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MSK/Derm > SM 243: Glucocorticoids > Flashcards

SM 243: Glucocorticoids Flashcards

1
Q

What is the classic cause of Inflammation?

A

A response to infection

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2
Q

What is the classic response to inflammation?

A

Vasodilation, increased vascular permeability, PMN transmigration into affected tissue

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3
Q

What are the signs of inflammation?

A

Increased warmth, pain, redness, and swelling that lead to disturbance of function

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4
Q

What hormonal axis and what class of hormones are essential in resolving the inflammatory porcess?

A

Hypothalmic-pituitary-adrenal axis + glucorcorticoids are needed to resolve the inflammatory process

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5
Q

What can excessive inflammation lead to?

A

Tissue destruction and disease

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6
Q

What can drive excessive inflammation?

A

Allergies, Asthma, Autoimmune disease, Sepsis

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7
Q

What receptor does the HPA axis use to control inflammation?

A

The Glucocorticoid receptor

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8
Q

Describe the signaling pathway along the HPA?

A

Multiple signals cause the Hypothalamus to secrete CRH

CRH stimulates the release of Corticotropin from the Pituitary

Corticotropin induces the synthesis and secretion of Cortisol by the Adrenal Cortex into the bloodstream

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9
Q

Does Cortisol exert genomic or nongenomic effects on target cells?

A

Both - nongenomic is faster

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10
Q

What nongenomic effects does Cortisol have on target cells?

A

Cortisol can activate anti-inflammatory proteins that inhibit inflammatory proteins over seconds to minutes

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11
Q

What genomic effects does Cortisol have on target cells?

A

After Cortisol binds to the Glucocorticoid Receptor, the two form a complex that translocates to the nucleus and initiates transcription of RNA Poly II while repressing activity of NFkB

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12
Q

What effect does Cortisol have on RNA Poly II and to what end result?

A

Cortisol + Glucocorticoid Receptor = Complex that translocates to Nucleus; Increased transcription of RNA Poly II produces antiinflammatory proteins

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13
Q

What effect does Cortisol have on NFkB and to what end result?

A

Cortisol + Glucocorticoid Receptor = Complex that translocates to Nucleus; Blocks NFkB to decrease production of inflammatory proteins

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14
Q

Is RNA Poly II pro or anti inflammatory?

A

Anti-inflammatory, hence the Coritsol + Glucocorticoid Receptor complex increases transcription

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15
Q

Is NFkB pro or anti inflammatory?

A

Pro-inflammatory, hence the Cortisol + Glucocorticoid Receptor complex blocks transcriptional activity

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16
Q

Describe the Arachidonic Acid cascade and it’s relationship to inflammation?

A

Cytosolic Phosphoplipase A2 (PLA2) converts Triglycerides into Arachidonic Acid

COX converts Arachidonic Acid into Prostaglandin percursors

5-Lipooxygenase (LOX) converts these Prostaglandin precursors into Leukotrienes = pro-inflammatory

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17
Q

How does Cortisol repress Leukotriene-mediated inflammation at a protein level?

A

The Glucocorticoid Receptor-Cortisol comples uses a cofactor, c-Src

c-Src phosphorylates Annexin 1 to inhibit PLA2 and reduce production of Arachidonic acid, a precursor for Leukotrienes

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18
Q

How does the Cortisol-Glucorcorticoid Receptor complex reduce inflammation at a genomic level?

A

The Cortisol-Glucocorticoid Receptor complex decreases expression of AP1 and NFkB, both of which are inflammatory transcription factors

19
Q

What disorders result from hyperactivity of the HPA axis?

A

Cushing’s Syndrome, Pain, Caloric Restriction, Immunosuppression

20
Q

What disorders result from hypoactivity of the HPA axis?

A

Adrenal insufficiency aka Addison’s Disease

21
Q

What is the strongest Corticosteroid?

A

Betamethasone and Dexamethasone

22
Q

What does the joint swelling in RA reflect and why do we use medication?

A

Swelling in RA reflects synovial membrane inflammation and the goal of using medications is to reduce inflammation

23
Q

What medications can be used as a first line for RA?

A

Methotrexate + Glucocorticoid

24
Q

How are Glucocorticoids used to treat RA?

A

Used in low doses wit Methotrexate to achieve Low Disease Activity, and then tapered off

Also can be injected in local areas for acute inflammation

25
Q

How does Polymyalgia Rheumatica present?

A

Shoulder +/- hip stiffness and pain with elevated ESR

26
Q

How should Polymyalgia Rheumatica be managed?

A

Predinose daily, tapering every 4 weeks until discontinuation

27
Q

What is Lumbosacral Radiculatopathy?

A

Radiating pain originated from a compressed or inflamed nerve root

28
Q

How can Lumboscaral Radiculopathy be treated?

A

Imaging-guided epidural injections of Glucocorticoids like Dexamethasone

29
Q

Can a Glucocorticoid steroid injection be done repeatedly?

A

Yes, up to 4 times a year, but consider risks as well

30
Q

Do glucocorticosteroids benefit Knee OA?

A

May be helpful for a few weeks, but not useful for signs of active inflammation

31
Q

Can glucocorticosteroids be used to treat Tendinopathy?

A

No, because tendon’s don’t show signs of inflammation

32
Q

What are tissue-specific side effects of high dose corticosteroids?

A

Adrenal atrophy, hypertension, dyslipedemia, immunosuppression, cataracts, and a lot of others

33
Q

How long does a single Corticosteroid dose suppress native Cortisol levels?

A

7 - 14 days after a single injection, and higher doses suppress longer

34
Q

How do Corticosteroids cause Osteoperosis?

A

Corticosteroids increase the number of bone-resorbinb osteoclasts, increasing the risk of Vertebral fractures within 3months after initiation

35
Q

What type of bone injury is common in people who take Corticosteroids?

A

Osteoperosis-mediated vertebral fractures

36
Q

How do Corticosteroids alter blood sugar levels?

A

Glucosteroids cause elevated blood sugars for up to 10 days

37
Q

How do Coricosteroids alter blood pressure?

A

Elevated blood pressure can occur from long term use of Corticosteroids due to renal sodium retention and potentiation of the Vasopressor responses to AngII and Catecholamines

38
Q

What 2 mechanisms do Corticosteroids use to raise blood pressure?

A

Increased Renal Sodium retention = increase blood volume

Potentiation of vasopressor responses to AngII and Catecholamines

39
Q

What patients tend to develop Glucocorticoid resistance?

A

Those with severe RA

40
Q

What mediates Gluoccorticoid Resistance?

A

Decreased expression of Glucocorticoid receptor alpha, increased expression of Glucocorticoid receptor beta, or phosphorylation of the glucocorticoid receptor to inhibit signaling

41
Q

What is Osteonecrosis and how does it relate to Glucocorticoids?

A

Necrosis of the bone, associated with daily Glucocorticoid use

42
Q

How are Glucocorticosteroids administered?

A

Orally, IV, and IM or directly into joints/soft tissue

43
Q

What is Osteonecrosis and how does it relate to Glucocorticoids?

A

Necrosis of the bone, associated with daily Glucocorticoid use

44
Q

How are Glucocorticosteroids administered?

A

Orally, IV, and IM or directly into joints/soft tissue

MSK/Derm (46 decks)

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