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Endo/Repro Block1 > Adrenal Pharm [TRH] > Flashcards

Adrenal Pharm [TRH] Flashcards

1
Q

How helpful are basal cortisol levels as Diagnostic tools?

A

not very…they oscillate w/ACTH levels

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2
Q

What is the Short ACTH stimulation test?

A

tests if the adrenal gland is functioning! [if yes, stop test]

  • compares cortisol levels b4 & after 250 mcg of tetracosactide [synthetic ACTH]
  • if 1 hr later: cortisol is 2x > normal = normal 1’ adrenal fxning
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3
Q

What is the Long ACTH stimulation test?

A

if short test is abnormal

  • possible that hypopituitarism = hypofxn but still responds to cortisol
  • used to differentiate b/w 1’ & 2’ adrenal insufficiency
  • 1 mg tetracosactide multiple administrations & measure blood at 1, 4, 8, & 24 hours later
    • in 1’ addison’s= cortisol low @ all times
    • 2’ corticoadrenal insufficiency [small adrenal but still responds (just delayed)] = eventually cortisol ^^
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4
Q

After a long ACTH stimulation test…

what would a pt with addison’s test results be?

a pt w/ 2’ corticoadrenal insufficiency’s results?

A
  • in 1’ addison’s= cortisol low @ all times
  • 2’ corticoadrenal insufficiency [small adrenal but still responds (just delayed)] = eventually cortisol ^^
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5
Q

What does a 24hr Urine cortisol measure?

-what Dx can it confirm?

A

free cortisol!!!

  • shouldnt be affected by conditions or medications that alter corticotropin binding protein
    • HIGH LEVELS: confirms hypercortisolism
    • ​11B-hydroxylase2 is overwhelmed & thus inactivation of cortisol–> cortisone doesnt happen

**need to have similar results >2 times? or in correlation w/ other Dx tests?

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6
Q

What does a late night salivary cortisol test tell us?

A

shows loss of circadian rhythm & absence of late night nadir

= indicates cushings syn!!

***also need 2+ tests of this

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7
Q

What tests can you do on pregnant ppl?

Which tests can be used on epileptics?

A

prego: urine free cortisol

epileptics: NOT dexamethasone [antiepileptic drugs ^^dexaM clearance]

  • use urine or salivary cortisol tests
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8
Q

What should you do once hypercortisolism has been established?

A

Do a baseline ACTH level!

  • LOW: ACTH independent disease
  • HIGH: ACTH dependent
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9
Q

What is a LOW dose Dexamethasone Challenge Test?

-

A

1mg DEX test or 2 mg/day over 48 hrs

  • GOLD STANDARD screening test for cushings
    • if blood cortisol > normal after test = failure to suppress [ACTH] cortisol w/ DEX –> ^^cushings suspicion
    • abnormal test should be followed up with a High dose DEX test
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10
Q

What is the high test DEX test?

A

give 8 mg DEX overnight

  • even pit. ACTH secreting tumor will show a decrease in cortisol prodxn with this high dose
  • distinguishes pit. ACTH secreting tumor CUshings from ectopic cells
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11
Q

How do we interpret the following results:

  • low dose DEX= no change in cortisol levels
  • ACTH level= low
A

Cushings caused by an adrenal tumor

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12
Q

How do we interpret the following tests:

  • low dose DEX test: no change [cortisol still ^^]
  • ACTH= high
  • High dose DEX= no change [cortisol still ^^]
A

Cushings related to ectopic tumor/cells secreting ACTH

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13
Q

How do we interpret these labs:

  • low dose DEX: no change [cortisol still ^^]
  • high dose DEX: normal suppression [cortisol decreases]
A

Cushings Syndrome caused by a pituitary tumor aka Cushings DIsease

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14
Q

What test do we use if Cushings Syndrome has already been Dx’d?

A

CRF/H stimulation test:

  • distinguishes Cushings disease [pit. origin] from ectopic ACTH-secreting tumors
    • pit tumors are responsive to CRH= ACTH/cortisol^^
      • >2.5x^^ in ACTH = cushings
    • ectopic tumors & adrenal tumors show NO response
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15
Q

How do glucoC’s effect the CV system?

A
  • positive inotropic effect
  • ^^BP [Na/h20 retention]
    • maintains sensitivity of small BV’s to catecholamines in order to retain tone & BP
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16
Q

How do glucoC’s effect the CNS?

A
  • lower seizure threshold [^^risk of seizure]
  • behavioral changes: mood depression/^^ is MC, euphoria, restlessness, anxiety & psychosis possible
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17
Q

How do glucoC’s effect the GI system?

A
  • increase gastric acid & pepsin
  • may suppress local immune response against h. pylori –> ulcer formation
  • decreased Ca++ absorption from the gut
18
Q

How do glucoC’s effect bone metabolism?

A
  • direct inhibition of osteoblasts
  • 2’ stimulation of PTH which stimul8s osteoclasts
  • net absorption of bone matrix ==> osteoporosis [long use]
19
Q

How do glucoC’s effect the M.Sk. system?

A
  • hypoK+
  • muscle wasting –> loss of protein
  • may result in greater disability than original inflammation?
20
Q

How do glucoC’s effect hematology aspects?

A
  • lympho’s decrease–> ^^ susceptibility to infxn
    • T cells decrease more than B cells
  • eos & baso-phils decrease
  • neutros & erythrocyte levels ^^
  • inhibits leukocyte extravasation
21
Q

What are the 3 main therapeutic effects of glucoC medication?

A
  1. anti-inflammatory
  2. immunosuppressant
  3. anti-allergic
22
Q

How are the anti-inflammatory effects of glucoC medication potentiated?

A
  • ArachA metabolites decrease–> COX2 express decrease
  • decrease in peripheral leuko & tissue mac [] –> depression of immune factor prodxn such as:
    • platelet activating factor, TNF, interleukins
  • reduce edema [leukos only allowed to extravasate to injured tissue] = cap wall integrity maintained
  • lysosomal membranes stabilized so proteases not released = less fibrosis [tissue break down and scarring]
  • reduce vasoactive factor release promoting vasoD & shock
  • max effect 6 hrs after Tx, gone after 24hrs
23
Q

HOw are the immunosuppressant effects of glucoC’s potentiated?

A
  • inflammation occurs @ boundary of donated tissue
  • inhibit the axn of immune factors
  • Ag release 4m grafted/donor tissue may be inhibited

–can result in increased susceptibility to infxn

24
Q

HOw are the anti-allergic effects of glucoC’s potentiated?

A
  • inhibits mast cell synthesis of Histamine–> limits allergic attack duration
  • NO affect on HistamineR or axn of already released Histamine
25
Q

Compare the activities of natural and synthetic glucoC’s!

A

synthetic > natural

  • ^^glucoC potency
  • synthetics are less bound to protein
  • synthetic glucoC metabolism is slower

**DEX & betamethasone have the highest activity of glucoC’s [administered in a way other than inhalation; beclometasone is inhaled and is higher]

26
Q

What is the difference between active and inactive synthetic glucoC’s?

A

active: reduced

  • prednisolone [synthetic], cortisol [natural]

inactive: oxidized

  • prednisone [synthetic], cortisone [natural]
    • also use 11Bhydroxylases to activate these
27
Q

in which pt’s should inactive preparations of glucoC’s be avoided?

A

pt’s w/ substandard liver fxns

[don’t give them prednisone]

28
Q

Which glucoC should you use in instances of substitution/replacement Tx of adrenal insufficiency?

A

When in doubt guess CORTISOL

  • its active already, & shortacting?
  • sometimes give fldrocortisone too
29
Q

What are some considerations with glucoC medication use that we should keep in mind?

A
  • can be toxic
  • dose is determined by trial and error for many inflam. conditions
  • high single doses can be used acutely
  • steroid w/drawal can happen after chronic admin is stopped
30
Q

What are glucoC toxicities associated with?

A

Acute adrenal insufficiency:

  • induced by rapid w/drawal after prolonged exogenous prep use
  • chronic Tx = adrenal gland shrinkage
  • in stressful times: pts may need supplementary Tx’s [2x dose in minor ones, 10x dose in major like accident/surgery]

iatrogenic Cushings Syn

  • effect of long term, hi-dose glucoC Tx [>2wks]
31
Q

SE’s of glucoC Tx’s

A
  • HYPERglycemia, glucosuria
    • may need insulin
  • Infxn
  • peptic ulcer- might have to discontinue steroids
  • Myopathy- discontinue
  • osteoporosis
  • cataracts
  • behavior changes
  • mineralcoricoid effect:
    • Na/H2o retention & K+ loss
32
Q

How does licorice affect glucoC’s?

A

licorice augments cortisol effect

  • licorice slows conversion of cortisol to cortisone
    • by reducing # of 11Bhydrox2
33
Q

What are the pharmokinetcis of ACTH [medication]?

A
  • t1/2= 10-15mins
  • injected only
  • hydrolyzed by blood & tissue enzymes mostly
34
Q

What can we use ACTH as a drug for?

A
  • distinguishes 1’ from 2’ adrenal insufficiency
  • anticonvulsant for infant spasms
  • prevent neurotoxicity with cisplatin
  • NOT used to ^^adrenoC levels for therapeutic benefits
    • replacement= unrealistic
    • prevention of adrenal atrophy during glucoC Tx= not useful
  • toxicity related to ^^glucoC’s
35
Q

What is the general hierarchy/standard of care approach to Tx’ing Cushings?

A
  1. Surgery, w/ glucoC until recovery of ACTH fxn
  2. Irradiation: for poor surgical candidates
  3. Medical Tx for those who fail surgery or are uneligible
36
Q

What are the 3 goals/methods of medical Tx of Cushings?

A
  1. inhibit adrenal steroidgenesis
    • ketoconazole, metyrapone, etomidate, & mitotan [for cancer pts]
  2. suppress ACT
    • pasireotide, cabergoline
  3. glucoC R antagonists
    • mifepristone
37
Q

Whate drugs used in the Tx of Cushings Disease are enzyme inhibitors of steroidogenesis?

[MEAK]

A

Ketoconazole: inhibits side-chain cleavage & other cyp’s

  • antifungal azole ==>inhibit fungal cyp
  • hepatotoxic

Aminoglutethimide: inhibits side chain cleavage enzyme

Etomidate: inhibits 11B-hydroxylase

Metyrapone: inhibits 11B-hydroxylase in adrenal w/ goal of interfering w/ cortisol prodxn

  • may be used while waiting for definitive Dx
38
Q

What medications are used for pituitary adenomas causing Cushings disease?

A

problem is with overproduction of ACTH in pituitary–>^^cortisol

  • pit adenomas usually have SS and D2 R’s
    • SS analog = paireotide
    • D2 analog= cabergoline
  • **D & SS inhibit release of H from pit **[normally just GH but maybe work for other H’s??]
39
Q

When would we use Mifepristone on a Cushings pt?

A

Mifeprostone= glucoC R antagonist

  • used for pt’s w/ inoperable disease
    • usually ectopic ACTH secreting tumors w/ failed other Tx’s
  • synthetic steroid w/ hi affinity for progesterone R’s that acts as an anti-progestin
  • @ hi doses it binds strongly to glucoC R’s and to lesser extent–>androgen R’s
40
Q

what is mitotane?

A

a DDT class of insecticide w/ non-selective adrenal toxicity–> adrenal carcinoma

41
Q
A

Endo/Repro Block1 (11 decks)

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