Chapters 22, 23

Front 1

What is the most important factor in raising airway resistance?

Back 1

airway radius, to the 4th power

Front 2

What two values are always high in the COPDs

Back 2

TLC and RV

Front 3

Definition of chronoic bronchitis

Back 3

Persistent productive cough daily for at least three consecutive months in at least two consecutive years

Front 4

Two means of increased resistance in chronic bronchitis

Back 4

either more mucus is being produced than there should be and therefore decreased radius or there is dramatic thickening of the bronchial wall (Reid Index - measures from peribronchium to the basement membrane)

Front 5

Most common causes of chronic bronchitis

Back 5

smoking and CF

Front 6

"blue bloaters"

Back 6

chronic bronchitis
usually stocky obese men who are cyanotic and have respiratory acidosis

Front 7

Emphysema definition

Back 7

permanent enlargement of the airspaces distal to terminal bronchioles

Front 8

general idea of whats going on in emphysema

Back 8

Normal airways are held open by elastic fibers. Small airways close at small volumes. These people have destroyed insterstitium of the lung thus the airways collapse at much high volume

Front 9

What molecule is the issue in "pure" emphysema

Back 9

a-1 antitrypsin

Front 10

temporary treatment for people with emphysema to breath better

Back 10

"pursed-lip" breathing
creates back pressure

Front 11

definition of asthma

Back 11

reversible airway obstruction. Reversibility with drugs depends on how reactive the patient is in the bronchi to various triggers

Front 12

what hypertrophy is seen in asthma

Back 12

smooth muscles, mucous glands, as well as inflammation and edema of bronchial wall.
asthma is an edema-permeability problem

Front 13

General parameters seen in obstructive lung dz

Back 13

decreased airflow from increased resistance
decrease FEV/FVC ratio
TLC IS NOT DECREASED

Front 14

general parameters seen in restrictive lung dz

Back 14

decreased expansion of the lung, increased TLC
Extrapulmonary - chest wall
Pulmonary - interstitium

Front 15

How is emphysema dianosed

Back 15

morphological appearance under microscope

Front 16

Bullae

Back 16

distended sacs of air that can form in emphysema and further obstruct/collapse airways

Front 17

Which type of emphysema attacks the apices of the lungs and is most associated with smoking

Back 17

centrilobular

Front 18

Which type of emphysema attacks the bases of the lungs?

Back 18

panlobular - a-1 antitrypsin problem

Front 19

most common mutation of a-1 antiprotease

Back 19

PiZZ

Front 20

What is a potential cause of spontaneous pneumothorax

Back 20

distal acinar emphysema
otherwise this is usually not clinically significant

Front 21

how is chronic bronchitis diagnosed

Back 21

based on clinical criteria: 3 consecutive months in 2 consecutive years

Front 22

What molecules/proteins are at play in emphysema

Back 22

generally increased protease or elastase and not enough antiprotease.

Front 23

What cells are particularly seen in the emphysema of smoking?

Back 23

centrilobular - you see neutrophils. They deposit elastase.

Front 24

"Pink puffer"

Back 24

emphysema. O2 stats are good but still tachypnic

Front 25

Extrinsic asthma

Back 25

lung based type 1 hypersensitivity rxn
atopic
allergic bronchopulmonary ASPERGILLOSIS

Front 26

Intrinsic asthma

Back 26

non-immune, usually after taking aspirin, and infection, a cold, or may be psychological

Front 27

T-Cells in asthma

Back 27

Cd4+ TH1 and TH1 cells
TH1 usually release interferon gamma to inhibit TH2 cells in the lung. This is decreased in asthma
Reaction becomes type 2, which stimulates inflammation and increased IgE production by B cells

Front 28

bronchiectasis definition

Back 28

permament dilation of large airways due to destruction of the tissue around them
combination of infection and obstruction
it is secondary to some other primary condition

Front 29

What are 2 conditions that can cause bronchiectasis

Back 29

Cystic fibrosis, primary ciliary dyskenesia (kartegeners)

Front 30

symptoms of bronchiectasis

Back 30

CLUBBING OF FINGERS, hemoptysis, severe cough, brain infection

Front 31

early phase of asthma

Back 31

30-60 minutes after exposure.
inhaled antigen binds IgE on mast cells
release of constrictive mediators, recruitment of EOSINOPHILS

Front 32

Late phase of Asthma

Back 32

4-8 hours after early phase.
Eosinophils release activators of mast cells
mediators increase and sustain inflammatory response

Front 33

What is an independent risk factor for the later development of asthma

Back 33

environmental tobacco smoke (fetal exposure)

Front 34

Samter Triad

Back 34

asthma, allergy to NSAIDS, and nasal polyposis

Front 35

Early childhood exposure in industrialized countries favoring the TH2 response are

Back 35

antibiotics, urban living, sensitization to cockroachs

Front 36

Exposure to what infection in particular is though to change people to more of a TH1 response

Back 36

mycobacterium tuberculosis

Front 37

symptoms of asthma

Back 37

chronic episodic cough that is worse at night, dyspnea, recurrent wheezing upon expiration

Front 38

PFT used in asthma

Back 38

methacholine challenge test with x ray

Front 39

_ is the clinical mainstay to objectively confirm the reversitiblity to airflow obstruction in patients with asthma

Back 39

spirometry

Front 40

FEV/FVC in obstructive dz like asthma

Back 40

LOW

Front 41

best treatment for most asthma

Back 41

short acting b2 agonist (inhaled)

Front 42

best treatment for chronic asthma

Back 42

"controller medications"
corticosteroids, long acting B2 agonists, leukotriene modifiers

Front 43

most widely used B2 agonist

Back 43

albuterol

Front 44

long acting B2 agonists

Back 44

formoterol, salmeterol

Front 45

What is the first line treatment for persistent asthma

Back 45

inhaled coriticosteroids

Front 46

anticholinergics used with b2 agonists

Back 46

Ipratropium, tiotropium

Front 47

secondary (add on) meds for persistent asthma

Back 47

zileuton, montelukast, zafirlukast

Front 48

Allergic asthma is characterized as

Back 48

elevation of specific IgE levels against one or more aeroallergens

Front 49

Humanized monoclonal antibody that blocks the binding of IgE to high affinity IgE receptors

Back 49

Omalizumab (allergic asthma)

Front 50

treatment for intermittent asthma

Back 50

b2 agonist inhaler

Front 51

persistent asthma symptoms

Back 51

daytime symptoms more than twice a week or 3-4 mornings a week

Front 52

asthma immunotherapy

Back 52

increase greater concentrations of allergen over time to decrease response
stimulates IgE blocking

Front 53

status asthamticus

Back 53

exacerbations of asthma not responding to initial therapy. Requires hospital admission
Can use heliox to help breathing (low gas viscosity decreases resistance)

Front 54

two vaccines asthmatics should def get

Back 54

yearly flu and 23-valent penumoccocal