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PHYL 4504 > Obstructive Diseases > Flashcards

Obstructive Diseases Flashcards

1
Q

name 2 obstructive lung diseases

A

Asthma and COPD (chronic bronchitis and emphysema)

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2
Q

increased resistance to airflow can be caused by conditions where?

A

inside the lumen, in the wall of the airway or in the peribronchial region

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3
Q

Obstructive lung disease is characterized by

A

obstruction to airflow

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4
Q

A) lumen i spartially blocked

A

ex: mucous

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5
Q

B) Airway wall is thickened

A

muscle hypertrophy in asthma, inflammation in bronchitis

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6
Q

C) abnormality outside airway

A

destoryed lung parenchyma with loss of radial traction - emphysema

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7
Q

obstructive lung diseases are increasingly important because

A

cause of mortaility

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8
Q

All PFT parameters in obstructive lung diseases are ___

A

decreased - because obstruction to air moving in and out

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9
Q

common airways diseases

A

obstructivr

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10
Q

Asthma is caracterized by

A

increased responsiveness of the airway to vairous stimuli

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11
Q

Asthma manifests as

A

widespread narrowing of the airways (bronchoconstriction), excessive mucous secretion, chronic inflammation, chest tightening and weezing and coughing

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12
Q

Asthmatics have more ____

A

muscle - tends to constrict inappropriately

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13
Q

Asthmatics also have more ____

A

mucous

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14
Q

Asthma is an _____ disease

A

inflammatory - increased edema fluid - inflammatory cells release cytokines

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15
Q

What is airway hyper-responsiveness

A

the capacity of the airways to undergo exaggerated narrowing in the response to stimuli that do not result in a comparable degree of airway narrowing in healthy subjects

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16
Q

what can be found in the mucous

A

epithelial cells that are sloughed off, inflammatory cells

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17
Q

structure and inflammatory changes thorughout the airway wall results in ____

A

bronchial thickening, edema and increased mucous production - airway remodeling

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18
Q

Test for asthma with

A

methacholine challenge

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19
Q

Explain methachloline test

A

methacholine given to patient via nebuliser and causes bronchocontriction via muscarinic receptors -d egree of narrowing quantified by spirometry - asthmatics will react to much lower dose

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20
Q

Bronchodilators administered to assess

A

degree of reversibility

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21
Q

Bronchoconstriction can be caused by

A

various agents or situaitons - allergens, NSAIDs, emotional stress, exercise, hypertonicity, cholinergic agonists

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22
Q

Why AHR?

A

increased presence of contractile mediators such as histamine due to inflammatory state, structural changes in ASM (mass and remodeling)

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23
Q

ASM contraction can be provoked by

A

Ca entering via voltage dependent Ca channels or form SR stores

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24
Q

What s the main source of Ca in ASM

A

intracellular SR stores

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25
Q

How does calcium get released from SR?

A

GPCR ligands coupled to Gaq induce PLC activation, leading to IP3 formaiton which binds to receptors on SR which triggers translocation of Ca into cytosol

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26
Q

What does increased calcium do?

A

activated calmodulin to phosphorylate myosin light chain kinase which directly phosphorylates myosin

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27
Q

What is activated by Calcium dependent and independent pathways

A

RhoA

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28
Q

What does RhoA do?

A

activates ROCK which phosphorylates and inactivates MLCP

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29
Q

ASM contractile force generation is mediated by

A

cyclic cross bridging of actin and myosin - which depend on phosphorylation of myosin light chain by MLCK

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30
Q

main source of calcium in ASM

A

SR stores

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31
Q

Process is negatively regulated by

A

myosin phosphatase

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32
Q

Asthma = _____ coupled with chronic ____

A

AHR and inflammation

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33
Q

Airway remodelling structural changes in epithelium include

A

airway wall thickening
epithelial hypertrophy goblet cell metaplasia subepithelial fibrosis
smooth muscle hyperplasia and hypertrophy

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34
Q

with bronchoconstriciton you will get more ___ of the airway

A

narrowing

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35
Q

Persistence of asthma driven by

A

ongoing host immune response that generates mediators responsible for this remodeling

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36
Q

Epithelium is a source of mediators and a source of ____

A

cells that respond to them

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37
Q

Lungs are usually hyper inflated because…

A

extensive mucous plugging

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38
Q

___ is a response ot ongoing tissue injury caused by infectious agents and allergens

A

remodeling

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39
Q

there is loss of ____, ____ and disruption of ____ and impariment of ____ and cell death

A

epithelial integrity and epithelial shedding, tight junctions, barrier function

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40
Q

Why AHR?

A

we don’t know

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41
Q

What response is lacking in asthma

A

bronchodilating effect of deep breaths

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42
Q

what are the 4 mechanical determinants of airways narrowing

A

increased ASM mass, increased ASM contractility, breathing dynamics, and lung elastic recoil is lost

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43
Q

ASM activity is affected by

A

asthmatic milieu - inflammatory cytokines

44
Q

breathing dynamics are different which means

A

no bronchodilating upon deep breath

45
Q

More ____ states predominate in asthma

A

proliferative

46
Q

ASM is triggered to proliferate by

A

EGFR ligands

47
Q

ASM in asthma proliferates more readily in response to ___

A

allergens

48
Q

What are the 2 phenotypes of ASM

A

contractile or secreotry/proliferative

49
Q

We dont know the contribution of ___

A

each change to athma in each person - what drives what? we dont know

50
Q

there is increased aviability of ____ like histamine

A

contractile mediators

51
Q

there is increased activation of the pro contractile ___ pathway

A

Rho

52
Q

There is inadequate ___ of ASM in asthmatics

A

relaxation

53
Q

Treatments

A

short acting beta agonist, inhled corticosteroids, leukotriene antagonists, long acting muscarinic antagonists, anti IgE antibody, bronchial thermoplasty

54
Q

Asthmatics are bad at compliance of taking

A

inhaled corticosteroids

55
Q

montelukast is useful if..

A

steroid dont work well

56
Q

there is a ___ between the drugs you give people

A

balance

57
Q

What is an unpopular treatmetn

A

long acting muscarinic antagonist

58
Q

What is an expensive treatment?

A

Anti IgE monoclonal antibody

59
Q

What is bronchial thermoplasty

A

go in with bronchoscope and burn away the tissue

60
Q

All pulmonary funciton indeces are __ and should ___ with bronchodilator

A

decreased, increase

61
Q

asthmatics have a bit of an ___

A

increased compliance

62
Q

increased complaince goes away with

A

bronchodilator - because of surface tension forces..?

63
Q

What is one of the most common diseases?

A

COPD

64
Q

define COPD

A

Progressive loss of lung function with airflow obstruction that is not fully reversible with bronchodilators

65
Q

Airflow obstruction is the result of __

A

pulmonary inflamation associated with bronchitis and mucous hypersecretion together with emphysema

66
Q

Emphysema

A

the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls. Destruction of the gas exchange surfaces

67
Q

in emphysema, what enzyme chops up the tissue

A

neutrophil elastase

68
Q

What causes COPD

A

smoking and alpha 1 antitrypsin deficiency

69
Q

Chronic bronchitis =

A

mucous

70
Q

clinically define chronic bronchitis

A

chronic productive cough for 3 months in each of 2 successive years in
a patient in whom other causes of productive chronic cough have been excluded.

71
Q

most COPD patients exhibit symptoms of ____

A

both, but BP more prevalent phenotype

72
Q

Why is there excessive mucous production

A

hypertrophy of mucous glands in large bronchi

73
Q

Reid index is normally

A

0.4

74
Q

what does the reid index express

A

gland/wall ratio

75
Q

there is ____ in small airways

A

chronic inflammation

76
Q

2 types of emphysema

A

centricinar, panacinar

77
Q

type of emphysema depends on

A

which part is destoryed

78
Q

what is an acinus

A

the parenchyma distal to the terminal bronchiole,

79
Q

in Centraiacinar, distruction is

A

limited to

the central part of the lobule and the peripheral ducts and alveoli may be fine.

80
Q

WHere is centracinar most often located

A

appex of the upper lobe - spreads downwards

81
Q

Panacinar emphysema more common where

A

bottom of the lung

82
Q

Panacinar emphysema characterized by

A

: distension and destruction of

entire lobule

83
Q

Alpha 1 antitrypsin

A

a major inhibitor of serine proteases, including neutrophil elastase.

84
Q

homozygotes of alpha 1 antitrypsin are mor elikely to ____

A

develop COPD earlier (age 40 instead of 65)

85
Q

who is more likely to get panacinar type of emphysema

A

alpha 1 antitrypsin homozygotes

86
Q

in lungs there is a lot of alpha 1 antitrypsin to ___

A

protect lung from neutrophil elastase

87
Q

deficiency of alpha 1 anti trypsin

A

neutrophil elastase is unibhibited

88
Q

what does alpha-1 anti trypsin normally do?

A

coats and protects lungs from neutrophil elastase

89
Q

where is alpha 1 antitrypsin synthesized

A

liver

90
Q

where is neutrophil elastase produced or by what

A

white blood cells

91
Q

what does neutrophil elastase do?

A

break down harmful bacteria - protentially damaging

92
Q

when circulating levels of alpha 1 AT are reduced, NE can____

A

destory the connective tissue of the lung

93
Q

Lung disease arises from a _____ mechanism

A

gain of function

94
Q

Liver diseases arises from a ______ mechanism

A

loss of function

95
Q

what is the pathogenesis of emphysema

A

things induce activation of proinflammatory singalling pathways resulting in recruitment of neutrophils and macrophages = additional source of cytokines and oxidants

96
Q

what do the neutrophils do in emphysema

A

destory the elastic matrix of alveoli via neutrophil elastase = cleaved type 4 collagen, essential for integirty of alveolar wall

97
Q

risk factors for emphysema

A

smoking, pollution, agricultural pesticides (ROS)

98
Q

What is the halmark of chronic bronchitis

A

gland hypertrophy

99
Q

how can gland hypertrophy be expressed?

A

reid index

100
Q

what is the reid index

A

fraction of line the lies over cross sectional profiles of gland - ratio fo gland thickness to wall thickness

101
Q

what are the problems with the reid index

A

subjective where to draw line, diseases that increase wall thicjness will minimize or hide effects of gland hypertrophy

102
Q

what are some clinical features of COPD presentation

A

all things are reduced, airway obstruction, excess mucus in lumen, thickening of wall due to inflammation or loss of radial traction

103
Q

Type A COPD

A

pink puffer

104
Q

Type B COPD

A

blue bloater

105
Q

pink puffer symptoms

A

no cough, increasing dyspnea, chest overexpansion, no cyanosis, quiet breahting sounds, no peripheral edema, arterial PO2 slightly depressed, arterial PCO2 normal

106
Q

blue bloaters symptoms

A

increasing dyspnea, frequent coughing with sputum, no increase in chest volume, cyanosis, peripheral edema, PO2 low and PCO2 raised

PHYL 4504 (8 decks)

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