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Derm Pharm 2020 > 1 - SYSTEMIC CORTICOSTEROIDS > Flashcards

1 - SYSTEMIC CORTICOSTEROIDS Flashcards

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1
Q

The inactive form cortisone is converted to the active form cortisol (hydrocortisone) by 11 beta-hydroxysteroid dehydrogenase in the liver

A

True (both cortisone and cortisol/hydrocortisone are short acting corticosteroid)

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2
Q

The addition of a 1,2 double bond to cortisol (hydrocortisone) results in prednisone with increased glucocorticoid activity and decreased rate of metabolic degradation

A

True (prednisone is an intermediate acting corticosteroid)

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3
Q

Prednisolone is the active analog of prednisone (both intermediate acting corticosteroids)

A

True (prednisone is converted to prednisolone through 11-hydroxylation)

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4
Q

Prednisone is converted to its active analog prednisolone through 11-hydroxylation

A

True (both are intermediate acting corticosteroid)

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5
Q

Methylprednisolone is formed through the addition of a 6-methyl group to prednisolone (active analog of prednisone), which leads to slightly increased glucocorticoid activity

A

True (Methylprednisolone is an intermediate acting corticosteroid)

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6
Q

Cortisone and cortisol (hydrocortisone) are short acting corticosteroids

A

True

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7
Q

Prednisone, prednisolone (active analog of prednisone), Methylprednisolone and Triamcinolone are intermediate acting corticosteroids

A

True

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8
Q

Dexamethasone and betamethasone are long acting corticosteroids

A

True

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9
Q

The addition of fluorine to cortisol (hydrocortisone) leads to increased glucocorticoid but also significant mineralocorticoid activity and results in fludrocortisone

A

True

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10
Q

By modifying fludrocortisone (high glucocorticoid and mineralocorticoid activity), 3 compounds (Triamcinolone, dexamethasone and betamethasone) with high glucocorticoid and low mineralocorticoid effects are formed

A

True (all 3 compounds are biologically active due to the 11-hydroxyl group and do not require 11 beta-hydroxysteroid dehydrogenase for conversion to active form)

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11
Q

All corticosteroids have a hydroxyl group at the 17 position (17-hydroxycorticosteroids)

A

True

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12
Q

The long acting corticosteroids (dexamethasone and betamethasone) have higher glucocorticoid potency than the shorter acting corticosteroids (cortisone and cortisol/hydrocortisone)

A

True (prednisone, prednisolone, methylprednisolone and Triamcinolone are intermediate acting corticosteroids)

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13
Q

The shorter acting corticosteroids (cortisone and cortisol/hydrocortisone) have mineralocorticoid activity as compared to the longer acting corticosteroids (dexamethasone and betamethasone) which have little/no mineralocorticoid activity

A

True (there is an inverse correlation between the duration of action I.e. Potency and the relative mineralocorticoid effects)

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14
Q

Exogenous corticosteroid are absorbed in the upper jejunum

A

True

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15
Q

Food does not reduce the amount of prednisone absorbed

A

True (only delays absorption)

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16
Q

Food delays the absorption of prednisone

A

True (but does not reduce the amount absorbed)

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17
Q

80-90% of endogenous cortisol/hydrocortisone is bound to cortisol-binding globulin

A

True (the free fraction represents the active form)

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18
Q

The free fraction of cortisol is the active form

A

True

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19
Q

The primary endogenous carrier protein for cortisol is cortisol-binding globulin and it is a low capacity high affinity binding system

A

True (in contrast to albumin which is a high capacity but low affinity reserve)

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20
Q

The binding of synthetic exogenous corticosteroids to plasma proteins (cortisol-binding globulin or albumin) is less than the avidity with which endogenous cortisol is bound, hence a greater free fraction of exogenous corticosteroid is available

A

True

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21
Q

Prednisolone (active analog of prednisone) binds to plasma carrier proteins with greater affinity to other exogenous forms, with resultant potential for displacement of endogenous cortisol from the protein-binding sites

A

True

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22
Q

Cortisol-binding globulin is decreased in hypothyroidism which may result in increased amount of the endogenous and synthetic corticosteroid free fraction

A

True

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23
Q

Cortisol-binding globulin is decreased in liver disease which may result in increased amount of the endogenous and synthetic corticosteroid free fraction

A

True

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24
Q

Cortisol-binding globulin is decreased in renal disease which may result in increased amount of the endogenous and synthetic corticosteroid free fraction

A

True

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25
Q

Cortisol-binding globulin is decreased in obesity which may result in increased amount of the endogenous and synthetic corticosteroid free fraction

A

True

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26
Q

Cortisol-binding globulin is increased by estrogen therapy which may reduce the endogenous and synthetic corticosteroid free fraction

A

True

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27
Q

Cortisol-binding globulin is increased by pregnancy which may reduce the endogenous and synthetic corticosteroid free fraction

A

True

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28
Q

Cortisol-binding globulin is increased by hyperthyroidism which may reduce the endogenous and synthetic corticosteroid free fraction

A

True

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29
Q

High dose corticosteroid therapy results in greater proportion of corticosteroid free fraction

A

True

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30
Q

Prolonged corticosteroid treatment increase the corticosteroid free fraction

A

True

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31
Q

All endogenous and synthetic corticosteroid are well distributed into Fetal tissue except prednisone (inactive form)

A

True

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32
Q

Gluconeogenesis is a glucocorticoid effect that generates glucose at the expense of amino acids derived from endogenous proteins (glucose metabolism)

A

True

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33
Q

The glucocorticoid effect of Corticosteroids produce peripheral insulin resistance which impedes glucose absorption by various body tissues (glucose metabolism)

A

True

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34
Q

The glucocorticoid effect of corticosteroids is to enhance glycogen storage in the liver (glucose metabolism)

A

True

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35
Q

The glucocorticoid effect of corticosteroids is to stimulate lipid stores to undergo lipolysis, thus generating increased amounts of triglycerides for which to derive energy (lipid metabolism)

A

True

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36
Q

The net glucocorticoid effect of corticosteroids is a catabolic state that produces carbohydrates at the expense of protein and fat stores

A

True

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37
Q

The glucocorticoid effect of corticosteroids is to redistribute fat to central locations resulting in lipodystrophy that’s is characteristic for the body habitus in Cushing’s syndrome (lipid metabolism)

A

True

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38
Q

Corticosteroids are metabolised in the liver and extrahepatic sites to form relatively water soluble metabolites which are then excreted in the kidneys

A

True

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39
Q

11 beta-hydroxysteroid dehydrogenase in the liver is necessary to covert cortisone to cortisol (hydrocortisone), and to convert prednisone to prednisolone

A

True (therefore only cortisol and prednisolone are biologically active here)

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40
Q

Severe liver disease may impair the conversion of cortisone to cortisol (hydrocortisone) and prednisone to prednisolone by 11 beta-hydroxysteroid dehydrogenase

A

True (therefore prednisolone is more appropriate in patients with liver disease than prednisone)

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41
Q

The administration of prednisolone rather than prednisone to patients with advanced liver disease is appropriate

A

True (as conversion of prednisone to prednisolone is mediated by 11 beta-hydroxysteroid dehydrogenase in the liver)

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42
Q

The plasma half lives of the various exogenous synthetic corticosteroids do not correlate well with the duration of biological activity I.e. Short, intermediate, long acting (potency)

A

True (a much more important measure of duration of activity is the duration of ACTH suppression after the administration of a single dose of corticosteroid)

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43
Q

The duration of activity of corticosteroids correlate well with glucocorticoid and anti-inflammatory effects (potency)

A

True

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44
Q

There is an inverse correlation between the duration of action and the relative mineralocorticoid effects of corticosteroids

A

True (long acting dexamethasone and betamethasone don’t have mineralocorticoid activity, in contrast to short acting cortisone and cortisol/hydrocortisone)

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45
Q

Prednisone and prednisolone (intermediate acting corticosteroid) have mild mineralocorticoid activity

A

True (in contrast to the other intermediate acting corticosteroid methylprednisolone and Triamcinolone which do not exhibit mineralocorticoid activity)

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46
Q

The hypothalamus secretes CRF (corticotropin-releasing factor) which stimulates the anterior pituitary gland to produce ACTH

A

True

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47
Q

The anterior pituitary gland secretes ACTH (adrenocorticotrophic hormone) which stimulates the zona fasciculata of the adrenal cortex to produce and release cortisol

A

True

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48
Q

ACTH from the anterior pituitary gland also stimulates adrenal androgen synthesis

A

True

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49
Q

ACTH from the anterior pituitary gland is not involved in stimulating the release of the mineralocorticoid aldosterone from the adrenal glands

A

True

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50
Q

The basal production of cortisol of 20-30mg daily is equivalent to 5-7.5mg of prednisone daily

A

True

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51
Q

The maximal stress production of cortisol of 300mg daily is equivalent to 75mg daily of prednisone

A

True

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52
Q

The minor stress production of cortisol is about 2-3 times the basal production of 20-30mg daily

A

True

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53
Q

The hypothalamus is the first to be suppressed and the first to recover full function in response to exogenous corticosteroids and stress

A

True (therefore the hypothalamus is the most important part of the HPA-axis in terms of stress responsiveness)

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54
Q

The adrenal gland is the slower to be suppressed and much slower to recover full function in response to exogenous corticosteroids and stress

A

True

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55
Q

CRF from the hypothalamus (and hence ACTH from the anterior pituitary gland) have innate diurnal variations tied to sleep cycle with the highest production in mid-sleep and the lowest production in late afternoon

A

True

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56
Q

Increased cortisol levels reduce CRF and ACTH production

A

True

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57
Q

In response to stress, there is increased CRF release from the hypothalamus and subsequently increased ACTH release from the anterior pituitary

A

True

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58
Q

The hypothalamo-pituitary-adrenal axis serves to maintain glucose homeostasis

A

True

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59
Q

Corticosteroids play a role in maintaining adequate glucose levels for brain function

A

True

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60
Q

ACTH has no role in endogenous mineralocorticoid (aldosterone) production

A

True (the control is through the renin-angiotensin system and and serum potassium levels)

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61
Q

Aldosterone is the primary endogenous mineralocorticoid hormone

A

True

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62
Q

The primary effect of aldosterone is sodium reabsorption resulting in water reabsorption at the proximal tubule in the kidneys

A

True (as sodium is exchanged for potassium, an excessive mineralocorticoid effect leads to hypokalaemia)

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63
Q

Corticosteroid with significant mineralocorticoid effects I.e. Hydrocortisone have a similar effect on sodium, potassium, and fluid balance as aldosterone

A

True

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64
Q

Potassium is exchanged for sodium at the proximal tubules of the kidneys as a result of mineralocorticoid effects of aldosterone, and excessive mineralocorticoid effect may lead to hypokalaemia

A

True

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65
Q

Aldosterone production and regulation is via the renin-angiotensin system

A

True

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66
Q

The major priority for mineralocorticoids is to maintain sodium and fluid homeostasis, including normal blood pressure

A

True

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67
Q

There is only 1 glucocorticoid receptor (located in the cytoplasm) which accounts for the endogenous glucocorticoid effects as well as the pharmacological effects of synthetic corticosteroids

A

True

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68
Q

There are rare cases of hereditary glucocorticoid resistance, in which there are mutations in the glucocorticoid receptor (GCR) gene

A

True (although there are also cases of relative resistance which lack mutations or polymorphisms in the GCR gene)

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69
Q

Relative resistance to corticosteroids is due to altered corticosteroid bioavailability, altered ligand binding to the cytosolic glucocorticoid receptor (GCR), or altered translocation of the activated GCR complex to the nucleus and could represent a negative feedback system, with downregulation of the GCR after prolonged or high dose corticosteroid therapy

A

True

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70
Q

The 2 well described transcription factors with a central role in the amplification on the inflammatory response as a result of corticosteroids are nuclear factor kappa B (NFkB) and Activating Protein-1 (AP-1)

A

True (there is tremendous overlap with the inflammatory response genes induced by NFkB and AP-1)

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71
Q

Nuclear factor kappa B (NFkB) is biologically inactive as long as it is bound to inhibitor kappa B (IkB), and NFkB is activated when any biological stimuli degrades IkB, thus freeing NFkB to be a biologically active transcription factor

A

True (coricosteroids increase production of IkB, therefore resulting in reduced free NFkB)

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72
Q

Corticosteroids reduces the effects of Nuclear factor kappa B (NFkB) in 2 ways - (1) increase the production of Inhibitor kappa B (IkB), resulting in more NFkB being bound to IkB leading to decreased free NFkB
(2) directly bind to free NFkB and thereby inhibiting the transcription factor

A

True

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73
Q

Corticosteroids can directly induce apoptosis in lymphocytes and eosinophils

A

True (this could explain the effect of corticosteroid in autoimmune disorders, allergic disorders, and neoplastic disorders)

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74
Q

The effect of corticosteroids in inducing apoptosis in lymphocytes and eosinophils may be an a underlying explanation for corticosteroid effects in autoimmune disorders (apoptosis of auto-reactive T cells), allergic disorders (apoptosis of eosinophils), and certain neoplastic disorders (apoptosis of malignancy T cells)

A

True

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75
Q

Systemic fungal infections is an absolute contraindication for systemic corticosteroid therapy

A

True

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76
Q

Herpes simplex keratitis is an absolute contraindication for systemic corticosteroid therapy

A

True

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77
Q

Hypertension is a relative contraindication for systemic corticosteroid therapy

A

True (mineralocorticoid effect of sodium retention and glucocorticoid induced vasoconstriction worsens hypertension)

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78
Q

Congestive cardiac failure is a relative contraindication for systemic corticosteroid therapy

A

True (mineralocorticoid effect of sodium reabsorption and water reabsorption causing fluid overload)

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79
Q

Prior psychosis is a relative contraindication for systemic corticosteroid therapy

A

True (corticosteroids possibly precipitate this due to electrolyte shifts, altered nerve excitability, mild cerebral oedema from sodium and water retention)

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80
Q

Severe depression is a relative contraindication for systemic corticosteroid therapy

A

True

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81
Q

Active peptic ulcer disease is a relative contraindication for systemic corticosteroid therapy

A

True (corticosteroid may cause reduced mucus production and increased acid secretion)

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82
Q

Recent bowel anastomosis is a relative contraindication for systemic corticosteroid therapy

A

True (glucocorticoid catabolic effects producing decreased wound healing)

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83
Q

Active TB is a relative contraindication for systemic corticosteroid therapy

A

True (immunosuppressive effect of corticosteroids)

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84
Q

A positive tuberculin skin test is a relative contraindication for systemic corticosteroid therapy

A

True (immunosuppressive effect of corticosteroid and TB reactivation)

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85
Q

Diabetes is a relative contraindication for systemic corticosteroid therapy

A

True (corticosteroid effect on glucose metabolism resulting in hyperglycaemia)

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86
Q

Osteoporosis is a relative contraindication for systemic corticosteroid therapy

A

True (corticosteroid effect on bone metabolism resulting in increased osteoclasts activity, decreased osteoblast activity, decreased GI absorption of calcium, increased renal excretion of calcium - secondary hyperparathyroidism and bone resorption)

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87
Q

Cataracts is a relative contraindication for systemic corticosteroid therapy

A

True (corticosteroids cause altered lens proteins)

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88
Q

Glaucoma is a relative contraindication for systemic corticosteroid therapy

A

True

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89
Q

Pregnancy is a relative contraindication for systemic corticosteroid therapy

A

True

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90
Q

Systemic Corticosteroids can cause hyperlipidaemia due to lipolysis and fat redistribution

A

True

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91
Q

Systemic corticosteroids cause Cushingoid changes due to altered fat distribution from overall fat catabolism

A

True

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92
Q

Systemic corticosteroids may case growth impairment due to reduced growth hormone production resulting in delays skeletal maturation

A

True

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93
Q

Systemic corticosteroids may cause myopathy due to reduced glucose and amino acid uptake by muscle cells, leading to muscle atrophy and wasting

A

True

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94
Q

Systemic corticosteroids have a greater effect on T cells than B cells

A

True (B cell effects are more evident with higher doses of corticosteroids)

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95
Q

Systemic corticosteroids inhibit granulation of mast cells, resulting in decreased histamine release

A

True

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96
Q

Systemic corticosteroids reduce angiogenesis in wound healing and in proliferative lesions I.e. Haemangiomas

A

True

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97
Q

Systemic corticosteroids causes vasoconstriction

A

True

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98
Q

Brief bursts of systemic corticosteroids for 2-3 weeks is surprisingly safe and useful in self-limiting dermatoses

A

True

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99
Q

Lower dose long term systemic corticosteroid regimens at or very near replacement/physiologic levels of corticosteroid are reasonably safe

A

True

100
Q

There is an increased risk for more serious complications with supraphysiologic/pharmacologic corticosteroid doses longer than 3-4 weeks

A

True

101
Q

Systemic corticosteroids adverse effects on the HPA axis include steroid withdrawal syndrome and addisonian crisis

A

True

102
Q

Systemic corticosteroids glucocorticoid adverse effects include hyperglycaemia and increased appetite/weight gain

A

True

103
Q

Systemic corticosteroids mineralocorticoid adverse effects include hypertension, CCF, excessive weight gain and hypokalaemia

A

True (due to sodium retention and potassium loss)

104
Q

Systemic corticosteroids lipid adverse effects include hypertriglyceridaemia, Cushingoid changes, and menstrual irregularity (decreased gonadotropin levels I.e. LH and FSH from the ovaries)

A

True (lipolysis and altered fat deposition = lipodystrophy)

105
Q

Systemic corticosteroids bone adverse effects include osteoporosis, osteonecrosis, and hypocalcaemia (indirect)

A

True

106
Q

Systemic corticosteroids GI adverse effects include peptic ulcer disease, bowel perforation, fatty liver, oesophageal reflux, nausea and vomiting

A

True

107
Q

Systemic corticosteroids ocular adverse effects include cataracts, glaucoma, infections, and refraction changes (from hyperglycaemia)

A

True

108
Q

Systemic corticosteroids psychiatric adverse effects include psychosis, agitation or personality change, depression (from prednisone phobia or dependency)

A

True

109
Q

Systemic corticosteroids neurological adverse effects include pseudotumour cerebri, epidural lipomatosis and peripheral neuropathy (? from hyperglycaemia)

A

True (interestingly pseudotumour cerebri is also an adverse effect of retinoids, and both glucocorticoid and retinoid receptors are part of the same receptor family)

110
Q

Systemic corticosteroids infectious adverse effects include TB reactivation and opportunistic infections (I.e. Deep fungi), and prolonged herpes virus infections

A

True

111
Q

IV methylprednisolone pulse therapy may cause electrolyte shifts leading to cardiac dysrhythmias and seizures

A

True

112
Q

IV methylprednisolone pulse therapy may cause cardiac dysrhythmias (from the electrolyte shifts) and cardiac monitoring is recommended

A

True

113
Q

IV methylprednisolone pulse therapy may cause seizures (from the electrolyte shifts)

A

True

114
Q

Systemic corticosteroids may result in opportunistic malignancies

A

True

115
Q

Prednisone bursts commonly cause increased appetite and weight gain

A

True

116
Q

Prednisone bursts commonly cause fluid retention with oedema and possibly weight gain

A

True

117
Q

Prednisone bursts commonly cause patients to be wired or weird

A

True

118
Q

Prednisone bursts commonly cause some patients to be be depressed during the tapering phase

A

True

119
Q

Prednisone bursts commonly cause mild GI symptoms

A

True

120
Q

Systemic corticosteroids may affect wound healing and result in non-healing wounds, ulcers, striae, atrophy and telengiectasia

A

True (from decreased collagen/ground substance/re-epithelialisation/angiogenesis)

121
Q

Systemic corticosteroids may affect the pilosebaceous unit and result in steroid acne and steroid Rosacea

A

True ( prom pityrosporum ovale and androgenecity)

122
Q

Systemic corticosteroids may affect the vascular system and result in purpura

A

True (due to catabolic effects on vascular smooth muscle)

123
Q

Systemic corticosteroids may affect the susceptibility for cutaneous infections and result in staphylococcal and herpes virus infections

A

True

124
Q

Systemic corticosteroids may affect hair growth and result in telogen effluvium and hirsutism

A

True (androgenic effects causing hirsutism, uncertain mechanism for telogen effluvium)

125
Q

Systemic corticosteroids may cause flare of pustular psoriasis and rebound of poison ivy/oak contact dermatitis

A

True

126
Q

Systemic corticosteroids may cause acanthosis nigricans

A

True (due to causing insulin resistance)

127
Q

Injectable corticosteroids may result in fat atrophy and crystallisation of injectable material

A

True (due to lipolysis of subcutaneous fat)

128
Q

Greater HPA axis suppression is observed with shorter intervals of low dose IM corticosteroid administration rather than with longer intervals of high dose treatment

A

True (low dose IM steroid at 2-4 week intervals produced greater suppression that’s higher doses at 6 week intervals)

129
Q

Oral corticosteroid is preferred over IM corticosteroid due to the precision of dosing and active patient participation

A

True (only exception would be in various subsets of hand dermatoses where there is thick stratum corneum on the palms and the general challenge of successfully treating this topically, long acting IM Triamcinolone I.e. Kenalog may be considered for 2-3 times a year)

130
Q

IM corticosteroids may cause cold abscess at the injection site

A

True

131
Q

IM corticosteroids may cause subcutaneous fat atrophy at the injection site

A

True

132
Q

IM corticosteroids may cause crystal deposition at the injection site

A

True

133
Q

Oral and IM corticosteroids may cause menstrual irregularities due to decreased gonadotropin levels

A

True (traditionally, menstrual abnormalities were thought to be due to IM corticosteroids only)

134
Q

IM corticosteroids may cause increased incidence of purpura as compared to oral regimens

A

True

135
Q

Sudden death of presumed cardiac origin is a notable complication of Pulse IV methylprednisolone, although the vast majority of cardiac complications have occurred outside of dermatologic settings

A

True (acute electrolyte shifts have been postulated)

136
Q

Careful potassium infusions may minimise the risk of potentially serious cardiac adverse effects from pulse IV methylprednisolone therapy

A

True (acute electrolyte shifts postulated)

137
Q

Pulse IV methylprednisolone may potentially cause life threatening anaphylaxis

A

True

138
Q

The suppression of lymphocyte subsets is greater with pulse IV methylprednisolone therapy than with standard doses of oral corticosteroid therapy, with corticosteroid induced apoptosis likely to play a key role in this effect

A

True

139
Q

The abrupt cessation of corticosteroid in patients undergoing major stressors I.e. Major surgery, trauma, illness, severe gastroenteritis with fluid and electrolyte loss may precipitate an adrenal crisis

A

True

140
Q

High systemic corticosteroid dose in patients with a family/personal history of diabetes, obesity may precipitate hyperglycaemia

A

True

141
Q

Administration of systemic corticosteroid with high mineralocorticoid effect (fludrocortisone, hydrocortisone, prednisone, prednisolone), prolonged therapy for over 1 year and pulse IV corticosteroid therapy in patients with a prior history of hypertension/elderly patients may precipitate hypertension

A

True

142
Q

Administration of a systemic corticosteroid with high mineralocorticoid effect in patients with prior well or partially compensated CCF may precipitate CCF

A

True

143
Q

High dose systemic corticosteroids in patients with a personal/family history of hyperlipidaemia, diabetes, hypothyroidism or high fat calorific intake may precipitate hyperlipidaemia

A

True

144
Q

Systemic corticosteroid therapy for at least 2-3 months in patients with excessive calorific intake due to increased appetite may precipitate Cushingoid changes

A

True

145
Q

Chronic pharmacologic dose systemic corticosteroids therapy in children with organ transplant or autoimmune condition requiring indefinite corticosteroid therapy may cause growth impairment

A

True (although catch up growth is possible when corticosteroids are reduced to physiologic levels or below)

146
Q

Systemic corticosteroid therapy in female patients who are elderly, thin, inactive may precipitate osteoporosis

A

True (men at risk as well)

147
Q

Continuous pharmacologic corticosteroid therapy for at least 2-3 months in patient with signifying trauma, smoking, alcohol abuse hypercoagulable conditions and hyperlipidaemia are at increased risk of osteonecrosis

A

True

148
Q

Dose and duration of corticosteroid therapy is not a key determinant of risk of bowel perforation

A

True (recent bowel anastomosis and active diverticulitis are main risks)

149
Q

Total corticosteroid dose of 1g in patients on concomitant aspirin, NSAID therapy, history of peptic ulcer disease or autoimmune connective tissue disease are at increased risk of peptic ulcer disease

A

True

150
Q

Corticosteroid dose of at least 40mg/day and particularly at doses above 80mg/day in patients with a family history of psychosis, baseline high anxiety and female gender are at increased risk for agitation and psychosis

A

True

151
Q

Prolonged high corticosteroid dose in patients on multi drug immunosuppression therapy and organ transplant patients are at risk of opportunistic infections

A

True

152
Q

Fluorinated corticosteroids and rapid tapering of corticosteroids in patients with lack of exercise are at risk of myopathy

A

Tru

153
Q

Sodium restriction and using a corticosteroid with low mineralocorticoid effect can prevent corticosteroid-induced hypertension

A

True (monitor blood pressure)

154
Q

Low calorie and low saturated fat diet can prevent corticosteroid-induced hyperlipidaemia

A

True (may need statins or gemfibrozil to treat resulting hyperlipidaemia)

155
Q

Calcium and vitamin D can prevent corticosteroid-induced osteoporosis

A

True (consider serial DEXA scans for monitoring, and bisphosphonates may be required to treat if result in osteoporosis)

156
Q

Avoidance of trauma/alcohol excess/smoking can prevent corticosteroid-induced osteonecrosis

A

True

157
Q

Caution with administration of corticosteroids after bowel surgery can prevent corticosteroid-induced bowel perforation

A

True

158
Q

Administration of H2 antihistamines in higher risk patients can prevent corticosteroid-induced peptic ulcer disease

A

True (history and consider upper GI endoscopy)

159
Q

Sunglasses may help prevent corticosteroid-induced cataracts

A

True (consider slit lamp exam every 6-12 months)

160
Q

Doxepin (if agitation present) and possible antipsychotics may be needed to managed corticosteroid-induced psychosis

A

True

161
Q

Exercise and caution with corticosteroid tapering after high dose therapy can prevent corticosteroid-induced myopathy

A

True

162
Q

Significant corticosteroid-induced hyperlipidaemia increases the risk of pancreatitis

A

True

163
Q

Adrenal crisis is a potentially fatal corticosteroid complication that can be avoided through aggressive emergency room or postoperative preventative and therapeutic measures

A

True (this complication is distinctively uncommon in the current era due to heightened awareness)

164
Q

Bowel perforation is a potentially fatal preventable corticosteroid complication where tremendous caution is needed with the use of systemic corticosteroid after recent bowel anastomosis and with active diverticulitis

A

True

165
Q

Peptic ulcer perforation (gastric ulcer more common than duodenal ulcer) is a potentially fatal corticosteroid complication most likely to occur in patients with adjunctive NSAID drugs and history of peptic ulcer disease

A

True (albeit controversial, proactive use of H2 antagonist or PPI for patients with prior history of peptic ulcer disease and for patients with symptoms even possibly related to peptic ulcer disease is suggested)

166
Q

Pancreatitis is a potentially fatal corticosteroid complication resulting from severe triglyceride elevations and the possible role of increased viscosity of pancreatic secretions leasing to obstruction

A

True (any reports of severe abdominal pain must be intervened promptly)

167
Q

Severe hyperglycaemia (diabetic ketoacidosis) is a potentially fatal corticosteroid complication most likely to occur with pre-existing diabetes mellitus

A

True (the widespread availability of home glucose monitoring has made this a rare complication)

168
Q

Opportunistic infections is a potentially fatal corticosteroid complication more likely in patients with multidrug immunosuppressive regimens common with organ transplantation

A

True

169
Q

Immunosuppression carcinogenesis/opportunistic malignancies predominantly from viral induced malignancies (Kaposi’s sarcoma, non-Hodgkins lymphoma, SCC) is a potentially fatal corticosteroid complication in patients on immunosuppression regimen in organ transplantation setting

A

True (although Kaposi’s sarcoma may be associated with corticosteroid use alone without HHV-8 aetiology)

170
Q

Multiple studies in humans concerning patients with corticosteroid-dependent systemic conditions during pregnancy have demonstrated no significantly increased risk of congenital malformations in humans I.e. Not teratogenic

A

True (although systemic corticosteroids should be used only when the drug is clearly indicated and if the potential benefits far exceed the potential risk to the mother and fetus)

171
Q

Fetal HPA-axis suppression is important to consider when systemic corticosteroid therapy is used near the time of delivery as there may an increased risk of stillbirth and spontaneous abortion

A

True

172
Q

Secondary exogenous adrenal insufficiency due to prolonged high dose corticosteroid therapy for at least 3-4 weeks results in no significant mineralocorticoid abnormalities (normal), no increased ACTH production (normal) and no pituitary tropic hormone abnormalities (normal)

A

True (significant mineralocorticoid reduction with resultant fluid and electrolyte abnormalities and increased ACTH production with resultant hyperpigmentation from stimulatory effect on melanocytes are noted only in primary adrenal insufficiency I.e. Addison’s disease)

173
Q

Corticosteroid doses exceeding physiologic levels for at least 3-4 weeks can produce clinically relevant mild HPA-axis suppression

A

True

174
Q

Divided dose regimens and single dose therapy given at a time other than the morning will increase the risk of HPA-axis suppression

A

True

175
Q

The longer acting corticosteroid preparations are more likely to produce HPA-axis suppression than are short and intermediate duration corticosteroid

A

True

176
Q

Even though alternate day corticosteroid therapy lessens the risk of HPA-axis suppression, it does not speed the recovery once this suppression occurs

A

True

177
Q

The direct corticosteroid effect in producing elevated blood glucose is much slower than the catecholamine response and both ACTH and cortisol can indirectly induce rapid glucose elevation through release of epinephrine/adrenaline

A

True

178
Q

The primary test of basal HPA-axis function is the morning cortisol level and this tests the function of the adrenal gland

A

True (peak level is at 8am and the trough level is late afternoon) - generally recommended to omit the morning corticosteroid dose on the day the cortisol level is checked

179
Q

With prolonged corticosteroid therapy, cortisol levels <10 mg/dL suggest impaired basal HPA-axis function

A

True

180
Q

The ACTH stimulation test is a provocative test of the function of the adrenal gland under stress, and not a test of the function of the entire HPA-axis

A

True

181
Q

In Steroid withdrawal syndrome there is no change in the serum cortisol level, although it has been postulated that there may be a sudden decrease in corticosteroid available at the cellular level

A

True

182
Q

Steroid withdrawal syndrome is precipitated by abrupt corticosteroid tapering with intermediate and chronic duration therapy

A

True (at pharmacologic doses beyond 2-3 weeks it is possible to develop steroid withdrawal syndrome) - the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms

183
Q

Mild to moderate steroid withdrawal syndrome is characterised by fatigue and lethargy

A

True (the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms)

184
Q

Mild to moderate steroid withdrawal syndrome is characterised by mood swings

A

True (the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms)

185
Q

Mild to moderate steroid withdrawal syndrome is characterised by headache

A

True (the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms)

186
Q

Mild to moderate steroid withdrawal syndrome is characterised by arthralgias and myalgias

A

True (the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms)

187
Q

Severe steroid withdrawal syndrome is characterised by the GI symptoms anorexia, nausea and vomiting

A

True (the return to higher corticosteroid doses with more gradual subsequent corticosteroid tapering will typically eliminate the symptoms)

188
Q

A systematic review noted that there was no perioperative haemodynamic compromise in the absence of corticosteroid stress doses in patients who have been on prolonged pharmacologic doses of corticosteroid therapy

A

True (therefore in the absence of primary/adrenal or secondary/hypothalamus or pituitary insufficiency, patients simply need to take their daily current maintenance dose of corticosteroid I.e. Physiologic doses would suffice) - this has challenged the traditional approach of supplementing higher doses during stress

189
Q

The majority of potentially serious drug interactions involving systemic corticosteroids are due to dexamethasone and methylprednisolone

A

True (few involve prednisone or prednisolone)

190
Q

Azole antifungal agents I.e. Ketoconazole may increase the levels and potential toxicity of various corticosteroids as it is a potent CYP3A4 inhibitor

A

True (metabolism of corticosteroids generally take place in the liver)

191
Q

Macrolide antibacterial agents I.e. Erythromycin > clarithromycin may increase the levels and potential toxicity of various corticosteroids as it is a potent CYP3A4 inhibitor

A

True (metabolism of corticosteroids generally take place in the liver)

192
Q

Sex steroids I.e. Estrogens and oral contraceptives may increase the half life and decrease the clearance of various corticosteroids

A

True (thus increasing the potential toxicity of corticosteroids)

193
Q

Anticonvulsants I.e. Phenytoin and phenobarbital may decrease the levels and activity of various corticosteroids as it is a CYP3A4 inducer

A

True (metabolism of corticosteroids generally take place in the liver)

194
Q

Anti-tuberculous therapy I.e. Rifampin may decrease the levels and activity of various corticosteroids as it is a CYP3A4 inducer

A

True (metabolism of corticosteroids generally take place in the liver)

195
Q

Aminoglutethimide may reduce the serum level and activity of various corticosteroids due to dexamethasone-induced adrenal suppression

A

True

196
Q

Cholestyramine may decrease the levels of hydrocortisone

A

True

197
Q

Ephedrine may decrease the half life and increase the clearance of dexamethasone

A

True

198
Q

Systemic corticosteroids may increase the serum levels and potential toxicity of diuretics (potassium-depleting ones) as the hypokalaemia potential of the diuretics may be aggravated by corticosteroid potassium loss

A

True (particularly in corticosteroids with mineralocorticoid activity)

199
Q

Systemic corticosteroids (primarily methylprednisolone) may increase the serum levels and potential toxicity of immunosuppressants I.e. Cyclosporine (similar to corticosteroids, CsA is also a substrate of CYP3A4)

A

True (cyclosporine in combination with corticosteroid is standard in transplantation and for autoimmune disorders)

200
Q

Systemic corticosteroids may increase the serum levels and potential toxicity of inotropic agents I.e. Digitalis glycosides due to corticosteroid-induced potassium loss

A

True (particularly for corticosteroids with mineralocorticoid activity)

201
Q

Corticosteroids may induce a state of insulin resistance, thereby reducing the efficacy of insulin and resulting in increased blood glucose

A

True

202
Q

Corticosteroids may reduce the serum levels and efficacy of salicylates

A

True

203
Q

Corticosteroids may reduce the serum levels of isoniazid antituberculous therapy

A

True

204
Q

Corticosteroids may increase or decrease warfarin anticoagulant activity

A

True (unpredictable effect)

205
Q

Concomitant usage of Corticosteroids and xanthine bronchodilators may result in alterations in either theophylline or corticosteroid activity

A

True

206
Q

When anticipating long term corticosteroid therapy, consider baseline screening blood pressure, weight and ophthalmoscopic examination for cataracts

A

True (risk of hypertension, weight gain and cataracts)

207
Q

When anticipating long term corticosteroid therapy, strongly consider baseline TB screening using the tuberculin skin test and chest X-Ray

A

True (risk of opportunistic infections I.e. tab and reactivation of latent TB)

208
Q

When anticipating long term corticosteroid therapy, consider baseline fasting glucose level and triglycerides as well as potassium level

A

True (risk of hyperglycaemia, hyperlipidaemia and hypokalaemia)

209
Q

During follow up of patients on long term corticosteroid therapy above physiologic/at pharmacologic doses, perform blood pressure and weight and a thorough history for adverse effects at 1 month and then every 2-3 months

A

True

210
Q

During follow up of patients on long term corticosteroid therapy above physiologic/at pharmacologic doses, consider ophthalmology examination for cataracts and glaucoma every 6 to 12 months

A

True (6 months initially and at least 12 months long-term)

211
Q

During follow up of patients on long term corticosteroid therapy above physiologic/at pharmacologic doses, monitor fasting glucose, fasting triglycerides and potassium levels at 1 month and then every 3-4 months

A

True

212
Q

Near the time of cessation of long term pharmacologic dose corticosteroid therapy, consider the morning cortisol level to assess basal adrenal function or a test of the entire HPA-axis

A

True (optional, and most clinical scenarios in dermatology do not require his morning cortisol testing)

213
Q

Consider cardiac monitoring during pulse IV methylprednisolone therapy

A

True (risk of fatal cardiac dysrhythmias due to electrolyte shifts)

214
Q

Consider daily electrolyte and glucose levels during pulse IV methylprednisolone therapy

A

True

215
Q

Seek to attain physiologic or alternate-day doses of corticosteroid therapy within 1-2 months, if this is not possible (or unlikely to be possible) then use ‘steroid-sparing therapy’

A

True

216
Q

To maximise the safety of systemic corticosteroids, use “attack” (quickly control the disease process), then reasonably quickly “retreat” (taper corticosteroid) philosophy

A

True

217
Q

In the presence of a relative contraindication for systemic corticosteroid therapy, medical management of this relative contraindication may allow careful corticosteroid therapy

A

True

218
Q

The careful clinician will anticipate risk factors and relative contraindications associated with systemic corticosteroid therapy

A

True

219
Q

The careful clinician will prevent adverse effects associated with systemic corticosteroid therapy by being proactive and take preventative measures

A

True (I.e. H2 antagonists or PPI for patients at risk of peptic ulcer disease)

220
Q

The careful clinician will diagnose the adverse effects associated with systemic corticosteroid therapy early by monitoring labs, encouraging home monitoring and educating patients and increasing their awareness about the potential adverse effects

A

True

221
Q

The careful clinician will manage adverse effects associated with systemic corticosteroid therapy

A

True

222
Q

Corticosteroid therapy given as a single oral dose in the morning with an intermediate-duration corticosteroid such as prednisone most closely approximates the body’s own diurnal variation of cortisol production

A

True (divided doses, typically given twice daily are reserved for acute therapy for severe potentially life threatening illnesses such as Pemphigus vulgaris)

223
Q

Divided doses of systemic corticosteroids, typically given twice daily are reserved for acute therapy for severe potentially life threatening illnesses such as Pemphigus vulgaris

A

True

224
Q

When a constant total daily dose is given, divided-dose regimens have greater therapeutic benefits than equivalent daily-dose regimens

A

True (although divided-dose regimens produce a greater risk of adverse effects than a comparable dose given as a single daily-dose)

225
Q

Divided-dose corticosteroid regimens produce a greater risk of adverse effects than a comparable dose given as a single daily-dose

A

True (although divided-dose regimens have greater therapeutic benefits)

226
Q

The briefer the duration for which corticosteroid therapy exceeds physiologic doses, the lower the risk of significant adverse effects

A

True

227
Q

Brief bursts of corticosteroid therapy are 2-3 weeks or less

A

True

228
Q

Intermediate-duration corticosteroid therapy is over 3-4 weeks and up to 3-4 months at the most

A

True

229
Q

Physiologic/replacement corticosteroid therapy is 5-7.5mg daily of prednisone or its equivalent

A

True

230
Q

Pharmacologic dosage ranges at the initiation of therapy include high dose (>60mg daily prednisone), moderate dose (40-60mg daily prednisone) and low dose (<40mg daily prednisone)

A

True (apart from potentially life threatening dermatoses such as Pemphigus vulgaris and bullous pemphigoid, most dermatologic conditions can be controlled by moderate to low dosage regimens)

231
Q

Prednisone is generally the systemic corticosteroid of choice for most dermatoses

A

True (the prednisone duration of action is optimal for allowing daily or alternate-day therapy)

232
Q

In Europe, prednisolone is commonly used instead of prednisone

A

True

233
Q

Prednisolone (1) requires no metabolic conversion to be active; (2) has a quicker onset of action; (3) has a cortisol-binding globulin affinity greater than that of prednisone

A

True (drawbacks to prednisolone use is its greater cost and smaller number of dosage options I.e. Only in 5mg tablets and liquid formulations)

234
Q

Overall, the mineralocorticoid effect and duration of action are much more important factors in the choice of corticosteroid therapy than is the anti-inflammatory potency of the product

A

True (as various preparations have equivalent anti-inflammatory efficacy at therapeutically equivalent doses)

235
Q

Prednisone and prednisolone share a reasonable profile of mineralocorticoid effect and duration of action compared to other short acting alternatives

A

True

236
Q

The mineralocorticoid effect of hydrocortisone is excessive (should the potential for sodium and fluid retention be deleterious to a specific patient) and may not allow for steady state day-long control of disease activity

A

True

237
Q

The prednisone dose should be increased to the last effective dose level if a significant disease flare occurs during the tapering process

A

True

238
Q

The risk of cataracts, osteoporosis and possibly osteonecrosis are not reduced by alternate-day corticosteroid therapy

A

True

239
Q

The type I Isoform of 11 beta-hydroxysteroid dehydrogenase catalyses conversion of endogenous cortisone (inactive) to cortisol (active), and converts exogenous prednisone (inactive) to prednisolone (active), whereas the type II Isoform of the same enzyme reverses this conversion and reverting the active forms back to the inactive forms

A

True (dexamethasone and betamethasone are active independently of this enzyme)

240
Q

Night time dosing of corticosteroid tends to produce greater HPA-axis suppression

A

True

241
Q

Cortisol (hydrocortisone) and cortisone have the greatest mineralocorticoid activity

A

True

242
Q

Dexamethasone, betamethasone and methylprednisolone have the least mineralocorticoid activity

A

True

243
Q

Prednisone and prednisolone have intermediate mineralocorticoid activity

A

True

244
Q

Hypertension from corticosteroid has recently been found to be largely independent of their naturetic effect, and is probably more related to vasoconstriction and increased myocardial contractility (duration of effect and thus HPA-axis suppression)

A

True (the long acting betamethasone and dexamethasone produce a much greater risk of HPA-axis suppression than intermediate acting prednisone, prednisolone and methylprednisolone)

245
Q

The relative risk of TB for prednisone doses of at least 15mg daily are 8 times higher than doses < 15mg daily

A

True

Derm Pharm 2020 (47 decks)

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