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Pharmacology Exam 1 > Corticosteroids > Flashcards

Corticosteroids Flashcards

1
Q

characteristic of glucocorticoids

A

stress hormones
increase circulating glucose
potent anti-inflammatory effects

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2
Q

characteristics of mineralocorticoids

A

Na+ retention
increase blood volume
increase blood pressure

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3
Q

regulation of mineralocorticoid synthesis

A

anterior pituitary does not control the synthesis of mineralocorticoids

RAA-system does

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4
Q

transport of steroids

A

transported in plasma by plasma transport proteins
corticoid-binding globulin - glucocorticoids & progesterone
sex hormone binding globulin - testosterone and estradiol

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5
Q

where are steroids metabolized

A

metabolized in the liver to soluble forms

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6
Q

excretion of steroids

A

excreted in bile (estrogen) or in the urine (progesterone, androgen, and glucocorticoids)

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7
Q

what are GRes

A

Glucocorticoid Resposive Elements - DNA binding domains that are targets of activated dimers

GREs are upstream of steroid responsive genes

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8
Q

what do glucocorticoids upregulate

A

glucocorticoids upregulate enzymes for gluconeogenesis & anti-inflammatory proteins

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9
Q

what catalyzes the rate-limiting step in gluconeogenesis

A

phosphoenolpyruvate carboxykinase (PEPCK)

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10
Q

function of lipocortin 1

A

suppresses phospholipase A2, critical role in eicosanoid synthesis

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11
Q

mechanism of suppression by glucocorticoids

A

activated glucocorticoid Rs binds to NFkB and prevents binding of NFkB to its response element
transcription of cytokine genes are repressed

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12
Q

physiologic effects of cortisol on liver

A

increases gluconeogenesis in short-term fasting

inreases glycogen storage in long-term fasting

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13
Q

physiologic effect of cortisol on muscle

A

promote protein degradation
decrease protein synthesis
decrease sensitivity to insulin

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14
Q

physiologic effect of cortisol on adipose tissues

A

promote lipolysis

decrease sensitivity to insulin

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15
Q

physiologic effect of cortisol on immune system

A

block the synthesis of cytokines (immunosuppression)

inhibits the production of eicosanoids (anti-inflammatory)

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16
Q

addison’s disease

A

hypoadrenalism

decreased secretion of steroid hormone by the adrenal cortex

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17
Q

causes of addison’s disease

A

destruction of the cortex by tuberculosis or atrophy

decreased secretion of ACTH due to diseases of anterior pituitary

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18
Q

symptoms of addison’s disease

A

extreme weakness

anorexia, anemia, nausea, vomiting

low blood pressure (primary Addison’s only)

skin hyperpigmentation (primary Addison’s only)

mental depression

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19
Q

what is another possible cause of Addison’s-like symptoms

A

cessation of long-term system glucocorticoid therapy can lead to Addisonian symptoms

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20
Q

characteristics of primary addison’s disease

A

adrenal defect

high CRH, high ACTH, low cortisol, low aldosterone

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21
Q

characteristics of secondary addison’s disease

A

pituitary defect

high CRH, low ACTH, low cortisol, aldosterone not affected

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22
Q

characteristics of tertiary addison’s disease

A

hypothalamic defect

low CRH, low ACTH, low cortisol, aldosterone not affected

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23
Q

Cushing’s disease

A

hyperadrenalism

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24
Q

causes of Cushing’s disease

A
  • tumors in the adrnal cortex
  • increased production of ACTH due to pituitary carcinoma
  • ectopic production of ACTH due to non-pituitary carcinoma
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25
Q

symptoms of Cushing’s disease

A

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

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26
Q

what else can cause Cushing’s symptoms

A

long-term therapeutic use of systemic glucocorticoids

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27
Q

characteristics of adrenal Cushing’s disease

A

low CrH, low ACTH, high cortisol

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28
Q

characteristics of pituitary Cushing’s disease

A

low CRH, high ACTH, high cortisol

29
Q

characteristics of ectopic Cushing’s disease

A

low CRH, low ACTH, high cortisol, high ectopic ACTH

30
Q

characteristics of ketoconazole

A

antifungal at lower concentrations (block synth of ergosterol)

inhibits P450scc, 17-alpha hydroxylase, and 11beta-hydroxylase

can tx hyperglucocorticoid states

may cause toxic side effects

31
Q

therapeutic uses of corticosteroids

A
  • primary adrenal insufficiency cause by atrophy of adrenal cortex
  • allergic rxns
  • inflammation & autoimmune diseases
  • asthma
  • immunosuppressive
  • anti-cancer
32
Q

requirements for glucocorticoid activity

A

4,5-double bond
C3 ketone
11-beta hydroxyl
C17 hydroxyl

33
Q

requirements for mineralcorticoid activity

A

4,5-double bond
C3 ketone
11-beta hydroxyl less important
C17 hydroxyl is NOT rquired

34
Q

cortisol vs cortisone

A

oxidation of 11 hydroxyl to ketone inactivates glucocorticoid

rxn catalyzed in liver by 11beta-hydroxysteroid DH (reversible)

35
Q

in whom should cortisone not be used

A

in patients with impaired liver functions

36
Q

short acting corticosteroids

A

t1/2 8-12 hrs
hydrocortisone
cortisone

37
Q

intermediate acting corticosteroids

A 
t1/2 12-36 hrs
prednisone
prednisolone
methylprednisolone
triamcinolone
38
Q

long-acting corticosteroids

A

t1/2 36-54 hrs
dexamethasone
betamethasone

39
Q

characteristics of fludrocortisone

A

9alpha-F
greater glucocorticoid activity
strong mineralocorticoid activity
intense Na+ retention leading to edema

40
Q

use for fludocortisone

A

used in mineralocorticoid replacement therapy

41
Q

characteristics of prednisone/prednisolone

A

extra double bound C1-C2
more potent, stronger binding to R
reduced mineralocorticoid act., interconvertable by 11beta-hydroxysteroid DH

42
Q

characteristics of methylprednisolone

A

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

43
Q

characteristics of triamcinolone

A 
9alpha-F and 16alpha-OH
GC act. similar to prednisone
reduced MC act.
increased hydrophilicty
low oral bioavailability
44
Q

characteristics of dexamethasone

A

16alpha-methyl group
increased lipophilicity -> ups R binding, stronger effect
increased stability in human plasma
reduced MC activity

45
Q

characteristics of betamethasone

A

enantiomer of dexamethasone at 16

similar properties to dexamethasone

46
Q

characteristics of 21-esters

A

hydroxyl group @ 21 can mod. to ester to control GC properties

47
Q

if modified 21 hydroxyl to ester with acetate & butyrate

A

switching to acetate and butyrate -> increased lipophilicity, prolonged action upon IM

48
Q

if modified 21 hydroxyl to ester with succinate

A

switch to succinate-> soluble, slow hydrolysis

49
Q

if modified 21 hydroxly to ester with phosphate

A

increased solubility
rapid hydrolysis by phosphatases
IV or IM injection for emergency conditions

50
Q

desired properties of topical GCs

A

high lipophilicity
minimal systemic effect
prolonged action
halogenated are more potent

51
Q

characteristics of topical GCs

A

once absorbed, metabolized primariy through the liver & excreted in the bile
low potentcy GC are safest for chronic applications
high potentcy GC for short term use

52
Q

why do acetonide or eseter forms have better potency for topical applications

A

high lipophilicity

eg traimcinolone acetonide > betamethasone valerate

53
Q

21-chlorocorticoids

A

greatly enhances topical anti-inflammatory activity

eg clobetasol proprionate, halobetasol proprionate, halcinonide

54
Q

characteristics of topical corticosteroids

A

only medium potency for topical corticosteroids
high lipophilicity and highest binding affinity but poor solubility
poor dissolution into inflamed tissue

55
Q

desired properties of inhaled GCs

A

high potency
minimal systemic effects
prolonged action

56
Q

characteristics of inhaled GCs

A

high lipophilicity
low oral bioavailability
rapid clearance

eg triamcinolone acetonide & beclomethasone diproprionate

57
Q

characteristics of triamcinolone acetonide

A

acetonide is resistant to hydrolysis

8x more potent than prednisolone

58
Q

characteristics of beclomethasone diproprionate

A

converted rapidly to 17-monoproprionate by hydrolysis

14x more potent than dexamethasone

59
Q

characteristics of flunisolide

A

rapid absorption from nasal or lung tissue
rapid metabolism by liver, extensive “first-path” metabolism
minimal systemic adverse effect with long-term therapy

60
Q

characteristics of budesonide

A

1:1 mixture of epimers at 16,17-butylacetal
faster topical uptake
low oral bioavailability
extensive first-path metabolism

61
Q

characteristics of mometasone furoate

A 
highly potent
more rapid onset of action
negligible systemic availability
rapid metabolism 
low oral bioavailability
62
Q

characteristics of fluticasone proprionate

A 
inactivated by hydrolysis of thioester
rapid first-path metabolism
highly lipophilic and insoluble
highly potent
poor absorption from GI
rapid topical uptake
63
Q

possible adverse crossover effects of corticoids

A

-crossover mineralocorticoid activity (Na+/H2O retention, HTN, correctible with synth. GCs)

64
Q

adverse metabolic effects of corticoids

A
  • metabolic effects (ups glucose produc)
  • -steroid myopathy - high doses cause wasting of prox muscles
  • -reduced long bone growth in kids-> premature closing of epiphyseal junction
  • -osteoporosis-inhibit osteoblasts, prevented by bisphosphonate
  • Cushing’s like effects (redistrib. of fat)
  • impaired glucose tolerance
65
Q

effects of corticoids on immune system

A

increased susceptibility to infections by suppressing immune system
impair wound healing

66
Q

corticoids on GI

A

greater peptic ulcer risk

67
Q

corticoids on CNS

A

linked to glucose metabolism
euphoria
depression
cataracts

68
Q

adverse effects of corticoids on withdrawal

A

adrenal insufficiency (addisonian crisis)

69
Q

symptoms of addisonian crisis

A

inability to withstand stress
hypotension
weakness

Pharmacology Exam 1 (7 decks)

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