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PHRM 825 > Asthma, COPD, EVALi and CF > Flashcards

Asthma, COPD, EVALi and CF Flashcards

1
Q

Factors Contributing to Growing Pulmonary Drug Market in the US

  • growing prevalence of ___
  • advantages of the ___ route as an alternative to oral and parenteral
  • rising incidence of ___ disease across the world
A
  • COPD (chronic obstructive pulmonary disease)
  • pulmonary
  • lung
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2
Q

factors contributing to recent pulmonary disease

A
  • EVALI (E-cigarette/Vaping use Associated Lung Injury)
  • COVID-19 and potentially long COVID
  • Post COVID-19 pulmonary fibrosis
  • ARDS (Acute Respiratory Distress Syndrome)
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3
Q

4 Hallmarks of a Normal Functioning of the Lung
1. ____ - expand/deflate
2. ___ exchange - O2 intake and CO2 exhaled
3. ___ - site of gas exhange
4. ____ and ___ - clean lungs from dust and microbes

A
  • elastic
  • gas
  • alveoli
  • cilia and mucus
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4
Q

Triad of Lung Disease Inducers

A

genetic, environmental, and medications

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5
Q

Defining Asthma

  • Wheezing, coughing, SOB
  • ___ of airway
  • inflammation and airway ___
  • release of ___ mediators
  • ___ of airway smooth muscle
  • ___ secretion of mucus
  • ___ of repiratory mucosa
A
  • narrowing
  • hyperreactivity
  • inflammatory
  • constriction
  • excess
  • edema
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6
Q

Pathogenesis of Asthma

Early Reaction - Immediate Bronchoconstriction
* antigen binding to ___ antibodies triggers release of ___, tryptase, ___, LTD4, and prostaglandins from ___ cells
* Bronchial smooth muscle ___ and vascular ___

A
  • IgE, histamine, LTC4, mast
  • contraction, leakage
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7
Q

Pathogenesis of Asthma

Delayed Reaction (2-___ hours)
* ___ bronchoconstriction
* activation of ___ lymphocytes (release of ___, IL-4, ___, and IL-13)
* mucus ___ : Goblet cells
* Cellular infiltration: ___

A

2-8 hours
* sustained
* TH2 (GM-CSF, IL-4, IL-5, IL-13)
* hypersecretion
* eosinophils

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8
Q

Mast Cell Activation

  • IgE is bound to ___
  • crosslinking by the antigen leads to mast cell ___
A
  • FcR
  • degranulation
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9
Q

IAR

A

immediate asthmatic response

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10
Q

LAR

A

late asthmatic response

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11
Q

FEV1

A

Forced Expiratory Volume

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12
Q

ECP

A

eosinophil cationic protein

cytotoxic secretory protein & marker of inflammation

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13
Q

PAF

A

platelet activating factor

hyper-responsiveness

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14
Q

Neutrophil Proteases may activate ___

A

eosinophils

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15
Q

Periostin

A

matrix protein that is used as an asthma biomarker

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16
Q

Phases of Asthma - IAR

Time: ___
Action: ___
Mechanism:
1. antigen triggers ___ cell to release mediators ( ___, PGD2, LTC4, LTD4, LTB4, and ___). These mediators play key roll in bronchoconstriction and activating immune cells in LAR.
2. antigen also triggers ___ cells which activate lymphocytes which play key roll in LAR and chronic asthma

A
  • minutes
  • bronchoconstriction
  • mast, histamine, PAF
  • antigen presenting
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17
Q

Introduction to Asthma

Oscillating pressure effect leads to ___

A

wheezing

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18
Q

Phases of Asthma - LAR

Time: ___
Action: ___
Mechanism:
1. Lymphocytes release ___, IL-4, and ___ to activate neutrophils, ___, and macrophages (respectfully)
2. mast cell mediators, ___ and ___, cause neutrophils, ___, and macrophages to release more mediators (PAF, LTC4, ___, and ___)

A
  • hours
  • submucosal edema, hyperresponsiveness
  • IL-8, IFN-gamma, eosinophils
  • LTB4, PAF, eosinophils
  • MBP and ECP
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19
Q

Phases of Asthma - Chronic Asthma

Time: ___
Action: ___
Mechanism:
1. lympocytes cause ___. More eosinophils means more mediators
2. lympocytes also release ___ and ___, which further increase eosinophil response
3. Both eosinophils and lymphocytes release PAF, LTC4, MBP, cytokines, and ___

A
  • days
  • epithelial cell damage, mucus hypersecretion, hyperresponsiveness
  • eosinophilopoesis
  • IL-5, GM-CSF
  • ECP

PAF = hyperresponsiveness
ECP = cytotoxic protein/inflammation

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20
Q

Goblet Cells and Hypersecretion in Asthma

4 factors that could cause goblet cell hyperplasia

A
  1. cytokines (TH2)
  2. bacterial products
  3. proteinases (neutrophil)
  4. oxidants (smoking)
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21
Q

Goblet Cells and Hypersecretion in Asthma

What 2 cell components are key in the development of goblet hyperplasia?

What maintains hyperplasia?

A
  • EGFR, CLCA
  • Bcl-2
22
Q

Genetic contribution to Goblet Cell Hyperplasia - R576 polymorphism

  • R576 polymorphism in the ___ receptor leads to enhanced response to ___
  • ___ binds to dimer of ___ and ___ recpetors
A
  • IL-4a, IL-13
  • IL-13, IL-4a, IL-13a1

IL-4a receptor also lets IL-13 bind

23
Q

Genetic contribution to Goblet Cell Hyperplasia - Q576R polymorphism

  • Q576R polymorphism in IL-4a receptors induces ___ to inhaled antigens.
  • Mechanism: amino acid change from ___ to ____
A
  • hyperreactivity
  • Q (glutamate) to R (Arganine)

Q576 turns into R576 = more goblet cells.

24
Q

Periostin promotes chronic allergic ___ in
response to ___ cytokines

A
  • inflamation
  • TH2
25
Q

Periostin is an extracellular matrix protein induced by ___ and ___

A

IL-13, IL-4

26
Q

Periostin is a ligand for alpha/beta ___ to support adhesion and cell migration

A

integrins

27
Q

Airway Remodeling in Asthma

Epithelium - mucous ___ and ___

A

hyperplasia and hypersecretion

28
Q

Airway Remodeling in Asthma

Basement membrane

A

thickening

29
Q

Airway Remodeling in Asthma

smooth muscle

A

hypertrophy

30
Q

Airway Remodeling in Asthma

  1. allergens trigger ___ (initiators)
  2. immune cells (amplifiers) - ___ mediated
  3. ___ and smooth muscle cells in the asthmatic airway wall (effectors)
A
  • epithelium
  • TH2
  • fibroblasts
31
Q

COPD vs. Asthma

COPD
* onset: late ___ hood
* ___ leading cause of death in the US
* Not linked to ___ response
* ___ are smokers
* ___ symptomatic
* emphysema and chronic ___
IRREVERSIBLE

A
  • adult
  • 6th
  • allergic
  • 85%
  • chronically
  • bronchitis

emphysema is the destruction of the alveolar wall

32
Q

COPD vs. Asthma

  • onset: often in ___
  • linked to specific triggers
  • ___ attacks
A
  • childhood
  • episodic
33
Q

COPD symptoms and assessment

  • chronic cough, sputum, dyspnea and ___ chest
  • ___ score related to everyday activities
  • ___ (COPD assessment test) considers mucus, chest tightness, sleep, breathlessness, etc
  • degree of airflow ___
  • comorbidities - ___, diabetes, cardiovascular, respiratory infections, and cancer
A
  • barrel
  • breathlessness
  • CAT
  • limitation
  • smoking
34
Q

Remodeling in COPD

  • ___ of small airways
  • ___inflation of lungs
  • alveolar ___
  • alveolar wall ___
  • mucus ___secretion
A
  • fibrosis
  • hyperinflation
  • enlargement
  • destruction
  • hypersecretion
35
Q

Remodeling in COPD

genetic deficiency of ___ causes emphysema and mucus hypersecretion

A

a1-anti-trypsin

36
Q

Asthma vs. COPD - site

Site of disease (COPD): ___, ___, and ___
Site of disease (asthma): ___

A

COPD: peripheral airways, lung parenchyma, and pulmonary vessels

Asthma: proximal airways

37
Q

Asthma vs. COPD - cells

COPD: ___, macrophages, and ___
Asthma: ___, macrophages, and ___

A

COPD: neutrophils, CD8 T cells (TH1)

Asthma: eosinophils, CD4 T cells (TH2)

38
Q

Asthma vs. COPD - key mediators

COPD: ___, ___ , ___ , and ___
Asthma: ___, ___, and ___

A

COPD: IL-8, TNF-a, IL-1B, IL-6

Asthma: IL-4, IL-5, IL-13

Asthma utilizes more NO than COPD

39
Q

Asthma vs. COPD - oxidative stress

Does COPD or Asthma have more oxidative stress?

A

COPD

40
Q

Genetic deficiency of a1-anti-trypsin

  • a1-anti-trypsin inhibits neutrophil ___ and limits lung tissue ___
  • deficiency causes increased neutrophil ___ and damage via ___ and ___ activity
  • ZZ allele results in disadvantageous ___ function
  • PI-MZ allele result in increased ___ and ___ function
A
  • elastase, damage
  • migration, inflammation, protease
  • lung
  • height, respiratory
41
Q

E-cigs and Vaping

Vaping generates an aerosol vapor that can alters indoor air quality and contains toxic
___ and other substance of unknown toxicity

A

aldehydes

42
Q

E-cigarette/Vaping product use associated lung injury (EVALI)

  • sterile exogenous ___ like reaction.
  • ___ immune response
  • vitamin ___ acetate
  • ___carbons in counterfeit vaping products
  • many of these compounds are involved in ___ stress and inflammatory responses in the lung
A
  • pneumonitis
  • innate
  • E
  • hydrocarbons
  • oxidative
43
Q

E-cigarette/Vaping product use associated lung injury (EVALI)

  • first responders: airway epithelial cells, ___ macrophages (AMs), and ___/neutrophils or ___ cells (PMNs)
  • ___ is initiated to trap particles/pathogens but adverse effect is tissue ___.
  • Dyregulated netosis leads to increased susceptibilty to ___
A
  • alveolar, granulocytes, polymorphonuclear
  • NETosis
  • infections
44
Q

Cystic Fibrosis

autosomal ___ , chronic disease that results from the mutation of the ____ gene

A

recessive, Cystic Fibrosis Transmembrane Conductance Regulator

45
Q

Cystic Fibrosis - stats

  • usually diagnosed by age __
  • 1:___ births in US
  • life expectancy: late ___
A
  • 2
  • 3200
  • 30s
46
Q

Cystic Fibrosis

CF patients secrete extremely viscous mucus that:
* ___ airflow to the lungs
* harbors ___ leading to lung infections
* obstructs the ___ duct that interferes with digestion

A
  • obstructs
  • pathogens
  • pancreatic
47
Q

Cystic Fibrosis Transmembrane Conductance Regulator

  • ___ amino acid protein
  • an ___ transporter
  • functions as a ___ channel
  • gated by ___ phosphorylation or ___ domain
  • CFTRs are expressed in: ___, sweat, and ___ duct epithelium
A
  • 1480
  • ABC
  • Cl-
  • PKA, R
  • airway, pancreatic
48
Q

Loss of CFTR function in sweat duct epithelium

Loss of CFTR function causes ___ NaCl concentration in sweat

A

increased

49
Q

T or F: excessively salty sweat is a sign of cystic fibrosis

A

True

There is an opposite effect on sodium in the lungs

50
Q

Loss of CFTR function in airway epithelium

CFTR function inhibits ENaC-mediated ___ influx.
CFTR dysfunction causes:
* increased ___ activities
* increased ___ uptake into epithelial cells

dehydration of ___ causes thickening of ___

A
  • Na+
  • ENaC
  • H2O
  • ASL, mucus

ASL = airway surface liquid

PHRM 825 (49 decks)

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