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Pharm 2 > E1. Drugs acting on the adrenal cortex > Flashcards

E1. Drugs acting on the adrenal cortex Flashcards

1
Q

Slides 1-7 review of adrenal physiology

A

.

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2
Q

What are the two possible effects glucocorticoids can have?

A

Genomic and non-genomic

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3
Q

For genomic effects where do you find your glucocorticoid receptors (GCR)? What are those receptors responsible for? What’s the feedback on the ACTH secretion?G

A

Find the receptors in the cytoplasm. They are responsible for trans-activation of genes and transrepression of genes. They have a ‘Slow feedback’ on ACTH secretion.

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4
Q

Where do you find the receptors responsible for the non-genomic effects? What’s the feedback on the ACTH secretion?

A

The receptors are found in membrane. They have a fast feedback on ACTH secretion.

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5
Q

List all of the effects on body systems that glucocorticoids have? (10)

A
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6
Q

What affects do glucocorticoids have on energy metabolism?

A

– Generally catabolic.
– Antagonistic to insulin.
(Increased gluconeogenesis, lipolysis, protein catabolism)

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7
Q

What affects do glucocorticoids have on water and electrolytes?

A

– Altered calcium metabolism (decreased G.I. absorption, increased urinary excretion).
– Polyuria (decreased ADH secretion).
– Polydipsia.
– Increased GFR.

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8
Q

What affects do glucocorticoids have on Cardiac and respiratory system?

A

– generally chronotropic and inotropic.
– Increase beta adrenoreceptors.
– Permissive to the effects of catecholamines.
– Indirect cardiac effects through water/electrolyte metabolism.

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9
Q

What affects do glucocorticoids have on Hematology?

A

– increased PCV and RBC life span.
– Increased platelets
– increased clotting/platelet function
– stress leukogram (decrease in circulating basophils, mast cells)

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10
Q

What affects do glucocorticoids have on Chemistry?

A

– Increase will usually be seen in: alkaline phosphatase (ALP)
– increase may be seen in: alanine aminotransferase (ALT), gamma glutamyl transferase (GGT), cholesterol/triglycerides, glucose (+/-).
– Decreases may be seen in: BUN, T3 and T4.

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11
Q

What affects do glucocorticoids have on Nervous system?

A

– mental dependency (humans)
– euphoria/depression
– Polyphagia
– peripheral neuropathies

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12
Q

What affects do glucocorticoids have on Decrease fever?

A

– Inhibition of PGE2 production in the thermoregulatory

center

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13
Q

What affects do glucocorticoids have on Skin(With chronic excess)?

A

– mineralization (

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14
Q

What affects do glucocorticoids have on Musculoskeletal system?

A

– increased osteoclast activity lash decrease osteoblast activity. (Osteoporosis, decreased bone growth, depletion of cartilage matrix)
– inhibitionof fibroblasts

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15
Q

What affects do glucocorticoids have on Reproductive system?

A 
– fetal maturation
– teratogenic (cleft palate)
– induce abortion/parturition (fetal glucocorticoid)
– inhibit spermatogenesis
– inhibit ovulation
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16
Q

What affects do glucocorticoids have on Gastrointestinal and hepatic system? (ONE OF THE BIGGEST AND MOST CONCERNING)

A

– G.I. alterations: increased gastric acid secretion, decreased gastric mucus secretion, significant risk if concurrent with use of NSAIDs.
– Fatty liver: increased absorption from GIT, increased fat deposition in the liver, alteration of liver enzymes.
– Pancreatitis (does not directly cause, but may indirectly cause)

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17
Q

What affects do glucocorticoids have on Immunologic effects – anti-inflammatory?

A
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18
Q

What affects do glucocorticoids have on Immunologic effects – immune suppression?

A
  • Different leukocytes have different sensitivity to

glucocorticoid concentrations

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19
Q

What are the clinical uses of glucocorticoids? (9)

A
20
Q

Look at slide 23 too much information.M

A

.

21
Q

What are your cautions/contraindications for glucocorticoids?

A 
– Diabetes mellitus
– pre-existing catabolic disease
– infections (most of the time)
– corneal ulceration
– young, growing animals
– pregnancy
– wounds (that you want to heal)
– concurrent use of NSAIDs
– caution with underlying liver, cardiac disease, etc.
22
Q

Look at slide 25 drug interactions. Lots of information.

A

.

23
Q

How long does short-term side effects last? (Look at slide 26 this question is not comprehensive)

A

3 – 5days

24
Q

How long does long-term side effects last? (Look at slide 27)

A

Greater than one week

25
Q

Look at slides 28 – 38.

A

.

26
Q

What happens when you combine glucocorticoids with salt esters?

A

It allows for larger volumes and IV injection.

*Onset may be faster with IV administration the duration will not change (similar to oral)

27
Q

What are some examples of the glucocorticoids combined with salt testers? (4)

A

–Dex sodium phosphate
– Methylprednisolone sodium succinate
– hydrocortisone sodium succinate
– prednisolone sodium succinate

28
Q

What happens when you combined glucocorticoids with insoluble esters?

How can these be given?

A

The less soluble the ester the longer it takes to absorb
(delayed onset of action) and the longer the duration.

They can be given IM, SC, as long as it’s not done through IV

29
Q

What glucocorticoid (suspensions) is used for topical use?

A

Fluorination.

30
Q 
What drug is an inhalant glucocorticoid?
A. Fluorination
B. Budesonide
C. Beclomethasone diproprionate
D. Fluticasone diprioprionate
A

D. Fluticasone diprioprionate

31
Q 
What drug has a week mineralocorticoid activity, and high topical activity in GIT?
A. Fluorination
B. Budesonide
C. Beclomethasone diproprionate
D. Fluticasone diprioprionate
A

B. Budesonide

32
Q

What are the two mineralocorticoid we would use to treat Addison’s disease?

Which of the two does not need to be given with a glucocorticoid?

A

Desoxycorticosterone pivalate (DOCP) & Fludrocortisone

Fludrocortisone

33
Q

What are the two major drugs that we will use to treat Cushing’s disease (Hyperadrenocorticism)?

A

mitotane and trilostane

34
Q

What type of Hyperadrenocorticism is mitotane able to treat?

A

Pituitary and adrenal

35
Q

What gland is mitotane cytotoxic to?

A

The adrenal gland (Zona fasciculata/reticularis)

36
Q

True or false: Mitotane is a very safe drug with a wide therapeutic index.

A

False. Mitotane is a drug with a narrow therapeutic index.

37
Q

How is mitotane taken?

A

Orally

38
Q

What is an issue if you overtreat an animal with mitotane?

A

You can cause primary Addison’s disease.

39
Q

What should you measure to monitor the treatment of Cushing’s disease with mitotane?

A

Monitor with ACTH stimulation testing.

40
Q

What type of Hyperadrenocorticism is Trilostane able to treat?

A

Pituitary and adrenal Hyperadrenocorticism

41
Q

How does Trilostane work?

A

Is a competitive inhibitor of steroid synthesis

42
Q

What can excessive dosing of Trilostane cause?

A

Over suppression

43
Q

What is the risk of using ketoconazole to treat hyperadrenocorticism?
What is its intended use?

A

The riskiest hepatotoxicity.

Intended use is as an anti fungal that inhibits cortisol synthesis along with inhibiting CYP 450 enzymes.

  • efficacy may be lower than mitotane or triostane
44
Q

Other than mitotane, triostane or ketoconazole, what drugs can be used to treat hyperadrenocorticism? (3)

A

L-deprenyl, Pergolide, Cabergoline.

45
Q

Look at slide 58, it has a picture to show you where the six drugs act.

A

.

Pharm 2 (17 decks)

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