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PHYL 4504 > Obstructive Diseases > Flashcards

Obstructive Diseases Flashcards

(106 cards)

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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
How does calcium get released from SR?
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
26
What does increased calcium do?
activated calmodulin to phosphorylate myosin light chain kinase which directly phosphorylates myosin
27
What is activated by Calcium dependent and independent pathways
RhoA
28
What does RhoA do?
activates ROCK which phosphorylates and inactivates MLCP
29
ASM contractile force generation is mediated by
cyclic cross bridging of actin and myosin - which depend on phosphorylation of myosin light chain by MLCK
30
main source of calcium in ASM
SR stores
31
Process is negatively regulated by
myosin phosphatase
32
Asthma = _____ coupled with chronic ____
AHR and inflammation
33
Airway remodelling structural changes in epithelium include
airway wall thickening epithelial hypertrophy goblet cell metaplasia subepithelial fibrosis smooth muscle hyperplasia and hypertrophy
34
with bronchoconstriciton you will get more ___ of the airway
narrowing
35
Persistence of asthma driven by
ongoing host immune response that generates mediators responsible for this remodeling
36
Epithelium is a source of mediators and a source of ____
cells that respond to them
37
Lungs are usually hyper inflated because...
extensive mucous plugging
38
___ is a response ot ongoing tissue injury caused by infectious agents and allergens
remodeling
39
there is loss of ____, ____ and disruption of ____ and impariment of ____ and cell death
epithelial integrity and epithelial shedding, tight junctions, barrier function
40
Why AHR?
we don't know
41
What response is lacking in asthma
bronchodilating effect of deep breaths
42
what are the 4 mechanical determinants of airways narrowing
increased ASM mass, increased ASM contractility, breathing dynamics, and lung elastic recoil is lost
43
ASM activity is affected by
asthmatic milieu - inflammatory cytokines
44
breathing dynamics are different which means
no bronchodilating upon deep breath
45
More ____ states predominate in asthma
proliferative
46
ASM is triggered to proliferate by
EGFR ligands
47
ASM in asthma proliferates more readily in response to ___
allergens
48
What are the 2 phenotypes of ASM
contractile or secreotry/proliferative
49
We dont know the contribution of ___
each change to athma in each person - what drives what? we dont know
50
there is increased aviability of ____ like histamine
contractile mediators
51
there is increased activation of the pro contractile ___ pathway
Rho
52
There is inadequate ___ of ASM in asthmatics
relaxation
53
Treatments
short acting beta agonist, inhled corticosteroids, leukotriene antagonists, long acting muscarinic antagonists, anti IgE antibody, bronchial thermoplasty
54
Asthmatics are bad at compliance of taking
inhaled corticosteroids
55
montelukast is useful if..
steroid dont work well
56
there is a ___ between the drugs you give people
balance
57
What is an unpopular treatmetn
long acting muscarinic antagonist
58
What is an expensive treatment?
Anti IgE monoclonal antibody
59
What is bronchial thermoplasty
go in with bronchoscope and burn away the tissue
60
All pulmonary funciton indeces are __ and should ___ with bronchodilator
decreased, increase
61
asthmatics have a bit of an ___
increased compliance
62
increased complaince goes away with
bronchodilator - because of surface tension forces..?
63
What is one of the most common diseases?
COPD
64
define COPD
Progressive loss of lung function with airflow obstruction that is not fully reversible with bronchodilators
65
Airflow obstruction is the result of __
pulmonary inflamation associated with bronchitis and mucous hypersecretion together with emphysema
66
Emphysema
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
in emphysema, what enzyme chops up the tissue
neutrophil elastase
68
What causes COPD
smoking and alpha 1 antitrypsin deficiency
69
Chronic bronchitis =
mucous
70
clinically define chronic bronchitis
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
most COPD patients exhibit symptoms of ____
both, but BP more prevalent phenotype
72
Why is there excessive mucous production
hypertrophy of mucous glands in large bronchi
73
Reid index is normally
0.4
74
what does the reid index express
gland/wall ratio
75
there is ____ in small airways
chronic inflammation
76
2 types of emphysema
centricinar, panacinar
77
type of emphysema depends on
which part is destoryed
78
what is an acinus
the parenchyma distal to the terminal bronchiole,
79
in Centraiacinar, distruction is
limited to | the central part of the lobule and the peripheral ducts and alveoli may be fine.
80
WHere is centracinar most often located
appex of the upper lobe - spreads downwards
81
Panacinar emphysema more common where
bottom of the lung
82
Panacinar emphysema characterized by
: distension and destruction of | entire lobule
83
Alpha 1 antitrypsin
a major inhibitor of serine proteases, including neutrophil elastase.
84
homozygotes of alpha 1 antitrypsin are mor elikely to ____
develop COPD earlier (age 40 instead of 65)
85
who is more likely to get panacinar type of emphysema
alpha 1 antitrypsin homozygotes
86
in lungs there is a lot of alpha 1 antitrypsin to ___
protect lung from neutrophil elastase
87
deficiency of alpha 1 anti trypsin
neutrophil elastase is unibhibited
88
what does alpha-1 anti trypsin normally do?
coats and protects lungs from neutrophil elastase
89
where is alpha 1 antitrypsin synthesized
liver
90
where is neutrophil elastase produced or by what
white blood cells
91
what does neutrophil elastase do?
break down harmful bacteria - protentially damaging
92
when circulating levels of alpha 1 AT are reduced, NE can____
destory the connective tissue of the lung
93
Lung disease arises from a _____ mechanism
gain of function
94
Liver diseases arises from a ______ mechanism
loss of function
95
what is the pathogenesis of emphysema
things induce activation of proinflammatory singalling pathways resulting in recruitment of neutrophils and macrophages = additional source of cytokines and oxidants
96
what do the neutrophils do in emphysema
destory the elastic matrix of alveoli via neutrophil elastase = cleaved type 4 collagen, essential for integirty of alveolar wall
97
risk factors for emphysema
smoking, pollution, agricultural pesticides (ROS)
98
What is the halmark of chronic bronchitis
gland hypertrophy
99
how can gland hypertrophy be expressed?
reid index
100
what is the reid index
fraction of line the lies over cross sectional profiles of gland - ratio fo gland thickness to wall thickness
101
what are the problems with the reid index
subjective where to draw line, diseases that increase wall thicjness will minimize or hide effects of gland hypertrophy
102
what are some clinical features of COPD presentation
all things are reduced, airway obstruction, excess mucus in lumen, thickening of wall due to inflammation or loss of radial traction
103
Type A COPD
pink puffer
104
Type B COPD
blue bloater
105
pink puffer symptoms
no cough, increasing dyspnea, chest overexpansion, no cyanosis, quiet breahting sounds, no peripheral edema, arterial PO2 slightly depressed, arterial PCO2 normal
106
blue bloaters symptoms
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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