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Endocrine > Therapeutic Use of Glucocorticoids > Flashcards

Therapeutic Use of Glucocorticoids Flashcards

1
Q

What are the 6 main uses for Glucocorticoids?

A
  1. Adrenal Insufficiency
  2. Inflammatory/ autoimmune disease
  3. Allergic Disease
  4. Infectious disease
  5. Blood malignancies
  6. Traumatic injury/organ transplantation.
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2
Q

What are the adrenal insufficiencies concerned with glucocorticoid use?

A
  1. Actue Adrenal Insufficiency
  2. Chronic adrenal insufficiency
  3. Congenital Adrenal Hyperplasia (CAH)
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3
Q

What are the Inflammatory/autoimmune diseases associated with therapeutic use of glucocorticoids?

A
  1. Systemic Lupus Erythematosis
  2. Vasculitis
  3. RA
  4. Asthma, Bronchitis, Emphysema
  5. Skin Disorders
  6. IBD
  7. Renal nephritis
  8. Thrombocytopenia
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4
Q

What Allergic diseases need the use of glucocorticoids?

A

Allergic Reactions: contact dermatitis/urticaria, bee stings, drug reactions, serum sickness.

Allergic rhinitis, allergic asthma.

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5
Q

What infectious diseases need glucocorticoids?

A

AIDS w/ opportunistic infections

Septic shock.

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6
Q

What Blood Malignancies need glucocorticoids?

A

Acute Lymphocytic Leukemia, Lymphoma.

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7
Q

What Traumatic injury/organ transplantation requires glucocorticoids?

A

Spinal Cord Injury (not effective with head injury)

Organ Transplantation.

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8
Q

What is Acute Adrenal Insufficiency?

A

A rapid decrease in blood corticosteroids secondary to bilateral adrenal injury, pituitary injury, withdrawal of glucocorticoids.

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9
Q

What are the characteristics of Acute Adrenal Insufficiency?

A

Nausea, Vomiting, dehydration, hyponatremia, hyperkalemia, wekaness/ lethargy, hypotension.

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10
Q

How is Acute Adrenal Insufficiency diagnosed?

A

Cosyntropin stimulation test to measure induction of cortisol secretion.

  • ACTH analog administered IV or IM
  • Can also measure plasma ACTH to determine cause (hypothalamus/pituitary vs. adrenal orgin)
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11
Q

What is Acute Adrenal Insufficiency treated with?

A

IV hydrocortisone + glucose

100 mg bolus followed by 50-100 mg/8hr (normal daily rate of cortisol production)

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12
Q

What is Addison’s Disease?

A

Chronic adrenal insufficiency.

-Corticosteroid deficiency secondary to adrenal autoimmune disease, anterior pituitary lesions (secondary adrenal deficiency), systemic infections incl. AIDS, Tb, Metastatic cancers.

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13
Q

What is the incidence of Addison’s disease?

A

1: 25,000 (relatively common)

- Familial presisposition.

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14
Q

What was formerly the most common cause of Addison’s disease?

A

Tb (infection and destruction of adrenals)

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15
Q

What are the symptoms of Addison’s Disease?

A

Same as for acute adrenal insufficiency but less severe.

  • Inability to maintain glucose, esp. in fasting (cant generate glucose from glycogen)
  • Excessive secretion of proopiomelanocortin-derived peptides (POMC –> ACTH, MSH)
  • Postural hypotension if ALDOSTERONE deficient also Increased renin/ANGII
  • Androgen deficiency in females.
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16
Q

What does excessive melanocyte-stimulating hormone (MSH) lead to?

A
  • Excessive pigmentation, reversible upon initiation of treatment.
  • Pigmentation of distal extremities: palms, knuckles.
  • Pigmentation of normally unpigmented skin: genitalia, buccal mucosa, tongue.
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17
Q

What is the treatment for Addison’s disease (Hypocortisolism)?

A
  1. Require daily oral tx w/ Hydrocortisone
  • 15-20mg/d 2-3doses to replicate diurnal variation.
  • Prednisone or Dexamethasone also used.
  1. Some patients = Hydrocortisone + Liberal Salt intake.
  • Many require mineralcorticoid replacement (primary AI)
  • Fludrocortisone, 0.05-0.2 mg/d
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18
Q

What should patients with Addison’s disease wear?

A

Med-alert bracelet or tag.

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19
Q

When do dosages need to be increased for patients w/ Addison’s disease?

A
  1. Co-administration of drugs that increase steroid metabolism.
    - P450 inducers - phenytoin, barbs, rifampin.
  2. Major and minor illnesses, surgery, stressful events.
  3. Nausea, vomiting can prevent absorption of steroid and may require IM admin.
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20
Q

What is the evaluation of therapy for glucocorticoid replacement?

A
  1. Adequate therapy should yield normal morning plasma ACTH levels.
  2. Hyperpigmentation and electrolyte abnormalities reversed.
  3. Sense of well-being should be taken into consideration.
  4. Over treatment can cause Cushing’s syndrome
    - Stunted growth in children, weight gain, sexual dysfunction.
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21
Q

What is Congenital Adrenal Hyperplasia?

A

Selective corticosteroid deficiency secondary to genetic defect in steroid synthesis.

  • Lack of cortisol production results in chronic high ACTH levels
  • Steroids “upstream” and parallel to defect are in excess.
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22
Q

What is the most common genetic defect associated with Congenital Adrenal Hyperplasia?

A
  1. CYP21 deficiency

- 90% of CAH patients, 1:14,000

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23
Q

What does CYP21 deficiency cause?

A

Prevents synthesis of Cortisol and Aldosterone.

  • 17-hydroxyprogesterone accumulates in blood (diagnostic)
  • Masculinization of females (pseudohermaphroditism at birth), precocious sexual development in males.
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24
Q

What do patients with a CYP21 deficiency require?

A
  1. Hydrocortisone.
  • Goal to restore normal serum cortisol and ACTH levels.
  • Severe cases require mineralocorticoid: fludrocortisone.
  • Table salt to infants in formula (1/5 tablespoon/bottle) to maintain Na+ levels.
  • Elevated renin levels indicate inadequate aldosterone levels.
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25
Q

What do elevated renin levels indicate?

A

Inadequate aldosterone levels.

26
Q

What does Prenatal diagnosis and treatment of CAH involve?

A
  1. Glucocorticoid in utero - avoid post-natal genital surgery
  2. Dexamethasone, 20 ug/kg by mother daily
  3. Adverse effects to mother include:
    - HTN
    - Weight gain
    - Edema
    - Mood effects.
27
Q

What are the specifics of Dexamethasone treatment pre-natally for CAH?

A
  1. Must begin less than 10 weeks gestation in susceptible fetus. (genotype and sex determined later)
  2. Therapy stopped if ONE wild type CYP21 allele, or sex is male!
28
Q

Signs and symptoms of CAH in Children?

A
  1. Moderate to severe recurrent sinus or pulmonary infections.
  2. Severe acne
  3. Hyperpigmentation, especially of genitalia
  4. Tall for age.
  5. Early onset of puberty.
29
Q

Signs and symptoms of CAH in Adults?

A
  1. Childhood history
  2. Syncope or near-syncope
  3. Shortened stature compared w/ either parent.
  4. Hypotension (21-hydroxylase deficiency)
  5. Hypertension (11B-hydroxylase deficiency)
30
Q

Signs and symptoms of CAH in Women?

A
  1. Clitoromeagaly
  2. Poorly developed labia
  3. Hirsutism
  4. Infertility
  5. Polycystic ovary syndrome
31
Q

What are other causes of CAH?

A
  1. CYP11B1 deficiency
  2. CYP17 deficiency
  3. 3B-hydroxysteroid dehydrogenase deficiency
  4. CYP11A1, StAR, CYPOR deficiencies.
32
Q

How is a deficiency in CYP11B1 related to CAH?

A
  1. causes 5-8% of CAH.
  2. Prevents Cortisol synthesis.
    - Increase ACTH leads to elevated androgens. aldosterone often increased.
    - Accumulation of 11-corticosterone and 11-deoxycortisol distinguishes disease from CYP21 deficiency.
  3. Treat with hydrocortisone.
33
Q

How is a deficiency in CYP17 related to CAH?

A
  1. 1% of CAH
  2. Decreased levels of cortisol and sex steroids, elevated Aldosterone.
  3. Diagnosis at puberty
  4. Treated w/ Hydrocortisone, sex steroids, and surgery.
34
Q

How is a deficiency in 3B-Hydroxysteroid dehydrogenase related to CAH?

A
  1. Very rare, patients present at infancy w/ apparent congenital lipoid adrenal hyperplasia.
    - ALL steroids lacking, fatal in 66%
    - StAR transports cholesterol into mitochondria
  2. CYPOR is electron transfer protein to CYP21 & CYP17
    - deficiency leads to elevated pregnenolone and progesterone, genital ambiguity,
    - Total loss of CYPOR is FATAL.
35
Q

What is Antley-Bixler Syndrome?

A

Deficiency in CYPOR that leads to elevated pregnenolone and progesterone, genital ambiguity.

36
Q

What are the characteristics of using Glucocorticoids in Inflammatory diseases?

A
  1. Provide symptomatic relief.
  2. Normally use high initial dose to reverse inflammation and prevent tissue damage.
  3. Oral dosing to treat severe exacerbations of Crohn’s disease, ulcerative colitis.
  4. Can also be injected into site of inflammation to minimize systemic effects.
  5. Low-moderate dose glucocorticoids are used to induce remission of sarcoidosis.
  6. Immunosuppressants may also be required.
37
Q

Do glucocorticoids cure inflammatory diseases?

A

NO they only provide symptomatic relief.

38
Q

When using glucocorticoids for inflammatory diseases how is the dosing done?

A

High initial dose to reverse inflammation and prevent damage.

  • Dose tapered over days to allow Adrenal Recovery
  • Alternate day tx may be initiated for long-term admin.
  • Intermediate acting steroids preferred: Methylprednisolone.
39
Q

When treating Crohn’s disease or ulcerative colitis what are other options when using oral dosing?

A
  1. Delayed release capsules deliver drug to ileum and ascending colon.
  2. Or use rectal admin to site of action.
40
Q

When are situations where you use low-moderate dose of glucocorticoids to induce remission of sarcoidosis?

A
  1. Granulomatous inflammation of lungs
  2. Muscle secondary to Crohn’s disease, Tb, RA, Vasculitis.
  3. Often require chronic treatment.
41
Q

How are glucocorticoids administered for use in Asthma patients?

A

By metered dose inhaler.

-places steroid at site of action, minimizes systemic effects.
-AE limited to hoarseness, oral candida infections
-

-Triamcinolone, Beclomethasone, Flunisolide, Fluticasone, ALL therapeutically equivalent.

42
Q

How to steroids help asthma?

A

Reduce asthma and reverse the inflammatory sequellae.

-Daily use is strongly recommended for even mild asthma patients to prevent progression of disease.

43
Q

When are oral steroids used in asthma?

A

Severe Exacerbations.

44
Q

When are MDI steroids less effective?

A

For chronic bronchitis and emphysema.

45
Q

What is the Anti-Inflammatory mechanisms of Steroids?

A
  1. Actions medicated through inhibition of cytokine, leukotriene, and prostaglandin synthesis.
46
Q

What are the characteristics of anti-inflammatory effect of steroids?

A
  1. Effects appear to be independent of DNA binding by GR.
  • mediated by GR interactions w/ transcription factors (NF-kB and AP-1)
  • Involved in suppression of cytokine expression (IL-1, IL-6, TNFa) leads to anti-inflammatory and immuno-supressive effects.
  1. Induction of LIPOCORTIN expression
47
Q

What does induction of Lipocortin do?

A

Inhibits phospholipase A2, blocking arachidonic acid release from the cell membrane (leukotriene/prostaglandin precursor)

48
Q

What is the anti-inflammatory potency, duration of action and equivalent dose of Cortisol?

A

1
8-12hr.
20mg

49
Q

What is the anti-inflammatory potency, duration of action and equivalent dose of Triamcinolone?

A

5
12-36hr.
4mg

50
Q

What is the anti-inflammatory potency, duration of action and equivalent dose of Betametasone?

A
  1. 36-72hr.
    0.75mg.
51
Q

What are the characteristics of the use of glucocorticoids in Allergic Disease?

A

Effectively suppress allergic (inflammatory) reactions.

  1. Onset of relief is delayed 12-24hr.
  2. Steroids are appropriate for severe/long lasting or systemic allergic reactions.
    - serum sickness, drug reactions, contact dermatitis that does not respond to anti-hist.
    - oral or IV
  3. Nasal spray steroids are 1st choice tx for allergic rhinitis.
52
Q

What is the first choice treatment for allergic rhinitis?

A

Nasal spray steroids.

53
Q

What are the characteristics for using glucocorticoids as topical preparations?

A

Very effective against inflammatory skin diseases.

  1. 1% hydrocortisone ointment, w/wo occlusive dressing applied BID. (minimal systemic)
  2. Systemic admin for widespread or severe exacerbations (prednisone, prednisolone most common, 40mg/d)
  3. Many preparations available (generally use lowest potency necessary for situation)
  4. Stronger steroids NOT on FACE
  5. Careful on thin skin areas
54
Q

Why should stronger steroids not be used on the face?

A

They can cause perioral dermatitis and rosacea.

55
Q

Why should topical preparations of glucocorticoids be used carefully on thin skinned areas?

A

Prolonged use on genitals, face, flexures can cause reversible dermal atrophy.

56
Q

What are AE of topical glucocorticoids?

A 
Telangectasia (superficial blood vessels, irreversible)
Fine hair growth (face)
Bruising
Hypopigmentation
Striae
systemic effects.
57
Q

How are topical glucocorticoids used for ocular inflammation?

A
  1. applied as 0.1% dexamethasone eye drops q4hr. OR dexamethasone ophthalmic ointment overnight.
  2. Can increase intraocular pressure and aggravate glaucoma. (pressure should be monitored if used longer than >2wks)
  3. Can mask underlying/developing bacterial/viral/fungal infections.
  4. NOT used for mechanical lacerations.
58
Q

How are glucocorticoids used in preterm labor?

A

Administered to mothers (up to 48hr) reduce preterm neonatal respiratory distress, intraventricular hemorrhage, and death.

  • 2 days treatment for wks 27-34
  • Combined w/ tocolytics (MgSO4, indomethacin) to prevent birth.
59
Q

How are glucocorticoids used in infectious disease?

A
  1. Counterintuitive, as steroids are immunosuppressive.
  2. AIDS patients w/ pneumocystic carinii pneumonia and hypoxia (reduce pulmonary inflammation)
  3. H. Influenzae type b meningitis in infants! (decrease neurologic impairment)
  4. septic shock (best early and moderate doses can reduce cytokines)
60
Q

How are glucocorticoids used in malignancies?

A

Used in acute lymphocytic leukemia and lymphomas.

-Anti-lymphocytic effects

61
Q

What are mescellaneous uses of glucocorticoids?

A
  1. Cerebral edema secondary to parasites and metastatic neoplasms (NOT effectiv w/ head injury edema)
  2. Spinal cord injury (high dose therapy within 8 hr of injury reduces neurologic deficits)
  3. Organ transplant (high dose prednisone w/ immunosuppressives.

Endocrine (9 decks)

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