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L 16 and 17 corticosteriods Flashcards

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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
cushing disease causes
-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)
26
symptoms of cushing disease
-increased protein catabolism (easy bruising, delayed wound healing, muscle wasting) and increased glucose levels -osteoporosis -opportunistic infections
27
adrenal cushing disease
-decrease in CRH and ACTH -decrease in cortisol
28
-pituitary cushing disease
-decrease in CRH -increase in ACTH and cortisol
29
ectopic cushing disease
-decrease in CRH and ACTH -increase in cortisol and ectopic ACTH
30
therapeutic uses of corticosteroids
-primary adrenal insufficiency (addisons diease) -allergic reactions -inflammation and autoimmune disease -asthma -immunosuppressive -anti cancer
31
allergic reactions treated by corticosteroids
insect stings angioedema
32
inflammation and autoimmune disease treated by corticosteroids
-Bursitis, synovitis, tendonitis -Rheumatoid arthritis -Systemic lupus erythematosus (SLE or lupus) -Inflammatory bowel disease -Chronic hepatitis
33
cortisol vs cortisone
-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
short acting systemic corticosteroids
-half life in tissues = 8 – 12 hrs -Hydrocortisone -Cortison
35
intermediate-acting systemic corticosteroids
-half life in tissues= 12-36 hrs -prednison -prednisolone -methylprednisolone -triamcinolone
36
long acting systemic corticosteroid
-half life in tissues= 36-54 hrs -dexamethasone -betamethasone
37
synthetic glucocorticoids: fludrocortisone
-9 alpha-F -greater glucocorticoid activity -strong mineralocorticoid activity (intense Na+ retention leading to edema) -used in mineralocorticoid replacement therapy
38
synthetic glucocorticoids: prednisone/ prednisolone
-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
synthetic glucocorticoids: methylprednisolone
-6 alpha-methyl group -potency similar to that for prednisolone -reduced mineralocorticoid activity
40
synthetic glucocorticoids: trimacinolone
-9 alpha-F and 16 alpha-OH -glucocorticoid activity similar to prednisone -reduced mineralocorticoid activity -increased hydrophilicity -low oral bioavailability
41
synthetic glucocorticoids: dexamethsone
-16 alpha-methyl group -increased lipophilicity (increased receptor binding and significantly stronger effect) -increased stability in human plasma -reduced mineralocorticoid activity
42
synthetic glucocorticoids: bethamethasone
-Enantiomer of dexamethasone at 16 -Has similar properties as dexamethasone
43
21 esters
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
21 esters acetate and butyrate
-increased lipophilicity -prolonged action upon IM or intra-articular injections
45
21 esters succinate
-soluble -slow hydrolysis (peak in 30-45 min)
46
21 esters phosphate
-increased solubility -rapid hydrolysis by phosphatases (10 min) -IV or IM injection for emergency conditions
47
mechanisms of glucocorticoid action in asthma
-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
Glucocorticoids ______ stop an asthma attack while it is happening
will not
49
how does glucocorticoids inhibit airway inflammation
-Modulation of cytokine and chemokine production -Inhibition of eicosanoid synthesis -inhibition of accumulation of immune cells in lung tissue -Decreased vascular permeability
50
how does Inhaled glucocorticoids are used prophylactically to control asthma
-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
inhaled glucocorticoids: desired properties
-High potency -Minimal systemic effects -Prolonged action
52
inhaled glucocorticoids: solutions
-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
inhaled glucocorticoids: triamcinolone acetonide
-acetonide is resistant to hydrolyisis -8x more potent than prednisolone
54
inhaled glucocorticoids: beclomethasone dipropionate
-converted rapidly to 12- monopropionate by hydrolysis -14x more potent than dexamethsone
55
inhaled glucocorticoids: flucisolide
-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
inhaled glucocorticoids: budesonide
-1:1 mixture of epimers at 16-17 butylactal -faster topical uptake -low oral bioavailability -extensive first pass metabolism
57
inhaled glucocorticoids: mometasone furoate
-highly potent -more rapid onset of action -negligible systemic availability *rapid metabolism *low oral bioavailability <1%
58
inhaled glucocorticoids: fluticasone propionate
-inactivated by hydrolysis of thioester *rapid first path metabolism -highly lipophilic and insoluble *high potent *poor absorption from GI * rapid topical uptake
59
topical glucocorticoids desired properties
-High lipophilicity for fast absorption -Minimal systemic effect -Prolonged action
60
topical glucocorticoids
-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
topical glucocorticoids actonide or ester forms have ____
better potency for topical applications due to high lipophilicity
62
21 chlorocorticoids
-Substitution of a chlorine atom for the 21 hydroxyl group greatly enhances topical anti-inflammatory activity.
63
topical glucocorticoids fluticasone propionate and mometasone furoate have only _____ potency
-medium -High lipophilicity and the highest binding affinity, but poor solubility -Poor dissolution into inflamed tissue
64
adverse effects of glucocorticoids
-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
adverse effects of glucocorticoids: cross over mineralocorticoids activity
-Sodium and water retention -Development of hypertension -Correctable with selective synthetic glucocorticoids
66
adverse effects of glucocorticoids; metabolic effects
-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
adverse effects of glucocorticoids: cushing life effects
-redistribution of fate -moon face -buffalo bump
68
adverse effects of glucocorticoids: impaired glucose tolerance
-Hyperglycemia from gluconeogenesis -Decreased insulin response *A special problem with diabetes mellitus *May unmask diabetes mellitus.
69
adverse effects of glucocorticoids: suppression of immune system
-Increased susceptibility to infections -Impaired wound healing
70
adverse effects of glucocorticoids: gastrointestinal
-greater peptic ulcer risk
71
adverse effects of glucocorticoids: cental nervous system
-linked to glucose metabolism -euphoria -depression
72
adverse effects of glucocorticoids: adrenal insufficiency upon withdrawal
-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
systemic corticosteroids
-Hydrocortisone -Cortisone -Prednisone -Prednisolone -Methylprednisolone -Dexamethasone -Betamethasone
74
systemic mineralocorticoid
Fludrocortisone (Florinef®
75
inhaled glucocorticoids
-Triamcinolone acetonide (Azmacort®) -Beclomethasone dipropionate (Vanceril ®, Qvar ®) -Flunisolide (Aerobid ®) -Budesonide (Pulmicort ®) -Mometasone furoate (Asmanex®) -Fluticasone propionate (Flovent ®
76
topical glucocorticoids
-Triamcinolone acetonide -Fluocinonide -Betamethasone valerate -Clobestasol propionate -Halobetasol propionate -Halcinonide

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