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Glucocorticoids and anti-allergics Flashcards

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1
Q

What zone of the adrenal medulla produces glucocorticoids (cortisol, corticosterone, cortisone)

A

zona fasiculata

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2
Q

what zone of the adrenal medulla produces mineralocorticoids (aldosterone)

A

zona glomerulosa

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3
Q

Why is it rare to have a spontaneous adrenal-origin glucocorticoid deficiency without a concomitant mineralocorticoid deficiency

A

Because of the proximity of the two zones that produce them

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4
Q

What axis controls the release of cortisol from the adrenal cortex?

A

Hypothalamic-pituitary-adrenal (HPA) axis

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5
Q

describe the HPA axis

A

CRH produced by the hypothalamus -> CRH acts on the anterior pituitary -> POMC is converted into ACTH in the anterior pituitary -> ACTH enters blood stream and acts on adrenal cortex -> ACTH stimulates the release of cortisol

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6
Q

What is POMC

A

Proopiomelanocortin. POMC is a precursor protein with multiple cleavage sites, in which post translational modification gives rise to ACTH, beta-endorphin, and alpha-MSH.

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7
Q

What molecule, belonging to the HPA axis, is an important aspect of pituitary pars intermedia dysfunction (PPID) in horses

A

POMC

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8
Q

What is the main stimulus for cortisol release?

A

stress (like this exam amiright)

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9
Q

What two parts of the HPA exhibit negative feedback?

A

Cortisol inhibits both CRH and ACTH.

ACTH inhibits itself.

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10
Q

What is the primary mineralocorticoid?

A

aldosterone

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11
Q

How do exogenous glucocorticoids/corticosteroids decrease cortisol production?

A

exogenous glucocorticoids also give negative feedback to the hypothalamus and pituitary, inhibiting the release of CRH and ACTH

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12
Q

What stimulates the release of aldosterone?

A

Aldosterone is the final production of activation of the RAAS system in response to decreased renal blood pressure. Its secretion is stimulated by angiotensin II

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13
Q

Describe the RAAS system (im so sorry)

A

decreased blood pressure -> renin converts angiotensinogen in the liver into angiotensin I -> angiotensin converting enzyme (ACE), produced in the lungs, converts angiotensin 1 into angiotensin II -> angiotensin II results in aldosterone production from the zona glomerulosa

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14
Q

What are the four “emia”s caused by a lack of aldosterone (eg hypoadrenocorticism/Addison’s)

A

hyponatremia, hypochloremia, hyperkalemia, and hypovolemia

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15
Q

What does aldosterone do

A

increases sodium and water retention and increases potassium excretion

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16
Q

What is the precursor for all steroid hormones

A

cholesterol

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17
Q

What are the predominant glucocorticoids of mammals

A

cortisol, corticosterone

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18
Q

Adrenal steroidogenesis of cortisol

A

cholesterol -> pregnenolone ->progesterone -> cortisol

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19
Q

adrenal steroidogenesis of aldosterone

A

cholesterol -> pregnenolone -> progesterone -> corticosterone -> aldosterone

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20
Q

Where are glucocorticoid receptors found

A

in cell membrane and cytoplasm

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21
Q

when bound, a cytoplasmic glucocorticoid receptor translocates to the _____ to affect _____

A

nucleus, gene transcription

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22
Q

What are the 7 effects of glucocorticoids

A

-antiinflammatory
-immunosuppressive
- vasoconstrictor/positive inotrope/chronotrope
-bronchodilator
-catabolic (increase glucose production from amino acids)
- maintain fluid homeostasis
-neuroprotective

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23
Q

What two affects of glucocorticoids only occur at supraphysiological doses?

A

anti-inflammation and immunosuppression

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24
Q

what cell type do glucocorticoids act on?

A

ALMOST EVERY CELL TYPE/BODY SYSTEM

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25
How are glucocorticoids anti-inflammatory
inhibition of arachidonic acid by inhibiting phospholipases. This reduces both the COX and lipoxygenase pathways products that are inflammatory mediators. They also decrease histamine production and antagonize kinins and toxins.
26
Which negative affects are greater and why: NSAIDS or glucocorticoids?
Glucocorticoids. They act higher up in the arachidonic acid pathway
27
How are glucocorticoids catabolic
promote fat utilization (lipolysis), promotes glucose production from amino acids (gluconeogenesis), antagonizes insulin (increases blood glucose), and inhibits bone formation/promotes bone loss
28
What does glucocorticoids deficiencies lead to in terms of blood glucose?
hypoglycemia. Glucocorticoids increase blood glucose by antagonizing insulin, so if they are deficient, insulin will take up all the glucose from the blood.
29
how do glucocorticoids maintain fluid homeostasis
promote salt and water retention due to the fact that they have some mineralocorticoid activity
30
What causes the classic PU/PD seen with glucocorticoids?
increased sodium and glucose levels, plus retention of more water than sodium, leads to increased plasma volume and lost of the renal medullary concentration gradient
31
How are glucocorticoids immunosuppressive
they alter leukocyte numbers. (Think about a stress leukogram - the acronym I use to remember is SMiLEd -> segmented neutrophils and monocytes are increased, lymphocytes and eosinophils are decreased)
32
What are the cardiorespiratory affects of glucocorticoids
They block increased capillary permeability induced by acute inflammation (this ties into their immunosuppressive properties), enhance vasoconstriction, are slight positive inotropes, and increases B-2 affects (bronchodilation)
33
What does a glucocorticoids deficiency lead to in terms of blood pressure?
glucocorticoid deficiencies lead to hypotension. This is because glucocorticoids enhance vasoconstriction, and if this is impaired, blood pressure drops.
34
What is chronic glucocorticoid use associated with in cats, particularly those with pre-existing disease?
Chronic glucocorticoid use increases the risk of CHF in cats
35
How are glucocorticoids neuroprotective
they protect against hypoxic/ischemic brain damage
36
What is the (fricking long) list of the effects of glucocorticoid deficiency
Hypotension hypoglycemia anorexia vomiting diarrhea weightloss muscular weakness increased susceptibility to stress inability to maintain endothelial integrity and tone +/- hyponatremia and +/- polyuria
37
Which is the active form: prednisone or prednisolone
prednisolone
38
What are the two forms of glucocorticoid esters
phosphate and succinate esters acetate and acetonide esters
39
What do the ester forms of glucocorticoids affect in terms of pharmacokinetics
speed of onset and duration of action
40
Which esters have rapid onset: phosphate and succinate esters or acetate and acetonide esters
phosphate and succinate esters. These are highly water soluble
41
Which esters have delayed onset: phosphate and succinate esters or acetate and acetonide esters.
acetate and acetonide esters. These are poorly water soluble
42
What form of prednisone/prednisolone should be given to cats and horses? why
Prednisolone. Horses and cats don't metabolize prednisone well because it is a CYP450 dependent process
43
What are the four most commonly used glucocorticoid drugs?
prednisone prednisolone dexamethasone fluticasone
44
Which form (prednisone vs prednisolone) is not suitable for topical administration in any species, and why?
prednisone because it requires hepatic metabolism to get to its active form
45
Which typically require a higher glucocorticoid dose: cats or dogs
cats
46
glucocorticoid routes of administration
IV/IM/SQ/oral/local(intraarticular)/inhaled/topical
47
What are the top 3 adverse affects of glucocorticoids
immunosuppression GI ulcers Elevated liver enzymes/steroid-induced hepatopathy
48
What glucocorticoid is commonly used in SA for anti-inflammatory/antiallergic treatment
prednisone/prednisolone
49
What glucocorticoid is commonly used in LA for anti-inflammatory/antiallergic treatment
dexamethasone
50
Why should you taper glucocorticoid administration withdrawal if their was a chronic administration
HPA axis suppression often occurs, so quitting cold turkey will mean the animal wont produce any endogenous glucocorticoids
51
How can you reduce HPA axis suppression?
alternate day therapy
52
What happens if you co-administer an NSAID with a steroid
Because they act on the same arachidonic acid pathway, any adverse affects will be amplified/doubled. This includes things like GI lesions and renal abnormalities
53
What skin condition is commonly treated with glucocorticoids
atopic dermatitis
54
What blood condition of dogs is commonly treated with glucocorticoids
immune-mediated hemolytic anemia
55
What neoplasia is commonly treated with glucocorticoids
lymphoma
56
What respiratory condition is commonly treated with glucocorticoids
equine/feline asthma
57
What are contraindications/cautions for glucocorticoid use
systemic fungal disease laminitis in horses concurrent infection corneal ulcers
58
What is ciclesonide
a new inhaled corticosteroid that was released and then pulled from the market.
59
What treatments for hyperadrenocorticism (PPID, cushing's) target the adrenal gland
Trilostane and mitotane
60
MOA of trilostane
inhibits pregnenolone conversion into progesterone, preventing the production of cortisol in the adrenal gland
61
Mitotane MOA
inhibits the conversion of cholesterol into pregnenolone, and inhibits the conversion of pregnenolone into progesterone, preventing the production of cortisol in the adrenal gland
62
What are the adverse affects of trilostane and mitotane?
signs associated with HYPOadrenocorticism: lethargy, vomiting, diarrhea, inappetance, weakness
63
What treatments for hyperadrenocorticism (PPID, cushings) target the pituitary
Selegiline and pergolide mesylate
64
What are selegiline and pergolide mesylates
dopamine agonists that reduce cortisol production at the level of the pituitary
65
What dopamine agonist is used to treat hyperadrenocorticism in dogs
selegiline, although it is only effective in 20% of dogs
66
What dopamine agonist is the standard treatment for PPID in horses
pergolide mesylate
67
Selegiline MOA
acts as a dopamine agonist to cause feedback inhibition to ACTH
68
Pergolide mesylate MOA
acts as a dopamine agonist and inhibits production of POMC derived hormones
69
What are the symptoms of hypoadrenocorticism (addisons)
lethargy, vomiting, diarrhea, inappetance, weakness
70
What mineralocorticoid replacements are used to treat addisons (hyopadrenocorticism)
Desoxycorticosterone pivalate (DOCP) Fludrocortisone acetate
71
What glucocorticoid replacement is used to treat hypoadrenocorticism (addisons)
Dexamethosone for acute crises, pred for chronic
72
What are the two components of atopic dermatitis
IgE-mediated mast cell degranulation Cytokine dysregulation
73
What type of T helper cells is most responsible for the initial response in atopic dermatitis
Th-2
74
What do Th-2 cells release
interleukins
75
what do Th-1 cells release
IFN-y, TNF-a
76
What are the two H1 antagonists used to treat atopic dermatitis (perhaps ineffectively)
Diphenhydramine (benadryl) Hydroxyzine
77
What is the top adverse affect of antihistamines
CNS depression
78
What should you not give CNS depressants (like antihistamines) with
monoamine oxidase inhibitors
79
What is oclacitinib?
brand name Apoquel, is a JAK-1 selective inhibitor
80
How does oclacitinib work for atopic dermatitis
it blocks the action of IL-31, an interleukin specifically associated with pruritis
81
How is oclacitinib administered
typically orally
82
when should you not dive oclacitinib
during active infections, due to the immunomodulatory effects
83
What are the adverse effects of Oclacitinib
Mostly GI (diarrhea, anorexia, vomiting) Immunosuppression Possibly worsens pre-existing tumors
84
What is cyclosporine
an immunosuppressive drug used to treat a variety of conditions, includingg transplant rejection
85
what immunosuppresive drug can be used to treat atopic dermatitis
cyclosporine
86
What are the adverse affects of cyclosporine
Gi upset, but usually decreases with time
87
What is Lokivetmab
aka cytopoint, is a monoclonal antibody against IL-31
88

Pharmacology (23 decks)

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