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Module 9 > Corticosteroid & Respiratory Systems > Flashcards

Corticosteroid & Respiratory Systems Flashcards

1
Q

what are the arachidonic acid pathway

A
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2
Q

how are corticosteroids produced

A

synthesized and released as required –> no storage needed

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3
Q

what is endogenous control of corticosteroids

A

hippocampus <——> amygdala

hypothalamus –> corticotropin releasing hormone –> pituitary –> adrenocorticotropic hormone –> adrenals –> cortisol

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4
Q

what are exogenous corticosteroids useful for

A

treating symptoms of conditions

but do not treat underlying cause

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5
Q

what is the mechanism of action of corticosteroids (5)

A
  1. binding of steroid hormone to receptor
  2. translocation of steroid-receptor complex to nucleus
  3. binding of complex to DNA regulatory site
  4. transcription
  5. translocation
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6
Q

what is the structure of corticosteroids

A

basic structure is: 3 hexane rings and a pentone ring

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7
Q

what are examples of proteins whose synthesis is induced by glucocorticoids

A
  1. angiotensin converting enzyme
  2. B2-adrenoceptro
  3. lipocortin 1 (inhibits phospholipase)
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8
Q

what are examples of protein synthesis is inhibited by glucocorticoids

A
  1. cytokines
  2. cyclo-oxygenase
  3. collagenase
  4. inducible NOS
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9
Q

what are mechanism of action of glucocorticoids

A
  1. metabolic effects and systemic effects –> normal physiological actions
  2. anti-inflammatory effects and immune suppressive effects –> pharmacological actions

physiological function –> anti-inflammatory activity –> immunosuppression –> cytotoxicty

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10
Q

what are the duration of action of corticosteroids

A

different glucocorticoids have different inherent durations of action

prenisolone, prednisone, methylprednisolone are short acting (<24 hours)

dexamethasone, betamethasone, triamcinolone are all long acting (>24 hours)

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11
Q

what are water soluble salts ideal for and why

A

ideal for IV

readily absorbed and eliminated within 8-24hrs

high concentrations, rapidly

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12
Q

what are examples of water soluble salts

A

sodium phosphate salts and soluble esters (succinate)

ex. betamethasone sodium phosphate (betsolan soluble), dexamethasone (axium, colvasone, dexadreson)

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13
Q

what are insoluble esters useful for

A

more sustained therapy

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14
Q

what are examples of insoluble esters

A

acetate, adamantoate, diproprionate, pivalate, phenylproprionate, isonicotinate, adamantoate

dexamethasone isonicotinate (voren 14)

methylprednisolone acetate (depo-medrone V)

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15
Q

what are the general principles of corticosteroid therapy (5)

A
  1. minimal mineralocorticoid activity preferred
  2. use a low dose
  3. withdraw treatment gradually
  4. long acting compounds greater risk of toxicity
  5. treat underlying cause of problem
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16
Q

how is the HPA axis suppressed

A
  1. negative feedback of exogenous corticosteroids
  2. suppression of ACTH followed by atrophy of adrenal gland
  3. sudden termination of exogenous corticosteroid –> life-threatening crisis

essential for gradual reduction in corticosteroid dose

17
Q

what are some side effects of corticosteroids (11)

A
  1. gastric and corneal ulceration
  2. suppression of responses (injury or infection)
  3. muscle and cutaneous atrophy
  4. hyperglycemia
  5. osteoporotic effect
  6. sodium and water retention (blood pressure) and loss of potassium
  7. polyuria and polydipsia
  8. increased susceptibility to infection
  9. iatrogenic cushing’s disease
  10. suppression of HPA leading to Addison’s disease on drug withdrawal
  11. laminitis
18
Q

what is addison’s disease

A

deficiency of adrenocortical steroid production

mineralocorticoid and glucocorticoid deficiency

usually immune mediated destruction of adrenal cortices

most commonly iatrogenic

19
Q

what are the symptoms of addison’s disease

A

anorexia, vomiting, diarrhea, weakness, exercise intolerance, polydipsia and polyuria

20
Q

what breeds are predisposed to addisons

A

standard poodles

west highland terriers

great danes

some collies

21
Q

how is addison’s diagnosed

A

circulating ACTH concentrations increased in primary (adrenal) addison’s but not so in central hypoadrenocorticism

22
Q

how is addison’s disease treated

A

acute hypoadrenal crisis is a medical emergency

hydrocortisone sodium succinate IV

chronic therapy requires permanent mineralcorticoid therapy (fludrocortisone acetate orally)

23
Q

what is cushing’s disease

A

hyperadrenocorticism

overproduction of glucocorticoids due to a pituitary adenoma (ACTH increased) or due to an adrenal tumour (ACTH very low)

Iatrogenic cushing’s can result from prolonged treatment with glucocorticoids

24
Q

what are common symptoms of cushing’s diease in dogs

A

polydipsia, polyuria, polyphagia

elevated liver enzymes

pot belly

thin skin

coat changes

muscle wastage

25
Q

what are breeds most commonly affected by cushing’s

A

poodles

dachshunds

terriers

german shepherds

golden retrievers

26
Q

what are the two types of cushing’s in dogs

A
  1. pituitary: 80% –> increase in ACTH, increase in cortisol
  2. adrenal: 20% –> decrease in ACTH, increase in cortisol
27
Q

what are the 3 tests for cushing’s (3)

A
  1. ACTH test: elevated corticosteroids before ACTH and a rise after admin
  2. low dose dexamethasone suppression test: in cushing’s it won’t suppress cortisol
  3. high dose dexamethasone suppression test: sometimes used to differentiate between pituitary and adrenal problem (if pituitary high dose will suppress cortisol production, if adrenal –> will not)
28
Q

what are pharmacological interventions in cushing’s disease (3)

A

enzyme blockers

  1. trilostane (vetoryl): oral, well tolerated, careful monitoring required
  2. ketoconazole (antifungal): interferes with synthesis of adrenal steroids (expensive)
  3. mitotane: cytotoxic –> easy to use, inexpensive but potentially very serious side effects, requires regular monitoring

Module 9 (43 decks)

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