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pt > L 16 and 17 corticosteriods > Flashcards

L 16 and 17 corticosteriods Flashcards

1
Q

what hormones does the cortex of the adrenal glands produce

A

glucocorticoids, mineralocrotoids, androgens

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2
Q

what hormones does the medulla of the adrenal glands produce

A

epinephrine, norepinephrine

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3
Q

what are glucocorticoids

A

-stress hormone
-increase circulating glucose concentrations
-potent anti inflammatory effects

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4
Q

what are mineralocorticoids

A

-Na+ retention
-increase blood volume
-increase blood pressure

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5
Q

what does epinephrine do in the action of stress hormones

A

-binds to beta-adrenergic receptor (GPCR)
-initiates signal transduction cascade
-induces immediate response
-breaks down glycogen and release glucose

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6
Q

what does cortisol do in terms of action of stress hormones

A

-binds to glucocorticoid receptor (nuclear hormone receptor)
-regulates gene transduction, and thus translation and protein production
-induces long term, persistent biological response
-induces gluconeogenic enzymes
-inhibit pro inflammatory processes

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7
Q

CRH?

A

corticotropin releasing hormone

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8
Q

ACTH?

A

-corticotropin
-adrenocorticotropic hormone

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9
Q

regulation of mineralocorticoids synthesis

A

-when the pituitary glands is surgically removed in animals, aldosterone synthesis is not affected significantly
-the anterior pituitary does not control the synthesis of mineralocorticoids
-renin-angiotensin-aldosterone system

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10
Q

hormone response elements

A

-DNA binding of activated dimers bind to specific DNA sequences called GRE, upstream of steroid responsive genes
-binding alters rate of transcription

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11
Q

GRE?

A

glucocorticoid responsive elements

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12
Q

what kinds of enzymes do glucocorticoids up-regulate for gluconeogensis and anti inflammatory proteins

A

-PEP carboxykinase: catalyzes the rate limiting step in gluconeogensis
-lipocortin I: suppresses phospholipase A2, which has a critical role in eicosanoid synthesis

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13
Q

mechanisms of immunosuppression by glucocorticoids

A

-activated glucocorticoid receptor (GR) binds to NFkB and prevents binding of NFkB to its response element
-transcription of cytokine genes are repressed

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14
Q

physiologic effects of glucocorticoids on the liver

A

-increase gluconeogensis
-increase glycogen storage
-increase blood glucose levels

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15
Q

physiologic effects of glucocorticoids in the muscle

A

-promotes protein degradation
-decrease protein synthesis
-decrease sensitivity to insulin
-increase blood glucose levels

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16
Q

physiological effects of glucocorticoids in the adipose tissues

A

-promote lipolysis
-decrease sensitivity to insulin
-increase blood glucose levels

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17
Q

physiologic effects of glucocorticoids in the immune system

A

-block the synthesis of cytokines (immunosuppression)
-inhibit the production of eicosanoids (anti-inflammation)

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18
Q

adrenal insufficiency

A

-hypoadrenalism
-decreased secretion of steroid hormones by the adrenal cortex
-cessation of long-term systemic glucocorticoid therapy can lead to addisonian symptoms

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19
Q

causes of adrenal insufficiency

A

-destruction of the cortex by tuberculorsis or atrophy (primary; addison’s disease)
-deceased secretion of adrenocorticotropin (ACTH) due to disease of anterior pituitary (secondary; no hypoalderosteronism)

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20
Q

symptoms of adrenal insufficiency

A

-extreme weakness
-anorexia, anemia, nausea, vomiting
-low blood pressure (only in primary)
-hyperpigmentation of the skin (only in primary)
-mental depression

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21
Q

primary adrenal insufficiency

A

-adrenal defect
-increase in CRH and ACTH
-decrease in cortisol and aldosterone

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22
Q

secondary adrenal insufficiency

A

-pituitary defect
-increase in CRH
-decrease in ACTH and cortisol
-aldosterone is not affected

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23
Q

tertiary adrenal insufficiency

A

-hypothalamic defect
-decrease in CRH, ACTH, and cortisol
-aldosterone is not affected

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24
Q

cushing disease

A

-hyperadrenalism
-long term therapeutic use of systemic glucocorticoids can lead to Cushing symptoms

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25
Q

cushing disease causes

A

-tumors in the adrenal cortex (adrenal cushing disease)
-increased production of ACTH due to pituitary carcinoma (pituitary cushing disease)
-ectopic production of ACTH due to non-pituitary carcinoma (ectopic cushing disease)

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26
Q

symptoms of cushing disease

A

-increased protein catabolism (easy bruising, delayed wound healing, muscle wasting) and increased glucose levels
-osteoporosis
-opportunistic infections

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27
Q

adrenal cushing disease

A

-decrease in CRH and ACTH
-decrease in cortisol

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28
Q

-pituitary cushing disease

A

-decrease in CRH
-increase in ACTH and cortisol

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29
Q

ectopic cushing disease

A

-decrease in CRH and ACTH
-increase in cortisol and ectopic ACTH

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30
Q

therapeutic uses of corticosteroids

A

-primary adrenal insufficiency (addisons diease)
-allergic reactions
-inflammation and autoimmune disease
-asthma
-immunosuppressive
-anti cancer

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31
Q

allergic reactions treated by corticosteroids

A

insect stings
angioedema

32
Q

inflammation and autoimmune disease treated by corticosteroids

A

-Bursitis, synovitis, tendonitis
-Rheumatoid arthritis
-Systemic lupus erythematosus (SLE or lupus)
-Inflammatory bowel disease
-Chronic hepatitis

33
Q

cortisol vs cortisone

A

-oxidation of 11 hydroxyl to ketone inactivated glucocorticoids
-cataylzed by 11 beta-hydroxysteroid dehydrogenase in the liver
-the reaction is reversible
*cortisone is as effective as cortisol, when used systemically
*cortisone should not be used to patients with impaired liver functions

34
Q

short acting systemic corticosteroids

A

-half life in tissues = 8 – 12 hrs
-Hydrocortisone
-Cortison

35
Q

intermediate-acting systemic corticosteroids

A

-half life in tissues= 12-36 hrs
-prednison
-prednisolone
-methylprednisolone
-triamcinolone

36
Q

long acting systemic corticosteroid

A

-half life in tissues= 36-54 hrs
-dexamethasone
-betamethasone

37
Q

synthetic glucocorticoids: fludrocortisone

A

-9 alpha-F
-greater glucocorticoid activity
-strong mineralocorticoid activity
(intense Na+ retention leading to edema)
-used in mineralocorticoid replacement therapy

38
Q

synthetic glucocorticoids: prednisone/ prednisolone

A

-extra double bond between C1 and C2 (altered ring structure)
-more potent glucocorticoid activity (stronger binding to the glucocorticoid receptor)
-reduced mineralocorticoid activity
-interconvertible by 11 beta-hydroxysteroid dehydrogenase

39
Q

synthetic glucocorticoids: methylprednisolone

A

-6 alpha-methyl group
-potency similar to that for prednisolone
-reduced mineralocorticoid activity

40
Q

synthetic glucocorticoids: trimacinolone

A

-9 alpha-F and 16 alpha-OH
-glucocorticoid activity similar to prednisone
-reduced mineralocorticoid activity
-increased hydrophilicity
-low oral bioavailability

41
Q

synthetic glucocorticoids: dexamethsone

A

-16 alpha-methyl group
-increased lipophilicity (increased receptor binding and significantly stronger effect)
-increased stability in human plasma
-reduced mineralocorticoid activity

42
Q

synthetic glucocorticoids: bethamethasone

A

-Enantiomer of dexamethasone at 16
-Has similar properties as dexamethasone

43
Q

21 esters

A

the hydroxyl group at 21 can be modified to an ester to control the property of glucocorticoid
-prodrugs activated through the hyrolysis by esterases

44
Q

21 esters acetate and butyrate

A

-increased lipophilicity
-prolonged action upon IM or intra-articular injections

45
Q

21 esters succinate

A

-soluble
-slow hydrolysis (peak in 30-45 min)

46
Q

21 esters phosphate

A

-increased solubility
-rapid hydrolysis by phosphatases (10 min)
-IV or IM injection for emergency conditions

47
Q

mechanisms of glucocorticoid action in asthma

A

-glucocorticoids do not directly relax airway smooth muscle; little effect on acute bronchoconstriction
-effective in inhibiting airway inflammation
-inhaled glucocorticoids are used prophylactically to control asthma

48
Q

Glucocorticoids ______ stop an asthma attack while it is happening

A

will not

49
Q

how does glucocorticoids inhibit airway inflammation

A

-Modulation of cytokine and chemokine production
-Inhibition of eicosanoid synthesis
-inhibition of accumulation of immune cells in lung tissue
-Decreased vascular permeability

50
Q

how does Inhaled glucocorticoids are used prophylactically to control asthma

A

-Beneficial effects may be seen within 1 week; maximal improvement in lung function may not occur until after several weeks of treatment.
-Compliance is a significant concern

51
Q

inhaled glucocorticoids: desired properties

A

-High potency
-Minimal systemic effects
-Prolonged action

52
Q

inhaled glucocorticoids: solutions

A

-High lipophilicity
* Tighter binding to the receptor
*Better tissue penetration
*Prolonged action by forming poorly soluble microcrystals
-Low oral bioavailability
*70-90% of inhaled glucocorticoids is swallowed.
-Rapid clearance
*Short half-life

53
Q

inhaled glucocorticoids: triamcinolone acetonide

A

-acetonide is resistant to hydrolyisis
-8x more potent than prednisolone

54
Q

inhaled glucocorticoids: beclomethasone dipropionate

A

-converted rapidly to 12- monopropionate by hydrolysis
-14x more potent than dexamethsone

55
Q

inhaled glucocorticoids: flucisolide

A

-rapid absorption from nasal or lung tissue
-rapid metabolism by the liver
*extensive first pass metabolism
*minimal systemic adverse effect with long term therapy

56
Q

inhaled glucocorticoids: budesonide

A

-1:1 mixture of epimers at 16-17 butylactal
-faster topical uptake
-low oral bioavailability
-extensive first pass metabolism

57
Q

inhaled glucocorticoids: mometasone furoate

A

-highly potent
-more rapid onset of action
-negligible systemic availability
*rapid metabolism
*low oral bioavailability <1%

58
Q

inhaled glucocorticoids: fluticasone propionate

A

-inactivated by hydrolysis of thioester
*rapid first path metabolism
-highly lipophilic and insoluble
*high potent
*poor absorption from GI
* rapid topical uptake

59
Q

topical glucocorticoids desired properties

A

-High lipophilicity for fast absorption
-Minimal systemic effect
-Prolonged action

60
Q

topical glucocorticoids

A

-Halogenated analogues are usually potent topical glucocorticoids.
-Once absorbed through the skin, topical glucocorticoids are metabolized primarily
in the liver and excreted into the urine or in the bile.
-Glucocorticoids with low potency are safest for chronic application.
*Hydrocortisone cream
-Glucocorticoids with high potency can have a risk of systemic exposure; should be used only for a short duration of treatment.

61
Q

topical glucocorticoids actonide or ester forms have ____

A

better potency for topical applications due to high lipophilicity

62
Q

21 chlorocorticoids

A

-Substitution of a chlorine atom for the 21 hydroxyl group greatly enhances topical anti-inflammatory activity.

63
Q

topical glucocorticoids fluticasone propionate and mometasone furoate have only _____ potency

A

-medium
-High lipophilicity and the highest binding affinity, but poor solubility
-Poor dissolution into inflamed tissue

64
Q

adverse effects of glucocorticoids

A

-crossover mineralocorticoid activity
-metabolic effects (increased glucose production)
-cushing like effects (redistribution of fat)
-impaired glucose tolerance
-suppression of immune system
-gastrointestinal
-central nervous systems
-cataracts
-adrenal insufficiency upon withdrawal (addisons crisis)

65
Q

adverse effects of glucocorticoids: cross over mineralocorticoids activity

A

-Sodium and water retention
-Development of hypertension
-Correctable with selective synthetic glucocorticoids

66
Q

adverse effects of glucocorticoids; metabolic effects

A

-increased glucose production
-Steroid myopathy
*High doses over period of time cause wasting of proximal muscles (e.g. shoulder).
-Reduced long bone growth in children
*May cause premature closing of epiphyseal junction and stop growth.
-Osteoporosis
*Pharmacological doses of glucocorticoids inhibit osteoblasts.
*Can be prevented by bisphosphonate

67
Q

adverse effects of glucocorticoids: cushing life effects

A

-redistribution of fate
-moon face
-buffalo bump

68
Q

adverse effects of glucocorticoids: impaired glucose tolerance

A

-Hyperglycemia from gluconeogenesis
-Decreased insulin response
*A special problem with diabetes mellitus
*May unmask diabetes mellitus.

69
Q

adverse effects of glucocorticoids: suppression of immune system

A

-Increased susceptibility to infections
-Impaired wound healing

70
Q

adverse effects of glucocorticoids: gastrointestinal

A

-greater peptic ulcer risk

71
Q

adverse effects of glucocorticoids: cental nervous system

A

-linked to glucose metabolism
-euphoria
-depression

72
Q

adverse effects of glucocorticoids: adrenal insufficiency upon withdrawal

A

-addison crisis
-Due to negative feedback on hypothalamus and pituitary from prolonged pharmacological doses of glucocorticoids
-Delayed recovery of hypothalamus and pituitary
-Depressed ACTH release and adrenal response to ACTH
-Directly related to dose and duration of therapy
-Symptoms
*Inability to withstand stress
*Hypotension
*Weakness

73
Q

systemic corticosteroids

A

-Hydrocortisone
-Cortisone
-Prednisone
-Prednisolone
-Methylprednisolone
-Dexamethasone
-Betamethasone

74
Q

systemic mineralocorticoid

A

Fludrocortisone (Florinef®

75
Q

inhaled glucocorticoids

A

-Triamcinolone acetonide (Azmacort®)
-Beclomethasone dipropionate (Vanceril ®, Qvar ®)
-Flunisolide (Aerobid ®)
-Budesonide (Pulmicort ®)
-Mometasone furoate (Asmanex®)
-Fluticasone propionate (Flovent ®

76
Q

topical glucocorticoids

A

-Triamcinolone acetonide
-Fluocinonide
-Betamethasone valerate
-Clobestasol propionate
-Halobetasol propionate
-Halcinonide

pt (17 decks)

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