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Endo/Repro: Week 2 > Rose: Adrenal Pharmacology > Flashcards

Rose: Adrenal Pharmacology Flashcards

1
Q

What is an ACTH stimulation test? What does it tell you?

A

Compares blood cortisol levels before and after 250 micrograms of tetracosactide (synthetic ACTH) (IV) is given.

If cortisol exceeds normal levels (↑ by at least 2x) by 1 hour, then primary adrenal gland fxn = normal

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2
Q

When do you do a long ACTH Stimulation test?

A

if short test reveals that cortisol is abnormal

used to differentiate between primary and secondary adrenal insufficiency

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3
Q

How do you do a long ACTH stimulation test? What does it tell you?

A

1 mg tetracosactide (IV/IM) multiple administrations → blood taken 1, 4, 5, and 24 hrs later

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4
Q

How does a LONG ACTH stimulation test allow you to differentiate between primary and secondary adrenal insufficiency?

A

o In 1- Addison’s Dz → cortisol level is ↓ at all time points

o In 2- corticoadrenal insufficiency (adrenal gland is small but still responsive) → delayed but normal response of ↑ cortisol is seen

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5
Q

What are the 5 steps to establish hypercortisolism and determine the origin of Cushing syndrome?

A
  1. 24 hr urine sample measurement of FREE cortisol
  2. Late night salivary cortisol (>2 tests)
  3. Special populations (prego and epilepsy)
  4. Once hypercorisolism is established a baseline plasma ACTH is obtained
  5. Dexamethosone challenge test
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6
Q

High levels of cortisol in a 24 hr urine sample indicate….

A

Hypercorisolism (overwhelms metabolism conversion to inactive cortisone)

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7
Q

Late night salivary cortisol tests that show a LOSS of circadian rhythm and ABSENCE of late night nadir are indicative of…

A

CUshings syndrome

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8
Q

What should you not use to test a pregnant women that you suspect may have hypercortisolism?

A

Urine sample–urine tends to be FREE of cortisol

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9
Q

What test should not be used in epileptics in that you suspect have hypercortisolism?

A

dex text (antiepileptic drugs ENHANCE dex clearance)

Use urine or salivary cortisol

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10
Q

Once hypercortisolism is established a baseline ACTH is obtained. What is hte difference between a high and low level?

A

LOW ACTH> ACTH indep disease

HIGH ACTH> ACTH dep disease

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11
Q

What is the gold standard screening test for hypercortisolism?

A

A. Low Dose Dex Test: 1 mg dexamethasone test overnight or 48 h 2 mg/d dexamethasone test

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12
Q

How do you interpret a low dose dex test?

A

o If blood levels of cortisol are lower than normal (post-test) → Cushing Syndrome can be ruled out

o If blood levels of cortisol are NOT lower than normal (post-test) → fail test

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13
Q

How does estrogen affect dex drug clearance?

A

Estrogen ↑ the cortisol-binding globulin (CBG)
→ result in false positive rates with dex test

(estrogen containing drugs like OCPs should be stopped 6 weeks before test)

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14
Q

How do antiepileptics affect dex drug clearance?

A

(phenytoin, carbamazepine, and EtOH)

→ induce hepatic enzymatic clearance of dexamethasone

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15
Q

How does liver disease affect dex drug clearance?

A

DECREASES clearance of dex

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16
Q

What test is used to distinguish Cushing pituitary ACTH secreting tumor from ectopic cells?

A

High Dose Dex Text

pituitary ACTH secreting tumor will show ↓ to dexamethasone in cortisol

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17
Q

What will Cushing syndrome caused by an adrenal tumor show on a dex test?

A
  • Low dose test: no change
  • ACTH level: low

In most cases, the high dose test is not needed

18
Q

What will Dex tests show in a pt with Cushing Syndrome related to ectopic ACTH producing tumor?

A

Low dose test: no change

ACTH level: high

High-dose test: no change

19
Q

What will dex tests show in a pt with CS cuased by a pituitary tumor (Cushing disease)?

A

Low dose test: no change

High dose test: normal suppression (if there is no suppression → another test is needed)

20
Q

How do glucocorticoids affect the CVS?

A
  • Positive inotropic effect (↑ strength of muscular contraction)
  • Na+/H2O retention → ↑ BP
  • Maintains the sensitivity of small vessels to catecholamines → retains tone and BP
21
Q

How do glucocorticoids affect the CNS?

A
  • ↓ seizure threshold

* Behavioral Δs: mood depression/elevation (common), euphoria and restlessness (some), anxiety and psychosis (possible)

22
Q

How do glucocorticoids affect the GI System?

A
  • ↑ gastric acid and pepsin
  • may suppress the local immune response against H. pylori → ulcer formation
  • ↓ Ca++ absorption from the gut
23
Q

How do glucocorticoids affect bone metabolism?

A
  • direct inhibition of osteoblasts
  • 2o stimulation of parathyroid hormone → stimulates osteoclasts
  • Net absorption of bone matrix
24
Q

How do glucocorticoids cause skeletal muscle wekaness and fatigue?

A
  • Hypokalemia
  • Muscle wasting – loss of protein
  • May result in a greater disability than the original inflammation
25
Q

What are the hematologic effects of glucocorticoids?

A
  • Lymphocyte levels ↓ → ↑ susceptibility to infection
  • Eosinophil and basophil levels ↓
  • Neutrophil and erythrocyte levels ↑
  • Inhibits leukocyte extravsation
26
Q

Why are glucocorticoids often used to treat non-adrenal disorders?

A

o ↓ in AA metabolites
o ↓ in peripheral LEUKOCYTE and tissue MPHAGE concentration → ↓ immune factor production of interleukins, TNF, and platelet activating factor
o ↓ EDEMA
o lysosomal membranes stabilized → proteases not released → less FIBROSIS
o ↓ in release of VASOACTIVE FACTORS that promote vasodilation and shock
o maximal effect is 6 hr after treatment and completely cleared by 24 h

27
Q

What is the role of glucocorticoids in organ transplants?

A

inflammation occurs at boundary of donated tissue>
glucocorticoids acts as an immunosuppressant>
decreases action of IMMUNE FACTORS>
INHIBITS Ag release from grafted donor tissue

Downside is that it increases suscpetibility to infection

28
Q

Why do glucocorticoids have anti-allergic effects?

A

Inhibit synthesis of histamine by mast cells → limits duration of an allergic attack

There is NO effect at the histamine receptor or with the action of released histamine

29
Q

Why are synthetic glucocorticoids better than natural?

A

↑ glucocorticoid POTENCY (ratio of glucocorticoid to mineralocorticoid effect)

synthetics are LESS protein bound

SLOWER metabolism

30
Q

Synthetic glucocorticoids often have many biochemical substitutions. What side chains are added on to enhance potency?

A
  • C1-C2 double bond
  • Methyl or fluoride at C6 or fluoride at C9
  • Hydroxyl group rather than a keto group at C11
  • Alpha-methyl or beta-hydroxy at C16
31
Q

What converts inactive prednisone to prednisolone?

A

Liver 11b-hydroxydehydrogenases

**if liver fxn is BAD avoid giving inactive form

32
Q

What is iatrogenic cushing syndrome?

A

effects of long-term, high-dose glucocorticoid therapy (>2 wks)

33
Q

What are SE of glucocorticoid treatments?

A
  • Hyperglycemia, glucosuria (insulin)
  • Infection
  • Peptic ulcer (Tx or DC)
  • Myopathy (DC)
  • Osteoporosis
  • Behavioral disturbances
  • Cataracts (↑ risk for kids)
  • Mineralcorticoid effect (Na+/H2O retention and K+ loss)
34
Q

How must ACTH analogs be given? What is their t1/2? What must they be hydrolyzed by to be active?

A

injected

10-15 mins

blood and tissue enzymes

35
Q

What are ACTH analgos used for?

A

• Distinguishes 1o and 2o adrenal insufficiency
• Anticonvulsant for infantile spasms
• Prevent neurotoxicity with cisplatin
o Prevention of adrenal atrophy during chronic glucocorticoid therapy – not useful
• Toxicity related to increase glucocorticoids

36
Q

What are ACTH analogs NOT used for?

A

Not used to increase adrenocorticoid levels for therapeutic benefits
o Replacement – not realistic
o Prevention of adrenal atrophy during chronic glucocorticoid therapy – not useful

37
Q

What is the treatment for Cushing Syndrome?

A

1) Surgery w/ support of glucocorticoids until recovery of ACTH function
2) Irradiation for those that are poor surgical candidates
3) Medical treatment for those who fail surgical treatment or are ineligible

38
Q

What does ketoconazole do? SE?

A

inhibits side chain cleavage and other CYP enzymes → blocks glucocorticoid and androgen synthesis

(SE: hepatotoxicity)

39
Q

What does metyrapone do?

A

inhibits 11b-hydroxylase in the adrenal gland with the goal of interfering with cortisol production

40
Q

What meds are used to suppress ACTH from pituitary adenomas?

A

SST analog: pasireotide

D2 analog: cabergoline

41
Q

When is Mifepristone used?

A

Pts w/ inoperable disease

42
Q

What is mifepristone?

A

Glucocorticoid receptor antagonist

synthetic steroid w/ a high affinity for progesterone receptors but at higher doses binds strongly to glucocorticoid receptors

Endo/Repro: Week 2 (11 decks)

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