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E2T1 > Adrenal Corticosteroids Drugs DSA > Flashcards

Adrenal Corticosteroids Drugs DSA Flashcards

1
Q

adrenal corticoid drugs

A
  • mineralocorticoids

- glucocorticoids

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2
Q

Mineralocorticoids- drug

A

-Fludrocortisone

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3
Q

Glucocorticoids- short to medium acting (<12 h)

A
  • hydrocortisone
  • cortisone
  • prednisone
  • prednisolone
  • methylprednisolone
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4
Q

Glucocorticoids- intermediate acting (12-36 hrs)

A

-triamcinolone

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5
Q

Glucocorticoids- long acting (>36 hrs)

A
  • betamethasone

- dexamethasone

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6
Q

Inhibitors of adrenal corticosteroid action

A
  • steroid syn inhibitors
  • glucocorticoid antagonists
  • aldosterone antagonists
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7
Q

steroid syn inhibitors- drugs

A

-aminoglutethimide
-ketoconazole
-metyrapone
-mitotane
(AKMM)

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8
Q

glucocorticoid antagonists- drugs

A

-mifepristone

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9
Q

aldosterone antagonists- drugs

A
  • spironolactone

- eplerenone

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10
Q

mineralocorticoids- induced by? regulate?

A
  • Ang II and K

- reg electrolyte, H2O balance and BP

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11
Q

Glucocorticoids- induced by? regulate?

A
  • ACTH

- reg metabolism and immunity

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12
Q

weak androgens- converted into?

A
  • potent androgens in males

- estrogens in females

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13
Q

adrenal corticosteroids- pharmacokinetics- transporters

A
  • hydrophobic- transported by protein carriers
  • transcortin (corticosteroid binding globulin- CBG)- high affinity, low capacity transporter- high during pregnancy and hyperthyroidism; low in liver dz
  • 90% of blood cortisol, 60% of blood aldosterone
  • remainder bound to albumin (low affinity/high capacity)
  • albumin- main carrier for synthetic corticosteroid drugs
  • plasma cortisol > 20-30- transcortin is saturated
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14
Q

adrenal corticosteroids- pharmacokinetics- liver

A
  • liver produces transcortin

- 80% of cortisol is metabolized by liver

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15
Q

adrenal corticosteroids- t1/2 of cortisol

A
  • 60-90 min

- inc in liver dz, hypothyroidism

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16
Q

adrenal corticosteroids- moa

A
  • ligands at nuclear R’s- TF’s (ligand act) that modulate gene expression
  • corticosteroids produce their effects after a lag period
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17
Q

mineralocorticoid effects- target cell types

A

principal cells of CT and CD of kidney and other epit cells involved in electrolyte transport:

  • inc epit Na channel (EnaC)
  • inc Na/K pump
  • retention of water and Na, loss of K
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18
Q

Direct effects of mineralocorticoids on CV system

A

-target non-epit tissues of heart and vasculature
Gene expression effects:
-NADPH reductase- ox stress
-collagen, TGFB- fibrosis, cell senescence
-IL-6, cell adhesion molecules- infl
-PAI-1- inhibition of fibrinolysis, blood clotting
Excess aldosterone causes:
-cardiac fibrosis and hypertrophy
-vascular remodeling and infl

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19
Q

glucocorticoid effects- 2 mechanisms

A
  • transactivation- GR-ligand complex binds to GRE in gene promoters to act gene expression- effects on carb, lipid, protein metabolism
  • transrepression- GR-ligand complex binds to other TF complexes to suppress their act of gene transcription- NF-KB, AP-1 TF’s; anti infl, immunosuppressive, anti-growth effects
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20
Q

glucocorticoid R isoforms

A
  • GRalpha- prototypical isoform

- GRbeta- doesnt bind ligands, inactiv- induced by TNF-alpha

21
Q

role of 11B-hydroxysteroid dehydrogenase (11B-HSD) in adrenal corticosteroid action

A
  • aldosterone and cortisol bind the MR with equal affinity
  • daily prod rates are predominantly corticosteroids
  • 11B-HSD converts cortisol into inactive at MR coritsone- making tissues mineralocorticoid responsive
  • dec 11B-HSD activity- results in excessive act of MR mediated by cortisol!!
22
Q

inhibition of 11B-HSD- causes what?

A
  • inc act of MR by cortisol- causes HTN and edema
  • Glycyrrhizin (in licorice) and carbenoxolone inhibits this enzyme
  • inact mutations- cause AME (mineralocorticoid excess syndrome)- leads to HTN
23
Q

Glucocorticoids- metabolic effects- carbohydrates

A
  • inc gluconeogenesis
  • inc glucose output into circulation (inc G6P)
  • inc glycogen syn (inc glycogen synthase)
  • dec glucose uptake by m and adipose tissues (dec GLUT4)
  • development of hyperglycemia!!
24
Q

Glucocorticoids- metabolic effects- lipids

A
  • inc lipolysis- stim of hormone-sensitive lipase in adipose tissue
  • inc mobilization of free fa and glycerol into the gluconeogenic pathway
  • inc lipogenesis- inc insulin secretion
  • net inc in fat deposition!!!
  • fat accum in upper body!! thinning arms and legs
25
Q

Glucocorticoids- metabolic effects- proteins

A
  • dec aa uptake into cells
  • dec prot syn
  • mobilization of aa’s into gluconeogenic pathway
  • skeletal m- suppressed prot syn- myopathy and m wasting
26
Q

Glucocorticoids- effects on intermediary metabolism antagonize actions of insulin

A
  • favor lipid and prot breakdown to supply substrates for gluconeogenesis
  • interference with insulin R signal transduction
27
Q

Glucocorticoids- effects on immune system and infl

A

(due to transrepression of NF-kB and AP-1 effects)

  • dec PLA2 and COX2- dec prod of prostaglandins and leukotrienes
  • dec prod and inc apoptosis of immune cell types
  • dec prod of cytokines and their R’s
  • dec expression of cell adhesion molecules
  • dec transmigration of neutrophils and macrophages from blood into tissues
28
Q

Glucocorticoids- effects on immune system and infl- consequences

A
  • dec infl
  • immune suppression
  • dec allergic/hypersensitivity rxns
29
Q

glucocorticoids effects on other systems- CV

A
  • inc prod of Epi and NE
  • inc R sensitivity to Epi and NE
  • residual mineralocorticoid activity of glucocorticoids
  • dec in capillary permeability
  • inc HR and CO
  • elevated BP
30
Q

glucocorticoids effects on other systems- GI

A
  • dec prod of gastro-protective prostaglandins
  • dec immune response against H pylori
  • inc in gastric acid and pepsin secretion
31
Q

glucocorticoids effects on other systems- CNS

A
  • insomnia
  • irritability
  • euphoria, followed by depression
  • dec sexual libido in males
32
Q

glucocorticoids effects on other systems- bone/growth

A
  • dec activity in osteoblasts
  • dec intestinal and renal Ca absorption
  • inc in osteoclast activity
  • growth retardation in children
  • osteoporosis, bone fractures
33
Q

glucocorticoids effects on other systems- skin

A
  • dec collagen syn
  • dec fibroblast prolif
  • dec wound healing, inc bruising
  • fragile and skin thin with stretch marks (called striae)
34
Q

common clinical indications of adrenal corticosteroid drugs

A
  • replacement therapy
  • immunosuppression
  • infl and allergic conditions
35
Q

common clinical indications of adrenal corticosteroid drugs- replacement therapy

A
  • adrenal insuff (Addison’s dz)- glucocorticoid and a mineralocorticoid used!
  • congenital adrenal hyperplasia
36
Q

common clinical indications of adrenal corticosteroid drugs- immunosupression

A
  • after organ or HSC transplantation
  • autoimmune dz
  • hematological cancers
37
Q

common clinical indications of adrenal corticosteroid drugs- infl and allergic conditions

A
  • rheumatoid arthritis
  • IBD
  • asthma and COPD
  • allergic rhinitis
  • skin dizes- infl dermatoses (psoriasis)
  • hypersensitivity rxns
38
Q

mineralocorticoids- adverse effects

A
  • retention of Na and H2O- edema
  • HTN
  • inc preload and cardiac enlargement- CHF
  • K loss and alkalosis
39
Q

glucocorticoids- adverse effects

A
  • suppressed ability to fight infections- opportunistic infections!
  • hyperglycemia
  • skin- striae, easy bruising
  • m wasting, steroid myopathy
  • HTN
  • steroid-induced glaucoma
  • cataracts
  • peptic ulcers
  • psychiatric disorders- euphoria, mania, anxiety
  • inc appetite and weight gain
  • osteoporosis
  • retarded growth in children
40
Q

adrenal corticosteroid drugs- dosing

A
  • use lowest dose for shortest duration possible!!
  • reduce distribution of drugs into systemic circulation (use topical, inhalational routes)
  • give single daily doses in morning
  • alternate day, short-course, pulse therapy admin
  • dose tapering
41
Q

pt populations in which systemic glucocorticoids admin is problematic

A
  • immunocompromised pts
  • diabetics
  • infections
  • peptic ulcer
  • CV conditions- HTN, CHF, angina
  • psychiatric conditions
  • osteoporosis
  • children
42
Q

Aminoglutethimide- moa, indications, SE’s

A
  • blocks conversion of chol to pregnenolone
  • reduces prod of all steroid H’s
  • indications- was used for breast cancer tx, adrenocortical cancer
  • drowsiness, GI upset
43
Q

inhibitors of adrenal corticoid action- drugs

A
  • aminoglutethimide
  • ketoconazole
  • metyrapone
  • mitotane
  • mifepristone
  • spironolactone
  • eplerenone
44
Q

Ketoconazole- moa, indications, SE’s

A
  • P450 inhibition
  • reduces syn of adrenal and sex H’s
  • antifungal drug, Cushing’s syndrome, suppresses androgenic hair loss, prostate cancer
  • SE’s- hepatotoxicity, gynecomastia in males
45
Q

Metyrapone- moa, indications, SE’s

A
  • inhibition of steroid 11-hydroxylation
  • suppresses formation of cortisol and corticosterone
  • Cushing’s syndrome! (can be used in pregnant woman!!)
  • accum of 11-deoxycortisol- inc aldosterone- Na and H2O retention; inc androgens- hirsutism in women
  • GI upset
  • dizziness
46
Q

Mitotane- moa, indications, SE’s

A
  • Na ionofore, Ca ionofore
  • PKC and AC inhibitor
  • non-selective cytotoxic action of adrenal cortex
  • used for adrenal carcinoma!!
  • depression, GI upset, rashes
47
Q

Mifepristone- moa, indications, SE’s

A
  • glucocorticoid R antagonists
  • prevents nuclear translocation of GR
  • progesterone R antagonist
  • Hypercortisolism in pts with cushing’s syndrome
  • medical termination of intrauterine pregnancy (anti-progesterone action)
  • dizziness, GI upset, fatigue
48
Q

Spironolactone- moa, indications, SE’s

A
  • aldosterone R antagonist
  • also antagonist at androgen R’s
  • primary hyperaldosteronism, hirsutism in women, diuretic (tx HF and HTN)
  • hyperkalemia, gynecomastia and impotence in men, menstrual abnormalities in women
49
Q

Eplerenone- moa, indications, SE’s

A
  • antagonist of aldosterone at mineralocorticoid Rs
  • lower affinity for androgen Rs vs spironolactone
  • used for HTN, HF (reduces cardiac remodeling)
  • SEs- hyperkalemia

E2T1 (6 decks)

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