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Pharmacology > Corticosteroids > Flashcards

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
Q

Corticosteroid effects on Phospholipase A2?

A

Corticosteroids
⬆️synthesis of annexin-1
which inhibits
phospholipase A2

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26
Q

Phospholipase A2 function?

A

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).

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27
Q

Which genes does glucocosteroids suppress?

A

-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

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28
Q

NFKB function

A

Switches on PLA2, COX-2 and IL2

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29
Q

Interleukin-2 (IL-2) function?

A

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.

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30
Q

Glucocorticoid effect on IkB and function on NFKB?

A

Increases synthesis of IκB, which binds to NFκB and inhibits it.

NFKB is important because it switches on PLA2, COX-2 and IL2

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31
Q

Corticosteroids Function on monocytes/lymphocytes?

A

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

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32
Q

Corticosteroids effect on COX?

A

Decreases COX-2, inducible nitric oxide synthase (NOS2), and inflammatory cytokines

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33
Q

Glucorticosteroids CNS effects?

A

-Adrenal insufficiency – slowing of the alpha rhythm lead to depression

-Glucorticoids cause insomnia and euphoria followed by depression

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34
Q

Glucocorticosteroids CNS effects in large doses?

A

-intecranial pressure (pseudotumor cerebri)

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35
Q

Glucocorticosteroids ulcer effects?

A

-Peptic Ulcers by suppressing immune response to H.Pylori

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36
Q

Glucocorticosteroids chronic use effects?

A

-Chronic use ↓ release of ACTH, growth hormone, TSH, luteinizing
hormone

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37
Q

Glucocorticosteroids blood calcium effects?

A

-Fat redistribution
-Decrease Vitamin D and calcium absorption

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38
Q

Glucocorticosteroids renal function effects?

A

Renal function: Cortisol deficiency – impaired renal function,
⬆️vasopressin secretion & ⬇️water secretion

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39
Q

Vasopressin Function?

A

Vasopressin down regulates blood pressure and plasma osmolarity

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40
Q

Glucocorticosteroids fetal lung development effects?

A

Glucocorticorticoids stimulates the production of pulmonary
surfactant – lungs – breathing

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41
Q

Glucocorticosteroids epigenetic regulation effects?

A
  • 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
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42
Q

Aldosterone water and electrolyte effects ?

A
  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
Q

Hyperaldosteronism?

A

Excessive ALDOSTERONE
SECRETION

44
Q

Hyperaldosteronism effects?

A

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
Q

Mineralocorticoid deficiency?

A
  • leads to Na+ wasting
  • Contraction of the extracellular fluid volume, hyponatremia,
    hyperkalemia, and acidosis.
  • Aldosterone deficiency can lead to hypotension and vascular collapse
46
Q

Adrenocortical insufficiency ?

A

Chronic Addisons disease

47
Q

Therapeutic Uses of cortisol?

A
  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
Q

Treatment of chronic addison’s disease?

A

*20 – 30g hydrocortisone daily

49
Q

What is hydrocortison supplemented by?

A

*Supplemented with salt-retaining steroid - fludrocortisone

50
Q

Hydrocortisone Admin?

A
  1. Oral
  2. Injectable
  3. Topical
51
Q

Hydrocortisone duration?

A

Short-acting

52
Q

Chronic Addison’s symptoms ?

A

*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
Q

Why must hydrocortisone
be supplemented fludrocortisone?

A

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
Q

Hydrocortisone CI?

A
  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
Q

Hydrocortisone DI?

A
  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
Q

Fludrocortisone - Adverse Effects?

A
  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
Q

Acute adrenocortical insufficiency drug?

A

Hydrocortisone 100mg I/V - 8hrly

58
Q

Acute adrenocortical insufficiency drug administration ?

A

I/V hydrocortisone & correction of fluid and electrolyte balance

59
Q

Congenital Adrenal Hyperplasia?

A

Defects in the synthesis of cortisol in children

60
Q

Congenital Adrenal Hyperplasia Tx?

A

hydrocortisone or prednisone

61
Q

Prednisone duration?

A

Intermediate-acting

62
Q

Which drug is administered to congenital Adrenal Hyperplasia to maintain BP?

A

Fludrocortisone also added to maintain BP, plasma renin-activity &
electrolytes

63
Q

Cushing’s syndrome?

A

Excess Corticosteriods

Possible causes: Bilateral adrenal hyperplasia or adrenal gland tumors

64
Q

Cushing’s syndrome Tx?

A

removal of tumor, irradiation of the pituitary tumor, resection of
both adrenals

65
Q

Primary Aldosteronism?

A

Excessive aldosterone production – adrenal adenoma,
hyperplastic glands, malignant tumor, disorders of adrenal
steroid biosynthesis

66
Q

Primary aldosteronism symptoms ?

A

Symptoms: HT, weakness, tetany due to renal loss of K+
hypokalemia, alkalosis, serum sodium, low levels plasma
renin and Ang II

67
Q

Primary Aldosteronism Rx?

A

Rx: fludrocortisone, spironolactone (aldosterone antagonist)

68
Q

CORTICOSTEROIDS AND
STIMULATION OF LUNG FUNCTION?

A

Cortisol regulates lung maturation in fetus

69
Q

CORTICOSTEROIDS AND
STIMULATION OF LUNG pathophysiology?

A

Premature infant – Respiratory distress syndrome

70
Q

Tx of corticosteriods?

A

*Tx – mother with high doses of glucocorticosteroid e.g.
betamethasone when delivery is before 34 weeks

71
Q

Why is Na+ retaining potency important to consider when giving patients corticosteroids ?

A

You do not want to give to patients who have oedema or that will increase pathological water retention

72
Q

Hydrocortisone salt form?

A

Hydrocortisone sodium succinate

73
Q

Hydrocortisone sodium succinate

A

IV

74
Q

Hydrocortisone sodium succinate I?

A

Acute bronchospasm, hypersensitivity reactions (anaphylactic shock),
drug sensitivity reactions

75
Q

Prednisolone/Prednisone I?

A

inflammatory and allergic dise

76
Q

Prednisolone/Prednisone Duration?

A

Intermediate-acting

77
Q

Dexamethasone potency?

A

Dexamethasone is very potent

78
Q

Dexamethasone duration ?

A

Long acting, minimal salt-retaining actions

79
Q

Dexamethasone Uses?

A

Anaphylaxis
Cerebral oedema
Used for lung maturation - Neonatal respiratory distress syndrome
(NRDS)
Combined with anti-emetics – nausea and vomiting induced by
chemotherapy

80
Q

Betamethasone duartaion?

A

Long duration of activity

81
Q

Betamethasone uses?

A
  • NRDS
  • intracranial pressure
  • Arthritis
  • Dermatitis
82
Q

Methylprednisolone uses?

A
  • Asthma
  • Anaphylaxis
  • Rheumatoid arthritis
  • Used when mineralocorticoid activity is undesirable
83
Q

Systematic corticosteroids?

A

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
Q

What causes adrenal atrophy?

A

Steroid therapy suppresses corticotrophin secretion leads to
adrenal atrophy.

85
Q

How long does it take to recover normal adrenal function?

A

6–12 months to recover normal adrenal function

86
Q

When do we administer steroids to increase stress?

A

Since the patient’s response to stress is suppressed,
additional steroid must be administered in times of severe
stress (e.g. surgery, infection).

87
Q

Which type of adrenal suppression is preferred ?

A

Gradual withdrawal

88
Q

Which withdrawal causes adrenal insufficiency ?

A

*Abrupt withdrawal causes adrenal insufficiency

89
Q

Prescribing corticosteroids?

A

Lowest appropriate dose, shortest time

90
Q

Why shouldn’t you prescribe to patients high doses in the evening?

A

High doses – late evening → insomnia

91
Q

Prednisone or betamethasone time of day precription?

A

morning

92
Q

Which pathologies should you caution against when using corticosteriods?

A

Peptic ulcer, heart disease, HT with HF, certain infectious diseases: varicella, TB,
* Psychosis, diabetes, osteoporosis, glaucoma

93
Q

Why should we limit children dosage?

A
  • Limit dose and duration of steroid exposure – children – growth
    retardation
  • If needed for an extended period – prednisone/methylprednisolone
    single dose on alternate mornings
94
Q

Immunisation and corticosteroids?

A

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
Q

WITHDRAWAL OF STEROID THERAPY?

A

*High dose, short term (7-14 days) can be withdrawn abruptly
or tapered slowly over a week
*Therapy >14 days, taper

96
Q

TOPICAL CORTICOSTEROIDS -
POTENCY GROUPS?

A

Group 1-weak
Group 2-moderately potent
Group 3-Potent
Group 4-Very potent

97
Q

Which drug is a weak potent?

A

Hydrocortisone

98
Q

Which drug is moderately potent?

A

Betametasone as a valerate,
half strength (0.05%)

99
Q

Which drug is potent?

A

Betametasone as a valerate
(0.1%)
* Betamethasone dipropionate
* Diflucortolone
* Fluocinolone acetonide
* Fluticasone, hydrocortisone
butyrate, methylprednisolone
aceponate, mometasone

100
Q

Which drug is very potent?

A

clobetasol

101
Q

Which combination of drugs should we avoid?

A

corticosteroid + antimicrobial
*Dermatophyte infection (imidazole + corticosteroid)
*Infected eczema- quinoline antiseptic + corticosteroid.
*Once under control – move to single most appropriate
agent.

102
Q

Whats the problem with increased skin absorption of drugs?

A

Skin barrier function compromised
⬆️absorption ⬆️the risk of systemic side-effects

103
Q

Topical Corticosteroids CI?

A

Rosacea
*Acne
*Peri-oral dermatitis
*Skin lesions infected with fungi or bacteria
*Hypersensitivity
*Ulcerative conditions

Pharmacology (44 decks)

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