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Block 9 Week 4 > Pulmonary pharmacology-Singer > Flashcards

Pulmonary pharmacology-Singer Flashcards

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1
Q

What can occur with asthma?

A
  • epithelial shedding
  • subepithelial fibrosis
  • brochoconstriction hypertrophy/hyperplasia
  • edema
  • asodilation of vessels
  • mucus hypersecretion and hyperplasia
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2
Q

What is characteristic of the late phase of asthma?

A

leaky vessels, esoinophils and neutrophils

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3
Q

What do airway smooth muscle cells have on them that can lead to even worse asthma?

A

They have receptors for Ig, cytokines, and chemokines and when bound release more cytokines and chemokines.

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4
Q

What is the immunopathogenesis of asthma?

A

exposure to allergen-> synthesis of IgE-> binds to mast cells-> upon reexposure of antigen, the antigen-antibody interaction on mast cell trigerrs release of mediators of anaphylaxis.

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5
Q

What are the mediators of anaphylaxis?
What will these cause?
What IL are common in asthma?

A

histamine, tryptase, prostaglanding D, leukotrience C and platelet activating factor (PAF).

  • contraction of airway smooth muscle causing the immediate fall in FEV1 and release of cytokines
  • IL4 and IL5
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6
Q

Reexposure to allergen also causes the synthesis and release of a variety of cyto-kines: interleukins (blank and blank) and (Blank X 3) from T cells and mast cells.
These cytokines in turn attract and activate (blank and blank), whose products include eosinophil cationic protein (ECP), major basic protein (MBP), proteases, and platelet-activating factor.

A

IL4 and IL5
GM-CSF
TNF
TGF

eosinophils and neutrophils

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7
Q

THe Vagus causes (blanK). How?

A

bronchoconstriction via transmission of ACH.

-trigger release of chemical mediators from mast cells, and tachykinin release

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8
Q

What is the FEV1 like in mild cases of asthma? How about moderate?
How about severe?

A

132% (due to smooth muscle hypertrophy and hyperplasia)
83%
34%

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9
Q

What is COPD?
Do corticosteroids help?
What is common in COPD?

A

emphyseama
chronic bronchitis

-no (no effective anti-inflammatory therapies exist)

systemic symptoms and comorbid diseases

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10
Q

How can you tell the difference between asthma and COPD via meds?

A

COPD wont response to anti-inflammatories cuz there is a very small inflammatory component.
However asthma will respond

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11
Q

Why does COPD cause fibrosis?
Why does it cause alveolar wall destruction (emphysema)?
Why does it cause mucus hypersecretion?

A
  • Fibroblast
  • Th1, TC1 and proteases
  • proteases
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12
Q

What are some epigenetic modifications that cause asthma? Why do they occur?

A

DNA methylation
Covalent modification of cytosine in CpG dinucleotides
Posttranslational modifications of histones

Environmental exposures to allergens, antibiotics, air pollution, environmental toxicants, diet

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13
Q

Why do you get systemic effects from using an inhaler?

A

because you breath in 10-20% and swallow the rest (80-90%

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14
Q

What are the 5 major agents used to treat asthma?

A
  1. bronchodilators
    - B2 adrenergic agonists
    - Theophylline
    - Anti-cholinergics
  2. corticosteroids (Inhaled corticosteroids)
  3. Leukotriene Antagonists
  4. Cromolyn & Nedocromil
  5. Immunomodulatory Therapies
    - IgE antibodies
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15
Q

What are the three most commony used B2 agonists?

What are the other B2 agonists you can use?

A

Albuterol, sameterol, formoterol

-Norepinpehrine, epinephrine, isoproterenol

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16
Q

How do B2 agonists work?

A

Decrease intracellular Ca2+

increase cAMP-> increase PKA-> decrease intracellular Ca2+

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17
Q

What are some other effects of B2 adrenergic agonists besides bronchodilation?

A
  • prevents mast cells from releasing stuff
  • prevents leakage and edema
  • increase in mucus secretion from submucosal glands and ion transport across airway epithelium
  • inhibition of ACh release in airways by blocking presynaptic nerve terminal
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18
Q

What is a short acting b2 agonist? What is its duration of action? How often do you use it?

A

Albuterol
3-4 hour duration
used 4-6X daily

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19
Q

What is a long acting B2 agonist? What is its duration of action? How often do you use it?

A

Salmeterol and formoterol
>12 hours
Used BID

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20
Q

If you are using Salmaterol and Formoterol for asthma how do you use it?
What about if you are using it for COPD?

A

always used in combo with ICS

Use alone or combo with ICS or anticholinergics

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21
Q

What are the side effects of B2 agonists?

A
  • Muscle tremor
  • Tachycardia
  • Hypokalemia
  • Restlessness
  • Hypoxemia
  • Increased mortality with LABA
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22
Q

(blank) is associated with seizures

A

Theophyilline

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23
Q

What are four methylxanthines?

What is the MOA of methylxanthines?

A

xanthine
theobromine
caffeine
theophylline

Inhibit phosphodiesterase (increases cAMP)
and
are antagonists of adenosine receptors

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24
Q

What are the inflammatory cell effects of methylxanthines in the lung?

A

Decrease Eosinophils (increased apoptosis)
Decreased T lymph cytokines and T lymph traffic
Decreased mast cell mediators
Decreasd macrophage cytokines

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25
What are the structural cell effects of methylxanthines in the lung?
- Bronchodilation of airway SM - Decreased leak of endothelial cells - Increased strength of respiratory skeletal muscle
26
What are the overal effects of methylxanthines?
decreased inflammation increased muscle strength increase bronchodilation
27
What are the effects of methylxanthines on the CNS? On the cardiovascular system? On the metabolism?
increased alterness, reduced fatigue, tremor, insomnia, anxiety increased cardiac contractility, reduced PVR diuresis, increased basal metabolic rate I.e the same effects as coffee!
28
Theophylline is basically like (blank) in its effects
coffee
29
How do you give theophylline? | Who do you give it to?
Orally or IV in combo with ICS Pnts with severe symptoms and in COPD patients who need to reverse corticosteroid resistance as an HDAC (histone deacetylateses deacactivator)
30
Theophylline has increased clearance in (blank and blank). WHy? So how do you fix this?
children and marijuana smokers - due to induction of CYP12 which also metabolizes phenytoin, rifampin, and phenobarbital - increase the dose
31
When will you have reduced clearance of Theophylline?
liver disease heart failure pneumonia co-admin of antibiotics like erythromycin, ciprofloxacin, cimetidine
32
What do you have to do when using theophylline?
therapeutic monitoring of serum levels to reduce toxicity risks
33
What are the side effects of theophylline?
``` nausea and vomiting headaches gastric discomfort diuresis behavioral disturbances cardiac arrhythmias epileptic seizures ```
34
How does Theophylline cause nausea, vomiting, headaches, gastric discomfort?
PDE4 inhibition
35
How does Theophylline cause diuresis?
A1 receptor antagonism
36
How does Theophylline cause cardiac arrhythmias and epileptic seizures?
PDE3 inhibition and A1 receptor antagonism
37
What muscarinic receptors are in the airway?
M1mAChRs- facilitate neurotransmission Neural M2mAChRs-limit further ACh release M3mAChRs on airway muscles-Contraction of airway smooth muscle M2mAChRs- on airway muscles-Counteract airway muscle relaxation
38
What are the three anti-cholinergics used in bronchodilatory therapy?
- Atropine - Apratropium (atrovent) - Tiotropium (spiriva)
39
What kind of inhibitor is atropine? | What is it made of?
prototypical nonselective inhibitor | -tertiary ammonium derivate that has system effects
40
What kind of inhibitor is Ipratropium (atrovent) and what is it made up of? What can you combine it with? What is the half life?
Nonselective inhibitor quarternary ammonium derivative Combined with albuterol (combivent) 4-6X/day (short half life)
41
What kind of inhibitor is tiotropium (spiriva)? | What is it made up of?
Inhibits M1, M2, M3 receptors but dissociates quickly for M2 | -also quaternary ammonium derivative
42
What are the side effects of ipratropium?
bitter taste | precipitate glaucome when nebulized with a face mask
43
What is the side effect of triotropium?
dry mouth
44
Beta agonists affect (blank) Theophylline affect (blank) Muscarinc antagonists affect (blank)
upregulate AC inhibit PDE and adenosine inhibit acetylcholine
45
What are the ICS (inhaled corticosteroids)? | These are all derivats of (blank)
- beclomethasone dipropionate - budesonide - fluticasone propionate Hydrocortisone
46
What is the MOA of corticosteroids?
ligand-activated transcription factors (intracellular)
47
Inflammatory stimuli increases gene transcription via acetylation. You can give (blank) to inhibit this acetylation and therefore inhibit gene expression
Corticosteroids by binding glucocorticoid receptors
48
Most corticosteroids repress (blank) gene expression
inflammatory
49
What are the anti-inflammatory effects of ICS in asthma?
- decreased inflammatory cells (eosinophils, T lymph, mast cell, macrophage, dendritic cells) - decreased cytokines and mediators from epithelial cells - decreased endothelial leaking - increased transcriptionof B2 receptors on smooth muscles - decreased cytokines on smooth muscles - decreased mucus secretion
50
Beclomethasone diproprionate is a (blank) cleaved by esterases in the lung to an active steroid (i.e helps to reduce systemic effects)
Prodrug
51
(blank and blank) has a greater 1st pass metabolism thatn Beclomethasone diproprionate. Does it have more or less systemic effects of Beclomethasone diproprionate?
Fluticasone and Budesonide | less systemic effects and less adverse effects
52
What is advair? | What is symbicort?
Fluticasone/salmeterol | Budesonide/formoterol
53
Advair and symbicort are (blank and blank)
long acting beta agonists + an ICS
54
What are the local side effects of ICS?
Dysphonia Oropharyngeal candidiasis Cough
55
What are the systemic side effects of ICS (similiar to prednisone orally)?
- adrenal suppression and insufficiency - growth suppression - bruising - osteoporosis - cataracts - glaucoma - metabolic abnormalities (glucose, insulin, triglycerides) - psychiatric disturbances (euphoria, depression) - pneumonia
56
What are the leukotriene antagonists?
Montelukast
57
What does Zileuton inhibit?
5-lipoxygenase inhibitor
58
What does Montelukast, Pranlukast, and Zafirlukast inhibit?
``` LT antagonists (it inhibits plasma exudation, mucus secretion, bronchoconstriction, eosinophil recruitment) ```
59
How do you give montelukast? Widely used to treat (blank). You have a significant improvement in (blank)
orally administered Children mild-moderate asthma and aspirin-sensitive asthma
60
Montelukast is indicated as an add-on therapy in patients not responding to an (blank)
ICS
61
What are the side effects of Montelukast?
rare cases of hepatic dysfunction | Churg-Strauss syndrome
62
What is an Anti-IgE used as bronchodilatoro?
Omalizumab
63
When do you use omaluzimab? How do you give it? How is the dose determined?
for severe asthma not responding to ICS/LABA - via S.C injection every 2-4 weeks - by titering IgE antibody in patients (ITS EXPENSIVE AND TAKES MORE TIME)
64
If you asthma control test (ACT) equals 20 what do you give your patient?
Rapid onset B2 agonist
65
If your asthmal contro test (ACT) equals 16-19?
Recommended Low-dose ICS
66
If your asthma control test is less than 16 ACT?
recommended Low-medium dose ICS + LABA Aternative is medium-high dose ICS Low to medium dose ICS+LTRA Low medium dose ICS + theophylline
67
If your patient is in step 4 asthma what do you give them?
high dose ICS +LABA +/- LTRA (leukotriene receptor antagonists) OMalizumab in allergic asthma
68
IF your patient is in step 5 asthma, what do you give them?
Omalizumab in allergic asthma and/or long-term oral corticosteroids
69
What are the mediator antagonists for bronchodilatory therapy?
Th2 cells Cytokines, chemokine receptors Antioxidants NOS inhibitors
70
What are the anti-inflammatories for bronchodilatory therapy?
``` Specific PDE inhibitors NF-kB inhibitors MAPK inhibitors Statins Mucoregulators ```
71
What is bronchothermoplastly?
burns tissue inside of a persons airway=destroys extra SM and inflammatory cell bulidup

Block 9 Week 4 (9 decks)

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