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62 Cards in this Set

  • Front
  • Back
What changes in lung volumes are seen in airway obstruction?
Increased TLC
Increased RV
Increased FRC
Increased ERV

Decreased TV
Decreased inspiratory capacity
Decreased reserve volume
What is summer hypersensitivity pneumonitis?
A unique form of hypersensitivity pneumonitis in which clinical symptoms appear in the summer and subside spontaneously in the mid-autumn.

Most prevalent HP in Japan

Classically caused by Trichosporon cutaneum in moldy rugs.
Describe the findings in ARDS.
Severe hypoxemia, respiratory failure, pulmonary infiltrates, small tidal volumes.

BAL:
--TGFB, IL2, IL6
--surfactant proteins, von willebrand factor
--PMNs, IL8, NFKB
--proinflammatory (alveolar) macrophages
What is Tranfusion Related Acute Lung Injury (TRALI)?
Transfusion of blood with antigranulocyte antibodies --> recipient becomes cyanotic, respiratory failure (mimics anaphylaxis)

Avoidance - no allo-antibodies in blood
--no transfusion from multiparous women
What is Toxic Organic Dust Syndrome?
(not HP)

Toxic alveolitis occurs in 12 hours with inhalation --> fevers, chills, myalgias, crackles

Pulmonary mycotoxicosis - severe form of ARDS
What causes Silo-unloaders Diease?
Oxides of nitrogen: NO, NO2, N2O2

Dangerous --> damage to respiratory epithelium --> dyspnea, death

Oxides form with few days of crop storage (don't enter silos soon after filling it)
What is Byssinosis?
(not HP)

Form of occupational asthma.

Caused by exposure to cotton, flax, hemp or sisal.

Bronchoconstriction (symptoms) occur early in the work week and then improve while away from the workplace, or later in the work week (tachyphylaxis with continued exposure).

Risk - processing of raw cotton.
What is Reactive Airways Dysfunction Syndrome (RADS)?
(non-immunologic lung disease)

~Irritant Induced Asthma

Criteria:
1) No prior history of bronchoconstrictive lung disease
2) Onset with increased levels of exposure (i.e. World Trade Center cough)
3) Symptoms - abrupt onset
4) Symptoms - last at least 3 mo
5) Bronchial hyperreactivity present (PFTs show obstruction)
6) Symptoms suggest asthma
7) Other conditions excluded

+methacholine
Not associated with atopy, eosinophils, cigarretes/smoking, or increased WBCs on BAL
What is Occupational Asthma?
Immunologic - IgE, has latency period (mo-yrs)

--immediate + late phase reactions

--high molecular weight antigens (plant, animal, food) or low molecular weight + carrier (platinum, penicillin, epoxy) --> IgE

Polyimmunogenic (IgE, IgG) from low molecular weight antigens (isocyanate, acid anhydride, plicatic acid [cedar])

NON-immunogenic - no latency period (i.e. RADS), may have isolated late phase.
What causes this response?
Allergen challenge with early + late phase.
What causes humidifier HP?
May be caused by fungi or thermophilic bacteria.

Penicillium, Thermoactinomyces vulgaris, Bacillus cereus
What is Malt Workers Lung?
Caused by barley spread on floor that is then flooded with water --> germination --> heated --> malt

Aspergillus clavatus, Aspergillus fumigatus
What are the stages of HP?
Acute/Subacute - fever, myalgias, cough, decreased DLCO, restriction, rales

Chronic - +/- reversibility, decreased DLCO --> fibrosis
What are the CT findings of HP?
alveolitis - ground glass opacities
end stage - honeycombing, irreversible
What causes Avian Hypersensitivity Pneumonitis (Bird Fanciers Lung)?
Aspergillus fumigatus

Smoking exposure --> less intense immunologic (clinical?) responses
What causes Hot Tub Lung?
Mycobacteria
What causes Bagassosis?
Hypersensitivity pneumonitis from sugar cane.

Thermoactinomyces sacchari/vulgaris
What causes Machine Operator's Lung?
Pseudomonas flouorescens
What causes Farmer's Lung?
Thermophilic actinomycetes
Saccharopolyspora rectivirgula
What causes Ventilation Pneumonitis?
Naegleria gruberi, Acanthamoeba (amoebae)
What happens with histone acetylation + deacetylation, and how does it related to asthma?
Acetylation - opens up DNA
--increased in asthma and COPD
--increased IL8 - evidence of increased acetylation --> proinflammatory cytokines --> PMNs

Deacetylation - closes up DNA
--prednisone increased deactetylation in patient with asthma, but not COPD
--theoplylline - increased deacetylation in COPD patients
What are the ABPA diagnostic criteria?
In a patient with fleeting infiltrates...

Major criteria in asthma:   
--Asthma         
--Immediate cutaneous hyperreactivity to Aspergillus antigens (+SPT)
--Central bronchiectasis         
--Elevated IgE (>1000)
--Elevated A fumigatus-specific IgG and/or IgE
--Eos >1000

***if no bronchiectasis may have ABPA-S (seropositive)

in CF:
--deterioration
--IgE >1200 
--Immediate cutaneous hyperreactivity to Aspergillus antigens (+SPT)
--Fixed pulmonary infiltrates on chest radiograph         
--Elevated A fumigatus-specific IgG and/or IgE
What are the stages of ABPA?
What causes this response?
Aspirin - caused by mediator release --> longer onset/duration
What causes this response?
Methacholine (non-selective challenge)
What happens in ABPA with steroid treatment?
Decreased IgE by 33% after 6 weeks of prednisone
What leads to genetic susceptibilty to ABPA?
HLA-DR2, HLA-DR5
Name diseases caused by Aspergillus fumigatus
1) ABPA
2) Allergic asthma
3) HP (malt workers lung)
4) Invasive aspergillus (immunocomprimised)
5) Aspergilloma
6) Chronic necrotizing pneumonia
7) Allergic fungal sinusitis (nasal polyps, peanut butter sputum)
8) Heat tolerance
What are the components of the Asthma Predictive Index (API)?
Major Criteria (need 1):
--Parental asthma
--Diagnosis of atopic dermatitis
--Sensitization of aeroallergens

Minor Criteria (need 2):
--Sensitization to foods
-->4% eosinphils
--wheezing outside of colds
What is Lofgren's Syndrome?
in women with Sarcoid:

Erythema nodosum
HIlar adenopathy
Polyarthritis
What are the pro/con and examples of different methods of bronchoprovocation?
Non-selective:
--Increased sensitivity
--Direct - methacholine (high NPV for asthma), histamine, PGD2, leukotrienes
--Indirect - exercise, mannitol, hypertonic saline, cold air, eucapnic voluntary hyperventilation, adenosine monophosphate [AMP], propranolol

Selective:
--useful to confirm, but not rule out asthma (high specificity, low sensitivity)
--Immunologic - allergen
--Non-immunologic - ASA, NSAIDs
What increases risk for asthma mortality?
1) history of sudden severe exacerbations
2) history of intubation/ICU
3) hospitalization in last month
4) 2 or more hospitalizations for asthma in the past year
5) >/= 3 ED visits in last year
6) >2 alb inhalers/month
7) Poor perception
8) Alternaria + cockroach sensitization
9) African American or Latino
10) Low social economic status
11) Illicit drug use
12) Inner city
13) Psych co-morbidity
14) Current use of or recent withdrawal from oral steroid

ADAM33 - increased risk of bronchial hyperreactivity +remodeling
Describe airway remodeling in asthma.
Contributes to accelerate lung function loss in asthma.

No data supports treatment to prevent remodeling.

--> smooth muscle hypertrophy
--angiogenesis
--thickening of lamina reticularis (type 3 + 4 collagen)
--Mucus plug - glandular hypertrophy under influence of IL9
--Epithelial damage
What type of Occupational Asthma occurs with Platinum salts?
Platinum:

Immunologic Occupational Asthma - IgE specific for platinum

Smoking is a risk factor for Occupational Asthma in this group
What is the symptom progression for high molecular weight (HMW) vs low molecular weight (LMW) allergens?
Occupational Asthma

HMW Occupational Asthma is usually preceded by allergic rhinitis, LMW Occupational Asthma is not.
When is Asthma not well controlled?
Albuterol >2/wk
Asthma symptoms >2/wk
Night time symptoms 1-3/wk

Some limitation
FEV1 60-80%
ACT<20

2-3 exacerbations/year = not well controlled

>3 exacerbations/year = poor control
What physiologic changes occur in the lung during pregnancy?
Minute ventilation increases --> respiratory alkalosis (normal pH in a pregnant asthmatic = bad)

Lung volumes:
--increased TV
--decreased RV
--decreased FRC
What medications can/cannot be used during pregnancy for asthma?
Category B medications:
--budesonide
--chromones
--omalizumab (!)
--leukotriene modifiers (except Zileuton)

NO decongestants

Exacerbations - most common in wks 24-36
What are some major causes of indoor air pollution?
Biomass burning (tobacco, wood stoves, fireplace, gas stove) --> increased nitric oxide (NO)

Cleaning products --> volatile organic compounds (VOCs)
--increased benzene from dry cleaning --> increased risk of asthma

O3 cannot enter building, EXCEPT some electrostatic air purifiers give it off
What is the Air Quality Index (AQI)?
Based on 5 pollutants:
Particulate matter 2.5um-10um
CO
SO2
O3
NO2

(not Lead)
What are the effects of Diesel Exhaust Particles?
Allergens cling to diesel exhaust particles (DEP)
--act as adjuvant in healthy people --> increased inflammatory cells, increased neutrophils, increase IL6, IL13, IL8, VCAM, ICAM

In mild asthma
--increased methacholine response, increased airway resistance, increased IL6, increased IL10
What 6 pollutants have set standards?
1) Ground-level ozone (O3) - leads to asthma exacerbations, 24-36 hrs after exposure, increased neutrophils; peak on warm sunny nights (VOCs + UV light --> O3)
2) Particle pollution (particulate matter) 2.5 um - 10 um
3) Carbon monoxide (CO) - mobile sources
4) Sulfur dioxide (SO2) - bronchoconstriction, onset = 2 min, tachyphylaxis, nasal breathing = protective; point sources
5) Nitrogen dioxide (NO2) - airway inflammation, increased response to allergen, increased late phase to allergen, point sources
How do you use exhaled nitric oxide (FeNO)?
>20 ppb = asthma

Good NPV for asthma - normal FeNO , no asthma or well controlled

Good measure of adherence

False positive + (high FeNO): viral URI, AR, increased nitrate diet

False negative - (low FeNO): CF, smoking, pulmonary hypertension, EtOH, recent spirometry maneuvers
When should controller medications for asthma be started in children <4 years old?
1) 4 wheezing episodes in last year with + asthma predictive index (API)
2) Need symptom treatment more than 2 days/wk for >4 wks
3) Oral steroids x2 in last 6 mo
4) During seasons of previously documented risk
What are some Asthma susceptibility genes?
ADAM33 - metalloproteinase - increased risk of bronchial hyperreactivity + remodeling

CD14 - coreceptor with TLR4 for LPS; polymorphism of soluble CD14 (sCD14) --> influences Th1/2 balance - increased asthma, decreased IgE (?)

Chitinase - (chitin found in fungi and arthropods) - area of interest

Chromosome 5q (B2-adrenegric receptor) - Arg-Arg - regular SABA use --> risk of death, no LABA influence
What are the lower airway changes in Asthma and COPD?
What are the causes of Eosinophilia?
I AM SAD HELP

G(I) - EGIDs

Allergy
Malignancy - Hodgkin's lymphoma

Skin - atopic dermatitis, pemphigoid
Arteritis - Churg Strauss
Drugs

Hematologic disorder - HES, mastocytosis
Endocrine - Addison's disease
Lung disease - ABPA, eosinophilic pneumonia
Parasites + HIV
What is a normal CD4/CD8 ratio in BAL, and what is it in some common disease states?
Normal CD4/8 = 2

Increased CD4/8 ratio:
--asthma
--sarcoid

Decreased CD4/8 ratio (<1)
--COPD
--hypersensitivity pneumonitis
What are Curschmann's spirals?
spiral shaped mucus plugs, associated with excess mucous plugs.

**Characteristic in asthmatic sputum
What are Creola bodies?
clusters of airway epithelia cells (ciliated columnar cells) sloughed from the bronchial mucosa of a patient with asthma.

**Characteristic in asthmatic sputum
What are Charcot Leyden crystals?
Charcot Leyden crystals made by eosinophils, colorless, needle shaped structures

**Characteristic in asthmatic sputum
Name 3 characteristic findings in asthmatic sputum.
Charcot Leyden crystals
Curschmann's spirals
Creola bodies
How does treatment effect a specific allergen challenge?
if on immunotherapy (IT) --> blocks immediate + late phase + hyperreactivity that follows

Chromones - block immediate + late phase

ICS - blocks late phase
Methacholine Challenge
excellent NPV for asthma

Exercise induced bronchospasm cannot be excluded by negative test (need exercise challenge)

False negative with elite athletes.

+ = PC20 <4 mg/ml
borderline = PC20 between 4-16 mg/ml

Blocked by:
--theophylline
--B agonist
--anticholinergics (hold tiotroprium for 48 hrs)

Not blocked by:
--antihistamines
--chromones
--antileukotrienes

+ test w/o asthma:
--AR
--family history of atopy
--asthmatic siblings
--COPD
--CF
--viral URI
--smokers
--recent exposure to allergens
Mannitol challenge
+ test = FEV1 decreased by 15% at cumulative dose <635 mg

On ICS --> negative test --> can check compliance

Blocked by B2 agonist, chromones, LTRA, antihistamines

Mannitol is associated with leukotriene and prostaglandin production

Indirect challenge
What is Exercise Induced Bronchospasm (EIB)?
EIB diagnosed by decreased FEV1 >/= 15% after exercise challenge

OR

hx + bronchodilator response

Cannot be excluded by negative methacholine/histamine challenge
Vocal cord dysfunction (VCD)
Functional airway obstruction, stridor

Associated with psych, GERD, asthma, irritants

FEF50/FIF50 = increased in VCD, decreased in asthma

Treatment - pursed lip breathing (Speech), heliox, topical lidocaine, Botox to vocal cords

Vocal cord anatomy:
posterior cricoarytinoids abducts
lateral cricoarytenoids adducts
What happens with Trimellitic anhydride (TMA)?
Occupational asthma/disease

TMA - used in plastics, resins, coatings

Low molecular weight sensitizers - needs a carrier

TMA flu - late respiratory systemic syndrome, pulmonary disease, anemia
What is Plicatic acid?
Sensitizers for occupational asthma in Western red cedar mill workers

Activates complement
What is Diisocyanate?
Occupational asthma

found in spray paints, adhesives, body, insulation

Can be an immunologic or non-immunologic sensitizers
Hypersensitivity Pneumonitis
history of exposure + precipitating abs (confirms only exposure)

improves with cessation of exposure

PFTs - restrictive, decreased TLC, decreased FVC, decreased DLCO

CXR - recurrent/fleeting infiltrates mid/upper lungs

BAL or biopsy (for diagnosis) - poorly formed non-caseating granulomas near bronchioles (T cell)

Increased CD8 --> decreased CD4/8 ratio (compared with sarcoid which has increased CD4 + increased CD4/8 ratio)
Sarcoidosis
Systemic inflammatory disease that can affect any organ.

CXR/CT Stages
--Stage 1: bihilar lymphadenopathy
--Stage 2: bihilar lymphadenopathy and reticulonodular infiltrates
--Stage 3: bilateral pulmonary infiltrates
--Stage 4: fibrocystic sarcoidosis typically with upward hilar retraction, cystic & bullous changes

BAL - CD4/8 ratio --> 8:1 (normal 2:1)

Labs:
increased ACE, ESR, Ca2+, IgG

Lofgren's syndrome - erythema nodosom, hilar adenopathy, polyateritis, which affects women with sarcoid