Pulm review Flashcards
Development stages
from lung bud (distal divirticulum)
Every Pulmonologist Can See Alveoli.
Embryonic stage, Pseudoglandular, Canalicular, Saccular, Alveolar
Embryonic stage
Embryonic stage (wk4-7): lung bud-> trachea-> bronchial buds-> main stem bronchi-> secondary Lobar bronchi-> tertiary (segmental bronchi)
Bronchi have hyaline cartilage
Broncioles have no cartilage, Terminal–> respiratory
Alveoli (capillaries and gas exchange
If theresa mistake–> transesophageal fistula
Pseudoglandular stage
Wk 5-17
Lung resembles gland, endodermal tubules–> terminal bronchioles surrounded by capillaries
Respiratory bronchioles and alveoli are NOT present, not compatible with life
Fetal respiration- fetus breathes in utero takes up amnion–>stimulates lung development and growth of respiratory muscles, important to growth in pseudoglandular phase
Oligohydroamnios- pulmonary hypoplasia, potters sequence, fetal kidney abnormalities
Canalicular phase
wk 16-25, terminal bronchioles divide–> respiratory bronchioles–> alveolar ducts
Respiration capable at the end of the canalicular phase airway diameter increases, pneumocytes start to develop
Type 1 are for respiration
Type 2 secrete surfactant to lower the surface tesnsion and keeps the alveoli open
Saccular phase
phase wk 26 to birth terminal sacs (primitive alveoli) form, capillaries multiply to prep for gas exchange
Alveolar period
Week36 to 8 years old
At birth, only 1/3 of alveoli are present , following birth theres an increase in the number of respiratory bronchioles and alveoli
Alveolarization and airspaces subdivide, new walls form septa
Bronchopulmonary dysplasia
premature babies need surfactant and O2 with mechanincal ventilation (they dont have surfactant and stong enough muscles to breath)
Ventilation and O2 can cause toxicity, alveolarization doesnt progress normally but during childhood they can do better
Pulmonary hypoplasia
oligohydramnios (potters sequence). congenital diaphragmatic hernia- defective formation of pleuroperitoneal membrane (leads to a hole in diaphragm, abdominal organs herniate into chest –> pulmonary hypoplasia Fatal
Broncho genic cysts
abnormal budding of foregut and dilitation of terminal/ terminal large, discrete, round fluid filled destension CXR asymptomatic
usually in mediastinum, contain clear fluid –> air when infected No communication of lungs, columnar ciliated
Pulmonary vascular resistance in utero is high, hypoxemia–> vasoconstriction at birth PVR goes down
Upper respiriatory tract and lower respiratory tract
Upper: nasal cavity, pharynx and larynx
Lower: trachea, brocni and lungs
Conducting zone
NO GAS EXCHANGE, large airways: nose, pharynx, trachea and bronchi
Filters, warms humidifies the air, anatomic dead space
cartilage and goblet cells–> bronchi, pseudostratified ciliary epithelium–> terminal bronchioles “mucociliary escalator”–> cuboid cells
Smooth muscles: sympthetic activation (beta 2) activation–> bronchodilation
Parasympathetic activation M3 –> bronchoconstriction
Respiratory zone
GAS EXCHANGE, respiratory bronchioles, alveolar ducts and alveoli
CUBOID in bronchioles–> simple squamous in alveoli
NO cilia, Alveolar macrophages clear debris and immune response
Difference between bronchi and bronchioles
Bronchi has cartilage: left and right primary, secondary/tertiary aka lobar or segental,
Bronchioles have NO cartilage: loular /large, terminal respiratory feed alveoli
Airway cells
- Goblet cells: secrete mucus (moslty glycoproteins and water) protects against particles and infections
- Ciliated epithelial cells: beating cilia moves mucus to epiglotis, so you can swallow it
- Club cells in bronchioles: non ciliated epithelial cells, secrete protective proteins, detoxify P450
- Trachea and bronchi cells: ciliated pseudostratified columnar cells and GOBLET cells
- Bronchiole cells: epithelium transitions to ciliated simple squamous cuboidal epithelial, and club cells
Resistance to air flow
UPPER airways (nose, mouth, pharynx): 50% Airway resistance LOWER airways- highest in medium bronchi (turbulent flow); lowest in terminal bronchioles- slow turbulent flow
ALVEOLI histology
small sacs, separated by septa, simple squamous Pneumocytes, gas exchange, surrounded by capillaries
Type 1 pneumocytes- vast majority of cells in alveoli, thin for gas exchange
Type 2 pneumocytes- produce surfactant, proliferate to form other cell types, key for regeneration after injury
Alveolar Macrophages- phagocytose foreign material, release cytokines and proteases
Surfactant when you exhale, alveoli shrink and want to collapse–> atelectasis, decreases efficiency for gas exchange. Surfactant prevents collapse: mix of lecithins–> DipalmitolPTcholine
Neonatal respiratory distress syndrome
Fetal lung maturity: lungs mature when adequate surfactant is present 35 WEEKS
Lecithin-sphingomyein L:S ratio both are 1:1 until 35 weeks, when the ratio is >2:1 its considered mature
NRDS: is a surfactant deficiency, increased surface tension–> alveolar collapse–> atelectasis, ground glass look, hypoxemia an increased CO2 due to poor ventilation, poorly responsive to O2 (lungs are collapsed, intrapulmonary shunting- no gas exchange)
Risk factors: prematurity, maternal diabetes (high insulin decrease surfactant) C section (decreases cortisol, decreases surfactant)
Complications: bronchopulmonary dysplasia (O2 toxicity, no alveolarization) patent ductus arteriosus– hypoxia keeps shunt open, Retinopathy of prematurity (O2 –> free radicals, neovascularization in retina, retinal detachment –> blindness
Treatments: BETAMETHASONE (Corticosteroid given to mom), direct surfactant administration
Foreign body aspiration
Commonly with peanuts and kids, Right lung is more common. Site of aspiration is the RIGHT lung (wide, less of angle, more verticle), right 60%, in main bronchus, sometimes in right lower lobe, Left 23% main bronchus small number in left lower,
Adequacy of effort and diffusing capability of membrane
Adequacy of effort- the volume of inspired air should be >90% of the largest Vital capacity
Diffusing capacity of membrane: volume of gas that diffuses per minute per mmHg 21 ml/min/mmHg norm
Lung volumes: Tidal volume Inspiratory volume Expiratory volume Residual volume Total lung capacity Inspiratory capacity Vital capacity Functional residual capacity
Capacity= is multiple volume
Tidal volume: air that moves into lung with each quiet inspiration 500 mL
Inspiratory volume: air that’s still breathed in after tidal inspiration
Expiratory volume: air thats expired out after tidal expiration
Residual volume: air after maximum expiration (expiratory volume) cant be measured by spirometry
Total Lung capacity: all air in lungs at maximum inspiration, Inspiratory reserve volume+ Tidal volume + expiratory volume + residual volume
Inspiratory capacity: air that can be inspired after tidal expiration, IRV + TV
Vital capacity: air that can be expired after maximum inspiration
Functional residual capacity: residual volume after quiet expiration (RV + ERV) volume when system is relaxed
Lung pressures
atmospheric pressure, alveolar pressure, intrapleural pressure, transpulmonary pressure
atmospheric pressure: 760 mmHg
Alveolar pressure (PA) pressure in the alveoli
Intrapleural pressure: pressure in pleural space
Transpulmonary pressure: Alveolar pressure-intrapulmonary pressure (need it to keep alveoli OPEN): Negative during normal quiet breathing, alveoli and lungs tend to collapse in on themselves, pull inward /recoild and need an outward force to keep the walls open. Chest wall tends to expand, creates a NEGATIVE pressure in pleural space–> you need to suck the alveoli open
PNEUMOTHORAX: TPP=PA-Pp in pneumothorax Pp goes from -5 to 0 the lung collapses in on itself
AIRFLOW and pressure changes (Quiet Breathing)
Inhalation: intrapleural pressure becomes more negative, alveolar pressure becomes negative airflows into the lungs
Exhalation: intrapleural pressure becomes less negative, alveolar pressure becomes positive, airflow out of lungs
Lung compliance
Decreased compliance issues, increased lung compliance issues
for a given pressure how much volume changes
Compliance: small amount of diaphragm effort, generates small pressure change across lungs, large volume change, easy to move air in and out
= change of Volume/ change of pressure
A non compliant lung: large amount of diaphragm effort to get a big pressure change across lung and only a small amount of volume change, harder to move air in/out-> decreases Functional reserve capacity
Decreased lung compliance: decrease FRC: Pneumonia, pulmonary edema, pulmonary fibrosis
Increased lung compliance: increased FRC: Emphysema (floppy lungs), Aging, surfactant
Emphysema
floppy chest, Increased FRC/lung compliance, increased volume in chest–> Barrel chest
Forced exhalation
when pleural pressure becomes positive, compresses airway pressure on alveoli-> positive pressure in airway pushes air out–> air flows from airways
Equal pressure point
why forced exhalation does not cause collapse/atelectasis
Pleural pressure= airway pressure, beyond the point the airway would collapse, but at that point there is cartilage preventing it from collapsing
Diseased lungs: equal pressure point, moves toward alveoli. Obstruction (bronchitis) more pressure drop, tmphysema leads to a loss of elastic recoli, collapses
COPD
Slow exhalation, prevents large rise in pleural pressure, forceful exhaaltion would increase pleural pressure, pursed lips–> increased airway and alveolar pressure, prevents collapse
Hemoglobin
Dissolved o2 equation
O2 transport- Dissolved O2 (determined by Henry’s law: PaO2 x solubility= Dissolved o2
Very small amount (2%) of total blood O2)
Bound O2= hemoglobin 98%, positive cooperativity
Right Curve shift: unloading of O2, releases R=Release,
Things that rise metabolic activity (increased CO2, decreased pH, increased temp, increased 23BPG_
Left curve shift: Latches on the O2, low metabolic activity, decreased CO2, increased pH, decreased temp and decreased 23BPG
Chronic hypoxia, CO poisoning, Methemoglobinemia
Chronic hypoxia: increased 23 BPG, COPD, High altitudes, anemia
CO poisoning: standard pulse ox, cherry red lips, normal < 3% smokers usually 10-15%, poisoning>15
Methemogglobinemia: oxidized iron Fe cant bind O2, –> hypoxia, anesthetics, Nitric oxide, Dapsone, Methylene blue Chocolate brown blood
pulmonary circulation pressure and O2 levels
low pressure system: systemic (120/80), pulmonary artery (24/12), walls of pulmonary artery are very thin, little smooth muscle, low resistance to flow, very distensible
Blood O2 levels: system (decrease PaO2)–> vasodilation to increase blood flow
in pulmonary: PaO2–> vasoconstriction decrease blood flow to non ventilated areas “hypoxic vasoconstriction”, shunts blood away from poorly ventilated areas, more blood to well ventilated areas, key for fetal circulation, low O2 constricts pulmonary arteries in womb–> dilate at birth
Gas exchange, perfusion and diffusion limited gas exchange
Inspired air in trachea- PO2=150 mmHg, PCO2 0 mmHg
Alveoli air in alveoli: PAO2= 100 mmHg, PACO2 40mmHg
Venous blood: Vein PO2= 40 mmHg, PVCO2 46 mmHg
Arterial blood PaO2= 90mmHg, PaCO2 40 mmHg
Perfusion limited gas exchange: gas transport limited by perfusion (blood flow) more blood flow–> more uptake of gas
Diffusion limited gas exchange: gas transport limited by diffusion
Diffusing capacity of CO (DLCO) test
measures the ability of lungs to transfer gas, essentially the patient takes up CO (diffusion limited gas). Machine measures the CO exhaled, Normal 75%- 140% predicted , severe disease if <40%
Emphysema: destruction of alveoli, decreases surface area
Fibrosis/pulmonary edema: thickness increases and distance
Resistance to blood flow, vessels in pulmonary vasculature
As blood moves thru pulmonary vasculature, 2 types of vessels: alveolar (capillaries), extra Alveolar (arteries and veins)
Increased lung volumes: crushes alveolar vessels–> high resistance, pulls extra-alveolar vessels open
Pulmonary hypertension
normal pulmonary Artery P=24/12, Males 10-14 mmHg,
considered Pulmonary HTN when mean Pulmonary HTN> 25 mmHg–> Loud P2 at upper left
Dyspnea, untreated –> COR pulmonale (Chronic high pressure in right ventricles, right ventricle hypertrophies, eventually dialates and fails, JVVD, lower extremity edema, hepatomegaly, death from heart failure, or arrythmia
Diagnosis made via right heart catheterization and non invasively by ECG and ultrasound
Pulmonary arteriosclerosis: PpA equations
thickened artery walls, proliferation of smooth muscle cells, thickened media, and narrowing of lumen
PpA= CO x PVR + PLA
Causes: high left atrial pressure “pulmonary venous HTN”, heart failure, valve disease
High pulmonary vascular resistance- pulmonary arterial HTN, hypoxemia–> vasoconstriction, COPD, sleep apnea, high altitiudes
Chronic pulmonary emboli, scleroderma, cocaid and idiopathic in females
Plexiform lesions: pathopneumonic of idiopathic pulmonary arterial hypertension, endothelial proliferation forms multiple tumors BMPR mutations
Ventilation/perfusion
Ventilation equation
ventilation= volume x frequency respiratory rate
500cc per breath x 20 breaths a minute = 10000 breaths of cc per minute
Alveolar ventilation= useful for gas exchange
Dead space ventilation: wasteful ventilation
Dead space: anatomy- volume of conducting portions of respiratory tract, nose, trachea
Physiologic- anatomic plus volume in alveoli that dont participate in gas exchange, includes functional dead space, insufficient perfusion leads to increased dead space, apex is largest contributor, increases in disease
Increased dead space increases CO2
Bohrs Dead space equation VD
Vd/ VT= (PaCO2- PeCO2)/ PaCO2
Vt= tidal volume
PaCO2= arteria; blood gas
PeCO2= exhaled air
Alveolar Ventilation equation
predicts alveolar CO2 Total Ventilation: TV= volume/min Volume IN is Slighly > Volume OUT due to O2 uptake Minute ventilation, alveolar ventilation= TV - dead space VA= Alveolar ventilation VCO2= rate of CO2 production PACO2= Alveolar CO2 TV= total ventilation Vds= Dead space ventilation K is a constant
PACO2= (VCO2 x K)/ VA = (VCO2 x K) / (TV -Vds)
3 major causes of increased CO2= increased Co2, decreased VA, incresed Vds
Alveolar Gas equation
Predicts Alveolar O2, PAO2= alveolar O2 PIO2= inspired O2, R= rate of exhalation CO2 production/ O2 consumption varies with diet, metabolic rate
PAO2= PIO2- PAO2/R
Lung perfusion
In upright position= blood flow distribution is uneven, caused by gravity at apex= lowest blood flow, base highest, same with ventilation but less change than perfusion
Ventilation/Perfusion V/Q ratio
V/Q ratio: alveolar ventilation/ pulmonary blood flow
NORMAL= .8
lowest at base, highest at apex
at apex highest V/Q–> increased PaO2 and PaCO2, Tb likes O2 where it lives
With exercise only venous blood changes
hypoxia
O2 delivery to tissues: depends on CO2 and O2 content, need both to be normal O2 content (mlO2)= (O2 binding capacity) (% saturation) + (dissolved O2)
Hypoxemia= decrease O2 content of blood
Hypxia= decreased O2 delivery to tissue
Ischemia= no blood flow
hypoxia w/o hypoxemia: HF, anemia, CO
HF (cant pump oxygenated blood to tissue), Anemia blood is oxygenated carrying capacity decreases, All Hb is staurated but theres not much Hb
CO= takes up Hb sites
Hypoxemia
defect in oxygenating blood, categorized by A-a gradient
norma A-a O2 gradient= 10-15
PAO2 from alveolar gas equation and Pa from blood gas
hypoxemia w/ normal A-a gradient
ALWAYS due to low Alveolar O2 content (low PA), decreased Oxygen content of air- high altitude, PIO2 at sea level 150 mmHg, in colorodo - 100 mmHg
Hypoventilation: decreased respiratory rate, reduced tidal volume, causes increased PACO2–> decreased PAO@ narcotics, NM weakness, obesity, improves with O2
Hypoxemia with increased A-a gradient
LOW arterial O2 content (PaO2), most primary lung diseases–> pneumonia, pulmonary edema
Diffusion defects, shunt, V/Q mismatch
Diffusion defects: decreased area (emphysema), increased thickness (fibrosis, and edema)
Shunting: no ventilation, venous –> arterial bypasses lung, not really improved with O2,
Mismathc, gets better with O2
Obstructive lung diseases
Air trapping, slow flow out, less air out
Decreased forced expiration (FEV1) , slow flow out in 1st second, decreased FVC (forced vital capacity, less air out)
Low FEV1/ FVC RATIO HALLMARK (ratio is less than 70%)
Chronic bronchitis, emphysema, COPDs, asthma bronchiectasis, alpha 1 antitrypsin deficiency, primary ciliary dyskinesia, kartageners syndrome, allergic bronchopulmonary aspergillosis
Chronic bronchitis
BLUE BLOATERS- enlarged heart and is placed horizontal
Chronic cough, productive of sputum, at least 3 months over 2 years
No other cause of cough present
SMOKERS
Hypertrophy of mucosecretory glands, REID index (thickness of gland/ total wall)> 50%
Can lead to mucous plug, increased risk of infection
poor ventilation of lung–> increased CO2 and decreased O2, hypoxic vasoconstriction, pulmonary HTN Right heart failure–> cor pulmonale
Clinical presentation: Cough, wheezing, crackles, dyspnea, cyanosis, Shunting –> hypoxemia O2 doesnt help
Emphysema
PINK PUFFERS- ventricle heart, depressed diaphragm
SMOKERS, too many proteases are created, overwhelm the anti proteases, upper lung damage
alpha 1 anti trypsin deficiency- ineffective- ineffective anti proteases, lower lobe damage
Destruction of alveoli: smoke activates Macrophage, recruitment of PMNS, release of proteases
Loss of elastic recoil, small airways collapse on exhalation, air is trapped in the lungs
Clinical presentation: Dyspnea, cough, hyperventilaiton weight loss, cor pulmonale, BARREL chest, upper lobe,
SMOKERS get centriacinar damage (the bronchiole portion of aciner), alpha 1 trypsin deficiency (PAN ACINAR damage the bronchiole and the alveoli)
COPD
Chronic Bronchitis, emphysema and asthma, DO NOT GIVE O2 because will lose the loss of the drive to breath
Alpha 1 antitrypsin (AAT) deficiency
inherited, Autosomal co-dominant
Decreased dysfunctional AAT, balances naturally occuring proteases
Proteases is an elastase in PMNs and alveolar Macrophages that stops it from destroying alveoli
LUNGS: Panacinar emphysema, imbalance between PMN and elastase inhibitor (AAT)–> lower lung damage
Liver cirrhosis- abnormal alpha 1 builds up in liver , only occurs in phyenotypes with pathologic polymerization of AAT in ER of hepatocytes
Asthma
REversible bronchoconstriction, usually due to allergic stimulus, type 1 hypersensitivity RXN
AIRWAYS hypersensitive, common in kids, associated with atopic rhinitis, eczema, may have family Hx of allergies
Triggers: allergens, stress, URI, exercise, cola, aspirin
Aspirin- exacerbated asthma asthma, chronic rhinosinusitis, nasal polyposis
Chronic asthma/ rhinusinusitus symptoms, acute exacerbation after ingestion of aspirin or NSAIDs, dysregulation of arachidonic acid metabolism, over production of leukotrienens, Treatment (LT receptor antagonist, monteleukasts, zafirlukast), I/E ratio is lowed, mucous plug
CURSHMANNS SPIRALS AND CHRO LEYDANOLUS
Bronchiectasis
Results of chronic, recurrent, airway inflammation, airways become permanantly dilatated
large airways dilates, small medium airways are thickened, recurrent infections, cough, excessive sputum production smells bad, bronchiectasis leads to hemoptysis, corpulmonale, amyloidosis, TUMOR, SMOKERS, CF, kertagners syndrome, allergic aspergillosis
Primary ciliary dyskinesia, kertagners syndrome
immotile cilia syndrome, cilia unable to beat, beat normally or absent, inherited (autosomal recessive), gene mutation in dyenin structure formation, dynein is a motor protein creates flow
Kertageners syndrome: chronic sinusitis, bronchiectasis, malinfertility, situs infersus
Allergic bronchopulmonary aspergillosis
HS type 1 to aspergillus, lungs become colonized with aspergillus, fumigatus
low virulence fungus, only infects immuno copromised
Asthma/ Cystic fibrosis pts
APDA ptients, increased Th2 CD4, synthesis interleukins, eosinophila IGa Ab, treat with steroids
Restrictive lung disease
Ratio is normal of (FEV1/FVC) because both are reduced.
Interstitial lung disease, dry cough, cant get air in –> less air out decrease FVC, decrease FEV1)
Causes : poor breathing mechanics and interstitial lung disease leads to decreased lung compliance, decreased lung expansion (during inspiration)
Poor breathing mechanics: not a pulmonary tissue problems, under ventilation of lungs, alveoli working Aa gradient normal neuromuscular problems (ALS POLIO MG) structural problems, (scoliosis and morbid obesity)
Interstitial lung disease (bilateral, diffuse pattern, small irregular, opacities, reticulonodular, honey comb appearance
DLCO (diffuces capacity (lung CO, normal= extralveolar, decreases interstitium)
Low DLCO conditions: interstitial lung disease, emphysema, abnormal vasculature, pulmonaty HTN, embolism, prior lung resection anemia
Idiopathic pulmonary fibrosis
most common idiopathic interstitial pneumonia, slow onset dyspnea, typically affect adults>40
Pneumoconioses
Coal minors lung: inhalation of coal dust: CXR small round nodules opacities, UPPER LOBES, simple<1cm, complicates> 1 cm with corpulmonale
Silicosis: inhaled silica from quartz, granite, sandstone, most US people, FOUNDRIES, Mines, Macrophages respond to silica–>inflammation/fibrosis, TB, no Macrophage killing, cancer, eggshell, Corpulmonale
ASbestosis: goes in bronchioles- inhalaltion of asbestos fibers, ship building/ roofing, plumbing, LOWER LOBES, (I) 3 clinical problems (interstitial lung disease, pleural plaques, lung cancer
Asbestosis
mainly causes Bronchogenic carcinoma (also mesothelioma is the only risk factor that includes asbstosis), occurs decades after exposure, pleural thickening, pleural effusion, slow onset of symptoms, (dyspnea, cough, chest pain) poor prognosis
Hypersensitivity pneumonitis
HS reaction to environmental Ag, agriculture dusts, microorganisms, (fungal bacterial protozoa)
Chemicals, mixed type 3 and 4 HS
Farmers lung, moldy hay, granier inexposure, also common in bird and pultry handlers
Diffese crackles, steroids exposure, chronic granuloma
Sarcoidosis
immune mediated granuloma all over the body
CD4 TH4 non caseating necrosis in the lungs, skin, eyes and heart
Hilar lymphadenopathy
Cough dyspnea infiltrates and fibrosis
Skin erythema nodosum, uveitis, hypercalcemia, (Vit D) high AC levels Af am females, steroids and immunosuppresants
pneumoconioses beryilioses
Beryillium in nuclear and airspace, granulomatous inflammation like TB sarcoidoses, complication corpulmonale and lung cancer
Cystic fibrosis
A form of bronchiectasis, inherited genetic diseases, AR both parents carry it, thick sticky mucous in lung and GIT
Kids disease
Diagnosis via sweat chloride test, pilocarpine, nasal transepithelium, more negative
Cystic fibrosis Transmembrane Regulator protein Defect (CFTR), gene encodes, for abnormal protein, ATP ion transporter, epithelial cell function functions ( allows CL ou of ion channel), draws out Na H20, hydrates mucosa and mucus in lungs GIT
F508 abnormal folding, CFTR cant get to the membrane
Thick mucus in lungs, recurrent pulmonary infection, pseudomonas, S aureus, chronic bronchitis, and bronchiectasis, impaired flow bile and pancreatic secretions, malabsorption of fats
Pancreatitis and diabetes (meconum ileus, abdomnial distensionvomiting and clubbing,
DNAse is a good treatment, Ivacoftor gets the CFT up there
Omalizumab
asthma
IgE binder, prevents mast cell degranulation used for sever asthma despite high dose steroids and dilator
Beta 2 adrenergic agonists
asthma
RElax airways via smooth muscle dilation
SABA: Alburterol immediate reversal of obstruction
LABA: salmetorol and formoterol
Never use a LABA alone
Theophyllines
asthma methylxanthine MOA (non selective inhibitor of Phosphodiesterase receptor antagonist of aadenosine
SE: headache, tachycardia, arrythmias and seizures
Steroids
asthma
Prednisone only for asthma thats really bad, ICs 1st line for mild asthma
Steroids and Beta 2= better than mutually beneficially
Leukotriene modifiers
asthma
add on therapy, monteleukast anatgonist of cys L 1 receptor
zileuton 5 LO enzyme inhibor
Mepolizumab
asthma
anti IL 5
COPD treatments
SABAs, anticholinergics (ipratropium), short
LABA s can actually be used as a monotherapy, anticholinergics (tiotropium- long acting)
ICS (fluticasone and budesonide)
Anticholinergics decrease mucus secretion and relaxes airways, SE dry mouth blurred vision,
ICSs are better than asthma for COPD
Cystic fibrosis treatments
antibiotics and anti inflammatoroy and bronchodilators
DNAase alpha- inhaled infiltrating PMNS release thick DNA, dnase breaks it up
IVACOFTOR- G551D mutation, opens chloride channel
LUM-IVACFOTR: gets the channel up to the membrane
