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Pharmacology: Exam 2 > Lecture 5: Asthma + COPD > Flashcards

Lecture 5: Asthma + COPD Flashcards

1
Q

Which drug(s) are B2 agonists?

A

Albuterol and Salmeterol

incr cAMP

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2
Q

Which drug is a leukotriene antagonist?

A

Montelukast

“luk” for LEUKotriene antag, block glucotrienes

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3
Q

Which drugs are muscarinic antagonists (2)?

A

Ipratropium, Tiotropium

blocks ACh

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4
Q

Which drug(s) are inhaled corticosteroid?

A

Fluticasone

blocks cytokines

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5
Q

Which drug(s) are monoclonoal anti-IGE antibodies?

A

Omalizumab

blocks abs

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6
Q

Which drugs are used as a RESCUE for asthma ONlY (2)?

A

Ipratropium and Tiotropim

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7
Q

Which drug is used as a RESCUE for BOTH asthma and COPD?

A

Albuterol

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8
Q

Which drugs are used as a control for ASTHMA only (2)?

A

Montelukast, Omalizumab

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9
Q

Which drugs are used as a control for COPD only (2)?

A

Ipratropium and Tiotropium

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10
Q

Which drug(s) are used as control for BOTH asthma and copd?

A

Salmeterol, Fluticasone

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11
Q

Incr in airway resistance is a hallmark of what type of lung disease?

A

Obstructive

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12
Q

What are 2 characersistics of obstructive lung disease?

A
  1. Decr airflow (b/c decr elasticity or incr raw in zone 0-10)
  2. Limited airflow during EXPIRATION
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13
Q

Low lung-cw compliance is a hallmark of what type of lung disease?

A

Restrictive

parenchyma fibrosis

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14
Q

A pt with restrictive lung disease has
a.Low FEV1/FVC
b. High FEV1/FVC
c. Normal FEV/FVC

A

Normal FEV/FVC

equal decr in fev1 andfvc

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15
Q

What is asthma

A

spasmodic contrctiion of smooth muscle in the bronchi

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16
Q

What is COPD

A
  1. Bronchitis: inflammation of the bronchi and bronchioles (inr mucus)
  2. Emphysema: alveolar destruction
  3. Combination

also cystic fibrosis and bronchiectasis

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17
Q

Which zone has higheset resistanace to airflow?
a. CZ
b. RZ

A

CZ (zone 1-10)

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18
Q

Alveoli does not have ____

A

smooth muscle

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19
Q

The further down we go in the airway towards the RZ the ____ the cross-sectional area

A

higher

lower resistance

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20
Q

What are the factors that determine airway resistance?

A
  • Structure of airways
  • Airway smooth muscle contraction
  • Lumen obstruction (mucus)
  • Elasticity of Lung parenchyma
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21
Q

For airway smooth muscle contraction, when receptors actiates, they will incr ____ by g protein ____ causing smooth muscle contraction

A

Intracellular Ca2+
G protein Q

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22
Q

What are diff receptors that can lead to airway smooth muscle contraction when activated?

A
  1. Histamien
  2. Muscuranic
  3. LTD4
  4. Substance P

you can have histamine induced bronchospasm

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23
Q

What does autonomic control of airway resisitance to the airways?

A
  1. Provides reflex arc for airway constriction following inhalation of irritants
  2. Provides airway dilation during exercise
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24
Q

Explain the reflex arc for autonomic control of airway resistance

A
  1. You have an irritant come in
  2. Signal travels up to the medualla via afferent neurons
  3. Activates PNS and ACh is released
  4. Constriction of airway to remove irritant
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25
Q

Explain how autonomic control of airway resistance can dilate airways during exercise

A
  • Decr PNS influence
  • incr CIRCULATING epi (no direct SNS innervation of smooth airway muscle)
  • Bronchodilation
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26
Q

Airway diameter depends on ____ of tisssue surrounding airways in lung parenchyma.

A

retractile force

as the lung expands, retractile force on airways incr

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27
Q

As the lung expands the what is pulling on the airway to keep it open, and if we loose this what can occur?

A

Alveoli, airway can collapse (emphysema)

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28
Q

Fxn of spirometry

A

used to acess lung parameters (airway resistance)

measures airflow

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29
Q

A pt with COPD (obstructive lung disease) has a high, low, or normal FEV1/FVC ratio?

A

Low, this is because with higher resitance it takes longer and it is harder for them to breathe out

men and taller ppl have higher FVC
FVC decr as you age from 45 on

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30
Q

Emphysema
a. major pathological changes
b. High or low resistance
c. high or low FEV1/FVC

A

a. airspace enlargemnent, destruction of alveoli
b. High resistance
c. Low FEV1/FVC

LOW eleastic recoil reduces structural support for bronchioles

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31
Q

Chronic Bronchitis
a. major pathological changes
b. High or low resistance
c. high or low FEV1/FVC

A

a. mucus gland hyperplasia, hypersecretion, bronchiole fibrosis
b. low resistance due to clogged bronchioles
c. low FEV1/FVC

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32
Q

Asthma
a. major pathological changes
b. High or low resistance
c. high or low FEV1/FVC

A

a. smooth muscle hyperplasia/spasmodic contraction, mucus inflammation, AHR
b. High resistance due to contracted bronchi
C. Low FEV1/FVC

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33
Q

Chronic disroder of the airfways that is complex and characterized by variable and recurring symptoms, airflow obstruction (bronchospasm). bronchial hyperresponsiveness, and underlying inflammation.

A

Asthma

lot of endotypes, we don’t know why some ppl have mild or severe asthma

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34
Q

What is the “hallmark” of asthma?

A

Reversibility with bronchodilator.

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35
Q

True or false: Airway obstruction may be absent between attacks

A

True

pt is not constanly breathless, or having attacks

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36
Q

Explain the concept of airway hyperactivity

A

For a given concentration of chemical that causes bronchospasm, they will have a much bigger bronchospams

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37
Q

Muscurininc agonist, will activate ____ receptor and cause constriction

A

M3

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38
Q

You can test the severity of asthma my measuring airway responsiveness using what?

A

Methacholine

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39
Q

How do we measure the severity of asthma/airway responsiveness using methacholine?

A

We look at the amount of methacholine given to drop FEV by 20%

incr dise until FEV dropped by 20%

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40
Q

How can you tell if someone has severe asthma using methacholine?

A

If 0.3 mg/ml of methacholine causes a drop of FEV by 20%

asthmatis react to low dose of methocholine

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41
Q

How is asthma linked to allergy?

A
  1. Allergen sensitization
  2. Allergen-induced mast cell activation

allergen sensitization: B cells produce IGE instead of IGG (antigen becomes an allergen
Allergen-induced mast cell activation: IGE binds to mast cells and basophills which has a receptor called FCeR1. They release their granules with infla,,atory agents

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42
Q

What is allergen sensitization?

A

B cells produce IGE instead of IGG

an antigen becomes an allerefen

43
Q

Early reaction of asthma involves what?

A

smooth muscle

44
Q

Late reaction of asthma involves what?

A

cell infiltration

  1. Hisamine release and cytokine release
  2. Histamine causes quick constriction, cytokine causes late cell infiltration
45
Q

What occurs to the lungs with asthma?

A

it remodels you keep repairing it

46
Q

What are some characteristics of a severe asthamtic lung?

A
  1. epithelial damage
  2. goblet cell hyperplasia
  3. smooth muscle hypertrophy and hyperplasia
  4. basement membrane thickening
  5. collagen deposition
  6. submucosal fibrosis
  7. angiogenesis
  8. mucus plug formation
47
Q

What is the role of vagal afferent nerves in respiratory diseases?

A

Sensory nerves that are activated by inflammation, irritants and pollutants

sense irritant

48
Q

What is the role of vagal efferent nerves in respiratory diseases?

A

They are PNS nerves (cholinergic) innervating smooth muscle and mucosal glands

49
Q

Activation of sensory nerves causes what 4 CNS reflexes?

A
  1. Cough
  2. Dyspnea
  3. Bronchospasm (PNS)
  4. Hypersecretion (PNS)

asthamtic subkects are hyperreflexive to inhaled irritants

50
Q

COPD is linked to what?

A

Smoking

51
Q

What occurs to your lung function when you smoke and why?

A

you have a decr in lung fxn bc you Decr your FEV1 at a faster rate than normal and there is limited reversibility

limited reversibility: a bronchodilator will not change FEV1

52
Q

If you stop smoking at the age of 45, what occurs to your FEV1?

A

It can somewhat return to normal

53
Q

If you stop smoking at the age of 65, what occurs to your FEV1?

A

It incr slightly, but not much

54
Q

lWhat are the presenting symptoms associated with a pt who smokes and now has copd?

A
  • cough, dyspnea
  • lower lung fxn (lower airflow and hyperinflation)
  • worse with exercise (6-min walk test)
  • Exacerbation (infections)
  • Airway hyperractivity (limited)

lungs have a higher RV

55
Q

Pts with COPD tend to die from what?

A

bacterial infection

56
Q

What role does neutrophils play in COPD?

A

They come in to get rid of damaged tissue but in the process, they damage normal cells in the lugns

neutrophilia: neutrophil elastase, matric mellatoproteinases, ROS-> leads to tissue destruction

57
Q

As a result of neutrophils being released, what damages can occur?

A
  • remodeling
  • smooth muscle metaplasia
  • fibrosis
  • cell death
  • higher resistance and lower elastic recoil leading to decr in airflow
  • lower gas exchange
58
Q

2 COPD subtypes

A

chronic bronchitis and emphysema

59
Q

Chronic bronchitis is blue bloater or pink puffer? and why?

A

Blue Bloater
because lack of ventilation: Hypoxia (blue), edema (bloater)

60
Q

What clinical manifestations do you see with chronic bronchitis and how does this affect resistance and airflow?

A

Excessive mucus production and fibrosis of bronchioles. You see incr in resistance and decr in airflow

mucus stuck in conducting airway so no O2 delivery

61
Q

Chronic bronchitis is blue bloater or pink puffer? and why?

A

Pink puffer because lack of perfusion (mild hypoxia-pink) and bronchiole collapse (hard to breath-puffer)

62
Q

What clinical manifestations do you see with emphysema and how does this affect resistance and airflow?

A

parenchymal/alv damage this incr resistance and decr airflow

lower alveolar structure, lower elastic recoil, lower structural support

63
Q

Asthma summary table
1. age of onset
2. smoking history
3. atopy (allergy)
4. drop on FEV1
5. incr resistance reversible with B2 agonist:?
6. Hyperactivity
7. Family history
8. cough
9. cell infiltration
10. immunological paradigm

A
  1. age of onset: usually < 40 (CHILDREN)
  2. smoking history: not required
  3. atopy (allergy): common (IgE)
  4. drop on FEV1: episodic
  5. incr resistance reversible with B2 agonist?: YES
  6. Hyperactivity: very high
  7. Family history: frequent
  8. cough: yes (dry)
  9. cell infiltration: eosinophils, mast cells, basophils
  10. immunological paradigm: CD4+ Th2 cells, B cells
64
Q

COPD summary table
1. age of onset
2. smoking history
3. atopy (allergy)
4. drop on FEV1
5. incr resistance reversible with B2 agonist:?
6. Hyperactivity
7. Family history
8. cough
9. cell infiltration
10. immunological paradigm

A
  1. age of onset: usually > 40
  2. smoking history:> 10 pack-years
  3. atopy (allergy): no correlation
  4. drop on FEV1: chronic
  5. incr resistance reversible with B2 agonist?: Minimal
  6. Hyperactivity: high
  7. Family history:uncomoon
  8. cough: yes (wet)
  9. cell infiltration: neutrophils, macrophages
  10. immunological paradigm: CD8+ Thcyt cells
65
Q

What disease?
a. Gap is filled with mucus
b. Gap closes with bronchonstriction
c. Loss of strutural support, bronchi collapse

A

a. bronchitis
b. asthma
c. emphysema

all incr resistance

66
Q

What are 4 ways drugs can incr airflow/decr resistance for obstructive diseases?

A
  1. Actively cause bronchodliation (B-adrenoreceptor agonist)
  2. Inhibit specific inflammatory mediators (leukotriene and muscarininc antagonits)
  3. reduce inflammation (corticosteroids)
  4. prevent inflammation (anti-IgE antibodies-for asthma only)

  1. albuterol, salmeterol
  2. montelukast, ipratropium, tiotropium
  3. fluticasone
  4. omalizumab
67
Q

MOA for B2 adrenoceptor agonists

A
  • Activation of b2 adrenorecptors on bronchial smooth muslce, incr cAMP ->relaxation->bronchodilation

  1. facilitates sequestration of Ca2+
  2. inacticates MLCK
  3. Inactivates MLC20
68
Q

Therapuetic uses for B adrenoceptor agonists

A
  • Short acting (albuterol): rescule for asthma and COPD
  • Long acting (LABA e.g. salmeterol): control for asthma and copd

salmeterol=everyday use

69
Q

What do you give if you have an asthama attack?

A

Albuterol

70
Q

Side effect of B adrenoceptor agonists is tachycardia, why?

A

B/c B2 also in heart and these drugs are not completely B1 inactive

71
Q

Does albuterol and salmeterol work the same way?

A

Yes, its just that albuterol works more quickly than salmeterol

72
Q

Asthama has a ____ increase in FEV1 while COPD has a very ____ increase in FEV1

A

robust, mild

complete reversal to 100% predicted with Asthma

73
Q

Cysteinyl leukotrienes (LTC4, LTD4, LTE4) are known as the slow reacting substances of anaphylaxis, where can de novo synthesis occur?

A

Occurs in mast cells and basophils following allergen binding IgE and also in eosinophils and neutrophils.

LTC4 easilt converted into LTD4 then slowly in LTE4

74
Q

Drugs can block cysteinyl leukotriences by what?

A

Being a 5-lipoxygenase inhibitor or being a cyst, T receptor antagonist

5-lipoxygenase causes the cascade leading to LTs being made
Cyst T receptor antags block receptor that leukotrienes are binding to, blocking signal cascade

75
Q

Which has the highest concentration?
a.LTC4
b.LTD4
c. LTE4

A

LTD4

76
Q

What does LTD4 bind to?

A

GPCR CysLT1 and CysLT2

77
Q

CysLT1 and CysLT2 are G ____ coupled and activation leads to what

A

Gq coupled leadinng to
1. PLP C activation
2. IP3 and Dag production
3. Incr Ca2+ and PKC
4. Bronchospasm

all cysteinyl leukotrienea re effective at both receptors

78
Q

Expression of bronchial smooth muscle (CysLT1) causes what?

A

Contractinn-> bronchospasm-> incr hyperplasia

also immune cells and mucus cells (incr inflammation)

79
Q

Expression of bronchial smooth muscle (CysLT1) causes what?

A

Contractinn-> bronchospasm-> incr hyperplasia

also immune cells and mucus cells (incr inflammation)

80
Q

Leukotriene antagonist

A

Montelukast

given orallu

81
Q

MOA for Montelukast?

A
  • CysLT1 antagonist
  • Prevents CysLT1-induced bronchospasm, decr immune cell infiltration, no decr in AHR, very mild reveral of remodeling
82
Q

Therapuetic use for Montelukast?

A

Control for asthma

NOT used for COPD b/c its not a TH2 disease
TH2 leads to production of IGE

83
Q

reflec bronchospasm and hypersecretion via cholinergic activation of ____ receptors

A

M3

84
Q

Nonselective muscurinic antagonist

A

Ipratropium bromide

given : inhalation
quartenery amine derivatice of atropine-charged-stays in lung when inhaled

85
Q

What does tiotropium bromide inhibit?

A

M1, M3, but NOT M2

does not binds to M2

given: inhalation

86
Q

MOA for Ipratropium bromide and tiotropium bromide

muscuranic antag

A

Blocks ACh induced acttivation of muscurinic receptors on
1. Airway smooth muscle (M3)-decr bronchospasm
2. Epithelial mucosal glands (goblet cells) (M3)- decr mucous secretion

87
Q

Therapuetic use for Ipratropium bromide and tiotropium bromide

A

Rescue for asthma
control for COPD

88
Q

Inhaled corticosteroids

A

Budesomide, Fluticasone

given: nasal or inhalation
analogs of corticosterone, steroid hormone (adrenal cortex)

89
Q

MOA for Fluticasone

A

Steroid molecule binds to cytoplasmic gluticorticoid receptor (GR), dimerizes, enters nucleus, binds to DNA at specific sites leading to

DECR in pro-inflammatory protein production and
INCR in anti-inflammatory protein production

90
Q

Modulation of protein expression of corticosteroids are slow-onset or fast onset and why?

A

Slow onset (more than 12 hours) because it alters the transcription of both pro and anti inflam

slow onset= not a rescue drug

91
Q

Corticosteroid (fluticasone) ____ de novo transcription of PRO-inflam proteins ___

A

decr
IL4 and IL5

KNOW THIS

92
Q

Corticosteroid (fluticasone) ____ transcription of ____ a potent ANTI-inflam protein that inhibits ____

A

INCR
IkB
NFkB

KNOW THIS

93
Q

Steroids ____ IgE production from B cells and ____ mast cell degranulation

A

decr
inhibit

far less immune cell infiltratiom
pretty much eradicates late response

94
Q

For asthma, what do steroids decr?

A
  • Decr airway eosinophilia
  • decr IgE production from B cells and inhibit Mast cell degranulation

decr Immune system

95
Q

How does Corticosteroids affect COPD?

A
  • have little effect on neutrophilia
  • have no effect on mortality (will still die)
96
Q

Corticosteroid side effects are due to what?

A
  1. GR signaling (glucocorticoid/cortisol)
  2. MR signaling (mineralcorticoid/aldisterone)
  3. Both in multiple tissues
97
Q

What are the side effects of corticosteroids if inhaled?

A

Incr risk of inf (oropharyngeal candiasis)
COPD: bacterial lung infections

incr risk for inf bec decr immune system

98
Q

What are the side effects of corticosteroids if taken orally?

A
  1. Hyperglycemia
  2. Dyslipidemia
  3. Hypertension
  4. Osteoporosis
  5. Cataracts
  6. Glaucoma
  7. Teratogenic
99
Q

Anti-IgE antibodies

A

Omalizumab

given: subcutenous inj
monoclonal antibody IgG

100
Q

MOA for Omalizumab anti-IgE antibody

A

binds to free IgE (Fc region), promoted destruction
* decr IgE from binding ro FCeR1 and FCeR2
* decr expression of FCeR1 on mast cells/basophils
* decr allergen-induced IgE crosslinling on mast cells/basophils

basically, we get rid of the reserves AKA circulating IgE and there is protein turnover which takes a few weeks. This means that the FceR gets lonely bc no more ige is coming over so it gets destroyed

101
Q

MOA for Omalizumab anti-IgE antibody leads to what effects?

A
  • prevents allergen-induced bronchospas,
  • decr immune cell infiltration
  • decr exacerbations
  • no defect on AHR
  • effect on remodeling unclear
102
Q

Therapeutic use for Omalizumab anti-IgE antibody

A

control for severe steroid resistant asthma

103
Q

Rate of onset for Omalizumab anti-IgE antibody

A

Circulating IgE destroyed in hours/days
Takes more than a weel for mast cell attached IgE to reduce

Pharmacology: Exam 2 (10 decks)

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