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Therapeutics > Hazbun lecture 1 > Flashcards

Hazbun lecture 1 Flashcards

1
Q

definition of asthma

A

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

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2
Q

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

A

Narrowing and inflammation of airway and release of inflammatory mediators

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3
Q

Effect of asthma on mucus secretion and respiratory mucosa

A

Excess mucus secretion and edema of respiratory mucosa

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4
Q

What are the two phases of asthma

A

Early and late phase

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5
Q

characteristics of early phase asthma

A

Immediate bronchoconstriction

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6
Q

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

A

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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7
Q

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

A

leads to bronchial smooth muscle contraction and vascular leakage

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8
Q

characteristics of delayed reaction?

A

sustained bronchoconstriction.

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9
Q

What cytokines are released during delayed reaction

A

TH2 cells, neutrophils, macrophages and eosinophils

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10
Q

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

A

PAF and ECP

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11
Q

What is PAF

A

PAF is a potent proinflammatory mediator

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12
Q

What is ECP

A

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

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13
Q

What are some triggers of asthma

A

Bacteria
proteinases and neutrophils
TH2 cells and cytokines
oxidants and smoke

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14
Q

pollutants like cigarettes can activate________

A

Neutrophils

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15
Q

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

A

Normally there are a lot more ciliated cells than goblet cells

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16
Q

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

A

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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17
Q

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

A

development- EGFR, CLCA
maintained by-BCL-2

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18
Q

the Q576R polymorphism in IL-4a receptor induces

A

hyperreactivity to inhaled antigens

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19
Q

Example for genetic factor involved in goblet cell hyperplasia

A

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

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20
Q

what is periostin? what is it induced by?

A

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

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21
Q

Periostin is secreted by

A

Fibroblast cells

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22
Q

fibroblasts are triggered by______ cells that release ____&_________

A

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

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23
Q

periostins bind to______

A

Integrins

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24
Q

What are integrins?

A

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

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25
Q

onset of asthma vs COPD

A

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

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26
Q

Asthma vs COPD link to allergic response

A

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

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27
Q

Asthma vs COPD progressive vs episodic

A

Asthma is episodic but COPD is progressive

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28
Q

which one is irreversible? Asthma or COPD

A

COPD

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29
Q

Symptoms of COPD

A

chronic cough, sputum dyspnea, barrel chest

30
Q

What are the different ways COPD is diagnosed?

A

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

31
Q

comorbidities of COPD

A

smoking, diabetes, CV disease, respiratory infection

32
Q

What does the CAT take into consideration when assesing COPD

A

mucus, chest tightness, sleep and breathlesness

33
Q

effect of cigarette smoke or other irritants on epithelial cells

A

Damages epithelial cells

34
Q

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

A

inflammation

35
Q

TH-1 vs TH-2

A

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

36
Q

What does TGF-b trigger

A

Fibroblasts

37
Q

What does TGF-b lead to

A

fibrosis

38
Q

what is fibrosis?

A

proliferation of fibroblasts lining the airways, makes them stiff

39
Q

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

A

COPD is TH-1 driven and asthma is TH2 driven

40
Q

What leads to the activation of the alveoli?

A

macrophages activating TH-1 cells

41
Q

release of which proteases will destroy alveoli

A

elastase and MMP9

42
Q

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

A

release of elastase and MMP9
activation of TH-1 cells

43
Q

1-2% of COPD patients have ____________ deficiency

A

a1-anti trypsin

44
Q

Asthma vs COPD site of disease

A

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

45
Q

Cells involved in asthma vs cells involved in COPD

A

More eosinophils in asthma
more neutrophils and macrophages in COPD

46
Q

More oxidative stress in COPD or asthma?

A

COPD

47
Q

key mediators in COPD?

A

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

48
Q

Key mediators in asthma

A

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

49
Q

More alveolar destruction and fibrosis in COPD or asthma

A

COPD

50
Q

normal role of a-1 anti trypsin

A

inhibiting lung tissue damage and protease

51
Q

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

A

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

52
Q

EVALI acronym

A

Electronic/vaping associated lung injury

53
Q

What type of reaction in the lungs is caused by EVALI

A

Pneumonitis

54
Q

The pneumonitis caused by EVALI is triggered by _________immune response

A

innate

55
Q

type of immune response in Asthma and COPD vs EVALI

A

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

56
Q

which immune response is incolved in EVALI

A

Innate

57
Q

4 First responders in EVALI

A

Airway epithelial cells
alveolar macrophages
granulocytes/neutrophils
polymorphonuclear cells

58
Q

How does NETosis occur?

A

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

59
Q

_________ is a major response in EVALI

A

NETosis

60
Q

What is Cystic fibrosis (CF)

A

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

61
Q

CF effects on mucus thickness

A

CF patients secrete viscous thick mucus

62
Q

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

A

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

63
Q

How do CF patients also suffer in interference with digestion

A

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

64
Q

CFT-R functions as a _______ channel

A

Cl

65
Q

3 tissue types CFT-R is expressed in?

A

Airway epithelium
sweat duct epithelium
pancreatic duct epithelium

66
Q

Does CFT-R behave the same at all times?

A

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

67
Q

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

A

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

68
Q

Name of the two layers of ASL in airway CF

A

Mucus
PCL (pericilliary layer)

69
Q

CFT-R function in airway on mucus

A

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

70
Q

What happens in airway if CFT-R function is lost

A

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.

Therapeutics (46 decks)

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