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Pharmacology > Glucocorticoids and anti-allergics > Flashcards

Glucocorticoids and anti-allergics Flashcards

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
Q

How are glucocorticoids anti-inflammatory

A

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.

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26
Q

Which negative affects are greater and why:
NSAIDS or glucocorticoids?

A

Glucocorticoids. They act higher up in the arachidonic acid pathway

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27
Q

How are glucocorticoids catabolic

A

promote fat utilization (lipolysis), promotes glucose production from amino acids (gluconeogenesis), antagonizes insulin (increases blood glucose), and inhibits bone formation/promotes bone loss

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28
Q

What does glucocorticoids deficiencies lead to in terms of blood glucose?

A

hypoglycemia. Glucocorticoids increase blood glucose by antagonizing insulin, so if they are deficient, insulin will take up all the glucose from the blood.

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29
Q

how do glucocorticoids maintain fluid homeostasis

A

promote salt and water retention due to the fact that they have some mineralocorticoid activity

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30
Q

What causes the classic PU/PD seen with glucocorticoids?

A

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

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31
Q

How are glucocorticoids immunosuppressive

A

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)

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32
Q

What are the cardiorespiratory affects of glucocorticoids

A

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)

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33
Q

What does a glucocorticoids deficiency lead to in terms of blood pressure?

A

glucocorticoid deficiencies lead to hypotension. This is because glucocorticoids enhance vasoconstriction, and if this is impaired, blood pressure drops.

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34
Q

What is chronic glucocorticoid use associated with in cats, particularly those with pre-existing disease?

A

Chronic glucocorticoid use increases the risk of CHF in cats

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35
Q

How are glucocorticoids neuroprotective

A

they protect against hypoxic/ischemic brain damage

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36
Q

What is the (fricking long) list of the effects of glucocorticoid deficiency

A

Hypotension
hypoglycemia
anorexia
vomiting
diarrhea
weightloss
muscular weakness
increased susceptibility to stress
inability to maintain endothelial integrity and tone
+/- hyponatremia and +/- polyuria

37
Q

Which is the active form: prednisone or prednisolone

A

prednisolone

38
Q

What are the two forms of glucocorticoid esters

A

phosphate and succinate esters

acetate and acetonide esters

39
Q

What do the ester forms of glucocorticoids affect in terms of pharmacokinetics

A

speed of onset and duration of action

40
Q

Which esters have rapid onset:
phosphate and succinate esters or acetate and acetonide esters

A

phosphate and succinate esters. These are highly water soluble

41
Q

Which esters have delayed onset:
phosphate and succinate esters or acetate and acetonide esters.

A

acetate and acetonide esters. These are poorly water soluble

42
Q

What form of prednisone/prednisolone should be given to cats and horses? why

A

Prednisolone. Horses and cats don’t metabolize prednisone well because it is a CYP450 dependent process

43
Q

What are the four most commonly used glucocorticoid drugs?

A

prednisone
prednisolone
dexamethasone
fluticasone

44
Q

Which form (prednisone vs prednisolone) is not suitable for topical administration in any species, and why?

A

prednisone because it requires hepatic metabolism to get to its active form

45
Q

Which typically require a higher glucocorticoid dose: cats or dogs

A

cats

46
Q

glucocorticoid routes of administration

A

IV/IM/SQ/oral/local(intraarticular)/inhaled/topical

47
Q

What are the top 3 adverse affects of glucocorticoids

A

immunosuppression
GI ulcers
Elevated liver enzymes/steroid-induced hepatopathy

48
Q

What glucocorticoid is commonly used in SA for anti-inflammatory/antiallergic treatment

A

prednisone/prednisolone

49
Q

What glucocorticoid is commonly used in LA for anti-inflammatory/antiallergic treatment

A

dexamethasone

50
Q

Why should you taper glucocorticoid administration withdrawal if their was a chronic administration

A

HPA axis suppression often occurs, so quitting cold turkey will mean the animal wont produce any endogenous glucocorticoids

51
Q

How can you reduce HPA axis suppression?

A

alternate day therapy

52
Q

What happens if you co-administer an NSAID with a steroid

A

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
Q

What skin condition is commonly treated with glucocorticoids

A

atopic dermatitis

54
Q

What blood condition of dogs is commonly treated with glucocorticoids

A

immune-mediated hemolytic anemia

55
Q

What neoplasia is commonly treated with glucocorticoids

A

lymphoma

56
Q

What respiratory condition is commonly treated with glucocorticoids

A

equine/feline asthma

57
Q

What are contraindications/cautions for glucocorticoid use

A

systemic fungal disease
laminitis in horses
concurrent infection
corneal ulcers

58
Q

What is ciclesonide

A

a new inhaled corticosteroid that was released and then pulled from the market.

59
Q

What treatments for hyperadrenocorticism (PPID, cushing’s) target the adrenal gland

A

Trilostane and mitotane

60
Q

MOA of trilostane

A

inhibits pregnenolone conversion into progesterone, preventing the production of cortisol in the adrenal gland

61
Q

Mitotane MOA

A

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
Q

What are the adverse affects of trilostane and mitotane?

A

signs associated with HYPOadrenocorticism:
lethargy, vomiting, diarrhea, inappetance, weakness

63
Q

What treatments for hyperadrenocorticism (PPID, cushings) target the pituitary

A

Selegiline and pergolide mesylate

64
Q

What are selegiline and pergolide mesylates

A

dopamine agonists that reduce cortisol production at the level of the pituitary

65
Q

What dopamine agonist is used to treat hyperadrenocorticism in dogs

A

selegiline, although it is only effective in 20% of dogs

66
Q

What dopamine agonist is the standard treatment for PPID in horses

A

pergolide mesylate

67
Q

Selegiline MOA

A

acts as a dopamine agonist to cause feedback inhibition to ACTH

68
Q

Pergolide mesylate MOA

A

acts as a dopamine agonist and inhibits production of POMC derived hormones

69
Q

What are the symptoms of hypoadrenocorticism (addisons)

A

lethargy, vomiting, diarrhea, inappetance, weakness

70
Q

What mineralocorticoid replacements are used to treat addisons (hyopadrenocorticism)

A

Desoxycorticosterone pivalate (DOCP)
Fludrocortisone acetate

71
Q

What glucocorticoid replacement is used to treat hypoadrenocorticism (addisons)

A

Dexamethosone for acute crises, pred for chronic

72
Q

What are the two components of atopic dermatitis

A

IgE-mediated mast cell degranulation

Cytokine dysregulation

73
Q

What type of T helper cells is most responsible for the initial response in atopic dermatitis

A

Th-2

74
Q

What do Th-2 cells release

A

interleukins

75
Q

what do Th-1 cells release

A

IFN-y, TNF-a

76
Q

What are the two H1 antagonists used to treat atopic dermatitis (perhaps ineffectively)

A

Diphenhydramine (benadryl)
Hydroxyzine

77
Q

What is the top adverse affect of antihistamines

A

CNS depression

78
Q

What should you not give CNS depressants (like antihistamines) with

A

monoamine oxidase inhibitors

79
Q

What is oclacitinib?

A

brand name Apoquel, is a JAK-1 selective inhibitor

80
Q

How does oclacitinib work for atopic dermatitis

A

it blocks the action of IL-31, an interleukin specifically associated with pruritis

81
Q

How is oclacitinib administered

A

typically orally

82
Q

when should you not dive oclacitinib

A

during active infections, due to the immunomodulatory effects

83
Q

What are the adverse effects of Oclacitinib

A

Mostly GI (diarrhea, anorexia, vomiting)
Immunosuppression
Possibly worsens pre-existing tumors

84
Q

What is cyclosporine

A

an immunosuppressive drug used to treat a variety of conditions, includingg transplant rejection

85
Q

what immunosuppresive drug can be used to treat atopic dermatitis

A

cyclosporine

86
Q

What are the adverse affects of cyclosporine

A

Gi upset, but usually decreases with time

87
Q

What is Lokivetmab

A

aka cytopoint, is a monoclonal antibody against IL-31

88
Q
A

Pharmacology (11 decks)

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