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PHarm > Adrenocorticosteroids > Flashcards

Adrenocorticosteroids Flashcards

1
Q

Steroidal hormones, enter the cell and bind to ________

Hormone-receptor complex translocates into the _____ to modulate _____.

A

Steroidal hormones, enter the cell and bind to cytosolic receptors.

Hormone-receptor complex translocates into the nucleus to modulate transcription.

Glucocorticoid receptor (GR)  
Mineralocorticoid receptor (MR)
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2
Q

Cortisol (Hydrocortisone MOA)

A

Due to time lag for changes in gene expression and protein synthesis –> most effects of corticosteroids are delayed

Once the appropriate protein synthesized –> effects persist much longer than steroid itself

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3
Q

Short acting (t1/2 = 8-12h) : ?

Intermediate acting (t1/2 = 12-36 h) : ?

Long acting: (t1/2 = 36-72 h): ?

A

Short acting (t1/2 = 8-12h) : Hydrocortisone (cortisol), Cortisone)

Intermediate acting (t1/2 = 12-36 h) : Prednisone, Prednisolone, Methylprednisolone, Triamcinolone, Fluticasone

Long acting: (t1/2 = 36-72 h). Betamethasone, Dexamethasone

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4
Q

Action of glucocorticoid

A

Effects on metabolism, anti inflammatory and immunosuppressant

Permissive actions: facilitates actions of other hormones e.g., response of vascular and bronchial smooth muscles to catecholamines is diminished in the absence of cortisol

Anti-inflammatory & immunosuppressive effects (most imp. property of glucocorticoids) - inhibit all the classic signs of inflammation (erythema, swelling, pain, and heat)

promote synthesis of lipocortins *** which inhibit phospholipase A2 (this inhibits production of arachidonic acid and hence of prostaglandins and leukotrienes)

additionally, inhibit protein-translation of inducible COX -II

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5
Q

Action of corticosteroid

A

salt retaining

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6
Q

Prednisone

A

(pro-drug) lacks glucocorticoid activity until converted to Prednisolone by hepatic enzymes

patients with liver function impairment should be treated with prednisolone rather than prednisone

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7
Q

Anti-inflammatory and immunosuppressive effects of glucocorticoids

A

inhibit the release of IL-1, IL-2, IL-3, IL-6, TNF-alpha and granulocyte-macrophage colony-stimulating factor (GM-CSF)

reduce migration of inflammatory cells to site of injury

Decrease vascular permeability by reducing histamine release and the action of kinins

inhibit the antigenic response of macrophages and leucocytes

decrease lymphocyte production

impair delayed type hypersensitivity reactions

Decrease in the lymphocyte count due to migration of lymphocytes to the lymphoid structures.

Long-term therapy results in involution and atrophy of all lymphoid tissues

also decrease the circulating monocytes, eosionophils and basophils.

Increase neutrophil count in the blood due to decreased migration to the site of injury

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8
Q

Metobolic effects of glucocorticoids

A

Hyperglycemia - increase blood glucose level by stimulation of gluconeogenesis (peripheral amino acids are utilized for gluconeogenesis), decrease peripheral glucose utilization
net effect: hyperglycemia

Protein catabolism - cause protein breakdown and lead to negative nitrogen balance

increase lipolysis (result in increased plasma free fatty acid and ketone body formation).

causes re-distribution of fat (moon face’, ‘buffalo hump’ as seen in Cushing’s syndrome)

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9
Q

Glucocorticoids on CVS

A

Promotes Na+ and water retention ► HTN (mineralocorticoid action)- distal & collecting tubules

Maintains the tones of arterioles and myocardial contractility

due to permissive effect on pressor actions of epinephrine and angiotensin, produce rise in blood pressure

Adrenal insufficiency (Hypoadrenalism) = reduced response to vasoconstrictors (Epi, NE, Angiotensin) = hypotension

Cushing’s syndrome (excess glucocorticoids ) = hypertension

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10
Q

Glucocorticoid on stomach

A

Increased gastric acid and pepsin secretion – may aggravate peptic ulcer
possibly suppress the immune response against H. pylori & also increase the secretion of pepsin & gastric acid

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11
Q

Glucocorticoid on skeletal muscle

A

Optimum concentration is required for the normal functions of skeletal muscles (permissive actions)

Weakness occurs in both hypo- and hypercorticism

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12
Q

Hypocorticism

A

(adrenal insufficiency):

reduced work capacity, weakness and fatigue due to the inadequacy of the circulatory system

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13
Q

Hypercorticism

A

increased mineralocorticoid action -> hypokalemia -> weakness

increased glucocorticoid action -> muscle wasting and myopathy (steroid myopathy in Cushing’s syndrome) -> weakness

increased glucocorticoid action -> muscle wasting and myopathy (steroid myopathy in Cushing’s syndrome ) -> weakness

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14
Q

Glucocorticoids on electrolyte and water balance

A

Aldosterone, natural mineralocorticoid, most potent with respect to fluid and electrolyte balance

Mineralocorticoids act on distal tubules and collecting ducts of the Kidneys

Reabsorption of Na+, water, bicarbonate and increased urinary excretion of K+ and H+ - hypokalemia and alkalosis

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15
Q

Glucocorticoid actions on calcium

A

Inhibits intestinal absorption, and enhances renal excretion of Ca2+

Loss of Ca2+ from bones, negative calcium balance -> Calcium deficiency -> weak & fragile bones (resulting in osteoporosis)

Long term use necessitates calcium supplement**

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16
Q

Glucocorticoid on CNS

A

Mild euphoria, insomnia, anxiety, increased motor activity and restlessness

Adrenal insufficiency (Addison’s disease): apathy, depression and irritability

High doses of glucocorticoids lower seizure threshold: cautiously used in epileptics.

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17
Q

What are the effects of glucocorticoids on ACTCH, fibroblast, collagen and surfactant

A

Inhibition of plasma ACTH and possible adrenal atrophy**

Inhibition of fibroblast growth and collagen synthesis

Induction of surfactant production in the fetal lung **

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18
Q

Glucocorticoid use for Addisonian crisis

A

Replacement therapy
Acute adrenal insufficiency (Addisonian crisis): due to acute lack of corticosteroids
An emergency; characterized by
- GI symptoms (Nausea, vomiting, abdominal pain)
- Dehydration, Hyponatremia
- Hyperkalemia- Weakness and Lethargy
- Hypotension and hypoglycemia, death (if failure to control the disease)

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19
Q

Drugs given to treat addisonian crisis

A

Dexamethasone, Hydrocortisone (cortisol)

Fludrocortisone may also be necessary

20
Q

Glucocorticoid use for addison disease

A

Similar symptoms as seen in Addisonian crisis, with lesser severity

Hydrocortisone orally in dose of 20-30 mg/day + salt & water

2/3rd dose in morning & 1/3rd dose in afternoon: to mimic diurnal rhythm of cortisol secretion – mostly in the early morning

Some patients may need Fludrocortisone for mineralocorticoid activity

21
Q

Glucocorticoid use in congenital adrenal hyperplasia

A

(Adrenogenital syndrome)
a group of genetic disorders in which the activity of one of the several enzymes (21α-hydroxylase**, 11β- hydroxylase and 17α-hydroxylase) required for biosynthesis of corticosteroids is deficient

Less production of hydrocortisone and aldosterone -> increased ACTH secretion -> adrenal hyperplasia

Replacement by Hydrocortisone and Fludrocortisone
Decreased ACTH production and decreased stimulation of adrenal cortices.

22
Q

General principles for uses of glucocorticoids in non endocrine disease

harmful dose?
withdrawal?
infection?

A

Single dose (even excessive) is not harmful

Short courses (even high doses) are not likely to be harmful in the absence of contraindications

Long term use is potentially hazardous: keep the dose minimum, which is found by dose titration

No abrupt withdrawal after a corticosteroid has been given for >2 weeks: may precipitate Addisonian crisis and if not controlled, death can occur

Infection, severe trauma or any stress during corticosteroid therapy -> increase the dose

23
Q

Glucocorticoids in bronchial asthma

A

Inhalational route/other

24
Q

Glucocorticoids in autoimmune disease

A

Hemolytic anemia, Thrombocytopenia, etc

25
Q

Glucocorticoids in severe allergic reactions

A

Allergic rhinitis (Beclomethasone, Triamcinolone)
Anaphylaxis, angioneurotic edema, urticaria and serum sickness
Even IV injection of corticosteroids takes 1-2 hours to act
In case of anaphylactic shock and angioedema of larynx- Epinephrine is DoC

26
Q

Glucocorticoids for inflammation

A

Rheumatoid arthritis and osteoarthritis

27
Q

Glucocorticoids for infectious diseases

A

Severe forms of TB, severe lepra reactions, certain forms of bacterial meningitis (H. influenzae) and Pneumocystis jiroveci pneumonia in AIDS patients with hypoxia

28
Q

Glucocorticoids for eye diseases

A

In allergic and inflammatory diseases of eye, e.g., allergic conjuctivitis, iritis, iridocyclitis, keratitis, etc.

Topical application ophthalmic solution/ ointment

Prolonged use of corticosteroid eye drops can cause glaucoma

Posterior segment afflictions like retinitis, optic neuritis, uveitis require systemic steroid therapy

29
Q

What eye disease are glucocorticoids contraindicated in

A

Contraindicated in herpes simplex keratitis**

30
Q

Uses of glucocorticoids in skin diseases

A

Highly effective in many eczematous skin diseases

Topical application (e.g., hydrocortisone ointment n eczema)

Systemic steroids in severe skin diseases like Pemphigus vulgaris, Exfoliative dermatitis, Stevens-Johnson syndrome, etc.

31
Q

Uses of glucocorticoids in intestinal diseases

A

In ulcerative colitis, Crohn’s disease

Oral or retention enema (Hydrocortisone, prednisone)

32
Q

Uses of glucocorticoids in cerebral edema

A

Due to cerebral tumor, tubercular meningitis, encephalitis, trauma

33
Q

Which glucocorticoids used to treat cerebral edema

A

Dexamethasone, Betamethasone

34
Q

Uses of glucocorticoids in malignancies

A

In acute lymphocytic leukemia and lymphomas because of antilymphocytic affects

Also offer symptomatic relief in other advanced malignancies by improving appetite

35
Q

Glucocorticoids in organ transplantation

A

for immunosuppression

36
Q

Glucocorticoids for septic shock

A

glucocorticoids help in raising blood pressure by mineralocorticoid action and its permissive action

37
Q

Glucocorticoids for surfactant production

A

acceleration of lung maturation in a preterm fetus:

Fetal cortisol is an inducer of lung maturation; premature infants can develop respiratory distress syndrome

38
Q

How to prevent respiratory distress in premature infants

A

Betamethasone/Dexamethasone IM*** to mother

not in second trimester!

39
Q

Uses of glucocorticoids in renal disease

A

Nephrotic syndrome – Minimal change disease

40
Q

Uses of glucocorticoids for diagnostic use

A

Dexamethasone suppression test (DST) for Cushing’s syndrome

To see the functioning of hypothalamic-pituitary- adrenal axis (HPA-axis)

If low dose suppresses the normal production of hydrocortisone, the HPA- axis is intact

If high dose suppresses ACTH production: origin of increased ACTH is pituitary; if not, the origin is ectopic

41
Q

Glucocorticoid ADR

A

Hypothalamic-pituitary-adrenal axis suppression

Cushing’s like syndrome:‘moon face’, ‘fish (narrow ) mouth’, ‘buffalo’ hump, obesity of trunk with thin limbs.

Fragile skin, purple striae and easy bruising (typically on lower abdomen and thighs)

Hypertension

Hyperglycemia (DM)

Myopathy: weakness of proximal (shoulder, arm, pelvis, thigh) limb muscles – withdraw steroid

Susceptibility to infection: (risk of reactivation of latent TB and appearance of opportunistic infections (Candida, etc)

Peptic ulcer

Osteoporosis

Edema

Psychosis

Cataract, glaucoma

Delayed healing of wounds and surgical incisions

Growth retardation in children: by decreasing GH secretion

42
Q

Glucocorticoid contraindications

A 
Osteoporosis
Psychosis
Peptic ulcer
Diabetes mellitus
Hypertension
Viral / fungal infections 
Pregnancy (esp. 2nd trimester)
43
Q

Steroid Withdrawal after prolonged use

A

Gradual, NOT ABRUPT(weakness,fatigue, decreased appetite nausea/vomiting, abdominal pain, dehydration…)
Longer the duration of therapy, slower must be the withdrawal.

44
Q

Steroid withdrawal after use for 2 weeks

A

If rapid withdrawal is desired, a 50% reduction in dose/day
If a patient is treated for longer period, withdrawal should be done very slowly (e.g., 2.5-3 mg of prednisolone or equivalent at intervals of 3-7 days).
Alternatively, halve the dose weekly until 25 mg prednisolone or equivalent is reached, after which reduce 1 mg every 3-7 days

45
Q

Aldosterone

A

Control body water and electrolyte balance especially sodium and potassium

Aldosterone acts on the kidney tubules and collecting ducts.

Aldosterone: increases reabsorption of Na+, water and bicarbonate from renal tubules
decreases reabsorption of K+ and H+ ions from renal tubules
Hyperaldosteronism may result in alkalosis and hypokalemia, whereas retention of sodium and water leads to increase in blood volume and blood pressure

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