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Block 9 Week 4 > Pulmonary pharmacology-Singer > Flashcards

Pulmonary pharmacology-Singer Flashcards

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
Q

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

A
  • Bronchodilation of airway SM
  • Decreased leak of endothelial cells
  • Increased strength of respiratory skeletal muscle
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26
Q

What are the overal effects of methylxanthines?

A

decreased inflammation
increased muscle strength
increase bronchodilation

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27
Q

What are the effects of methylxanthines on the CNS?
On the cardiovascular system?
On the metabolism?

A

increased alterness, reduced fatigue, tremor, insomnia, anxiety

increased cardiac contractility, reduced PVR

diuresis, increased basal metabolic rate

I.e the same effects as coffee!

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28
Q

Theophylline is basically like (blank) in its effects

A

coffee

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29
Q

How do you give theophylline?

Who do you give it to?

A

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
Q

Theophylline has increased clearance in (blank and blank). WHy? So how do you fix this?

A

children and marijuana smokers

  • due to induction of CYP12 which also metabolizes phenytoin, rifampin, and phenobarbital
  • increase the dose
31
Q

When will you have reduced clearance of Theophylline?

A

liver disease
heart failure
pneumonia
co-admin of antibiotics like erythromycin, ciprofloxacin, cimetidine

32
Q

What do you have to do when using theophylline?

A

therapeutic monitoring of serum levels to reduce toxicity risks

33
Q

What are the side effects of theophylline?

A 
nausea and vomiting
headaches
gastric discomfort
diuresis
behavioral disturbances
cardiac arrhythmias
epileptic seizures
34
Q

How does Theophylline cause nausea, vomiting, headaches, gastric discomfort?

A

PDE4 inhibition

35
Q

How does Theophylline cause diuresis?

A

A1 receptor antagonism

36
Q

How does Theophylline cause cardiac arrhythmias and epileptic seizures?

A

PDE3 inhibition and A1 receptor antagonism

37
Q

What muscarinic receptors are in the airway?

A

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
Q

What are the three anti-cholinergics used in bronchodilatory therapy?

A
  • Atropine
  • Apratropium (atrovent)
  • Tiotropium (spiriva)
39
Q

What kind of inhibitor is atropine?

What is it made of?

A

prototypical nonselective inhibitor

-tertiary ammonium derivate that has system effects

40
Q

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?

A

Nonselective inhibitor
quarternary ammonium derivative
Combined with albuterol (combivent)
4-6X/day (short half life)

41
Q

What kind of inhibitor is tiotropium (spiriva)?

What is it made up of?

A

Inhibits M1, M2, M3 receptors but dissociates quickly for M2

-also quaternary ammonium derivative

42
Q

What are the side effects of ipratropium?

A

bitter taste

precipitate glaucome when nebulized with a face mask

43
Q

What is the side effect of triotropium?

A

dry mouth

44
Q

Beta agonists affect (blank)
Theophylline affect (blank)
Muscarinc antagonists affect (blank)

A

upregulate AC
inhibit PDE and adenosine
inhibit acetylcholine

45
Q

What are the ICS (inhaled corticosteroids)?

These are all derivats of (blank)

A
  • beclomethasone dipropionate
  • budesonide
  • fluticasone propionate

Hydrocortisone

46
Q

What is the MOA of corticosteroids?

A

ligand-activated transcription factors (intracellular)

47
Q

Inflammatory stimuli increases gene transcription via acetylation. You can give (blank) to inhibit this acetylation and therefore inhibit gene expression

A

Corticosteroids by binding glucocorticoid receptors

48
Q

Most corticosteroids repress (blank) gene expression

A

inflammatory

49
Q

What are the anti-inflammatory effects of ICS in asthma?

A
  • 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
Q

Beclomethasone diproprionate is a (blank) cleaved by esterases in the lung to an active steroid (i.e helps to reduce systemic effects)

A

Prodrug

51
Q

(blank and blank) has a greater 1st pass metabolism thatn Beclomethasone diproprionate. Does it have more or less systemic effects of Beclomethasone diproprionate?

A

Fluticasone and Budesonide

less systemic effects and less adverse effects

52
Q

What is advair?

What is symbicort?

A

Fluticasone/salmeterol

Budesonide/formoterol

53
Q

Advair and symbicort are (blank and blank)

A

long acting beta agonists + an ICS

54
Q

What are the local side effects of ICS?

A

Dysphonia
Oropharyngeal candidiasis
Cough

55
Q

What are the systemic side effects of ICS (similiar to prednisone orally)?

A
  • adrenal suppression and insufficiency
  • growth suppression
  • bruising
  • osteoporosis
  • cataracts
  • glaucoma
  • metabolic abnormalities (glucose, insulin, triglycerides)
  • psychiatric disturbances (euphoria, depression)
  • pneumonia
56
Q

What are the leukotriene antagonists?

A

Montelukast

57
Q

What does Zileuton inhibit?

A

5-lipoxygenase inhibitor

58
Q

What does Montelukast, Pranlukast, and Zafirlukast inhibit?

A 
LT antagonists
(it inhibits plasma exudation, mucus secretion, bronchoconstriction, eosinophil recruitment)
59
Q

How do you give montelukast?
Widely used to treat (blank).
You have a significant improvement in (blank)

A

orally administered
Children
mild-moderate asthma and aspirin-sensitive asthma

60
Q

Montelukast is indicated as an add-on therapy in patients not responding to an (blank)

A

ICS

61
Q

What are the side effects of Montelukast?

A

rare cases of hepatic dysfunction

Churg-Strauss syndrome

62
Q

What is an Anti-IgE used as bronchodilatoro?

A

Omalizumab

63
Q

When do you use omaluzimab?
How do you give it?
How is the dose determined?

A

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
Q

If you asthma control test (ACT) equals 20 what do you give your patient?

A

Rapid onset B2 agonist

65
Q

If your asthmal contro test (ACT) equals 16-19?

A

Recommended Low-dose ICS

66
Q

If your asthma control test is less than 16 ACT?

A

recommended Low-medium dose ICS + LABA

Aternative is medium-high dose ICS
Low to medium dose ICS+LTRA
Low medium dose ICS + theophylline

67
Q

If your patient is in step 4 asthma what do you give them?

A

high dose ICS +LABA
+/- LTRA (leukotriene receptor antagonists)

OMalizumab in allergic asthma

68
Q

IF your patient is in step 5 asthma, what do you give them?

A

Omalizumab in allergic asthma
and/or
long-term oral corticosteroids

69
Q

What are the mediator antagonists for bronchodilatory therapy?

A

Th2 cells
Cytokines, chemokine receptors
Antioxidants
NOS inhibitors

70
Q

What are the anti-inflammatories for bronchodilatory therapy?

A 
Specific PDE inhibitors
NF-kB inhibitors
MAPK inhibitors
Statins 
Mucoregulators
71
Q

What is bronchothermoplastly?

A

burns tissue inside of a persons airway=destroys extra SM and inflammatory cell bulidup

Block 9 Week 4 (9 decks)

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