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PHAR253 > Cushings and Addisons > Flashcards

Cushings and Addisons Flashcards

1
Q

What is the role of the adrenal glands?

A

produce hormones that react to stressors
regulate metabolism of fats, proteins, CHO
regulate BP and BG
help control kidney function
two major hormones produced: cortisol and aldosterone

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2
Q

Describe the release of aldosterone.

A

the major mineralocorticoid secreted by the adrenals
secretion mainly controlled by RAAS; less so by potassium, then ACTH
-release stimulation: low bp, low Na, CNS excitation

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3
Q

What are the actions of aldosterone?

A

maintains electrolyte (K, Mg, Na) and volume homeostasis
increases Na & H2O retention and K excretion
=expanded plasma volume, elevated BP, hypokalemia

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4
Q

What is the secondary site for androgen synthesis? Describe androgen synthesis at this secondary site.

A

adrenal cortex
-primary site is testes and ovaries
-primarily DHEA
-release increased with puberty, decreased with aging

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5
Q

What is the role of androgens?

A

helps with bone density
sexual desire and function
sex and body maturation

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6
Q

What is Cushing’s Syndrome?

A

disorder caused by persistent exposure to excessive glucocorticoids (exogenous or endogenous)
-primarily a result of exogenous use
-women>men

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7
Q

What is the etiology of Cushings?

A

ACTH dependent
-benign pituitary tumor over-producing ACTH (Cushings Disease)
-ectopic ACTH source (non-pituitary tumor)
ACTH independent
-adrenal gland tumors
exogenous administration of corticosteroids

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8
Q

True or false: the diagnosis of Cushings is often relatively quick due to the obscure symptoms

A

false
difficult and delayed because it mimics other conditions

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9
Q

What are the signs and symptoms of Cushings?

A

emotional disturbance
moon face
osteoporosis
hypertension
buffalo hump
abdominal obesity
thin, wrinkled skin
striae
muscle weakness
poor wound healing
decreased libido

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10
Q

What are the signs of Cushings that could help distinguish from obesity?

A

protein wasting
-thin skin
-muscle weakness
-bruising
suddenly appearing red striae
children: decreased linear growth

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11
Q

What are the treatment goals of Cushings?

A

remove the source of hypercortisolism
restore cortisol secretion to normal
reverse clinical features
prevent dependency on medications
with appropriate treatment, most signs and symptoms will resolve within 2-12 months

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12
Q

What are the treatment options for Cushings? (non-drug)

A

pituitary adenoma
-surgical resection
adrenal tumors
-surgical resection (radiation or chemo if theres metastases)
ectopic ACTH syndrome
-often multiple tumors, some are cured and some require medication
drug induced Cushings
-removal of the cause

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13
Q

What are the options when a transsphenoidal resection does not cure Cushings?

A

repeat the transsphenoidal surgery
medication therapy
radiation therapy
bilateral adrenalectomy

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14
Q

When is pharmacologic therapy initiated for Cushings?

A

when surgical removal of the tumor cannot be done or is ineffective
-to decrease cortisol levels pre-surgery
-treat severe symptoms
-adjunct treatment after unsuccessful surgery
-non resectable tumors

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15
Q

What are the pharmacologic options for Cushings?

A

steroidogenesis inhibitors
-ketoconazole
-metyrapone
-mitotane
inhibitors of ACTH secretion
-pasireotide

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16
Q

What is the MOA of ketoconazole for Cushings?

A

blocks synthesis of cortisol in adrenal gland via inhibition of 11 beta and 17 alpha hydroxylase

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17
Q

What is the drug of choice for Cushings?

A

ketoconazole
-effective and adverse effect profile not as bad as others

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18
Q

What is the dose of ketoconazole for Cushings?

A

start low and titrate based on lab results
typical: 200-400mg TID

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19
Q

What are the adverse effects of ketoconazole?

A

GI upset
gynecomastia
increased LFTs
headache
sedation
impotence
decreased libido

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20
Q

What are the drug interactions of ketoconazole?

A

many: 1A2, 2C9, 3A4
-CCBs
-grapefruit juice
-cyclosporine
-carbamazepine
-warfarin
-PPIs
-benzodiazepines
-aminoglycosides

21
Q

What is the MOA of metyrapone?

A

inhibits the enzyme 11 B-hydroxylase (cortisol pathway)

22
Q

What are the uses of metyrapone?

A

experiencing dose-limiting AEs with ketoconazole
adjunct therapy
diagnostic agent

23
Q

What are the adverse effects of metyrapone?

A

androgenic AEs (hirsutism and acne)
NV
abdominal discomfort
headache
dizziness
allergic rash

24
Q

What is the dose of metyrapone for Cushings?

A

wide range

25
Q

What is the MOA of mitotane?

A

decrease the synthesis of cortisol by inhibiting the hydroxylation of 11-desoxycortsiol and 11-desoxycorticosterone

26
Q

What is the indication of mitotane?

A

inoperable adrenal carcinoma
-in combination with irradiation, other steroidogenic inhibitors

27
Q

Where is mitotane used and why?

A

hospital
-greatly decreases cortisol synthesis
-adverse effects

28
Q

What are the adverse effects of mitotane?

A

GI: anorexia, NVD
depression, lethargy, somnolence
hypercholesterolemia, rash, hepatoxicity

29
Q

Are steroidogenic inhibitors effective as monotherapy long term?

A

not usually
often combined with one another if not providing adequate response on their own

30
Q

What is the MOA of pasireotide?

A

binds to somatostatin receptors
=inhibition of ACTH secretion in ACTH-producing adenomas

31
Q

What is the indication of pasireotide?

A

surgery not an option or failure of surgery

32
Q

What is the dosing of pasireotide?

A

0.6-0.9mg BID subq injection

33
Q

What are the side effects of pasireotide?

A

hepatotoxicity
CV events (bradycardia, QT)
hyperglycemia
gall-bladder events

34
Q

What are the drug interactions of pasireotide?

A

antiarrythmics
drugs that prolong QT interval

35
Q

What is Addisons disease?

A

primary adrenal insufficiency
-adrenal glands cannot synthesize enough glucocorticoids and mineralocorticoids
-destruction of all 3 zones of the adrenal glands (sx when >90% destroyed)

36
Q

What is the cause of Addisons?

A

autoimmune-mediated destruction
-most common in Western world
infectious diseases: TB, CMV, HIV, fungal
-more common in other parts of world
tumors
hemmorrhage
injury to adrenal glands

37
Q

What is the cause of secondary adrenal insufficiency?

A

most commonly in those taking chronic corticosteroids
-symptoms due to abrupt withdrawal of corticosteroids
other causes: tumors, surgical removal of pituitary, meds

38
Q

What are the signs and symptoms of Addisons?

A

glucocorticoid deficiency:
-fatigue
-weight loss
-loss of appetite
-N, V, abdominal pain
-muscle/joint pain
-hypotension
-depression
mineralocorticoid deficiency:
-dehydration
-hypotension
other:
-skin hyperpigmentation
-salt craving
-dry/itchy skin
-decrease axillary/pubic hair
-decreased libido

39
Q

What are the lab results for someone with Addisons?

A

hyponatremia
hyperkalemia
anemia
hypoglycemia

40
Q

Where is hyperpigmentation most prevalent for an Addisons patient?

A

sun-exposed areas
knuckles
elbows
knees
mucous membranes

41
Q

What is the treatment of chronic adrenal insufficiency?

A

glucocorticoids
-DOC: hydrocortisone*, cortisone, prednisone, dexamethasone
-HC: 15-30mg/d
-cortisone: 20-35mg
-dose adjustments based on pt well being, BP, weight
mineralocorticoids
-fludricortisone 0.05mg-0.1mg qd
-titrate based on BP, K, and Na

42
Q

How frequently are glucocorticoids dosed in Addisons?

A

BID-TID with majority of dose in AM

43
Q

What might be the stress dosing of an Addisons patient during strenous exercise? What about illness or trauma?

A

add 5-10mg HC
double dose until recovery

44
Q

What might be a third therapy a woman with Addisons may require?

A

DHEA 25-50mg/d if low libido is present
-adrenals are primary source of androgens in women

45
Q

What are the adverse effects of DHEA?

A

sweat odour
acne
hirsutism
itchy scalp

46
Q

What is the main cause of an acute adrenal crisis? What are some symptoms?

A

abrupt steroid withdrawal or lack of stress dosing (medical emergency)
sx: tachycardia, NV, fever, hypotension, dehydration, hypoglycemia

47
Q

What is the treatment of acute adrenal crisis?

A

IV glucocorticoids
-HC is DOC (combined gluco and mineralo activity)
fluid replacement to support bp
fludricortisone when pt can eat/drink and HC dose is decreased

48
Q

Which steroidogenesis inhibitor may require concomitant administration of glucocorticoids?

A

mitotane
-greatly decreases cortisol lvls

49
Q

What causes skin hyperpigmentation in Addisons?

A

high levels of ACTH binding to melanocortin 1 receptor on dermal melanocytes

PHAR253 (16 decks)

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