1. peak expiratory flow- flow rate
2. spirometry- lung volumes & rates
3. bronchoprovocation- airway reactivity (hyperresponsiveness)
4. plethysmography- lung volume
5. puls oximetry/diffusion capacity testing & arterial blood gases- gas exchange

1. neutraphils (typically in severe cases)
2. eosinophils, lymphocytes
3. mast cells
4. epithelial cell injuryy

1. airway smooth muscle constricts
2. inflammation leading to tissue edema causing the airway to shrink
3. mucus (small amount but blocks the allready narrowed airway)
4. over time collagen will deposit thickening the basement membrane
5. vascular dilation of the eipithelial layer

allergic and non-allergic triggers

inflammatory cells

inflammatory mediators

airwat cells and tissues

IgE

inflammation

airway construction

airway hyperresponsiveness

mast cell activation

inflammatory cell infiltration

eosinophils

B lymphocytes/TH2-like cells

macrophages

tissue edema

neutrophils (typically in death)

denuded airway epithelium (sloughing)

airway remodeling

airway inflammation (major) dysfunctional neuroregulation

structural changes

cigarette smoke

occupational dust/chemicals

environmental tobacco smoke

inddor outdoor air pollution

infections

genes nutriotin

age

socio-economic status

air way remodeling

shit ton of mucus enlargement of mucus secreting glands

mucousal rigidity/thickening

increased muscle tone

scarring of bronchial wall

ciliary loss

obstruction (leading to air trapping)

ALv macrophage

epithelial cells (slough off)

Cd8 cell (TC1)

neutrophils

80% due to infections

20% non-infections environmental noncompliance with drugs

• activates macrophage, which recruite neutraphil, which then secretes elastin causing elastse to degrades elastin causing the emphasemia pic
• another path is smoking releases oxidents and free radicals, (the macrophage causes a releases of H2O2), bothe od the prior two will lead to oxidazes of alpha antitrypsin which inhibits elasatase

centrilobular

panlobular (senile emphysema)

iniitially more the alveolar are preserved till the fenestrationis enlarge (these fenestrations develop in the walls initially

more common in men and is usually associated with chronic bonchitis

• this is the distal destruction  (aveoli's)
• os the end stage centilobular disease
• may not be true emphysemia since no clinical loss of impaired lung
• is not common, but is charecteristic of primary emphesema

• this is a genetic disorder, where 1/3 patients will develop emphysema as young adults (still needs concomitant factors)
• causes inhibition of neutrophil elastase

infection

right sided heart failure (Cor pulmonale)

ulcer

pneumothorax

arrhythmia

stimulation of RBC synthesis

coma

altered behavior

seizures

FEV1/FVC < 70%

FEV1 > 80% predicted

FEV1/FVC < 70%

50% < FEV1 < 80% predicted

FEV1/FVC < 70%

30% < FEV1 < 50% predicted

FEV1/FVC < 70%

FEV1 < 30% predicted

OR

< 50% WITH Chronic Respiratory Failure

(1) contraction of bronchial smooth  muscles

  (2) edema

  (3) mucus hypersecretion

inflammation

bronchospasm

mucous production

bronchoconstriction

beta 2 agonists

corticosteroids

methylzanthine

cromolyn

muscarinic antagonist

monoclonial antibodiea

leukotriene modifiers

reverse   bronchoconstriction irrespective of the contractile agent]

aside from beta two agonists what is another way to increase cAMP to cause bronchodilation

albuterol

biolterol

pirbuterol

terbutaline

bronchodilation for 4-8 hrs

formoterol

salmeterol

bronchodilation >12h

isoproterenol

metaproterenol

isoetharine

tolerance may affect b receptors on mast cells & lymphocytes   more than in bronchiolar smooth muscle;

     thus, lack of significant chronic antiinflammatory effects

theophylline

thebromine

cafeine

inhibits phosphodiesterase4

blocks adenosine (adenosine can produce bronchoconstriction)

the range 10-20 ug/ml

and you would use this in a patient who has poorly controlled symptoms

Ipratropium bromide (Atrovent) – short acting    

Tiotropium (Spiriva) – 24 hr duration of action

Affects bronchoconstriction caused by p-symp stimulation

  (occurs in asthma produced by irritant stimuli

  and allergy) ----  M3 receptor

inhibition of mast cell degranulation;   >     inhibit mediator release from bronchial mast cells;

  inhibit inflammatory response to allergens on eosinophils

  inhibition of parasympathetic & cough reflexes

they will bind to IgE and inhibit igE binding to mast cell t lymphocytes and macrophages

not used in acute attacks

inhibit degranulation of inflammatory cells

  decrease capillary permeability

decreasein accumulation in lung of basophils, eosinophils, etc

decrease in LT production & release

increase in  ­ b-AR synthesis [prevent & reverse b-AR desensitization

budesonide

fluticasone

mometasone

ciclesonide

beclomethasone

mast cells and basophils dgranulate to release

what kind of phases does anaphylaxis have

• can have one phase
• can have two phases (treated then goes into it again)
• can have a protracted anaphylaxis (extended over 24 hrs)

Urticaria/angioedema  88

Upper airway edema  56

Dyspnea/wheeze  47

Flush  46

Hypotension  10-33

pruritus of lips, tongue, and palate; edema of lips and tongue; metallic taste in mouth

flushing, pruritus, urticaria, angioedema, morbilliform rash, and pilor erecti; pruritus in unusual places (scrotum, vagina, ear) - ( > 90% of patients)

feeling of faintness, syncope, chest pain, dysrhythmia, hypotension.  (Shock: 10% of patients)

if they are having cardiac issues or respiratory issues

if you have 2 or more systemes involved

not used or not used properly or delayed use

people allow there epinephrine to outdate

cough

wheezing

breathlessness

especially if these are present at triggers (stron smells, animals etc...)

look ar severity

control

responsiveness

intermittent is>80%

mild is >80%

moderate it 60-80%

sever <60

• poor perceivers
• asthma history of intubation or icu admission
• 2 or more asthma hospitilizations in a month or>3 ER visits a year
• if they are filling more then 2 fills for short acting beta agonist
• drug use

• repiratory distress (can't speak right or walk), drowsiness nasal flaring, retractions
• severe exacerbation lung function below 60%
• if they don't respond to beta 2 agonist in promp and not sustained for 3 hours or no improvement after2-6 hours corticosteroid

• symptoms of asthma and ability of meds to control it
• asthma related to ER visists
• and related conditions
• things that effect severity like rhinitis/sinusitis

Asthma not controlled (persistent) if:

avoid triggers

don't begin immunotherapy

can try singulair

chlorphenrimne is drug of choice

avoid oral decongestants

consider cromolyn

acute is < 3 weeks

subacute is 3-8 weeks

chronic is >8 weeks

it acts centrally on the medulla to increase cough threshold

it is equipotent to codeine

it interacts with MAO's and can cause seratonin syndrome

• this works peripherally by numbing the cough reflex (this introduces a choking risk since you may lose gag reflex)
• works within 15-20 min

diphenhydramine

can use other sedating antihistamines like 1st generation)

}Antitussives

• avoidance measaures anti-inflammatory (every day control corticosteroids)
• bronchodilators (SABA for quick reliefe, quick onset anticholinergics, LABA in combo with corticosteroids) 
• systemic steroids (moderat to severe)

for beta agonists why use inhaled route

maybe swollowing the drug

too much, wrong technique

diuretics- hypokalemia

beta blockers

sympathomimetics-additive toxicity

MAOI and tricyclics

less effective

high rates of toxicity

must adjust doses for use

• it stunts by 1.54cm/year and they can catch up
• asthma can stunt growth
• if they are forced to take systemic steroids for acute exacerbation they will end up recieving more steroids

as a second line as an alternative to inhaled steroids

for moderate to severe disease

you can add on LABA

or less often add on leukotrienes

describre step2 therapy in

>12

ICS low dose or leukotriene cromolyn or theophylline

low dose ICS with a LABA

or medium strength ICS

alternative low dose ICS with leukatriene or (theophylline or zileuton)

medium dose ICS with LABA

alternative is to replace laba with either leukotriene theophylline or zileuton

ICS (high) + LABA

AND oral steroid

AND

Consider omalizumab if IgE allergy 

proper inhaler technique

adherance

be aware of any environmental changes

consider alternative diagnosis

symptoms

ER visits

risk factor exposure

monitor comorbidities

SABA

or use ipatropium

you use your PRN SABA or  ipatropium 

also use regular LABA, and roids

bronchodialator

if mucus turns green give antibiotics

if improved step down bronchodilators if not then you will give corticosteroids for 10 days

the pancreas and the lung

sweet glands (salty skin)

hepatobilliary

Genitourinary

is a mutlie system disease

sweat test (gold standard)

genotyping and neonatal screening

pancreatic enzymes, vitamins

flutter, vest

antibiotics

nebulizers

pulmozyme (recombinant human DNase)

hypertonic saline

bronchodilators

lung transplant