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Endo/Eye/Derm - Women/Men > EXAM 3 Adrenal Gland disorders Dr. Hess > Flashcards

EXAM 3 Adrenal Gland disorders Dr. Hess Flashcards

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1
Q

Why do Cushings cause diabetes?

A

too much cortisol -> glucose production ->
-> increase in insulin resistnace

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2
Q

What are the 3 adrenal gland produced corticosteroids?

A

-Cortisol (glucocorticoid)
-Aldosterone (mineralcorticoid)
-DHEA (androgen)

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3
Q

Which part of the adrenal gland secretes the corticosteroids?

A

adrenal cortex

(the adrenal medulla secrets catecholamines: NE and epinephrine)

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4
Q

What is the cause of adrenal insufficiency?

A

Addison’s disease
-auto-immune disease
-Effects all regions of the adrenal gland

secondary cause:
-abrupt d/c of exogenous glucocorticoids (meds)

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5
Q

What are the secondary causes of adrenal insufficiency?

A

-abrupt d/c of exogenous glucocorticoids (meds)
-most common cause
-> shuts down the HPA axis

patients may stop due to a stressful event (infection, couldn’t afford the meds, quit due to side effects)
-> risk for adrenal crisis

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6
Q

Which drug may cause adrenal insufficiency?

A

Ketoconazole

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7
Q

Functions of Cortisol

A

Cortisol:
-Regulates metabolism of fat, carbohydrates and
protein

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8
Q

Functions of Aldosterone and its effect in Addison’s disease

A

Maintains electrolyte balance and volume Aldosterone homeostasis (Na+ and fluid retention)

in Addisons’ disease:
-hypotension
-hyperkalemia, hyponatremia

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9
Q

Functions of DHEA and its effect in Addison’s disease

A

converted to testosterone or estradiol – expression
of primary and secondary sex characteristics

-women are more affected bc 25% of their testosterone comes from the adrenal gland vs in men only 5%

-in Addison’s disease: decreased libido and secondary sex characteritiscs

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10
Q

Clinical Presentation in Addison Disease - Symptoms

A

-fatigue, malaise, anorexia, weakness
-postural dizziness, syncope

-GI: N/V, diarrhea, constipation, abdominal pain

-myaglia, arthlagia

-decreased libido, amenorrhea

-> all related to low levels of cortisol, aldosterone, DHEA

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11
Q

Patient presentation

A

Look great feel awful
-thin and tanned

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12
Q

Signs of Addison’s disease

A

-Weight loss
-Hyperpigmentation
-Hypotension
-thinning of axillary and pubic hair
-vitiligo (loss in skin color in patches - no melanocytes due to autoimmune)

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13
Q

What causes hyperpigmentation in Addison’s disease?

A

due to increased ACTH release from the anterior pituitary gland that is upregulated in low cortisol
-> with ACTH the myelocyte-stimulating hormone is expressed

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14
Q

In what pattern is cortisol physiologically released?

A

pulsatile pattern in a circardian rythm

-naturally it is high in the morning
-patients should take it as the first thing in the morning to mimic physiologic release
-highest dose in the morning

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15
Q

What is the drug of choice and the starting dose in Addison’s disease?

A

Hydrocortisone
-starting dose: 15-20 mg per day

may also use: 5mg of prednisone (or equivalent) per day

-using a long-acting steroid (dexamethasone, highly cortical activity) may lead to overtreatment of the cortical compartment
-> leads to diabetes, cataracts, obesity, heart disease???

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16
Q

Which of the glucocorticoids have mineralocorticoid activity?

A

-Cortisone (the inactive form of cortisol) - 2
-Hydrocortisone (binds MR and GR) - 2

-Prednisone (prodrug) - 1
-Prednisolone - 1

1=less MR activity
2= more MR activity

-when dosing, we have to take the MR properties (Na and water retention) and the patient’s BP goal into account !!! (EXAM Q???)

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17
Q

Hypotension and corticostroid dosing

A

-when we dose to get their BP up we might overtreat the cortisol component (GR receptor)

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18
Q

Which of the corticosteroids are short and long-acting?

A

short-acting:
-Cortisone
-Hydrocrtisone

long-acting:
Dexamethasone

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19
Q

Which of the corticosteroids are intermediate acting?

A

-Prednisone (prodrug)
-Prednisolone
-Methylprednisolone

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20
Q

Advantages of the short-acting glucocorticoid steroids

A

-more flexible in making adjustments, since the effect is short
-more mineralocorticoid activity -> BP regulation

BUT effects wears off quickly, so it has to be dose multiple times a day

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21
Q

Advantage of intermediae-acting steroids

A

Prednisone, Prednisolone

-longer-acting -> once daily dosing
-smoother blood levels

BUT it is less adjustable and it may have too much glucocorticoid activity

22
Q

What do dose adjustments for glucocorticoids depend on?

A

Dose adjustments q 6- 8 weeks based on improvement of patient signs and symptoms

23
Q

What are the short-term ADRs?

A

may happen due to overtreatment

-Insomnia/excitability
-Elevated glucose
-GI upset
-Increased appetite/Weight gain

24
Q

What are the long-term ADRs?

A

may happen due to overtreatment

-Diabetes
-HTN
-Osteoporosis
-Cataracts
-Slow wound healing

25
Q

How would the dose of steroids change in stressful events?

A

Exercise (small stress)
- Extra 5mg hydrocortisone?

Sickness or injury (e.g., flu) (moderate stress)
-2-3x the usual GC replacement dose until recovery

Critically ill, Major surgery, Major trauma (High stress)
-Up to 10x usual GC replacement doses

-Refer to ER if vomitin, consider IV

26
Q

Which drug may be used to treat orthostatic hypotension?

A

Fludrocortisone

-> also used for Addison’s disease when we have reached the ideal glucocorticosteroid supplement but not enough mineralcorticoid supplementation

-used in combination with glucocorticoids
-it only has mineralocorticoid activity!!!

27
Q

What are the signs of overtreatment with Fludrocortisone?

A

too much mineralcorticoid activity

-increased BP
-edema
-Hypokalemia

28
Q

When is Androgen replacement therapy considered?

A

after 6 months of cortisol corticosteroid treatment
-fix the cortisol first
-make sure the BP is fine

-treat with DHEA if the patient is still complaining about androgen-related symptoms (decreased libido)

29
Q

What is the drug of choice for Androgen replacement therapy?

A

Dehydroepiandrosterone (DHEA)
-25 – 50mg daily (OTC)
-only for women (since men only produce 5% of androgens from their adrenal gland)

30
Q

Which labs should be monitored for Addison’s disease?

A

-Patient symptoms
-Vitals
-Electrolytes
-Signs/Symptoms of overdosin

-we dont check for ACTH bc

-remember we dose adjust based on patients’ symptoms

31
Q

What is an Acute Adrenal Insufficiency

A

-Addisonian Crisis after abruplty stopping steroid supplement -> HPA axis is not active

-5 S’s
-Steroids IV
-Salt (2-3L of NS or D5NS bolus, bc they are hypotensive)
-Sugar (they may have low blood sugar)
-Support and Search (find the cause)

-> to prevent this we use stress-dosing

32
Q

What is the treatment dose in Addisonian Crisis?

A

-Hydrocortisone 100mg IV bolus q 8 hrs x 24 hrs then 50mg q 6-8 hrs after hemodynamic stability.
-Taper to a maintenance dose after 4 -5 days

-Monitor symptoms, BP, Weight and Electrolytes

33
Q

When should we consider tapering when d/c steroids?

A

Supraphysiologic doses (> 7.5mg/day prednisone or equivalent) in long-term steroid therapy (> 3 weeks)

-there may be different ways (regimen) to taper down

-Taper by 5 – 20% every 1 – 2 weeks
-Increase dose and slow taper for disease
flare

34
Q

Clinical presentation of Cushing’s disease - Head

A

-thinning hair
-moon face
-cereblra atrophy
-fat deposition on the back

35
Q

Clinical presentation of Cushing’s disease - Inner

A

-diabetes
-osteoporosis (catabloic effect)
-HTN (too much mineralcorticoid activitiy)
-immunosuppression
-adrenal hyperplasia
-poor wound healing
-muscle weakness (catabolic effect)

36
Q
A

-obese (trunk area - too much cortisol and altered fat deposition)
-thin arms and legs (catabolic effects)
-moon face
-fat deposition on the neck
-strae on the skin

37
Q

What is the treatment of choice in Cushing’s Syndrome?

A

-Surgery (80-90% cure rate)

Pharmacotherapy for patients:
-Tumor can’t be localized
-Not surgical candidates
-Failed surgery
-relapse after surgery
-adjunctive therapy is needed for remission

38
Q

Pharmacotherapy targets

A

Hypothalamus: suppress the release of CSH

Anterior pituitary: suppress the release of ACTH
-Dopamine agonists
-Somatostatin analogs
-PPAR-gamma ligands

Adrenal gland: suppress the release of the steroids
-Ketoconazole
-Metyrapone
-Mitotane
-Etomidate

block cortisol receptor
-Mifepristone

39
Q

Which levels are monitored in Cushing’s disease

A

Urinary Free Cortisol (UFC)
-hypercortisolemia -> leads to increased cortisol in the urine

-a marker on how well a patient is responding to therapy
(reference ranges are provided on the EXAM)

40
Q

What is the drug of choice and the starting dose in Cushings disease?

A

Ketoconazole

400mg - 1.6g per day

41
Q

What is the BBW for Ketocanozole

A

hepatotoxicity

-> monitor liver function
monitor urinary free cortisol in Cushing’s treatment

42
Q

What is required for proper absorption of Ketoconazole and what are potential DDIs?

A

it needs an acidic environment (stomach pH)

DDIs:
-PPIs and H2R antagonist
-warfarin and many more
-Ketoconazole is a potent CYP3A4 inhibitor

43
Q

Which of the drugs is a adrenolytic agent?

A

Mitotane

tetragenic, avoid pregnancy for 5 years

44
Q

Which drug is indicated for Cushing’s and diabetes or glucose intolerance?

A

Mifepristone (Korlym)

45
Q

Hyperaldosteronism Quote

A

When BP can not be controlled with 3+ medications
(including a diuretic), think hyperaldosteronism

46
Q

What are the effects of Hyperaldosteronism on the cardiovascular system?

A

too much aldosterone -> Na+/K+ transporter synthesis

-Salt retention-> HTN
-detection of HTN leads to downregulation of Renin

-Hypokalemia

47
Q

Clinical Presentation in Hyperaldosteronism

A

Symptoms
-mood disturbance
-headache, tiredness

-Polyuria
-Nocturia

-Muscle weakness, Paraesthesia

Signs
-HTN

48
Q

What is the drug of choice in Hyperaldosteronism?

A

Spironolactone

-> overtreatment: hyperkalemia, impotence, gynecomastia, menstrual irregularities

-monitor potassium

49
Q

How is Spironolactone different from the other aldosterone antagonists?

A

it is not specific to aldosterone
it also has antitestosterone effects binding to androgen receptors

-useds for anti-testosterone effects: POCS, acne, hirsutism

-other uses: HTN, HF, ascites (fluid collection in the stomach)

50
Q

Which drugs to use if spironolactone has too many antitestosterone effects during therapy?

A

Eplerenone (Inspara)

-selective to MR -> fewer antitestosterone related side effects

51
Q

3rd line option for Hyperaldosteronism

A

Finerenone (Kerendia) - non-steroidal

-actually indicated for CKD in patients with diabetes

52
Q

Which patients should not be treated with Aldosterone antagonists?

A

patients with renal impairment
-risk for hyperkalemia

Endo/Eye/Derm - Women/Men (30 decks)

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