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Flashcards in Respiratory Deck (86):

Conducting Zone

Trachea, Bronchi, Bronchioles, terminal bronchioles
-No gas exchange
-Cartillage to Bronchi
-All lined with pseudostratified ciliated epithelium
-Goblet cells to Bronchi
-Clara Cells in bronchioles


Clara (Club) cell

Secrete GAGs, toxin degredation, can divide into pseudostratified epithelium
-Large ER secretory capacity


Respiratory Zone

Respiratory Brochioles (Cuboidal Epithelium)
-Alveoli squamous and cubidal


Type 1 pneumocytes

Make the majority of the surface of lung. Simple Squamous


Type 2

Secrete surfactant, clusters, cuboidal
-Also can divide in response to injury


Collapsing pressure

Surface tension/radius
-Smaller radius means more likely to collapse. Residual volume prevents collapse



Amphipathic and reduces hydrogen bonds and surface tension, decreases collapsing pressure
-Phosphatydlcholine most common
-2:1 phosphatydal choline to sphingmyelin ratio signals maturity
-Begin production around 26 weeks and complete by 36 weeks.
-Prematurity means immature lungs. Can give steroids to increase maturity


Diaphragmtic structures

IVC at T8 in central tendon
-Esophagus, vagus at T10
-Aorta, thoracic duct, aygous at T12


Lung relations

R bronchus is straight down, more likely to lodge in left lower lobe


Bronchi to pulmonary artery

Right side has three lobes so pulmonary artery is anterior to bronchi
-Left side has 2 lobes, so artery is superior to bronchi


Accessory respiration

-External Intercostals, Scalene, SCM: Inspiration
-Internal Intercostals, abdominal : Expiration


Anatomic Dead Space

-Volume of air in the conducting zone,
Does not participate in gas exchange


Physiologic Dead Space

-Volume of air in the alveoli that does not particiate in gas exchange
-generally from V/Q mismatches


Total Dead Space Calculation

-If perfect ventilation and no dead space, all alveolar CO2 will be expired CO2. In realiy, anatomic and physiologic dead space dilute the expired air
-Must make assumption that PaCO2 = PACO2
-Equation will be: (PACO2-PECO2)/(PACO@) essentially a dilution factor
-Using assumption allows for practical measurment
-(PaCO2-PECO2)/(PaCO2) * Vt
-There will always be dead space, so PECO2 will always be less than PaCO2


Alveolar Ventialation Equation

-Remember that PACO2 = PaCO2
-Under steady state, PaCO2 is inversely proportional to alveolar ventilaiton rate. All CO2 produced is ventilated (Steady state assumption)
-PAO2 or alveolar oxygen deliver is thus dependent on alveolar ventilation and inspired oxygen concentration
-More rapid ventilation (Hypervetilation) leads to drop in PaCO2 and
-Slowed or hypoventilation leads to increased PaCO2
-A correction factor is uniformaly provided

-PAO2 = PIO2 - (PaCO2/.8)


Lung and Chest Wall

-Elastic forces predominate, combination of system
-X interept is FRC, point where atmospheric and lung pressures are equal, end expiration of tidal volume.
-All graph motions are a function of the tissue to behave independently of external forces
-Lung always wants to collapse, chest wall changes
-At FRC tendency is for chest wall to expand and lung to collapse and forces are balanced (Highest blood flow)
-At a forced expiration the tendency of the chest wall to expand will be even more and the system will expand
-At forced inspiration, the chest wall is strethed more than it is comfortable with and will have a compressive force leading to exhalation



-Chest wall curve is more or less fixed
-Compliance of lungs can chage
-Compliance defined as volume change for a given unit of pressure change
-Increased compliance as seen in emphysema will lead to decreased compressive forces of the lungs and a higher FRC
-Decreased compliance as seen in restuctive lung disease will cause an increase in collapsing force and drop in FRC


Airway Resistance

R= nl/r^4
-Largest radius is in smaller airways because of large numbers
-Medium radius in traches
-Smalles radius in medium sized bronchi
-Larger lung volumes also have larger radius and have decreased resistance to flow
-Small lung vlumes have increased resistance to flow
-ANother purpose or residual volume



-Methemoglobin is Fe 3+ and can't bind O2. Oxidizing drugs (nitrates and sulfonamides)
-HgF has decreased affinity for 2,3BPG and leads to increased O2 affinity


Dissociation Curves

-COoperative binding allows sigmoidal curve
-R is relaxed and capable of binding O2, T is taught and lower affinity for O2
-In tissues pushed into T form by (H-deoxyhemoglobin, CO2-carbamino, increaesed T, increased 2,3BPG) altidude causes increased in 2,3 BPG
-In lungs exchange leads to opposite effects
-CO binding to O2 leads to a left shift because of cooperativity of O2 and CO occuring at a lower O2 concentration, but the shift will also be pushed down beause binding sites are occupied


CO2 transport

-Minor portion is dissolved
-Some in carbamino form which will decreasd O2 affinity
-Majority as bicarb. CA catalyzed reaction. HCO3 leaves the cell in exchange for Cl (Band 3), H stays in cells and is buffered by deoxyhemoglobin
-Reverse occurs in lungs
-In tissues H+ and Cl into cells and HCO3 out of cells, opposite occurs in lungs


Lung Embry

Conducting zone develops first with the respiratory later
-Alveoli are prodced during saccular phase and mature during alveolar phase
-Surfactant secretion mature at the end of sacular phase around 36 weeks


TE Fistula

Associaed with VACTERL
-Midline Defects
-Vertebral, Anal atreais, cardiac, TEF, renal, limb


Congenital Diaphragmatic Hernia

-Failure of left pleuroperitioneal folds to close
-GI into thorax and lung hypoplasia occurs


Hyaline Membrane Disease

-Premature infant without surfactant leads to widespread atelectasis
-Fibrin cellular debris and red cells make up hyaline membranes
-Give steroids and surfactant



Right anterior and Left superior. Is the relatinship of the pulmonary artery to the bronchi


Diaphragm structures

T8 is IVC
T10 is esophagus and vagus
T12 is Aorta, thoracic ducts, and azygous


Intercostal NAV

NAV from inferior to superior. Wil hit nerve first, artery closest to the rib
-Do thoracocentsis on upper border of rib



Superior coanae is respiratory epithelum
-Sensry cells are bipolar and can regenerate


Pulmonary vascular reistance

-At high lung volumes arteries will be compressed by alveolar pressure
-At low lung volumes there will be inadequate traction and closure (Atelectasis has closed arteries, kinda)
-Best flow is at FRC, atomospheric pressure leads to minimal compression from either
-Contriction with acidosis, endothelin and SANS
-Dilation with PG, NO, PANS, His


Respiratory control

Apneustic and chemotactic centers in pons
-Medullary centers integrate information


Obstructive Diseaes

Characterized by increasing TLC (air trapping) and decreased FEV1, FVC, and FEV1/FVC ratio
-Can see pulsus paradoxus


Chronic Bronchitis

-Caused by longterm bronchiole iritation leading to mucus cell hyperplasis (in bronchioles) Ried Index
-Hypermucus secretion leads to narrowing of Bronchi and high resistance to flow, air trapping may occur
-Mucus causes hypoventalation and there is often times hypoxemia (Blue Bloaters)
-Hypoxemia induces vasoconstriction leading to cor pulmonale
-Also mucus predisposes to infection
-Treatement can be supplemental O2 to decrease hypoxic vasoconstriction and decrease cor pulmonale
-Also can treat with steroids for acute attack and albuterol too
-DLCO will be normal
-Hypoventalation leads to VQ mismatiching and hypoxemia, can be corrected with O2



-Destruction of parenchyma of lung due to imbalance in pro elastase and anti-elastase functions
-Panacinar associated with congenital decrese in alpha 1 antitrypsin (Piz is mutatnt, heterozygote is risk, homo wil get, often accompanied by cirrhosis) will see PAS positive misfolded proteins in ER of Hepatocytes
-Cetnriacinar: chronic inflammation from smoking leads to destruction of lung parenchyma
-Destruction leads to loss of elastic recoil and increaed compliance
-Destruction also leads to loss of radial traction
-Combination leads to an obstructive pattern
-Parenchymal loss leads to decreased surface area, so there will be impaired DLCO
-Pink puffers do not get hypoxemia because of loss of vasculature along with alveoli
-Treatment is stop smoking and beta 2 agonists can be helpful for some patients.
-Patietns will breathe through puresed lips. This will decrase resistance to flow because airway radius is increased. It will also prevent collapsing as radius is increased



-Airway hyperresponsivness leads to trigger mediated smooth muscle constriction and arteriolar dilation leading to obstructive pattern
-Inflmmatory mediators such as histamine lead to vasodilation
-Leukotrienes lead to bronchoconstriction
-Chemotactic and cellular infiltrate lead to direct damage
-Can see mucus hyperplasia at times
-Crushman spirals are sloughed epithelial cells and Charcot-Leyden Crystals are MBP crystals
-Vasodilation: NO, His, PGE
-Growth factors lead to smoth muscle hypertrophy
-Can be diagnosed with methacholine challenge


ASA asthma

-ASA leads to imbalance in AA pathway and favors leukotrienes, leads to increase contriction C-E
-Also commonly see nasal polyps


Beta 2 agonists

-Albuterol is short acting
-Salmeterol is long acting
-Avoid non-specific beta blockers in heart treatment



-Ach Muscarinic antagonist


Inhaled steroids

-Decrease inflammatorry mediators
-Inhibit NF-KB leading to decreased B cell response
-Stabalize mast cells
-Decrease cytokines
-Long term use can cause glaucoma, cataracts, HTN, osteoporosis, etc



PDE inhibitors, rarely used because of narrow theraputic index



Stabalize mast cell membranes



Blocks leukotriene receptors
-Used for ASA asthma



-Blocks leukotriene synthesis



-Binds circulting IgE and prevents attachment to mast cells



-Chronic necrotizing inflammation in bronchi leads to dilated bronchi
-Productive of purlent sputum and hemoptysis
-ABPA, CF, KArterengers, Tumor, Smoking
-Can give patietns antibiotics to prevent future infection and also can give DNAses to losen sputum
-On physical exam very localized breath sounds will be heard


CF bugs

-S Aureus, PSeudomonnas, H Flu


Restrictive lung disease

-Decreased lung capacity with decreaed vital capacity and relatively spared FEV1
-Mechanical - normal Aa
-Interstitial increased Aa






Drugs: (Bleomycin/busulfan, amiodarone, MTX)



-Seen in coal miners
-Presents with DOE with restricive pattern, generally in upper lobes
-Main consequence is hypoxic vasoconstriction and cor pulmonale



-Mining, sandblasting, etc
-Silica depostis that become fibrosed in upper lobes
-There will be calcified hilar lymph nodes
-Increased risk of bronchiogenic carcinoma
-Also prevents phagolysosomal fusion and increases risk of TB



-ASsociated with aerospace or electronics
-Granuloma formation around beryllium, can look like sarcoid



-Ferruginous bodies inside macrophages of lower lobes
-Restrictive pattern from cytokine release
-Increase risk of carcinoma and mesothelioma, with smoking is massively increased
-Pathognomonic calcified pearly white pleural plaqes which are not cancer


Neonatal respirartory distress

-Alveoli form during saccular period from 24 weeks to 36 weeks
-Prematurity leads to immature type 2 pneumocytes that can't produce surfactant leading to atelectasis and dilation
-Increased risk with prematurity. C-Section (lack of steroids), DM mother, insulin inhibits
-Can give intrapartum, prepartum steroids to increase maturity (give to mother)
-Can give surfactant
-After birth, O2 is usually required. Can cause retinopathy of prematurity and bronchopulmonary dysplasia
-NO can also be given with surfactat to dilate
-Low O2 tension will keep PDA open (maintains PGE secretion)
-CXR wil show diffuse ground glass appearance of atelectasis
-Heavy lungs because of increased fluid in capillaries
-Pathology will show immauter type 2 cells with hyaline membrane composed of exudated fibrin and RBC



-Many causes including pancreatitis and trauma
-Initial insult is from neutrophils which cause damage and increased permiablity of alveoli
-Exudation of fluid and firbin etc leads to pulmonary edema and hyaline membrane formation
-Leads to atelectasis and increased Aa gradient
-Diffuse alveolar damage with atelectasis and accumulation of fluid throughout lungs
-Type 2 pneumocyte damage leads to loss of surfactant and if cured impaired healing and fibrosis
-Check PCWP to rule out left failure as cause of exudates



-Noncasseating granulomas systemically, usually appear first in the lungs
-Look for african american femal
-Hilar lymphadenopathy
-Increased Ca (Vitamin D) and ACE levels
-Uveitis, Skin changes are common
-TX: steroids



-Very common cause
-Usually occurs in middle aged female and progession is inevitable
-Ground glass appearance of chest CT



Type two hypersensitivity to type 4 collagen in pulmonary and renal basement memrane
-Hemoptysis and RPGN
Tx: Plasmaphoresis



-Necrotizing small vessel granulomatous vasculitis leading to RPGN, Hemoptysis, Nasal bleeding
-Tx: Steroids


Eosinophilic Pneuomia

-Increased Eosinophils and restrictive pattern
-Tx steroids


Hypersensitivity pneumonitis

-Farmers lung, pigeon breeders lung
-Mixed type 3 and type 4 hypersensitivity
-Leading to progressive damage and may become bronchiectasis and restricitve pattern
-Will resolve with removal of antigen


Sleep Apnea

-Central: Lack of respiratory drive
-Obstructive: obesity and snoring
-Both will show increased daytime somnolence, can switch to O2 mediated respiratory drive
-Polycythemia could predispose to bud chiari
-pHTN, systemic HTN, arryhmias and death


Pneumothorax and atelectasis

-Atelectasis is alveolar collapse without collection of air
-Pneumothorax is rupture of lung parenchyma that leads to accumulation of air in pleural space
-Tension pneumo, sucking wound that causes tracheal deviation away from lesion, emergency thoracotomy is necessary



-Occurs in the deep vein legs (femoral, not saphenous)
-Can dislodge and cause PE (Majority of PE) or can cause paradoxical stroke due to PFO
-Hypercoagulable: Factor V Lieden, ATIII (Mutation or loss in nephrotic syndrom), Prothrombin 20210 (Upstream mutatino leads to increased expression), PNH (GPI anchor, inflammation and setting off cascade), Oral Contraceptives (especially with smoking and previous event), antiphospholipid
-Endotheilial damage: Turbulent flow
-Stasis: Surgery or long drives/plane flights



-Most common cause is DVT as stated above
-Can also be Fat (Fracutre), Amniotic (Can cause DIC), Gas (Caissons/diving), Tumor, Bacterial (Staph Tricuspid in IV drug user)
-Most are clinically silent, but larger defects can cause infarction
-Dual blood supply so smaller ones are inconsequential
-Large ones have a wedge shaped area of hemorrhagic necrosis (Bronchial Artery dual supply)
-Saddle will cause electrical mechanical dissociation
-Physical exam may show localized changes in breath sounds, Loud P2 with parasternal heave, JVD, Friction rub from fibrinous exudate
-V/Q mismatching, areas of hyperventialation leading to hypocapnia from blowing off, ventialtion with minimal perfusion


Primary pulmonary hypertension

-Most commonly occurs in females and is due to mutations in BMPR2 and TGF-beta signalling that causes smooth muscle hypertrophy and vascular constriction, endothelial dysfunction
-Treat with NO, PGE, Endothelin antagonists, Sildenafil (PDE inhibitor), O2


Secondary pHTN

-Many causes
-Cor Pulmonale, hypoxic vasoconstriction
-Organizing clots
-Valvular disease
-Left heart failure


Lung Cancer

Most common cause of cancer death in the US
-Highly metastatic and cause significant local destruction
-Hemoptysis, DOE, bronchial obstruction
-generally present with a non calcified coin lesion that wasn't seen on previous X rays
-Smoking is main risk factor as is asbestos and silicosis
-Metastasis to lungs is common
-Lung commonly metastasizes to adrenals resulting in addisons adrenal failure
-Also metastasize to liver and bone



-Most common
-Most common in female smokers and nonsmokers
-Located at lung periphery and is an adenocarcionma with mucin cells
-Better prognosis than most
-Associated with K-Ras mutations
-Presenting sign is usually due to parenchymal destruction and hypoxemia leading to clubbing



-Subtype of adenocarcinoma that appears like pneumonia with a diffues interstitial thickening
-Good prognosis and responds to chemo


Squamous Cell Carcinoma

-Very common and seen alomst exclusively in smokers
-Centerally located cavitary lesion
-Requires squamous metaplasia
-Most commonly arises from the bronchi and can cause local obstuction
-Metastatic and poor prognosis
-Will have keratin pearls and intercellular bridges
-Associated with PTHrP and hypercalcemia
-Commonly metastasizes first to hilar nodes
-Presents as hilar mass
-Also often presents as a caviatry lesion


Small cell carcinoma

-Centrally located and highly associated with smoking
-Small poorly differentiated oat cells with high nucelar to cytoplasm ratio
-Neuroendocrine in origin and chromogranin positive
-SIADH, ACTH, Lambert Eaton
-Highly metastatic and surgery is not possible
-L-Myc associated


Large Cell Carcinoma

-Large anaplastic an pleomorphic cells located peripherally
-Surgical resection is possible if caught early, but poor prognosis


Bronchial Carcinoid

-Neuroendocrine origin arises from bronchus, chromogranin positive
-Rarely malignant and causes mass effect but not metastasis
-May cause carcionoid syndrome



-Tumor of mesothelila cells highly associated with asbestos and smoking
-Pleural adhesions leading to hemorrhagic effusions
-Poor prognosis
-Psamomma bodies


Pancoast Tumor

-Located in superior pole of lung
-Causes shoulder pain and compresion of superior cervical ganglion leading to horners syndrome


Superior Vena Cava syndrome

-Tumor or thrombosis on indwelling catheter leads to SVC blockage
-Drains upper limbs and face, backup leads to venous congestion and cyanosis
-JVD is also present and present with headache and dizziness
-Surgical emergency due to increased ICP and risk of anyeurism or rupture


laryngeal Carcnoma

-Benign nodules seen in singers and heavy smokers
-Benign growhts associated with HPV 6,11
-Malignant SCC associated with HPV 16,18


Lobar Pneumonia

-Most commonly cause by strep pneumo, klebsiella
-Lobar involvment with effusion possible and localized consolidation and breath sound changes
-Exudate into alveolar spaces leads decreased ventilation, also there is inflammatory vascular dialtion leading to V/Q mismatches
-Strep pneumo is gram + diplococcus, rusty sputum
-Klebsiell: increased risk with diabetics and alcoholics, currant red sputum, can cause abcesses and is risk of death, Aminoglycosides. Currant jelly sputum due to thick capsule


Bronchial Pneumonia

Patchy infiltrates that involve more than one lobe
-Inflammation and infection is localized to the bronchioles
-Commonly occur post flu infection
-Staph aureus: Can cause abcesses and disseminate to brain etc. Treat with vanco. Seen nosocomial and post flu. Can also spread hematogenously from endocarditis in IV drug users
-Klebsiella can cause this too
-H FLu, common after flu and also in kids
-Psedommonas: CF and nosocomial causes hemorrhage and necrosis leading to bronchiectasis
-Moraxella also possible


Intersitial Pneumonia

-Diffuse patchy infiltates in all lobes, does not involve bronchioles or cause exudate, stays in sepatae. Therefore a more indolent course
-Mycoplasma pneumonia is most commn: no cell wall, macrolides, cold agglutanins
-Legionalla: water supply, high fever and GI pain with penuomina. CYBE, SIADH, needs iron and cystine for grwoth, silver stain, intracellular. macrolides
-Adenovirus: military recruits
-CMV: Tranplants
-Coxiella: Fever and sheep exposure
-Chylamydia: Second most common, obligate intracellular, lives in epithelial cells
-Measles (Rubeolla)-gian cell pneumonia



Intralveolar cysts
-Diffuse infiltrates on CXR



-Candida: Rare, and only occurs with hematogenous spread in immunocompromised patients (neutrophils)
-Histoplasmosis: Common and assymptomatic, intramacrophages. Midwest caseating granuloma, splunking disease
-Blastomyces: Chills and fever with pulmonary symptoms, broad based budding yeast, great lakes area. Can disseminate to skin, bones, etc
-Cocciodes: fever, GI pain, headache, flu like symptoms: Spherules in southwest
-Cryptococcus: Mild symptoms in AIDS patients, worry is dissemiation and meningitis, pigeon droppings, latex agglutination
-Aspergillus: Branching yeast that commonly colonizes cleared spaces. Fungus balls in cavitary TB. Also causes BPA (invasion and 45 degree branches into spaces)



-Primary infection is a ghon complex with a casseating granuloma in the periphery or lower lobe
-Secondary infection reactivates in upper lobes
-milliary is disseminated



Dissemiated non TB disease in AIDS patients
-Prophylax with azithromycin


M Kansasii

-Can cause a TB appearing disease that is not TB