI

Tertiary

A

Conditions that cause deficiency in the hypothalamic secretion ofcorticotropin-releasing hormone (CRH)

33
Q

Primary disease – Addison’s Disease

etiology

A

Autoimmune
Most common cause – 70% of cases
Adrenal cortex is gradually destroyed → loss of mineralocorticoids, glucocorticoids, and adrenal androgen hormone production

Infection (tuberculosis)
Hemorrhage (rupture of the adrenal cortex blood vessels due to ↑ BP leading to tissue ischemia)
Metastatic cancer

34
Q

secondary AI

etiology

A

Hypopituitarism - ↓ ACTH
Pituitarytumors and surgery

35
Q

tertiary AI

etiology

A

Prolonged high-dose glucocorticoid use suppresses thehypothalamus–pituitary–adrenalaxis

Effects of Cushing’s syndrome treatment

36
Q
A
37
Q

AI

hormonal regulation

A

Hypothalamic–pituitary–adrenal (HPA)axis:

Hypothalamus secretes CRH →releaseof ACTH from the anteriorpituitary gland
ACTHrelease:
Like CRH,the releaseis pulsatile, following thecircadian rhythm
↑ in the early morning hours (before awakening), with peak levels in the morning (approximately 8:30 a.m.) and ↓ in the evening

Adrenal gland (cortex):
ACTH mainly stimulates thezona fasciculata (cortisol) andzona reticularis (androgens)
Thezona glomerulosa(aldosterone) is primarily regulated by therenin–angiotensin system andpotassiumlevels

38
Q

Addison’s Disease

Clin man

A

Symptoms relate to the degree of hormonal deficiency – ≥ 90% destruction of adrenal tissue by the time symptoms appear

Hyperpigmentation from ↑ ACTH
Most characteristic symptom

39
Q

addisons

↓ Glucocorticoids Sx

A

Fatigue
Weakness
Weight loss/anorexia
Myalgia/jointpain
Abdominalpain/diarrhea
Hypoglycemia

40
Q

addisons

↓Mineralocorticoids Sx

A

Hypotension, dizziness
Hyperkalemia,hyponatremia (salt craving)
Metabolic acidosis

41
Q

addisons

↓Androgens:

A

↓ Axillary and pubic hair
Loss of libido
Amenorrhea in women

42
Q

AI

Morning serum cortisol test value that suggests Adrenal Insufficiency

A

Morning serum cortisol
Normal: 10–20 µg/dL
↓ serum cortisol levels (≤ 3 µg/dL): strongly suggests AI

43
Q

AI

ACTH levels for primary, secondary, tertiary

A

Obtain baseline level simultaneously with morning cortisol
↑ ACTH: suggests primary AI
↓ or normal ACTH: suggests secondary/tertiary AI

44
Q

AI

High-dose ACTH stimulation test

A

Measure a baseline serum cortisol and plasma ACTH
Administer 250 mcg of cosyntropin (synthetic ACTH) IV or IM

Measure serum cortisol at 30 and 60 minutes
↓ cortisol level; ↑ ACTH = primary adrenal insufficiency
↓ cortisol level; ↓ or low normal ACTH = secondary adrenal insufficiency

45
Q

Addisons

Tx
Glucocorticoid replacement

A

Use the lowest tolerated dose to control symptoms
Oral hydrocortisone in 2-3 divided doses

Stress dosing
Used for illnesses and before surgery
Dose is 3x the maintenance dose x 3 days

46
Q

Addisons

Tx
Mineralocorticoid replacement

A

Fludrocortisone (Florinef)
Mineralocorticoid agonist, but also stimulates glucocorticoid receptors
Increase sodium and water reabsorption
Duration of action 8-12 hours
Side effects: fluid retention, hypertension, edema, hypokalemia, hyperglycemia

46
Q

Adrenal Crisis

general

A

Medical emergency
More likely to occur in primary disease than secondary disease
Usually precipitated by severe stress (infection, trauma, surgery

47
Q

Adrenal crisis

Clin man

A

Profound weakness
Abdominal pain – mimics an abdominal emergency
Hypotension
Orthostasis
Shock
Fever – when precipitated by infection

48
Q

Adrenal crisis

Tx with dosing

A

IV fluid resuscitation
Hydrocortisone phosphate or hydrocortisone sodium 100-300 mg IV over 30 seconds, then 50 mg every 6 hours
Treat any electrolyte imbalances and hypoglycemia
Search for the underlying condition and treat accordingly

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