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Corticosteroids Flashcards

1
Q

Synthesis of corticosteroids?

A

In adrenal cortex

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2
Q

Corticosteroid Hs?

A

Cortisol
Aldosterone

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3
Q

Adrenal Deficiency ?

A

Addison’s Disease

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4
Q

Adrenal Excess?

A

Cushing’s Disease

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5
Q

Corticosteroids feedback?

A

Negative Feedback

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6
Q

Corticosteroids Negative Feedback Pathway?

A
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7
Q

ACTH response to sleep, meals and stress?

A

ACTH increase after meals, increased steroidogensis in response to meals and are lowest at night and highest at 8AM in the morning

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8
Q

What influences aldosterone levels in body?

A
  • ACTH
  • More by renin–angiotensin system and plasma potassium levels
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9
Q

Corticosteroids MOA?

A

Gene active hormones
* Diffuses into the cell and binds to cytoplasmic
glucocorticosteroid receptors
* Release of chaperone heat shock protein (hsp)
* Activated receptor translocates to the nucleus →
transcription → protein synthesis → steroid response

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10
Q

Why are corticosteroids effects not felt immediately?

A

Corticosteroids MOA are multi-stepped process there effects are only felt after several hours

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11
Q

Corticosteroids MOA?

A
  1. Glucocorticoids are carried via transporter, Glucocorticoid binding protein.

2.Glucocorticoids binds to a receptor complex coupled with two heat-shock proteins, HSP70 and HSP90, located in the cytoplasm.

  1. Activates receptor and dissociates the two proteins from complex allowing the activated glucocorticoid translocate in the nucleus where it binds to the glucocorticoid response element.
  2. This activates the complex and alters gene transcription.
  3. This causes up-regulation of lipocortin and down regulation of COX-2.
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12
Q

Lipocortin Function?

A

Lipocortin inhibits Phospholipase-A2 and prevents the liberation of arachnoid acid from membrane phospholipids and reduces production of Prostaglandins and Thromboxane-A2.

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13
Q

What is the physiological function of glucocosrticosteriods/cortisol?

A

BIG FIB

⬆️ Blood pressure
⬆️ Insulin Resistance
⬆️ Glucneogenesis, Glycogen synthesis
⬇️Fibroblast Activity
⬇️Inflammatory Response and ⬇️ Immunosupressant
⬇️Bone formation(osteoblast activitY)

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14
Q

What is the physiological function of mineralcorticosteroids/aldosterone ?

A

Electrolyte-water balance regulating

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15
Q

Steroid Effects?

A

6 S’s

Sugar(Hyperglycaemia)
Soggy bones(causes osteoporosis)
Sick(decreased immunity)
Sad(depression)
Salt(water and salt retention)
Sex(decreased libido)

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16
Q

Corticosteroid Metabolic Effects?

A
  • Dose-related
  • Carbohydrate, protein and fat metabolism

1.Increases Blood glucose
* formation of glucose from amino acids(gluconeogenesis)
* Glucogenolysis
* Decreased Cellular Uptake
*Glucose release- stimulates insulin release but inhibits peripheral
glucose uptake
* Increased Glucagon(pancreas)
* Promotes glucose storage as glycogen

  1. Increased Lipolysis
    * Increased FFA–release of fatty acids & glycerol into circulation
    * Inhibits lipolysis and causes fat depoisition
  2. Decreased Proteins
    * Inhibit protein synthesis and stimulate protein catabolism
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17
Q

Why are glucocorticoids vital in fasting?

A

During fasting, glucocorticoids are vital to prevent (possibly fatal)
hypoglycaemia.

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18
Q

Corticosteroids effect on liver?

A

Stimulate RNA and protein synthesis in the liver

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19
Q

Corticosteroids effect on muscle?

A

Degradation of skeletal muscle for gluconeogenesis and therefore causes: muscle wasting and atrophy
Larger amounts - ↓muscle mass,

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20
Q

Corticosteroids effect on children?

A
  • Children – inhibition of growth
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21
Q

Corticosteroids effect on bones?

A

Bone – osteoporosis, osteonecrosis

Decreased osteoclast activity

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22
Q

Corticosteroids effect on skin?

A

Decreases Collagen Synthesis and thus:
-easily bruises
-vessel fragility
-stretch marks
-thin skins
-peripheral fat because of fat deposition

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23
Q

Prostaglandins function?

A

Prostaglandins are hormone-like substances that affect several bodily functions, including inflammation, pain and uterine contractions.

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24
Q

Thromboxane A2?

A

Thromboxane A2 (TXA2) is a short-lived, lipid mediator synthesized by platelets from arachidonic acid and released from the phospholipid membrane upon platelet activation. Its main role is in amplification of platelet activation and recruitment of additional platelets to the site of injury.

Thromboxanes, a substance produced by platelets, lead to occlusion of blood vessels by fueling blood clots inside the vascular system.

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25
Corticosteroid effects on Phospholipase A2?
Corticosteroids ⬆️synthesis of annexin-1 which inhibits phospholipase A2
26
Phospholipase A2 function?
Phospholipase A2 (PLA2) catalyzes the hydrolysis of the sn-2 position of membrane glycerophospholipids to liberate arachidonic acid (AA), a precursor of eicosanoids including prostaglandins (PGs) and leukotrienes (LTs).
27
Which genes does glucocosteroids suppress?
-Phospholipase A2 -Cyclo-oxygenase-2 (COX-2) -Interleukin-2 (IL-2) receptor * These genes are switched on by NFκB. * synthesis of IκB, which binds to NFκB and inhibits it. * ↓monocyte/macrophage function * ↓ circulating T-cells, especially helper T4 lymphocytes * Prevents lymphocyte proliferation by inhibiting IL-1 and IL-2 * Inhibits transport of lymphocytes to the site of antigenic stimulation * Inhibits antibody production * ↓COX-2, inducible nitric oxide synthase (NOS2), and inflammatory cytokines
28
NFKB function
Switches on PLA2, COX-2 and IL2
29
Interleukin-2 (IL-2) function?
Interleukin-2 (IL-2) is a pleiotropic cytokine that drives T-cell growth, augments NK cytolytic activity, induces the differentiation of regulatory T cells, and mediates activation-induced cell death.
30
Glucocorticoid effect on IkB and function on NFKB?
Increases synthesis of IκB, which binds to NFκB and inhibits it. NFKB is important because it switches on PLA2, COX-2 and IL2
31
Corticosteroids Function on monocytes/lymphocytes?
Decreases monocyte and macrophage function Decreases.circulating T-cells, especially helper T4 lymphocytes * Prevents lymphocyte proliferation by inhibiting IL-1 and IL-2 * Inhibits transport of lymphocytes to the site of antigenic stimulation * Inhibits antibody production
32
Corticosteroids effect on COX?
Decreases COX-2, inducible nitric oxide synthase (NOS2), and inflammatory cytokines
33
Glucorticosteroids CNS effects?
-Adrenal insufficiency – slowing of the alpha rhythm lead to depression -Glucorticoids cause insomnia and euphoria followed by depression
34
Glucocorticosteroids CNS effects in large doses?
-intecranial pressure (pseudotumor cerebri)
35
Glucocorticosteroids ulcer effects?
-Peptic Ulcers by suppressing immune response to H.Pylori
36
Glucocorticosteroids chronic use effects?
-Chronic use ↓ release of ACTH, growth hormone, TSH, luteinizing hormone
37
Glucocorticosteroids blood calcium effects?
-Fat redistribution -Decrease Vitamin D and calcium absorption
38
Glucocorticosteroids renal function effects?
Renal function: Cortisol deficiency – impaired renal function, ⬆️vasopressin secretion & ⬇️water secretion
39
Vasopressin Function?
Vasopressin down regulates blood pressure and plasma osmolarity
40
Glucocorticosteroids fetal lung development effects?
Glucocorticorticoids stimulates the production of pulmonary surfactant – lungs – breathing
41
Glucocorticosteroids epigenetic regulation effects?
* Alter activity of DNA methyltransferases, other enzymes involved epigenesis * Consequences – pregnant mums, young infants and children- predispose to behavioural/somatic disorders e.g. depression, obesity, metabolic syndrome
42
Aldosterone water and electrolyte effects ?
1. Aldosterone is a Mineralocorticoids 2. Aldosterone acts on the Distal convoluted tubules and collecting ducts of the kidney 3. There is increaseed teh Sodium/Potassium Pump and causes reabsorption of Na+ from the tubular fluid and decreases potassium effects.⬆️ urinary excretion of K+ and H+. 4. Water follows the sodium and thus this will increase water retention and increases fluid volume and decrease body osmolarity
43
Hyperaldosteronism?
Excessive ALDOSTERONE SECRETION
44
Hyperaldosteronism effects?
Excessive (e.g. hyperplastic gland/adrenal adenoma/malignant tumor) * HT, weakness, tetany – loss of potassium → hypokalemia and alkalosis * Positive Na+ balance * Tx: surgery, Spironolactone * Chronically, hyperaldosteronism causes HT
45
Mineralocorticoid deficiency?
* leads to Na+ wasting * Contraction of the extracellular fluid volume, hyponatremia, hyperkalemia, and acidosis. * Aldosterone deficiency can lead to hypotension and vascular collapse
46
Adrenocortical insufficiency ?
Chronic Addisons disease
47
Therapeutic Uses of cortisol?
1. Anti-inflammatory(IBD, Asthma, COPD) 2. Immunosuppression(allergic rxns, organ transplant, cancer, autoimmune diseases, rheumatic and skin disorders) 3. Adrenal Insufficiency: Premature neonates, multiple sclerosis and renal diseases.
48
Treatment of chronic addison's disease?
*20 – 30g hydrocortisone daily
49
What is hydrocortison supplemented by?
*Supplemented with salt-retaining steroid - fludrocortisone
50
Hydrocortisone Admin?
1. Oral 2. Injectable 3. Topical
51
Hydrocortisone duration?
Short-acting
52
Chronic Addison's symptoms ?
*Weakness, fatigue, weight loss, hypotension, hyperpigmentation, *Can’t maintain blood-glucose levels during fasting *Minor trauma could precipitate acute adrenal insufficiency with circulatory shock and death
53
Why must hydrocortisone be supplemented fludrocortisone?
The available evidence suggests that a combination of fludrocortisone and hydrocortisone is more effective than adjunctive therapy and could be recommended for septic shock
54
Hydrocortisone CI?
1. Acute psychosis-presence of visual hallucinations and absence of mood congruent delusions.Cortico-induced psychosis is a serious A/E so we do not want to exacerbate it. 2.Ocular herpes simplex
55
Hydrocortisone DI?
1. Drugs that risk hypokalemia Amphotericin B, furosemide, thiazides, digoxin – risk of hypokalemia 2. Drugs that increase CYP450 interactions: Phenobarbital, carbamazepine, phenytoin, alcohol, rifampicin – may ↓efficacy 3. Caution with Sodium retaining agents – NSAIDs
56
Fludrocortisone - Adverse Effects?
1. Dizziness, headache, HT, raised intracranial pressure, cataracts 2. Sodium and water retention →weight gain, swelling of feet & ankles 3. Potassium depletion – weakness of limbs, fatigue, arrhythmias 4. Monitor – blood pressure and serum electrolytes
57
Acute adrenocortical insufficiency drug?
Hydrocortisone 100mg I/V - 8hrly
58
Acute adrenocortical insufficiency drug administration ?
I/V hydrocortisone & correction of fluid and electrolyte balance
59
Congenital Adrenal Hyperplasia?
Defects in the synthesis of cortisol in children
60
Congenital Adrenal Hyperplasia Tx?
hydrocortisone or prednisone
61
Prednisone duration?
Intermediate-acting
62
Which drug is administered to congenital Adrenal Hyperplasia to maintain BP?
Fludrocortisone also added to maintain BP, plasma renin-activity & electrolytes
63
Cushing’s syndrome?
Excess Corticosteriods Possible causes: Bilateral adrenal hyperplasia or adrenal gland tumors
64
Cushing’s syndrome Tx?
removal of tumor, irradiation of the pituitary tumor, resection of both adrenals
65
Primary Aldosteronism?
Excessive aldosterone production – adrenal adenoma, hyperplastic glands, malignant tumor, disorders of adrenal steroid biosynthesis
66
Primary aldosteronism symptoms ?
Symptoms: HT, weakness, tetany due to renal loss of K+ hypokalemia, alkalosis, serum sodium, low levels plasma renin and Ang II
67
Primary Aldosteronism Rx?
Rx: fludrocortisone, spironolactone (aldosterone antagonist)
68
CORTICOSTEROIDS AND STIMULATION OF LUNG FUNCTION?
Cortisol regulates lung maturation in fetus
69
CORTICOSTEROIDS AND STIMULATION OF LUNG pathophysiology?
Premature infant – Respiratory distress syndrome
70
Tx of corticosteriods?
*Tx – mother with high doses of glucocorticosteroid e.g. betamethasone when delivery is before 34 weeks
71
Why is Na+ retaining potency important to consider when giving patients corticosteroids ?
You do not want to give to patients who have oedema or that will increase pathological water retention
72
Hydrocortisone salt form?
Hydrocortisone sodium succinate
73
Hydrocortisone sodium succinate
IV
74
Hydrocortisone sodium succinate I?
Acute bronchospasm, hypersensitivity reactions (anaphylactic shock), drug sensitivity reactions
75
Prednisolone/Prednisone I?
inflammatory and allergic dise
76
Prednisolone/Prednisone Duration?
Intermediate-acting
77
Dexamethasone potency?
Dexamethasone is very potent
78
Dexamethasone duration ?
Long acting, minimal salt-retaining actions
79
Dexamethasone Uses?
Anaphylaxis Cerebral oedema Used for lung maturation - Neonatal respiratory distress syndrome (NRDS) Combined with anti-emetics – nausea and vomiting induced by chemotherapy
80
Betamethasone duartaion?
Long duration of activity
81
Betamethasone uses?
* NRDS * intracranial pressure * Arthritis * Dermatitis
82
Methylprednisolone uses?
* Asthma * Anaphylaxis * Rheumatoid arthritis * Used when mineralocorticoid activity is undesirable
83
Systematic corticosteroids?
CORTICOSTERIODS Cushing-syndrome Osteoporosis Retardation of growth Thin skin, easy bruising Immunosuppression Cataracts and glaucoma Oedema Suppression of HPA Axis Tetragenic Emotional Disturbance Rise in BP Obesity(truncal) Increased hair growth(hirsutism) Diabetes Mellitus Struae
84
What causes adrenal atrophy?
Steroid therapy suppresses corticotrophin secretion leads to adrenal atrophy.
85
How long does it take to recover normal adrenal function?
6–12 months to recover normal adrenal function
86
When do we administer steroids to increase stress?
Since the patient’s response to stress is suppressed, additional steroid must be administered in times of severe stress (e.g. surgery, infection).
87
Which type of adrenal suppression is preferred ?
Gradual withdrawal
88
Which withdrawal causes adrenal insufficiency ?
*Abrupt withdrawal causes adrenal insufficiency
89
Prescribing corticosteroids?
Lowest appropriate dose, shortest time
90
Why shouldn't you prescribe to patients high doses in the evening?
High doses – late evening → insomnia
91
Prednisone or betamethasone time of day precription?
morning
92
Which pathologies should you caution against when using corticosteriods?
Peptic ulcer, heart disease, HT with HF, certain infectious diseases: varicella, TB, * Psychosis, diabetes, osteoporosis, glaucoma
93
Why should we limit children dosage?
* Limit dose and duration of steroid exposure – children – growth retardation * If needed for an extended period – prednisone/methylprednisolone single dose on alternate mornings
94
Immunisation and corticosteroids?
Administration of vaccines/toxoids deferred till corticosteroid discontinued May diminish immunological responses to toxoids, inactivated or live vaccines * Replication of organisms - live attenuated vaccines may occur * High doses may aggravate neurological reactions to some vaccine
95
WITHDRAWAL OF STEROID THERAPY?
*High dose, short term (7-14 days) can be withdrawn abruptly or tapered slowly over a week *Therapy >14 days, taper
96
TOPICAL CORTICOSTEROIDS - POTENCY GROUPS?
Group 1-weak Group 2-moderately potent Group 3-Potent Group 4-Very potent
97
Which drug is a weak potent?
Hydrocortisone
98
Which drug is moderately potent?
Betametasone as a valerate, half strength (0.05%)
99
Which drug is potent?
Betametasone as a valerate (0.1%) * Betamethasone dipropionate * Diflucortolone * Fluocinolone acetonide * Fluticasone, hydrocortisone butyrate, methylprednisolone aceponate, mometasone
100
Which drug is very potent?
clobetasol
101
Which combination of drugs should we avoid?
corticosteroid + antimicrobial *Dermatophyte infection (imidazole + corticosteroid) *Infected eczema- quinoline antiseptic + corticosteroid. *Once under control – move to single most appropriate agent.
102
Whats the problem with increased skin absorption of drugs?
Skin barrier function compromised ⬆️absorption ⬆️the risk of systemic side-effects
103
Topical Corticosteroids CI?
Rosacea *Acne *Peri-oral dermatitis *Skin lesions infected with fungi or bacteria *Hypersensitivity *Ulcerative conditions

Pharmacology (44 decks)

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