Hazbun lecture 1 Flashcards by Matti Daniel

definition of asthma

Wheezing, coughing, shortness of breath that is caused by narrowing of airways.

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What are some features of asthma with regard to the airway of patients and inflammatory mediators

Narrowing and inflammation of airway and release of inflammatory mediators

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Effect of asthma on mucus secretion and respiratory mucosa

Excess mucus secretion and edema of respiratory mucosa

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What are the two phases of asthma

Early and late phase

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characteristics of early phase asthma

Immediate bronchoconstriction

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In early phase of asthma, what antibody do the antigens bind to? What effect does this have on mast cells?

In early, antigen is bound to IGE antibody. This triggers the release of histamine, trypase, LTC, LTD 4 prostaglandins from mast cells.

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What does the release of cytokines from mast cells in early phase of asthma lead to?

leads to bronchial smooth muscle contraction and vascular leakage

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characteristics of delayed reaction?

sustained bronchoconstriction.

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What cytokines are released during delayed reaction

TH2 cells, neutrophils, macrophages and eosinophils

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What two factors are measured to see what level of chronic asthma we are on

PAF and ECP

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What is PAF

PAF is a potent proinflammatory mediator

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What is ECP

ECP is a ribonuclease, but it also promotes inflammation and fibrosis

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What are some triggers of asthma

Bacteria
proteinases and neutrophils
TH2 cells and cytokines
oxidants and smoke

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pollutants like cigarettes can activate________

Neutrophils

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number of ciliated cells compared to goblet cells in non-asthmatic patients

Normally there are a lot more ciliated cells than goblet cells

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Number of goblet cells compared to ciliated cells in asthmatic patients? why? What does this lead to?

There less ciliated cells in asthmatic cells, this is due to inflammation and airway remodeling. This leads to hypersecretion of mucus

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hyperplasia of goblet cells is mediated by? What is it maintained by?

development- EGFR, CLCA
maintained by-BCL-2

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the Q576R polymorphism in IL-4a receptor induces

hyperreactivity to inhaled antigens

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Example for genetic factor involved in goblet cell hyperplasia

The Q 576 R polymorphism in the IL-4a receptor induces hyperreactivity to inhaled antigens

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what is periostin? what is it induced by?

Periostin is an extracellular matrix protein induced by IL-13 and IL-4

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Periostin is secreted by

Fibroblast cells

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fibroblasts are triggered by______ cells that release ____&_________

TH-2 cells that release IL-4 and IL-13

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periostins bind to______

Integrins

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What are integrins?

Cells that support adhesion and cell migration. Leads to pro-inflammatory cytokine release.

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onset of asthma vs COPD

Onset often in children in asthma onset in late adulthood in COPD

Asthma vs COPD link to allergic response

COPD is not linked to allergic response, but asthma is linked to specific triggers

Asthma vs COPD progressive vs episodic

Asthma is episodic but COPD is progressive

which one is irreversible? Asthma or COPD

COPD

Symptoms of COPD

chronic cough, sputum dyspnea, barrel chest

What are the different ways COPD is diagnosed?

breathlessness score related to everyday activities COPD assesment test (CAT) degree of airflow limitation

comorbidities of COPD

smoking, diabetes, CV disease, respiratory infection

What does the CAT take into consideration when assesing COPD

mucus, chest tightness, sleep and breathlesness

effect of cigarette smoke or other irritants on epithelial cells

Damages epithelial cells

The damage of epithelial cells by irritants in COPD triggers macrophages to ________ mode

inflammation

TH-1 vs TH-2

TH-1 interacts with macrophages and TH-2 interacts with B cells

What does TGF-b trigger

Fibroblasts

What does TGF-b lead to

fibrosis

what is fibrosis?

proliferation of fibroblasts lining the airways, makes them stiff

Asthma vs COPD. Which is Th1 driven and which is TH2 driven?

COPD is TH-1 driven and asthma is TH2 driven

What leads to the activation of the alveoli?

macrophages activating TH-1 cells

release of which proteases will destroy alveoli

elastase and MMP9

What two steps lead to the enlargement and destruction of alveolar wall and mucus hypersecretion of alveoli

release of elastase and MMP9 activation of TH-1 cells

1-2% of COPD patients have ____________ deficiency

a1-anti trypsin

Asthma vs COPD site of disease

Asthma- proximal airways COPD- peripheral, pulmonary, lung parenchyma

Cells involved in asthma vs cells involved in COPD

More eosinophils in asthma more neutrophils and macrophages in COPD

More oxidative stress in COPD or asthma?

COPD

key mediators in COPD?

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

Key mediators in asthma

Eotaxin, IL-4, IL-5, IL-13, NO

More alveolar destruction and fibrosis in COPD or asthma

COPD

normal role of a-1 anti trypsin

inhibiting lung tissue damage and protease

What happens in the case of deficiency of a-1 anti trypsin

increased neutrophil migration into the lungs. This leads to increased lung damage by less amount of elastase.

EVALI acronym

Electronic/vaping associated lung injury

What type of reaction in the lungs is caused by EVALI

Pneumonitis

The pneumonitis caused by EVALI is triggered by _________immune response

innate

type of immune response in Asthma and COPD vs EVALI

Asthma and COPD are adaptive, whereas EVALI is triggered by innate response

which immune response is incolved in EVALI

Innate

4 First responders in EVALI

Airway epithelial cells alveolar macrophages granulocytes/neutrophils polymorphonuclear cells

How does NETosis occur?

NETosis occurs when neutrophils die once they get to the inflammation site. They release strings that capture bacteria (suicide bombers)

_________ is a major response in EVALI

NETosis

What is Cystic fibrosis (CF)

CF is an autosomal recessive disease where there is a mutation in the cystic fibrosis transmembrane conductance regulator (CFT-R)

CF effects on mucus thickness

CF patients secrete viscous thick mucus

What is the effect of the the thick mucus in the body in CF patients

This increases the likelihood of a secondary infection in the lungs because the mucus is not being cleared effectively

How do CF patients also suffer in interference with digestion

This is because CF patients suffer from obstruction of the pancreatic duct

CFT-R functions as a _______ channel

3 tissue types CFT-R is expressed in?

Airway epithelium sweat duct epithelium pancreatic duct epithelium

Does CFT-R behave the same at all times?

No, the way CFT-R behaves differs depending on its location

Loss of CFT-R function in sweat glands vs lungs difference in Na

Increase in NaCl concentration in sweat (excessive salty sweat is a sign of CF) decrease in sodium in lungs

Name of the two layers of ASL in airway CF

Mucus PCL (pericilliary layer)

CFT-R function in airway on mucus

CFT-R in airway negatively regulates sodium channel (ENaC)

What happens in airway if CFT-R function is lost

there will be no negative regulation of sodium channel (ENaC), so it will bring in a lot of sodium into the cell, and this brings in a lot of water to compensate. This dehydrates the mucus and makes it thicker.