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PHRM 5001 > 3. Anti-inflammatory Medications > Flashcards

3. Anti-inflammatory Medications Flashcards

1
Q
  1. What kind of gland is the hypothalamus?
  2. What nerves does it receive sensory impulse from?
  3. What does the hypothalamus coordinate signals with?
  4. What does the hypothalamus release into the bloodstream?
A
  1. Endocrine gland
  2. Afferent nerves
  3. Hormonal feedback
  4. Chemical messengers
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2
Q
  1. What controls the pituitary gland?
  2. The posterior pituitary controls the ______, and what does it do?
  3. The anterior pituitary controls the ______, and what does it do?
A
  1. Hypothalamic cell nuclei
  2. Neurohypophysis, maintains fluid levels via ADH
  3. Adenohypophysis, stimulates/inhibits release of other hormones
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3
Q
  1. The hypothalamus is stimulated by ______ to release _______.
  2. What are some examples that could stimulate the hypothalamus?
A
  1. Stressors, corticotropin releasing factor (CRF)

2. Infection, trauma, emotional stress, exercise, surgery, thermal changes

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4
Q

HPA Axis

  1. ______ enters the ______, and is transported to the _______.
  2. Stimulates the release of ________.
  3. ______ travels via the ________ to the _______
  4. ACTH binds to specific _________ in the _______.
A
  1. CRF, pituitary portal system, transported to the adenohypophysis
  2. Adrenocorticotropin hormone (ACTH)
  3. ACTH, bloodstream, adrenal cortex
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5
Q

HPA Axis Cascade —> What are the 4 steps?

A
  1. Activates adenylyl cyclase
  2. ATP converted to cAMP
  3. ↑ cAMP stimulates adrenal cortex
  4. Hormones synthesized and released
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6
Q
  1. The adrenal glands are ____ and highly ____, and where are they found?
  2. What are the 2 distinct endocrine glands they contain?
A
  1. Small, highly vascularized, found on superior aspect of kidneys
  2. Adrenal medulla, adrenal cortex
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7
Q

What are the 3 layers of the adrenal cortex, and the steroid hormone that each layer synthesizes?

A
  1. Zona glomerulosa —> mineralocorticoids
  2. Zona fasciculata —> glucocorticoids
  3. Zona reticularis —> gonadocorticoids
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8
Q

What are the functions of each of the 3 steroid hormones?

A

Mineralocorticoids —> regulate plasma electrolytes
Glucocorticoids —> regulate blood glucose levels
Gonadocorticoids —> promote protein synthesis

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9
Q

Glucocorticoids do 2 main jobs… the first is increasing _____, and modifying the body’s __________, which influences ____ expression and protects from ______________.

A

Increases blood glucose, modifies the body’s inflammatory response which influences gene expression and protects from pro-inflammatory host defences

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10
Q

Glucocorticoids MOA

  1. Glucocorticoids are highly ______, which allows for what?
  2. Where are the receptors located that glucocorticoids bind to?
  3. Where does this steroid-receptor complex migrate to?
A
  1. Lipophilic, allowing for entry into cells in the airway
  2. Cytoplasm
  3. Cell nucleus
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11
Q

The glucocorticoid steroid-receptor complex binds to ______ in the nucleus, which induces production of ______, and suppresses production of ______.

A

Specific genes, induces production of anti-inflamm proteins and receptors, suppresses production of pro-inflamm proteins

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12
Q

What can lung inflammation occur in response to? (5 things)

A

Direct trauma, indirect trauma, inhalation of noxious stimuli, respiratory or systemic pathogens, allergens

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13
Q

S&S of airway inflammation (latin —> english), and what are these S&S caused by?

A

Rubor —> redness
Tumor —> swelling
Calore —> heat
Dolore —> pain

Caused by: ↑ vascular permeability, leukocytic infiltration, phagocytosis, mediator cascade

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14
Q

Glucocorticoid-receptor complex binds to genes that induce synthesis and up-regulation of anti-inflamm substances such as…..???

A

Lipocortin, neutral endopeptidase, secretory leukocyte protease inhibitor (SLPI), and inhibitors of plasminogen activator

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15
Q

Interaction of the glucocorticoid steroid-receptor complex with airway cell DNA inhibits the synthesis of….???

A

Inflammatory enzymes, cell adhesion molecules, cytokinesis, chemokines, and inflammatory receptors

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16
Q

What inflammatory enzymes are inhibited by the interaction of the S-R complex with airway cell DNA? (Hint: 3 of them)
What does each enzyme do if not inhibited?

A
  1. Nitric oxide synthase inhibition (NO damaging to airway epithelium in high conc)
  2. Cyclooxygenase-2 Inhibition (COX)
  3. Phospholipase A2 inhibition (reduce late phase inflamm)

NO: if not inhibited, high conc, damaging to airway epithelium
COX: If not inhibited, will convert arachidonic acid into prostanoid inflamm. mediators
Phospholipase A2: if not inhibited, arachidonic acid is converted to intermediate compounds that generate eicosanoid mediators

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17
Q

What molecules are inhibited to allow slower movement of leukocytes into inflammatory tissue? What does this mean for the inflammatory response?

A

Cell adhesion molecules, this decreases the amplification of the inflammatory response.

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18
Q
  1. What are cytokines?
  2. What do they do?
  3. What happens when cytokines are inhibited?
A
  1. Proteins secreted by various cells
  2. Regulate local and systemic inflammatory responses
  3. Prevents the recruitment and migration of inflammatory cells
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19
Q
  1. What are chemokines?

2. What happens when they are inhibited?

A
  1. Family of small cytokines that act as chemoattractants

2. Prevents the mobilization of inflammatory cells (eosinophils, monocytes, neutrophils)

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20
Q
  1. Inflammatory receptors normally interact with what? Give examples
  2. What happens when these are inhibited?
A
  1. Histamine-like mediators, such as bradykinin and substance P
  2. Reduces the total # of receptors available
21
Q

Endogenous Glucocorticoids

  1. What is released from the adrenal cortex, and what is it in response to?
  2. What effect does this have?
A
  1. Hydrocortisone, in response to ACTH

2. Potent anti-inflammatory effect

22
Q

Endogenous Glucocorticoids MOA (Part 1)

  1. Mobilize __________ for use in ________.
  2. Suppress the activity of _______, inhibiting _______ production
  3. Proteins in ______ tissue diverted to _________ pathway, ↓ ___ production
  4. Inhibit the production of ______ in target cells
A
  1. non-carbohydrate substances, gluconeogenesis
  2. fibroblasts, collagen
  3. lymphoid, gluconeogenesis, Ab
  4. histamine
23
Q

Endogenous Glucocorticoids MOA (Part 2)

  1. Stabilize ____ within ______, preventing _____ and ______ release
  2. Inhibit _________________and ___ enzymes, which ↓ _______ mediators
  3. Enhance responsiveness to __________ drugs by ↑ the # of _______, and ↑ the affinity for ________ drugs
A
  1. lysosomes, neutrophils, degranulation and mediator release
  2. phospholipase A2, COX, eicosanoid
  3. B2-agonist, receptors, B2-agonist
24
Q
  1. What does ↑ mineralocorticoid release lead to?
  2. What electrolyte(s) does it ↑? ↓?
  3. What else does the fluid retention lead to?
A
  1. Fluid retention and electrolyte imbalances
  2. Increases Na+, decreases K+
  3. Edema (moon face)
25
Q

What does ↑ glucocorticoid release lead to? (Hint: 4 things)

A
  1. ↑ blood glucose level
  2. Shifting of fat storage depots
  3. Immunosuppression –> less circulating Abs
  4. General weight gain (replace protein thru ↑ appetite and dietary intake)
26
Q

Who is ↑ gonadocorticoid release more visible in?

What does this do to the body?

A
  1. Women

2. Masculinization (facial hair, ↑ muscle mass, voice changes, disruption of menstrual cycle)

27
Q

What does ↓ mineralocorticoid (aldosterone) release lead to? (4 things)

A
  1. Excess elimination of Na+ and water
  2. Hyperkalemia
  3. Renal suppression
  4. Retention of toxic materials
28
Q
  1. What does ↓ glucocorticoid release lead to?

2. What does ↓ sex hormone (gonadocorticoid) release lead to?

A
  1. ↓ blood glucose levels, ↓ ability to resist physiological stress
  2. Muscle weakness
29
Q
  1. Exogenous glucocorticoids initiate a ____________, which suppresses the ___ axis.
  2. List the steps of axis suppression
A
  1. Negative feedback loop, HPA

2. Hypothalamus inhibited, ↓ CRF output, no ACTH release from ant. pituitary, adrenal cortex suppressed.

30
Q
  1. What kind of dependency do exogenous glucocorticoids create?
  2. The similarities with endogenous hormones lead to _____ effects.
  3. What must happen with patients on these medications, and why?
A
  1. Physiologic
  2. Cushingoid
  3. Patients must be tapered from exogenous steroids to avoid withdrawal and Addisonian crisis
31
Q
  1. What is the circadian rhythm? How often does it repeat?

2. Because of this, when are exogenous steroids taken during the day and why?

A
  1. Body’s way of optimizing hormone levels to meet physiologic stressors, repeats every 24 hrs
  2. In the morning, when natural hormone levels peak
32
Q

What is the purpose of alternate day therapy?

When is it indicated?

A
  1. To minimize disruption of the circadian rhythm

2. Pt is active during the day, sleeps at night, requires chronic steroid therapy

33
Q
  1. What type of glucocorticoid is Hydrocortisone (Solu-Cortef)?
  2. What is it considered?
  3. What preparations does it come in? DOA?
  4. What is its use limited in?
  5. It has _______ mineralocorticoid activity.
A
  1. Short-acting
  2. The prototype drug
  3. Oral and IM, 8-12 hrs
  4. Tx of resp disorders
  5. Significant
34
Q

Hydrocortisone:

  1. Indications?
  2. Contraindications?
  3. Precautions?
A
  1. Acute inflammatory responses (asthma, rheumatoid arthritis, bursitis)
  2. HTN, CHF (b/c fluid overload), serious infection, diabetes
  3. Behavioural disturbances, tapered withdrawals, interacts with barbs and phenytoin, pre-existing infection
35
Q
  1. What type of glucocorticoid is Methylprednisolone (Medrol)?
  2. Preparations? DOA?
  3. It has _______ mineralocorticoid activity.
  4. What is it used to treat?
  5. What else can it be used for?
A
  1. Intermediate-acting
  2. Oral, IV, IM, 12-36 hrs
  3. Minimal
  4. Allergic rxns/anaphylaxis
  5. Status asthmaticus, asthma prophylaxis
36
Q
  1. What type of glucocorticoid is Prednisone (Deltasone)?
  2. ____ x more potent than _____
  3. DOA? Preparation?
  4. Typical dose for asthma/COPD pts?
A
  1. Intermediate-acting
  2. 4-5x, cortisol
  3. 12-36 hrs, oral prep with systemic absorption, IV
  4. 50 mg dose
37
Q
  1. What type of glucocorticoid is Dexamethasone (Decadron)?
  2. Preparations? DOA?
  3. ___ x more potent than ________ steroids
  4. ____ mineralocorticoid activity.
  5. Used to treat??
A
  1. Long-acting
  2. Oral, IM, IV, nasal MDI, 36-72 hrs
  3. 25x, endogenous
  4. No
  5. Seasonal allergic rhinitis, asthma, status asthmaticus, upper airway inflammation
38
Q

Inhaled corticosteroids exhibit _____ systemic effects, resulting in what 5 improvements?

A

Minimal!

  1. ↓ severity of cushingoid effect
  2. No HPA suppression
  3. Circadian rhythm intact
  4. No immunosuppression
  5. Localized airway effects
39
Q
  1. What effect develops over time with inhaled corticosteroids?
  2. What are these contraindicated for?
  3. What are nasal formulations available for treatment of?
A
  1. Protective anti-inflammatory effect
  2. Acute treatment
  3. Nasal polyps, perennial and seasonal rhinitis, allergic/inflammatory nasal conditions
40
Q

What type of infection can inhaled corticosteroids cause? What is the most common etiologic agent
What can it be prevented by?

A
  1. Fungal infections
  2. Candida albicans
  3. Rinsing/gargling after ICS use
41
Q
  1. What type of inhaled corticosteroid is Beclomethasone (Qvar)?
  2. Available in what devices?
  3. Doses available? How many puffs and how many times a day?
  4. What % is deposited in the lung?
  5. Can this be administered to ventilated pts?
A
  1. Long-acting
  2. MDI with HFA propellant
  3. 50 mcg, 100 mcg, 1-2 puffs BID
  4. 50-60%
  5. Yes!
42
Q
  1. What forms of delivery is budesonide (pulmicort) available in? What are the strengths per dose in each form?
  2. How many times a day is it given?
  3. More potent than ______?
A 
1. DPI, inhalation solution 
DPI: 100 mcg, 200 mcg, 400 mcg
Pre-mixed "respules": 0.125 mg, 0.25 mg, 0.5 mg 
2. BID
3. Beclomethasone
43
Q
  1. Fluticasone (Flovent) has greater potency than ______
  2. Forms of delivery available & doses for each?
  3. How many times a day is it given?
  4. What happens when this medication is swallowed?
A
  1. Budesonide
  2. MDI, DPI
    MDI: 50 mcg, 125 mcg, 250 mcg
    DPI: 50 mcg, 100 mcg, 250 mcg
  3. 1-2 puffs BID
  4. Weak HPA suppression when swallowed
44
Q
  1. Fluticasone (Flovent) has greater potency than ______
  2. Forms of delivery available & strengths for each?
  3. How many times a day is it given, and how many puffs?
  4. What happens when this medication is swallowed?
A
  1. Budesonide
  2. MDI, DPI
    MDI: 50 mcg, 125 mcg, 250 mcg
    DPI: 50 mcg, 100 mcg, 250 mcg
  3. 1-2 puffs BID
  4. Weak HPA suppression when swallowed
45
Q
  1. Mometasone (Asmanax twisthaler) is available in what form, and what are the strengths?
  2. How many times a day is it given? (Hint: approved for 2 different methods)
  3. What form of prep of this med is frequently prescribed?
A
  1. DPI, 100 mcg, 200 mcg, 400 mcg
  2. OD, BID
  3. Nasal preparation
46
Q

Ciclesonide (Alvesco)

  1. What is this drug referred to as?
  2. 120x greater receptor affinity than _____?
  3. 50% of drug deposited in _____
  4. What does this med decrease the incidence of?
A
  1. Prodrug (inactive until converted in the body to des-ciclesonide)
  2. Endogenous steroids
  3. Lungs
  4. Oral candiasis
47
Q

What are the benefits of combination therapy? (Hint: 4 things, mostly to do with steroids)

A
  1. Steroids upregulate B2-receptors
  2. Steroids limit drug tolerance to B2-agonists
  3. Steroids enhance catecholamine action
  4. Some B2-agonists promote glucocorticoid-receptor binding
48
Q

What are the 4 combination LABA/ICS medications?

A

Salmeterol + Fluticasone = Advair
Formoterol + Budesonide = Symbicort
Formoterol + Mometasone = Zenhale
Vilanterol + Fluticasone = Breo Ellipta

49
Q
  1. What are the strengths of the triple therapy Trilogy Ellipta?
  2. What are the 3 types of inhalers within this one device?
    What dosing regimen is this designed for?
    What does this method improve?
A
  1. 25 mcg, 62.5 mcg, 100 mcg
  2. LABA + LAMA + ICS
  3. OD dosing
  4. Compliance!!

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