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P&T Exam 1 > Dr. Corey Lectures > Flashcards

Dr. Corey Lectures Flashcards

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1
Q

What are the divisions of the adrenal gland and their function?

A

Medulla synthesizes epinephrine and norepinephrine, cortex synthesizes adrenocortical hormones(steroids)

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2
Q

What are examples of adrenocortical hormones(steroids)?

A

Glucocorticoids, mineralcorticoids, and adrogenic and estrogenic activity

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3
Q

What do glucocorticoids do? Give an example of a glucocorticoid

A

Effect intermediary metabolism and immune functions, ex) cortisol

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4
Q

What do mineralocorticoids do? Give an example

A

Salt retaining, aldosterone

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5
Q

Describe mineralocorticoid synthesis

A

Acetate, cholesterol, pregnenolone, progesterone, 11-deoxy-corticosterone, corticosterone, aldosterone

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6
Q

Describe glucocorticoid synthesis

A

acetate, cholesterol, pregnenolone, 17-hydroxy-pregnenalone, 17-hydroxy-progesterone, 11B-deoxycortisol, cortisol

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7
Q

Describe androgen and estrogen synthesis

A

acetate, cholesterol, pregnenolone, 17-hydroxy-pregnenolone, dehydroepi-androsterone, delta4-androstene-3,17-dione, testosterone, estradiol

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8
Q

What causes release of aldosterone?

A

Angiotensin I gets converted to angiotensin II in lungs and high serum potassium levels

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9
Q

What happens when aldosterone is released?

A

Increases reabsorption of Na+ into kidneys

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10
Q

What happens when aldosterone is insufficent?

A

Lose sodium, decreased plasma fluid volume, blood volume, and blood pressure

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11
Q

Describe glucocorticoid synthesis and release

A

stressor release corticotropin(CRH) in hypothalamus, which causes release of adrenocorticotropic hormone (ACTH) in anterior pituitary, which leads to release of cortisol in adrenal cortex, this then is delivered to liver, fat, muscle, and lymphocytes(etc.)

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12
Q

Describe the negative feedback of glucocorticoid synthesis and release

A

Cortisol negatively regulates CRH and ACTH

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13
Q

What can suppress output of adrenocorticotropin hormone(ACTH)?

A

High plasma concentration of glucocorticoids

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14
Q

What happens in the absence of adrenocorticotropin hormone(ACTH)?

A

Decreased cortisol levels and adrenal cortex begins to atrophy, ACTH helps maintain gland

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15
Q

Describe the pharmacokinetics of cortisol

A

released on 24hr cycle that peaks at 8am and diminishes by 8pm, 90% of cortisol in plasma bound to corticosteroid binding globulin, 5-10% is free or bound to albumin(can affect target cells

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16
Q

What is the half life of cortisol and its metabolism breakdown in kidneys and liver?(pharmacokinetics still)

A

80min half life, kidney breaks down about 20%, liver degrades most with CYP3A4

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17
Q

What is the mechanism of cortisol on gene expression?

A

free glucocorticoid binds to cytosolic receptor, migrate to nucleus, regulate gene expression, modify synthesis of protein, get hormone response within hours

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18
Q

What percentage of genes are regulated by glucocorticoids?

A

10-20%

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19
Q

What is the metabolic effect of cortisol on protein?

A

Stimulates gluconeogenesis, increases blood glucose. Extended exposure leads to breakdown of proteins and wasting

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20
Q

What is the metabolic effect of cortisol on carbohydrates

A

Decreased uptake of carbohydrates by fat cells and inhibition of uptake of glucose by muscle cells, overall increase in blood glucose levels

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21
Q

What is the metabolic effect of cortisol on lipid metabolism?

A

Promote breakdown of fats which increases free FA in plasma, prolong administration or hypersecretion of cortisol and lead to redistribution of body fat to back, shoulders, face, and abdomen

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22
Q

What are the therapeutic uses of glucocorticoids?

A

Treat adrenal insufficiency and suppress inflammation ,allergic conditions, and autoimmune disorders and pharmacological doses

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23
Q

Describe the acute vascular phase of inflammation

A

Localized vasodilation, redness and warmth, increased capillary permeability, localized edema, swelling pain and tenderness, walling off inflamed area

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24
Q

What does release of histamine cause?

A

Relaxation of smooth muscle which leads to swelling, vasodilation, pain, and tenderness(etc.)

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25
Describe the subacute response of inflammation
Proliferation and infiltration of leukocytes, phagocytosis of bacteria and debris, release of chemical mediators involved in inflammation
26
Describe the tissue phase of inflammation
Repair of tissue damage and return of function, lymphocytic phase(interleukins and TNFa)
27
What causes chronic inflammation?
Caused by persistent infection or loss of homeostatic control of inflammatory process
28
What are diseases with chronic inflammation?
TB, rheumatic fever, glomerular nephritis, rheumatoid arthritis, psoriasis, ulcerative colitis, gout, periodontal disease
29
What are chemical mediators ofinflammation?
histamine, prostaglandins, leukotrienes, lymphocyte products, macrophage products, neutrophil release
30
What are the types of leukotrienes?
LTD4(bronchial constriction) and LTB4(chemotactic)
31
What are examples of lymphocyte products?
Cytokines, interleukins, chemotactic factors
32
Describe the synthesis of chemical mediators
Stimuli, disturbance of cell membrane, phospholipids, arachadonic acid, lipoxygenase turns into hydroperoxides which turn into leukotrienes OR cyclooxygenase turns into endoperoxides which turn into prostaglandins, prostacyclin, or thromboxane A1
33
What are mechanism of antiinflammatory effects of pharmacological doses of glucocorticoids?(5 things)
Increase synthesis of annexin 1 which decreases arachadonic acid(decrease chemical mediators), suppresses synthesis of COX2, inhibit synthesis of inflammatory cytokines, impairs leukocyte function, decreases phagocytic activity
34
What are anti inflammatory effects of glucocorticoids?
Suppress capillary permeability and vasodilation, decrease leukotrienes, decrease recruitment of lymphocytes, inhibit connective tissue phase
35
Why can glucocorticoids be dangerous with regards to inflammation?
Suppress symptoms of inflammation which are signs of infection
36
What are immunosuppresive actions of glucocorticoids?
decreased cytokine production, inhibit effects on immune cells, interfere with macrophage function(increased b and t lymphocyte proliferation), decreased phagocytosis, suppressed cell mediated immunity, decreased lymphocyte circulation
37
When we add a F group to cortisol, how does this affect the pharmacological activity?
F group increases the half life of the glucocorticoid
38
What does acetonide do when added to a glucocorticoid?
Allows for topical activation
39
Describe short acting glucocorticoids
High equivalent dose, same anti-inflammatory effect as cortisol, last for about 8-12 hours, about 1 in salt retaining
40
Describe intermediate acting glucocorticoids
lower equivalent dose than short acting, 5x higher anti-inflammatory effect as cortisol, last for about 12-36 hours, 0-0.3 in salt retaining
41
Describe long acting glucocorticoids
lowest equivalent dose, 30x higher anti-inflammatory effect as cortisol, last for about 36-72 hours, 0 in salt retaining
42
Describe function of fludrocortisone
Acts like aldosterone, high salt retention ability, 10x anti-inflammatory effect as cortisol
43
What are examples of short acting glucocorticoids
cortisol and cortisone acetate
44
What are examples of intermediate acting glucocorticoids
prednisone prednisolone, methylprednisolone, triamicinolone
45
What are examples of long acting glucocorticoids?
Dexamethasone and betamethasone
46
Describe the administration and dose of cortisol
oral, about 20-240mg/day
47
Describe the administration and dose of prednisone
oral, available in 21 day dose packs, 5-60mg/day
48
Describe the administration and dose of methylprednisolone
oral, 21 day dose packs, 4-48mg/day
49
What are special types of glucocorticoids
topical preparation, enema, aerosol, nasal spray, into synovial space, ophthalmic
50
What do special preparations of glucocorticoids do?
Increase the concentration of drug in the therapeutic site, decreases side effects by reducing systemic absorbtion
51
What is Addison's disease? Treatment?
deficiency of glucocorticoids and mineralcorticoids, 20-30mg hydrocortisone and fludrocortisone
52
What is Cushing's disease? Treatment?
Hyperplasia of adrenal glands, tumor of adrenal glands which lead to increase cortisol levels, remove tumor, treat with irradiation, remove adrenal glands(steroid therapy)
53
Describe emergency uses of glucocorticoids
High doses for few days, for shock severe acute asthma, autoimmune disease, and transplant rejection
54
How much glucocorticoid is considered an emergency dose?
1-2g methylprednisolone
55
Describe general guidelines for pharmacological doses of glucocorticoids
Used to relieve symptoms and may decrease progression of disease, smallest effective dose for shortest time, special dosage forms, disease indexes monitored for efficacy
56
What are inhaled glucocorticoids for bronchial asthma?
Beclomethasone(beclovent), budesonide(plumicort), trimcinolone(azmacort),flunisolide(aerobid), fluticasone(flovent)
57
What receptors, agonists, and pathways are affected when glucocorticoids are used for bronchial asthma
Not for acute attack, increases number of beta2 receptors, increases effect of beta agonists, decreases mucus, decreases airway edema
58
What are side effects of glucocorticoids for bronchial asthma and how can they be prevented?
Increased incidence of oral candidiasis, prevented with rinsing and use of spacer
59
When are oral steroids used for bronchial asthma?
For acute exacerbations unresponsive to bronchodilators, up to 10 days to decrease symptoms
60
When would you use parental corticosteroids for bronchial asthma?
severe acute attack, administer via IV injection or infusion
61
Describe the role of beta2 agonists for bronchial asthma
relax bronchiole smooth muscle and dilate bronchioles, relieve actue attack
62
What are examples of beta2 adrenergic agonists?
metaproterenol, terbutaline, albuterol, salmerterol
63
What are examples of intranasal steroids for allergic rhinitis and their availability
flunisolide(nasarel, rx), beclomethasone(beconase, rx), triamcinolone(nasacort, otc), fluticasone(flonase, otc), budesonide(rhinocort, otc), monetasone(nasonex, Rx 2+ yr)
64
What are examples of glucocorticoids that need to be administered via intraarticular injection
trimcinolone(keralog), dexamethasone(decadron-LA), methylprednisone(depo-medrol)
65
When would you use intraarticular injected glucocorticoids?
When NSAIDS and other pharmacologic measures fail
66
What are the increasing treatments of rheumatoid arthritis?
Initially treat with rest and PT, DMARDS may lead to remission, if DMARDS alone do not work add NSAIDS, if DMARDS and NSAIDS do not work, add corticosteroids to reduce symptoms to tolerable levels
67
What are other chronic inflammatory diseases besides rheumatoid arthritis?
Acute MS, Chron's disease, ulcerative colitis, SLE
68
What is considered a low versus high dose of prednisone for inflammatory conditions?
2-40mg/day is low, 40-60mg/day is high
69
What is the atenatal use of glucocorticoids?
Stimulate structural and functional changes in fetal lungs near term(produce surfactant), dexamethasone(4doses/12hours) reduce incidence of respiratory distress syndrome and mortality of premature babies
70
What are immunosuppressive effects of glucocorticoids in organ transpland?
Prevents rejection, effects lymphoid cells, anti-inflammatory effects
71
What are applications of glucocorticoids in dentistry?
Noninfections inflammation, ulcerative lesions of the oral mucosa, temporomandibular joint disorders, post operative, variety of dental diseases
72
What is orabase?
Topical paste that adheres to mucosa(maximizes contact time), cortisol 2-3x/day, trimcinolone acetonide(Kenalog in orabase) 2-3x/day
73
What are the ways to withdrawl steroid therapy
With taper(after symptoms are under control), Without taper in cases of steroid induced psychosis or herpesvirus induced corneal ulceration
74
What is toxicity of steroids dependent on?
Duration and dose of drug, age and condition of patient, disease type
75
When is it unlikely to get suppression of HPA axis when on steroids?
When a high dose is taken for a few days or any dose is taken for less than 3 weeks
76
What is the effect of intermediate acting glucocorticoids on toxicity?
Not as clear, 10-20mg prednisone for over three weeks. likely to get suppression of HPA axis if dose is comparable to greater than 20 mg prednisone for more than 3 weeks
77
How to dose taper prednisone
If dose is greater than 40mg/day, reduce by 5-10 mg every other week
78
How long can recovery of HPA axis take? How does this affect tapering
HPA recovery can take 2-12 mo and then an additional 6-9 mo to return to normal cortisol levels, tapering will be extremely slow if HPA is atrophied
79
Describe toxicity of glucocorticoids in infections
These drugs delay wound healing, suppress inflammation and the immune response. This makes patients more susceptible to serious infection or exacerbate an existing one. Greater effect on T cells but ab production is persevered
80
What are effects of prolonged therapy toxicity?
Ulcer formation, myopathy, osteoporosis, hyperglycemia, hyperlipidemia, protein wasting, Cushingoid appearance, weight gain, CNS effects, cataracts(in 1+ year treatment), decreased resistance to infection and poor wound healing, suppression of HPA axis

P&T Exam 1 (3 decks)

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