Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ENRP Exam 2 > Adrenal Corticosteroid drugs > Flashcards

Adrenal Corticosteroid drugs Flashcards

1
Q

what are the effects of glucocorticoids?

A

antiinflammatory
immunosuppressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

glucocorticoids can be produced naturally _

glucocorticoids can be produced synthetically _

A

cortisol

hydrocortisone/prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pharmalogical doses of corticosteroids are used to treat patients with

A

inflammation, allergic disorders, immunologic disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

in endocrine patients corticosteroids are give to? (3)

A

establish a diagnosis of cushings syndrome
treat adrenal insuficciency
treat congential adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the corticosteroid agonists

A

glucocorticoids and mineralcoticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is a glucocorticoid synthetic

A

prednisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is a mineralocorticocoid synthetic

A

fludrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the corticosteroid antagonists

A

receptor antagonsits and synthesis inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the corticosteroid sythensis inhibitors

A

ketoconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the corticosteroid receptor antagonists

A

glucocorticoid antagonists: mifepristone

mineralcorticoid antagonsits: spironolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

adrenal corticosteroids belong to the receptor _

A

superfamily

steroid nuclear receptor

ligand binds displacing HSP90 and the glucocorticoid receptors and mineralocorticoreceptors are activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

once the mineralocorticoid receptor is stimulated what is released

what about the glucocorticoid receptor

A

aldosterone

cortisol

they have equal affinities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the parent compound of steroids

A

cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what enzyme takes active steroids to their inactive form

A

11B dehydrogenase 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

side effects of corticosteroids

A

infections, myopathies, osteoporosis, skin thinning, HPA insufficiency , hypertension, hyperglycemia !

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are some factors that influence theraputic and adverse effects of corticosteroids

A

potency (inherent strength of steroid)
pharmokinetics (short vs long term)
daily dose (how frequently)
timing og dose (given in AM)
metabolism differences
duration of treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how do you treat primary adrenal insufficiency (addisons)

A

give a glucorticoid (hydrocotisone) and a mineralocorticoid (fludrocortisone)

this is the same way you would treat congential adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

give common examples of non-endocrine conditions we treat with steroids

A

following bone marrow transplant, autoimmune diseases (MS/psoriasis), hematological cancers, IBD, asthma, RA, hypersensitivity rxns, skin diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

can corticosteroids be given in medical emergencies?

A

yes, high doses for a few days with little risk

DO NOT GIVE MORE THAN A FEW DAYS AND DO NOT REPLACE OR DELAY PRIMARY THERAPIES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

can steroids be given for chronic conditions?

A

yes but you really must monitor your patients: you need to see if there is evidence for therapy in a particular preparation: dosem frequency, route of administration, and assessement of theraputic efficacy

closely monitor patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

steroids cannot be given chronically without the risk of

A

adverse events

22
Q

only initiate steroids id there is published evidence of objective theraputic _

A

benefit

23
Q

use steroids after other therapies have _

A

failed

24
Q

you must identify the specific _ objective and have criteria to gage the response of the steroid

A

theraputic

administer as much to get theraputic effect, taper off when no longer necessary, terminate if expected result has not be achieved, complications arise or maximum benefit has occurred.

25
Q

steroids decrease production of _ and _

A

prostaglandins and leukotrienes

26
Q

steroids _ production of proteolytic enzymes and _ apoptosis of immune cells

A

decrease

increase

27
Q

steroids _ transmigration of neutrophils and macrophages from the blood into tissues

A

decrease

28
Q

steroids _ expression of cell adhesion molecules

A

decrease

29
Q

consequences of steroids

A

decreased inflammation, immune suppresion, decreased allergies/hypersentitivity reactions

30
Q

metabolic effects of steroids

A

carbohydrate metabolism - hyperglycemia
lipid metabolism - lipolysis, fat redistribution (hump back)
protein metabolism- myopathy and muscle wasting, dreased AA uptake, decreased protein synthesis

31
Q

in what patient populations are systemic glucocorticoids problematic

A

immunocompromised, diabetics, people with infections, peptic ulcers, cardiovascular conditions, physciatric conditions, osteoporosis, children

32
Q

decreased activity/inhibition of the enzyme 11BHSD2 results in excessive activation of _ mediated by _

A

MR mediated by cortisol

this increases Na+ and water retention leading to K+ loss and increased BP

33
Q

what are known inhibitors of 11B-HSD2

A

glycyrrhizin (licorice root extract)
carbenoxolone

34
Q

glucocorticoids have an anti _ action

A

insulin

they increase gluconeogenesis, decrease glucose uptake, and increase lipolysis all leading to hyperglycemia

35
Q

what are the short to medium acting glucocorticoids (12 hrs)

A

hydrocortisone (cortisol) and cortisone

36
Q

what are the intermediate acting glucocorticoids (12-36 hrs)

A

prednisone
predinisolone
methylprenisolone
triamicnolone

37
Q

what is a long acting steroid (>36 hrs)

A

betamethasone, dexamethasone

38
Q

corticosteroid drug dosing

A

use the lowest doe for the shortest duration possible
use short/intermediate vs long acting
use topical/inhalation over systemic
give single doses in the AM
can do alternate day with short course pulse therapy
taper off- for HPA recovery

39
Q

how can you test the integrity of the HPA axis

A

morning cortisol
ACTH test
CRH test

40
Q

prednisolone MOA

applications

pharmaokinetics

toxicities

A

activates the GR receptors and alters gene transcription

inflammatory conditions, cancers, transplantation etc.

intermediate acting 12-36 hrs

adrenal suppresion, hyperglycemia, osteoporosis, salt retention (high blood pressure)

41
Q

mifepristone MOA

applications

pharmokinetics

effects (adverse)

A

anatagonist at glucocorticoid and progesterone receptors

medical abortion and CUSHINGS disease

oral administration

vaginal bleeeding, gi upset, diarrhea

42
Q

mineralocorticoids are a class of steroid hormones that influence _ and _ balance

A

salt and water

43
Q

mineralocorticoids primarily act on the _ where they cause sodium and water retnetion and excretion of _ and _

A

kidney

postassium and protons

44
Q

the primary mineralocortcoid is _

A

aldosterone (also progesterone and deoxycorticosterone )

45
Q

fludrocortisone MOA

applications

pharmokinetics

toxicities

A

agonsit at mineralocortioid receptors and glucocorticoid receptors

primary adrenal insuffuciency (addisons)

long duration of action

salt and fluid retention, hyperglycemia, CHF

46
Q

what are the mineralocorticoid receptor antagonisrs?

A

spironolactone and eplernone

47
Q

spironolactone MOA

applications

pharmokinetics

toxicities

A

antagonists at mineralocorticoid receptor and weak antagonist at androgen receptors

aldosteronism and hypokalemia (applications)

slow onsent and offset

toxicities: hyperkalemia, gynecomastia

48
Q

eplernone MOA

clinical applications

pharmacokinetics

toxicities

A

mineralocorticoid receptor anatgonist (specific)

HTN

cleared ny cypP450 metabolism

hyperkalamia and increased creatine

49
Q

ketaconazole MOA

application

pharmacokinetics

toxcicities

A

blocks fungal and mammalian CYP450 enzymes

inhbitis steroid hormone synthesis and fungal ergosterol synthesis

oral/topical administration

hepatic dysfunction, CYP450 interactions

50
Q

what is metyrapone

A

a medication used in the diagonsis of adrenal insufficiency and occasionally in the treatment of cushing disease

ENRP Exam 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions