Pulmonary Obstruction/restriction

Front 1

3 asthma components

Back 1

recurrent episodes of airway obstruction that resolve
airway hyperresponsibeness
inflammation of airways

Front 2

in asthma, what infiltrates the bronchial mucosa

Back 2

th2 lymphocytes, mast cells, and eosinophils

Front 3

Mediators of acute bronchospasm in asthma

Back 3

ach
histamine
kinins
leukotrienes
neuropeptides (substance P and neurokinin A)
Nitric oxide
Platelet activating factor

Front 4

Mediators of inflammation in asthma

Back 4

il5, il4, TNFa (major), GMCSF, LTB4(leukotriene)

Front 5

Asthma physical findings

Back 5

increased respiratory rate
pulsus paradoxus

Front 6

sounds of asthma

Back 6

wheezing
ronchi

Front 7

Arterial blood gasses in asthma
early vs. late

Back 7

early- resp alkalosis with normal or high po2
late-resp and metabolic acidosis b/c co2 not expelled

Front 8

Sputum of asthmatic

Back 8

charcot-leyden crystals
creola bodies

Front 9

Asthma reliever meds and side effects

Back 9

B-adrenergics -albuterol
tachycardia, tremor

Front 10

Controller medications for asthma

Back 10

inhaled corticosteriods,
antileukotrienes
theophylline
long-acting b-agnonists
systemic corticosteroids

Front 11

Inhaled corticosteroids
use
mechanism
side effects

Back 11

asthma- anti-inflamm therapy
effects mediator release, inflammatory cell activity, mucus production
se: growth retardation, bone loss cataracts, glaucoma
ORAL THRUSH

Front 12

Antileukotrienes
use
mechanism

Back 12

asthma-receptor antagonists/lipoxygenase inhibitor
antiinflammatory

Front 13

Theophylline
use
side effects
contraindicated for
disadvantages

Back 13

asthma
inhibits phosphodiesterase
se: gi, cardiac, cns toxicity, arrythmia, seizure
can't be on electroshock therapy
narrow thrapeutic index

Front 14

long-acting B agonists

Back 14

useful for nocturnal asthma

Front 15

Responsible for COPD inflammation

Back 15

oxidative stress
neutrophils
macrophages
cd8 lymphos
il8 and TNFa
protesase/antiprotease imbalance

Front 16

structural changes of COPD

Back 16

alveolar destruction
collagen deposition
glandular hypertrophy
airway fibrosis

Front 17

pathology of chronic bronchitis

Back 17

increase of mucus glands
increase smooth muscle
neutrophil infitration into bronchial mucosa
bronchiolar wall fibrosis
mucus and inflammatory cells filing small airway lumens

Front 18

where centrilobular is worse

Back 18

upper lobes - where smoke goes due to increased ventilation

Front 19

where panlobular is worse

Back 19

lower lobes - greater blood flow

Front 20

DLCO decreased in what obstructive disease?

Back 20

emphysema

Front 21

parasympas are located where in the lung vs. sympas

Back 21

paras are central and sympas are peripheral

Front 22

atropine
category
se

Back 22

anticholinergic
tachycardia, arrhythmia

Front 23

Ipatropium
use

Back 23

B blocker-induced bronchospasm treatment of choice
COPD

Front 24

B blocker-induced bronchospasm treatment of choice

Back 24

ipatropium

Front 25

2nd generation drug (anticholinergic) that causes increased lung function throughout the day for chronic bronchitis/emphysema

Back 25

tiatropium

Front 26

100% associated with cigarette smoke

Back 26

Respiratory bronchiolitis-associated interstitial lung disease

Front 27

chicken wire appearence of normal lung alveolar space

Back 27

UIP

Front 28

hallmark of UIP

Back 28

spatially and temporally heterogeneous

Front 29

feature of UIP

Back 29

fibroblastic foci -

Front 30

small proteinaceous plugs in the sub epithelial space

Back 30

fibroblastic foci of UIP

Front 31

Features of UIP

Back 31

hetero temporal
patchy collagen fibrosis
fibroblastic foci
honeycomb

Front 32

Features of NSIP (non-specific interstitial pneu)

Back 32

uniform temporal
interstitial inflammation
diffuse collagen fibers
organizing pneumonia

Front 33

Feature of AIP

Back 33

uniform temporal
hyaline membrane

Front 34

velcro crackles heard in

Back 34

interstitial lung disease

Front 35

Clinical features of interstitial lung disease

Back 35

most common: cough, dysnea

tachypnea, clubbing, crackles

Front 36

Age of onset
UIP v DIP v NSIP

Back 36

UIP in older males
DIP, NSIP younger (40's)

Front 37

Mortality of UIP v DIP v NSIP

Back 37

UIP = higher mortality rate

Front 38

Response to treatment
UIP v DIP v NSIP

Back 38

UIP responds poorly

Front 39

abnormal white thickenings around the periphery of the lung

Back 39

UIP

Front 40

diagnosis of ILD is made by

Back 40

history!!!

Front 41

Drug for UIP

Back 41

azathioprine

Front 42

drug for ILD

Back 42

corticosteroids

Front 43

Seen in biopsy of UIP

Back 43

end stage lung (honeycomb)
normal lung
active inflammation

Front 44

how NSIP differs from UIP

Back 44

inflammation is prominent and homogenous

Front 45

Plugs in alveolar space that aren't true granulation tissue but resepble it witha clump of myofibroblasts and a lot of inflammation around the airways

Back 45

BOOP

Front 46

cells appear to be desquaminating but are actually alveolar macrophages

Back 46

DIP

Front 47

associated with cigaretttes

Back 47

DIP

Front 48

HRCT shows ground glass

Back 48

hypersensitivity pneumonitis - acute

Front 49

path of hypersensitivity pneumonitis

Back 49

antigen
neutrophil/mast cell
chronic lymphociyic
granuloma
fibrosis or repair

Front 50

Chronic Hypersensitivity pneumonitis can mimic

Back 50

UIP/IPF

Front 51

HRCT shows reticular lacy stuff or honeycomb appearence

Back 51

hypersensitivity pneumonitis

Front 52

Definition of asbestosis

Back 52

interstitial pneumonitis and fibrosis caused by exposure to asbestos fiber

Front 53

presentatin is identical to IPF

Back 53

asbestosis

Front 54

low levels of silica v. high

Back 54

low = scarring
massive = ARDS-like

Front 55

Silica-associated illnesses

Back 55

Mycobacterial infection
Scleroderma
Lung Cancer

Front 56

On biopsy CTD people will show

Back 56

UIP

Front 57

RA ILD presents just like

Back 57

IPF (at the bases)

Front 58

predicts poor prognosis in scleroderma

Back 58

pulmonary htn

Front 59

raynauds phenomenon is associated with

Back 59

scleroderma

Front 60

Drugs of drug-induced ILD

Back 60

bleomycin (dose dependant)
cyclophosphamide
methotrexate
mitomycin

Front 61

non-cytotoxic agent that can cause IPF

Back 61

amiodarone

Front 62

characteristics of ARDS

Back 62

acute dypsnea
bilateral infiltrates
hypoxemia
no heart failure
appropriate trigger

Front 63

hypoxemia is defined by

Back 63

P/F ratio
P is PaO2 and F is O2 fraction

Front 64

P/F ratios
normal and lung injury and ards

Back 64

normal is 450
injury is less than 300
Ards is less than 200

Front 65

type of cell destroyed in ards

Back 65

type 1

Front 66

2 stages of ARDS and their components

Back 66

exudative
-flooding
-hypoxemia
-hyaline membranes
proliferative
-inflammation
-fibrosis

Front 67

hypoxemia in ards is a result of

Back 67

shunt