Systemic Steroids and Autoimmune Conditions Flashcards

1
Q

Why are steroids used in adrenal insufficiency?

A

to replace endogenous steroids that adrenal gland is not producing enough of

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2
Q

which endogenous steroids requirement replacement in adrenal insufficiency?

A

Cortisol -> replaced by any steroids

Aldosterone -> replaced by fludrocortisone

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3
Q

what does aldosterone/fludrocortisone do?

A

it has mineralocorticoid activity

AKA maintains the balance of water and electrolytes to keep blood pressure stable

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4
Q

what are the indications for fludrocortisone?

A

FDA: Addison’s

Non-FDA: orthostatic hypotension

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5
Q

What does glucocorticoid activity entail?

A

anti-inflammatory effects

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6
Q

What can systemic steroids with glucocorticoid activity cause the adrenal gland to do?

A

stop producing cortisol due to feedback inhibition

HPA axis suppression!

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7
Q

Why is it important to taper off steroids?

A

so the adrenal gland has time to resume cortisol production

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8
Q

Explain the HPA axis

A

Hypothalamus produces CRH (cortisol releasing hormone) which stimulates the pituitary gland to release ACTH (adrenocrticotropic hormone) which stimulates the adrenal glands to produce cortisol. Cortisol suppresses ACTH and CRH produces vai negative feedback

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9
Q

how does Cushing’s develop?

A

adrenal gland produces too much cortisol or exogenous drugs are taken in high doses

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10
Q

How does Addison’s develop?

A

opposite of Cushing’s! it’s when the adrenal gland is not making enough cortisol or if exogenous steroids are stopped suddenly (Addison’s crisis) = fatal!

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11
Q

Adverse effects of cushing’s

A
Psychiatric chcanges
acnes
glaucoma
moon face/buffalo hump
stretch marks 
muscle wasting 
impaired wound healing
diabetes
irregular periods/hirsutism 
poor bone health 
gi bleeding/ulcers
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12
Q

ways to reduce the adverse effect of steroids

A

alternate day dosing
use localized therapy (inhaltion for lungs, injection for joints)
lowest possible dose for shortest amount of time

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13
Q

which steroid has low systemic absorption?

A

budesonide

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14
Q

Steroids least to most potent and dose equivalence

A
Cortisone 25mg 
Hydrocortisone 20mg
Prednisone 5 mg
Prednisolone 5 mg 
Methylprednisolone 4 mg 
Triamcinolone 4 mg
Dexamethasone  0.75 mg 
Betamethasone 0.6 mg
"Cute Hot Pharmacists and Physicians Marry Together and Deliver Babies"
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15
Q

Contraindications for systemic steroids

A

Live vaccines, serious systemic infections

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16
Q

prodrug of cortisol

A

cortisone

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17
Q

prodrug of prednisolone

A

prednisone

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18
Q

which steroid is typically used in children?

A

prednisolone (liquid form)

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19
Q

At what dose and time period is a patient on steroids considered immunosuppressed

A

> 2mg/kg/day for > 2 weeks

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20
Q

lab tests that can detect inflammation in autoimmune disorders

A

ESR
CRP
RF
ANA (anti-nuclear antibody)

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21
Q

Why is a high dose given intially then tapered down?

A

to prevent Addison’s crisis AND

quickly reduce inflammation then treat remaining inflammation while preventing a rebound attack

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22
Q

what conditions does the use of strong immunosuppressants increase the risk of?

A

re-activating TB/HepB and C : test and treat before starting
live vaccine virus : vaccinate before starting immunosuppressants
Lymphoma/skin cancers
fungal/bacterial infections - monitor CBC

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23
Q

RA presents bilaterally/symmetrically or unilaterally?

A

bilaterally/symmetrically

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24
Q

OA presents bilaterally/symmetrically or unilaterally

A

unilaterally

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25
Q

Symptoms of RA

A
systemic! 
fever, weakness, loss of appetite, 
worsening stiffness after rest (morning stiffness) 
joint swelling
bone deformity 
edema 
redness
26
Q

does OA cause prolonged stiffness?

A

NO!

27
Q

how to diagnosis RA

A

test for ACPA (anti-citrullinated peptide antibdoy) and RF

if later in disease state will see joint erosion and rheumatoid nodules

28
Q

what should a patient be started on if symptomatic despite severity level?

A

DMARD

29
Q

how do DMARDs work?

A

slow disease progression and prevent further joint damage

30
Q

Preferred initial therapy in most patients?

A

Methotrexate

31
Q

What is preferred therapy in patients with mod-severe RA

A

combo of DMARD or TNF inhibitor biologic or a non-TNF biologic with/without MTX

32
Q

What should never be done with RA drug treatment

A

using 2 biologics together!

Risk of serious infections!

33
Q

when can you use a low dose steroid in RA patients/

A

when starting a DMARD in a moderate or severe patient to provide some relief while waiting for the DMARD to work
or in patients with hx of dmard failure

34
Q

MOA of MTX

A

inhibis dihydrofolate reductase inhbiting folate causing immune modulator and anti-inflammatory activity

35
Q

RA dosing for MTX

A

7.5 - 20 mg once WEEKLY!

daily dosing in RA leads to liver damage and intestinal bleeding

36
Q

monitoring with MTX use

A

cbc
lfts
chest x-ray
hep B and C serologies

37
Q

what can be given with MTX to decrease Gi and hepatic side effects

A

folate

38
Q

Warnings with hydroxychloroquine

A

irreversible retinopathy - eye exam needed!

39
Q

counseling note with sulfasalazine

A

yellow-orange color of skin/urine

40
Q

MOA of leflunomide (Arava) f

A

inhibits pyrimidine synthesis causing anti-proliferative and anti-inflammatory effects

41
Q

which traditional DMARDs are teratogenic?

A

MTX and Leflunomide

42
Q

Warnings with leflunomide

A

DNU in pregnancy
hepatotoxicity
SJS risk
Accelerated drug elimination process needed upon d/c to lower levels of teriflunomide (active metabolite)

43
Q

what DMARD requires accelerated drug elimination?

A

leflunomide

44
Q

what are the two accelerate drug elimination options with lefluomide?

A
  1. cholestyramine 8 g tid for 11 days

2. activated charcoal suspension 50 g q 12 h 11 days

45
Q

how long must a patient wait if wanting to get pregnant after using leflunomide?

A

2 years or use accelerated drug elimination procedure

46
Q

List of Janus Kinase Inhibitors (JAK)

A

Tofacitinib (Xeljanz)
Baricitinib (Olumiant)
Upadacitinib (Rinvoq)

47
Q

JAK inibitor MOA

A

Inhibit the enzyme janus kinase which stimulates immune cells

48
Q

Boxed warnings with JAK inhibitors

A

serious infections
malignancy risk increase
thrombosis risk

49
Q

Special warning with Xeljanz (tofacitinib)

A

increased mortality in patient >50 years old with 1 or more CV risk and taking higher dose

50
Q

Interactions with MTX

A
alcohol - liver tox
NSAIDs/beta lactams/probenecid - renal tox 
sulfonamides and topical tacrolimus 
loops
cyclosporines
51
Q

List of Anti-TNF (tumor necrosis factor) alpha inhibitors

A
etanercept (Enbrel) 
adalimumab (Humira) 
infliximab (Remicadde) 
certolizumab pegol (Cimzia) 
golimumab (Simponi)
52
Q

Etanercept (enbrel) dosing schedule

A

50 mg sc WEEKLY

53
Q

Adalimumab (humira) dosing schedule

A

40 mg sc EVERY OTHER week

without MTX: weekly

54
Q

Infliximab dosing (Remicade)

A

3 mg/kg IV weeks 0,2,6 then every 8 weeks

can do 10mg/kg or every 4 weeks but increased infection risk

55
Q

Remicade preparation

A

filter needed

only stable in Normal saline

56
Q

what’s something unique about hypersensitivity reactions with Remicade?

A

delayed (3-12 days) after administartion

57
Q

Simponi (golimumab) dosing

A

50 m gmonthy for sc

2mg/kg IV at week 0,4 then every 8

58
Q

Which anti-TNF biologic DMARDs require filters?

A

Simponi (golimumab) and Remicade (infliximab)

59
Q

CI specific for infliximab

A

doses >5 mg/kg in mod-severe heart failure

60
Q

CI specific for etanercept

A

sepsis

61
Q

role of anti-TNF biologics

A

add-on therapy with MTX unless the presentation is severe, then can be started as initial therapy with or without MTX