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74 Cards in this Set

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PFTs in COPD:
dec FEV1, inc FVC ==> dec FEV1/FVC ratio
extent of ciliated mucosal epithelium in respiratory tract
nose to terminal bronchioles
what protects alveoli from inhaled particles?
ciliated epithelium -> mucociliary clearance
pathogenesis of centriacinar emphysema
oxidative injury to resp bronchioles --> PMN recruitment --> elastase, proteinase, cathepsin, and MMPs released , along with oxygen free radicals which --| alpha1antitrypsin ==> protease-antiprotease imbalance --> acinar wall destruction
clearance of differnt sized particles from resp tract
10-15 um: trapped in URT; 2-10um: mucociliary xport; <2um (eg dust): phagocytosed by macrophages --> cytokine rleases --> tissue injury, inflammation --> fibrosis ==> PNEUMOCONIOSIS
3 causes of pulmonary hypertension
1) hypoxic vasocnstriction (eg following COPD); 2) volume overload (left heart, eg in decomensated cadiac disorder); 3) idiopathic dysfunction of the endothelium --> impaired apoptosis --> inc wall thickness
most common cause of lung abscess
aspiration of oropharyngeal contents (fusobacterium, peptostreptococcus, bacteroides); a/w LOC (EtOH, seizures, anesthesia)
clinical triad of fat embolism syndrome
1) hypoxemia (fat emoblus in lungs); 2) petechial rash (thrombocytopenia /petechiae from platelet adherence to and coating of fat microglobules; 3) neuro abnormalities (microinfarctions of brain tissue)
role of type II pneumocytes
1) secrete surfactant (dec alveolar surface tension); 2) presurcors of type I cells (proliferate during lung damage)
which lung more common for inhaled foreing bodies?
right lung (right main stem bronchus has less acute angle)
lobes of each lung
R: sup, middle, inf; L: sup, inf, Lingula, + space for heart
relation of pulm artery to bronchus at each lung
RALS (Right Anterior; Left Superior)
where do structures perforate the diaphragm?
"I 8 10 EGGS AT 12": T8: IVC; T10: EsophaGus + vaGus; T12: Aorta, Azygous, Thoracic duct
muscles of forced inspiration (3)
external intercostals, scalene muscles, SCM
muscles of forced expiration
"abs" + internal intercostals
diffusion limited
equilibrium not reached by the time blood reaches end of capillary -- seen in exercise, emphysema, fibrosis, and with CO
calculating physiologic dead space
V_D = V_T * (1 - PeCO2/PaCO2) = V_T * ( (PaCO2 - PeCO2)/PaCO2 )
changes in v/q with exercise
exercise --> vasodilation of apical arteries --> V/Q approaches 1
three methods of CO2 transport from tissue to lungs
1) as Bicarb (converted by CA) (90%); 2) bound to Hb as carbaminohemoglobin(5%); 3) dissolved CO2 (5%)
how does Hb unload CO2 in lungs?
Haldane effect: oxygenation of hemoglobin --> release of CO2
how does O2 get unloaded in the tissues?
tissues build up acid form metabolism; inc H+ --> shifts Hb curve to right --> unloading of O2 (Bohr effect)
how to calc A-a gradient
Aa gradient = PAO2 - PaO2; PAO2 = PiO2 - PACO2/R = 150 - PACO2/0.8
causes of emphysema
smoking (centriacinar) and alpha1-antitrypsin deficiency (panacinar + liver cirrhosis [accumulation of unreleased A1AT])
emphysema vs bronchitis
EMPHYSEMA: "pink puffer," decreased breath sounds, tachycardia, dec I/E ratio; BRONCHITIS: "blue bloater," wheezing, crackles, cyanosis
findings in asthma
wheezing, dec I/E ratio, pulsus paradoxus, Curschmann spirals, smooth muscle hypertrophy, mucous plugging
what causes bronchiectasis?
chronically infected/dilated bronchi/airways, often b/c of bronchial obstruction, CF, poor cilia motility, and Kartagener's syndrome
PFTs in obstructive vs restrictive lung disease
OBSTRUCTIVE: dec FEV1/FVC ratio; RESTRICTIVE: dec FEV1 and lung volumes (VC, TLC, FVC), but FEV1/FVC ratio > 80%
causes of interstitial lung disease (8)
ARDS, NRDS, IPF, Sarcoidosis, Pneumoconioses, Goodpasture, Wegener's, Eosinophilic Granuloma
in what population do you see asbestosis?
plumbers and shipbuilders
pathologic findings in asbestosis
Ferruginous bodies in lung (asbestos fibers coated in hemosiderin) + ivory-white plaques
pathogenesis of NRDS
surfactant deficiency --> inc surface tension --> atalectasis (alveolar collapse)
tx for NRDS
maternal steorids beore birth, artificial surfactant for infant
central bronchogenic carcinomas
squamos cell, small cell
peripheral bronchogenic carcinomas
1) ADENOCARCINOMA (most common); 2) BRONCHIOALVEOLAR (no smoking link); 3) LARGE CELL (undifferentiated)
where do lung tumors met to?
Brain (seizures), Bone (fractures), Liver (jaundice, hepatomegaly)
complications from lung cancer
SPHERE (SVC compression/invasion, Pancoast tumor, causes Horner syndrome (cervical sympathetic plexus dysfunction), Endocrine (paraneoplastic), Recurrent laryngeal symptoms (hoarseness), Effusions (pleural or pericardial)
lobar pneumonia: bugs and characteristics
pneumococcus; lobar consolidation (can be of whole lung)
bronchopneumonia: bugs and characteristics
S. aureus, H.flu, Klebsiella, S.pyogenes; patchy distribution, acute inflam infiltrates from bronchioles to alveoli
interstitial (atypical) pneumo: bugs and characteristics
viruses (RSV, adeno), mycoplasma, legionella, chlamydia; diffuse patchy inflam, localized to interstitla areas at alveolar walls
PFTs in asthma vs emphysema
both COPD so both have dec FEV1/FVC, inc TLC; however, EMPHYSEMA causes destruction of alveoli and adjoining capillary beds --> DECREASED DLCO, while ASTHMA INCREASE DLCO due to increased pulmonary blood volumes
how to rule out asthma?
METHACHOLINE: muscarinic agonist --> causes bronchioconstriction (sensitive but not specific)
extrinsic vs intrinsic asthma
extrinsic (atopic, allergic) asthma caused by Type I hypersensitivity to inhaled / ingested allergens, begins in childhood; INTRINSIC asthma is a/w chronic bronchitis, exercise, and cold-induced asthma; occurs in ADULT life, no a/w allergy
pathogenesis of ARDS
diffuse alveolar damage --> NEUTROPHILS --> leaky alveolar capillaries --> protein-rick fluid in alveoli ==> intra-alveolar hyaline membrane
chronic lung rejection
causes bronchiolitis obliterans -- lyphocytic inflam, necrosis, and fibrosis of small airways ==> eventual occlusion of bronchiolar lumen
MCC meconium ileus
CF
MCC death in CF
cardiorespiratory complications (pneumonia, bronchiectasis, cor pulmonale) -- 80%
embryologic origin of diaphragm
Some Parts Build Diaphragm (Septum Transversum, Pleuroperitoneal folds, Body Wall, Dorsal mesentary of the esophagus)
cheyne-stokes breathing
caused by pontine dysfunction, a/w drug OD, hypoxia, CNS depression, CHF, inc intracranial pressure
hyaline membranes
eosinophlic membranous structures lining alveolar wall; characteristic of both ARDS and NRDS
common description of pt with spontaneous PTX
tall, slender men 20-40 yo
bronchial obstruction vs pneumothorax: tracheal deviation
both have tracheal deviation; in PTX, trachecial deviation AWAY from lesion; in bronchial OBSTRUCTION, tracheal devation TOWARD lesion
increased Reid index
chronic BRONCHITIS (persistent irritation --> hyperplasia of goblet cells and submucosal glands)
what does "blue bloater" mean
BRONCHITIS: blue = cyanosis, bloater = peripheral edema from pulmHTN and RV overload (cor pulmonale)
what does "pink puffer" mean
EMPHYSEMA: pink = not cyanotic (PaO2 ~ nl); puffer = hypervent
3 MCC hemoptysis
TB, malignancy, Goodpasture
honeycomb lung
idiopathic pulmonary fibrosis
silicosis seen in what occupations?
mining, stone cutting, glass production (inhaled silica dust --> macrophages -> alveolar damage, scarring)
immune response in typical vs atypical pneumo
TYPICAL: PMNs, fibrin, RBCs (sputum = bac + PMNs); ATYPICAL: T cells and macrophages (intracellular orgs --> no sputum)
pneumo in dairy workers
coxiella burnetti
fungal ball of hyphae in preexisting lung cavity
aspergilloma (aspergillus)
most common location of TB
PRIMARY: upper lower lobe or lower upper lobe; SECONDARY: apical
rifampin interactions with other drugs
rifampin INDUCES p450, so it REDUCES HALF LIFE of: {oral contraceptives, warfarin, digitoxin, ketoconazole, propanalol, prednsione}
causes of viral rhinitis
Rhinovirus, coronavirus, adenovirus, parainfluenza virus
mech of action of streptomycin
same as aminoglycosides (--| initiation of ribosomal complex)
reid index
(thickness of mucous gland layer) / (thickness of bronchial wall between resp epithelium and bronchial cartilage) ==> measure of MUCOUS GLAND ENLARGEMENT, increased in CHRONIC BRONCHITIS
MCC cause and site of lung abscess
cause: aspiration; site: right lung (right bronchus is straighter than left), lower lobe if standing during aspiration, posterior if supine
immune response to TB
macrophage phagocytosis --> Ag presentation to CD4+ TH1 cells --> stim macrophages --> kill M.TB, form Langerhans giant cells
most common side effect of inhaled steroids
oral candidiasis (risne mouth to prevent)
epithelium of respiratory tree
pseudostratified ciliated columnar until respiratory bronchioles --> simple cuboidal ciliated until alveoli --> no cilia in alveolar sacs / terminal alveolar ducts
chronic obstructive disease with recurrent resp infections
chronic bronchitis
sweating in CF vs normal person
in normal people, CFTR makes sweat hypotonic (pulls Na/Cl back from isotonic sweat); this creates hypertonic volume loss in which ECF loss is compensated for by redistribution from ICF; in pts with CF, lack of CFTR causes secretion of isotonic sweat --> exclusively extracellular volume contraction --> hypovolemia, severe hypotension
minute ventilation vs alveolar ventilation
minute ventilation includes dead space, alveolar ventilation does not
source of gastrin, location
G cells in stomach/duodeneum
common locations of gastrinoma (zollinger-ellison syndrome)
pancreas (MEN I), duodenum