Term
| impedance of the respiratory system as a whole =? |
|
Definition
| pressure difference across the entire system (Prs). = Pao (airway opening) - Pbs (body surface) |
|
|
Term
| to measure the mechanical properties of the heart alone? |
|
Definition
| measure transpulmonary pressure = Pao - Ppl (pleural pressure measured with thin balloon catheter positioned in mid esophagus) |
|
|
Term
| airway resistance arises from what 2 sources of friction |
|
Definition
| airflow and tissue motion (tissue motion only accounts for 20% and can be clinically ignored) |
|
|
Term
|
Definition
| (change in pressure)/volume |
|
|
Term
| how do we measure resistance of the entire respiratory system? |
|
Definition
|
|
Term
| how do we measure resistance in the lungs? |
|
Definition
| Pao-Ppl (requires esophageal balloon for Ppl) |
|
|
Term
| how do we measure resistance of the airways? |
|
Definition
| Pao-Palv (measure with body plethysmography) |
|
|
Term
| what sized airways contribute the most to airway resistance? |
|
Definition
| the LARGE airways (bc combined cross sectional area of many thousand of peripheral airways is far greater than that of the trachea and large bronchi) |
|
|
Term
| describe expiratory flow limitation |
|
Definition
| during forced vital capacity, maximum expiratory flow becomes limited by mechanisms INTRINSIC to the lungs after ~30% of vital capacity has been exhaled. after this, modest expiratory effort allows us to reach maximal flow, and further increases in effort have no effect. it's related to dynamic compression of intrathoracic airways under positive pleural pressure. |
|
|
Term
| what are the inspiratory muscles (non-accessory)? |
|
Definition
| diaphragm, parasternal portions of internal intercostals, scalene muscles |
|
|
Term
| what are the accessory muscles of inspiratioN? |
|
Definition
| external intercostals, muscles of neck and shoulders (SCM) |
|
|
Term
| why do pts with paralyzed intercostals show paradoxical inspiratory breathing? |
|
Definition
| bc negative pleural pressure produced by diaphragm contraction is no longer counteracted by the rib cage muscles |
|
|
Term
| what are the main expiratory muscles? |
|
Definition
| TRANSVERSUS ABDOMINUS, external and internal obliques, rectus abdominis. (TA recruited earliest during exercise) |
|
|
Term
| what are the expiratory accessory muscles? |
|
Definition
|
|
Term
| endurance depends on what kind of muscle fiber? |
|
Definition
|
|
Term
| strength depends on what muscle fibers? |
|
Definition
|
|
Term
| muscles reach fatigue when they are called upon to sustain an average level of force that exceeds what fraction of the maximal force? |
|
Definition
|
|
Term
| what is the normal breathing movement we observe in supine and upright position? |
|
Definition
| in supine, abdomen expands visibly to a greater extent than the rib cage; in upright position, rib cage accommodates the majority of the tidal volume |
|
|
Term
| what is abdominal paradox? |
|
Definition
| when patient is in supine, inspiratory indrawing of the abdomen. this is abn and indicates malfunctioning diaphragm (weak, paralyzed, nerve injury, myopathy, intact diaphragm working against fatigued load) |
|
|
Term
| what is respiratory alternans? |
|
Definition
| alternating use of the diaphragm then inspiratory rib cage muscles to avert fatigue |
|
|
Term
| what is a "volume responder"? |
|
Definition
| (in response to bronchodilation in spirometry testing) they respond with a reduction in hyperinflation and air trapping. they can then breathe at lower lung volume (FRC decreases, RV decreases, IC increases ,and FVC may increase significantly, but there may be no apparent improvment in flow rates or FEV1) |
|
|
Term
| what is the optimal point in the inspiration expiration cycle to measure inspiratory muscle functioN? |
|
Definition
| inspiratory muscles generate pressure best at low lung volumes, so maximal inspiratory pressure is measured at RV or FRC |
|
|
Term
| when is the best point in the inspiration-expiration cycle to measure expiratory muscle function? |
|
Definition
| generate pressure best at high volumes, so maximal expiratory pressure is measured at TLC |
|
|
Term
| when do we see a scooping of the flow-volume loop? |
|
Definition
| obstructive diseases (decreased FEV/FVC ratio) |
|
|
Term
| what is the single best indicator of severity of an obstrutive disease? |
|
Definition
| FEV1 (falls 0.5-1.0 L in far advanced obstructive disease); FVC can fall later (progressive air trapping) but is better preserved |
|
|
Term
| what are 2 diseases that might in themselves cause a mixed obstructive-restrictive defect? |
|
Definition
| interstitial lung disease and neuromuscular disorders |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| what indicates that we're dealing with a combined restrictive-obstructive disorder? |
|
Definition
| low FEV1/FVC ratio with a TLC that is reduced or unexpectedly normal given the severity of the obstruction |
|
|
Term
| what is diffusion limitation (vs diffusing capacity)? |
|
Definition
| diffusing limitation is when a gas fails to equilibriate between airspaces and alveolar capillaries during the available blood transit time (most likely when a patient with a restircted pulm microvasculature undertakes physical activity, bc they cannot recruit alveolar capillaries to accommodate the increased CO) |
|
|
Term
| what are flow-volume loop abnormalities characteristic of upper airway obstruction? |
|
Definition
| marked truncation of peak flow, flattening of the expiratory and/or inspiratory limb and sawtooth irregularities of either limb |
|
|
Term
| what is static hyperinflation? |
|
Definition
| pulmonary elastic recoil decreased (i.e. widespread emphysema, long-standing asthma) |
|
|
Term
| what is dynamic hyperinflation? |
|
Definition
| when breathing pattern does not afford sufficient time to exhale the tidal volume through obstructed airways (COPD, uncontrolled asthma, other diseases that cause expiratory flow limitation) pt has to breathe at abn high lung volumes, which increases the inspiratory work of breathing |
|
|
Term
| what are the 3 main mechanisms of intrapulmonary hypoxemia? |
|
Definition
| v/q mismatch, shunt (microscopic or macroscopic), diffusion limitation |
|
|
Term
| what are the 4 main mechanisms of extrapulmonary hypoxemia? |
|
Definition
| alveolar hypoventilation, low inspired oxygen tension (low barometric pressure or hypoxic gas mixture), shunt (extra pulmonary right to left), low mixed venous arterial oxygen (exercise, circulatory impairment, anemia) |
|
|
Term
| which maximal respiratory muscle pressures are reduced in severe obstructive disorders? |
|
Definition
| inspiratory bc hyperinflation causes patients to have to breathe at higher lung volumes --> fatigue |
|
|
Term
| emphysema exhibits what effect on elastance? |
|
Definition
| decreases lung elastance (increases compliance) |
|
|
Term
| what is "ventilatory pump failure"? |
|
Definition
| inability of the inspiratory muscles to maintain adequate alveolar ventilation |
|
|
Term
| since we cannot measure directly the multiple forces (inspiratory muscles) that exert force on the chest wall, we express it as? |
|
Definition
| pressure developed within the pleural space during inspiration or expiration |
|
|
Term
|
Definition
| pressure/volume (measured best at rest, during mechanical ventilation) |
|
|
Term
| how do we measure compliance? |
|
Definition
| slope of the P-V curve (measure chord slope between FRC and FRC+0.5L. gives standardized index of lung distensibility over tidal breathing range, where PV curve is approx linear) |
|
|
Term
| which pressure increases during forced expiration? |
|
Definition
| pleural pressure (to expel air rapidly), transmitted to alveolar spaces and applied to airway walls tending to collapse them (luminal narrowing --> limits expiratory flow) |
|
|
Term
| what are 2 mechanisms for increased airway resistance? |
|
Definition
| intrinsic disease of the airways and decreased elastic recoil of lung parenchyma |
|
|
Term
|
Definition
| saturation of Hb with oxygen in arterial blood (dependent on PaO2) |
|
|
Term
|
Definition
| saturation of Hb with oxygen by pulse oximetry (important, gives real time assessment of oxygenation) |
|
|
Term
|
Definition
| content of oxygen in arterial blood |
|
|
Term
| alveolar-arteriolar oxygen difference =? what does it mean when its increased? |
|
Definition
| PalvO2-PaO2; normally zero; increased means there are gas exchange problems within the lung |
|
|
Term
| how do we calculate AaDO2? |
|
Definition
| alveolar oxygen - arterial oxygen. PaO2 from ABG. PAO2 = 150-s(PaCO2) where s = gas xc b/w oxygen and co2 |
|
|
Term
| what are some things that can lead to an increased AaDO2? |
|
Definition
| V/Q imbalance, shunt, and diffusion impairment |
|
|
Term
| is AaDO2 affected in generalized hypoventilation? |
|
Definition
| no (total or minute ventilation is reduced, but gas xc within the lung is unaffected) |
|
|
Term
| what effect does the concentration of inspired O2 (FiO2) have on AaDO2? |
|
Definition
| when FiO2 is greater than room aim (21%) --> normal value for AaDO2 increases. gradient goes up 5-7% for each 10% increase in FiO2 |
|
|
Term
| what is a useful ratio that we can use as an index of oxygen transfer regardless of FiO2? what are the normal and abnormal ratio values? |
|
Definition
| PaO2/FiO2 ratio. normally 100/0.21=470. acute lung injury = 200; ARDS <200. |
|
|
Term
| what are the 4 pathophysiological mechanisms affecting gas exchange? |
|
Definition
| right to left shunt, V/Q imbalance, diffusion impairment, alveolar hypoventilation |
|
|
Term
| what 2 things make up the arterial content of oxygen? |
|
Definition
| hemoglobin (blood factor) + amount of dissolved oxygen (lung factor aka PaO2) |
|
|
Term
| what are 4 factors that affect oxygen delivery to tissues? |
|
Definition
| lung factor (PaO2), blood factor (Hb), cardiac factor (CO), tissue factors (distribution and uptake) |
|
|
Term
| what does the dissolved oxygen determien? |
|
Definition
| the partial pressure of oxygen in the lung. it is the driving force that loads hemoglobin, increases the saturation and oxygen content of blood, but yet contributes very little to the amount of oxygen in the blood for transport |
|
|
Term
| how do we determine that hypoxemia is as a result of right to left shunt vs the other 3 causes? |
|
Definition
| have patient breathe 100% O2. normally this should raise the PaO2 to at least 550 mmHg and if the PaO2 is less than this value, it means blood is bypassing ventilated alveoli |
|
|
Term
| how come in right to left shunts, CO2 elevation can be offset but hypoxemia cannot be offset? |
|
Definition
| right to left shunt --> elevation in PCO2 and reduction in PO2. central chemoreceptors sense elevation in arterial PCO2 and increase ventilation so that we blow off more CO2 and keep that increased level from diseased lung offset by increased CO2 expulsion from normal lung. we cannot similarly compensate for hypoxemia bc we cannot increase oxygenation in normal lung areas (oxygen dissociation curve reaches a limit bc hemoglobin saturates, so at some point increasing PaO2 doesnt increase oxygen content of blood anymore) |
|
|
Term
| explain the 3 steps of V/Q imbalance and how it results in hypoxemia without increased PaCO2. |
|
Definition
| 1. normal situation, PO2=80-100 and PCO2=35-44. 2. disease causes V/Q mismatch --> hypoxemia and co2 retention 3. increased co2 affects chemoreceptors --> increase in total ventilation --> hypoxemia with normal CO2 |
|
|
Term
| in what situations with V/Q mismatch do we see hypoxemia WITHOUT corrected CO2 levels from increased ventilation? |
|
Definition
| when disease process increases the work of breathing (elevated airway resistance usually) --> pt unable to expend the extra energy to raise level of ventilation or elects not to bc of subnormal chemoreceptor responsiveness or there are not enough normal areas of lung left to hyperventilate and blow off CO2 |
|
|
Term
| how can V/Q mismatch be corrected? |
|
Definition
| give supplemental oxygen. this can help overcome hypoxemia with a modest increase in FiO2 |
|
|
Term
| how do we assess V/Q imbalance? |
|
Definition
| measurement of uneven ventilation using single breath or multiple breath nitrogen washout |
|
|
Term
| describe why reduction in diffusion capacity is sometimes only identifiable during exercise? |
|
Definition
| diffusion moderately impaired --> oxygenation can still be complete within .75s which is the normal capillary transit time. however, during exercise, transit time is decreased to .25 and in this short amount of time, the same diffusion abonormality results in decreased PaO2. therefore,abnormality in diffusion capacity usually has to be VERY low (less than 30% of predicted value) to impair O2 uptake at rest |
|
|
Term
| how do we determine if hypoxemia is d/t diffusion abnormality vs other 3 causes? |
|
Definition
| exercise test (6 min walk test) |
|
|
Term
|
Definition
| K (VCO2)/VA; VCO2 = amount of CO2 produced in the body, does not change much. VA = alveolar/effective ventilation |
|
|
Term
| dead space (VD) = ___+___? |
|
Definition
| anatomical dead space (conducting but non-gas exchanging airways) + alveolar dead space (areas where ventilation>perfusion) |
|
|
Term
| compare generalized/global alveolar hypoventilation with net alveolar hypoventilation |
|
Definition
| Ve=Va+Vd. generalized hypoventilation means a decrease in Ve (lungs intrinsically normal, just a problem with respiratory control i.e. CNS disease or neuromuscular problem that affect the bellow action of chest. AaDO2 normal); net alveolar hypoventilation = increase in Vd (severe pulm disease makes gas xc inefficient i.e. severe V/Q imbalance. AaDO2 abnormal. hyperventilation as compensatory mechanism not probable bc the conditions causing this degree of V/Q mismatch also result in marked increase in work of breathing and any increase in total ventilation would be costly in terms of energy expenditure) |
|
|
Term
| what is the definition of respiratory failure and what are the 2 types? |
|
Definition
| lung fails to maintain adequate ABG (PaO2<60 or PaCo2>50); type I = hypoxemic, decreased PaO2 and PCO2 normal or low; type II = alveolar hypoventilation, decreased PaO2 with increased PaCO2 |
|
|
Term
| what can cause type I respiratory failure? type II? |
|
Definition
| type I - any one or combination of mechanisms of hypoxemia (shunt, v/q imbalance, diffusion impairment); type II - alveolar hypoventilation (either generalized hypoventilation or net hypoventilation) |
|
|
Term
| how do we treat type I respiratory failure? what about if its ARDS (form of type I rf)? |
|
Definition
| supplemental oxygen; ARDS - supp oxygen not enough because the hypoxemia is d/t widespread shunting through areas of microatelectasis, so we should use endotracheal intubation and positive pressure ventilation with positive-end-expiratory pressure in order to reexpand areas of collapse, decrease shunt, and improve oxygenation |
|
|
Term
| how do we treat type II respiratory failure? |
|
Definition
| must improve alveolar ventilation - endotracheal intubation, mechanical ventilation, non-invasive positive pressure ventilation via face mask |
|
|
Term
| what are the main organisms we'd see on a throat culture of an asymptomatic patient? |
|
Definition
| strep viridans, nonhemolytic strep spp, diptheroids, nisseria, moraxella, haemophilus sp, candida albicans, enteric bacilli, pseudomonads |
|
|
Term
| what are a few organisms that normally colonize normal people's lungs and remain in a latent state untl TH1 defenses decrease (then symptomatic infection!) |
|
Definition
| CMV, pneumocystis jiroveci, TB, histoplasmosis |
|
|
Term
| what organisms colonize people in nosocomial settings? |
|
Definition
| gram neg enteric bacilli, psuedomonas, s. aureus |
|
|
Term
| what is the main physical component of respiratory tract defense? |
|
Definition
|
|
Term
| what are the main chemical components of respiratory tract defense? |
|
Definition
| lactoferrin and trasnferrin (starve pathogens of iron), lysozyme, complement, defensins, free fatty acids, antibodies (IgG and sIgA, sIgA constant domain as mucin receptors that enable clearance of IgA pathogen complexes via mucociliary escalator) |
|
|
Term
| what are the main cellular defenses of the respiratory tract? |
|
Definition
| mononuclear phagocytes (especially alveolar macrophages) and to a lesser degree, neutrophils (marginating pool - contained in pulmonary vascular bed and associated with endothelium) |
|
|
Term
| how small do organisms have to be to reach the alveoli? |
|
Definition
| <10 micrometers (usually 1-3) |
|
|
Term
| what stimulates mucociliary clearance? |
|
Definition
| inflammatory mediators (i.e. histamine, bradykinin) |
|
|
Term
| what is compound heterozygosity? |
|
Definition
| 2 different mutant alleles |
|
|
Term
| what is allelic heterogeneity? |
|
Definition
| same gene is affected by different mutations leading to differing degrees of disease severity (i.e. CF) |
|
|
Term
| most mutations in cystic fibrosis are of which one alele? |
|
Definition
|
|
Term
| how does cystic fibrosis cause respiratory failure? |
|
Definition
| inability of ciliary escalator to clear the thickened mucus (cl- inhibited from transport out of cell, so na and h20 are retained in the cell --> decrease in surface fluid and mucus dehydration) --> persistent colonization with pathogens --> chronic exaggerated inflammatory response to pathogens + bacterial toxin action --> bronchiectasis (chronic and irreversible dilatation of bronchioles leading to decreased surface to volume ratio of airways covered by cilia --> chronic colonization) --> pneumonia, lung scarring, decreased lung capacity and respiratory failure |
|
|
Term
| what does p. aeruginosa have to do with CF? |
|
Definition
| forms a mucoid exracellular matrix (alginate) rarely seen in other natural conditions (forms biofilm) --> increased resistance to drugs and host defenses in lung |
|
|
Term
| what are the features of primary ciliary dyskinesia? |
|
Definition
| failure of cilia to beat and clear mucous secretions (leads to chronic sinusitis and bronchiectasis with persistent bacterial colonization). normal life expectancy. immotile sperm in males, situs inversus of internal organs |
|
|
Term
| what is kartageners triad/syndrome? |
|
Definition
| situs inversus + sinusitis + bronchiectasis (assoc with primary ciliary dyskinesia) |
|
|
Term
| what is locus heterogeneity? |
|
Definition
| (primary ciliary dyskinesia) different genes are affected causing the same diseases with different specific manifestations (abnormalities are different from one loci defect to another bc different proteins get knocked out by different mutations) |
|
|
Term
| pattern of inheritance for CF vs. PCD? |
|
Definition
| cf autosomal recessive; PCD variable (usually autosomal recessive, sometimes x-linked or dominant) |
|
|
Term
| which substances recruit neutrophils? |
|
Definition
| complement factor C5a, IL-8 (released by airway epithelial cells), and leukotriene B4 (released by alveolar macrophages) |
|
|
Term
| what happens to a patient who is deficient in B2 integrins? |
|
Definition
| these are adhesion molecules that are used for neutrophil-endothelium binding. deficiency --> pt lacks neutrophil marginating pool and suffer recurrrent respiratory infections |
|
|
Term
| how is the neutrophil action in the lungs modified to minimize collateral damage by inflammation? |
|
Definition
| most of defense done by alveolar macrophages, neutrophils intervene occasionally and undergo apoptosis in the alveoli --> alveolar macrophages phagocytize these dead neutrophils |
|
|
Term
| how and when are lymphocytes recruited to lung? |
|
Definition
| lymphocyte recruitment may depend on antigen transport into the respiratory-associated lymphoid tissue (hilar lymph nodes and sub-epithelial lymphoid patches), where it can be processed by other macs and dendritic cells that are better signalers than alveolar macrophages. lys only recruited in large #s when constitutive defenses become overwhelmed and can no longer dispose of antigens before they reached sub-epithelial or interstitial tissue (M cells transport antigens from lumen to sub-epithelial APCs) |
|
|
Term
| we mostly acquire respiratory infections through large droplet nuclei that colonize the URT. which pathogens can we get from direct inhalation to alveoli? |
|
Definition
| TB, environmental organisms (histoplasmosis, coccidiodomycosis, aspergillosis and mucormycosis...fungi form conidial spores that are resistant to drying and scattered by wind), inhalation anthrax |
|
|
Term
| compare acquisition of community-acquired pneumonias to nosocomial pneumonias to inhalation-acquired pneumonias |
|
Definition
| community-acquired from resp secretions colonizing URT -->penetration to LRT; nosocomial - URT colonization (or tracheal colonization of intubated patients) --> frank infection with gram - bacilli and s. aureus, resistant strains; inhalation-acquired penumonias acquired thru inhalation i.e. zoonotic disaeses, avian influenzea, sars, chlamydia psittaci, hantavirus, q fever |
|
|
Term
| what is vincent's disease? what predisposes us to it? |
|
Definition
| aka vincents angina aka trench mouth - painful ulcerative disease of the oral mucosa caused by in situ overgrowth of a synergistic combination of anaerobic spirochetes and fusobacteria. poor oral hygiene and general debility predispose to it |
|
|
Term
| what are the characteristics of aspiration pneumonia? |
|
Definition
| polymicrobic infection, poor oral hygiene (dirty saliva), anaerobic lung abscess |
|
|
Term
| how are pneumonias acquired hematogenously? |
|
Definition
| (embolic pneumonia) following bacteremia. s. aureus endocarditis, bacteroides abdominal infections, ecoli pelvic or UTI |
|
|
Term
| what are 3 ways a baby can get congenital pneumonia? |
|
Definition
| transplacental (rubella, CMV, hsv, rpr, toxoplasma); aspiration from infected birth canaL (group B strep, chlamydia); hospital environment infection (s. aureus, gram neg bacilli, rsv, influenza, parainfluenza, enterovirus) |
|
|
Term
| what is the example of a respiratory infection caused by an adult helminth? |
|
Definition
| paragonimus westermani (oriental lung fluke) ingested in undercooked infected crustaceans. migrate directly from intestine to lung through body cavities and mature in the lung |
|
|
Term
| the major bacterial and fungal meningitides are acquired via resp tract. what are the pathogens? |
|
Definition
| strep pneumoniae, h influenza type b, neisseria meningitidis, and the yeast cryptococcus neoformans |
|
|
Term
| which systemic viral diseases begin as symptomatic of asymptomatic URT infections |
|
Definition
| measles, mumps, rubella, varicella, variola |
|
|
Term
| what are the intestinal helminths that use the resp tract as a means of infection? |
|
Definition
| hookworms, strongyloides, schistosoma, ascaris, wuchereria, brugia |
|
|
Term
| what does a person with inhalation anthrax usually die of? |
|
Definition
| hemorrhagic mediastinitis |
|
|
Term
| what does a person with inhalation anthrax usually die of? |
|
Definition
| hemorrhagic mediastinitis |
|
|
Term
| neutrophil and complement defects and humoral defects lead to pneumonia caused by? |
|
Definition
|
|
Term
| cell mediated immune defects lead to increased infections with? |
|
Definition
| mycobacteria, hsv, and orgs with low virulence like pneumocystis jiroveci |
|
|
Term
| genetics of asthma: susceptibility locus for asthma where in the genome? |
|
Definition
|
|
Term
| which genetic polymorphism has the strongest association with asthma/allergies? |
|
Definition
|
|
Term
| describe the TT genotype of CD14 and its effect on asthma susceptibility |
|
Definition
| protective against asthma/allergies with low household endotoxin levels, assoc with increased risk of asthma/allergies w/high household endotoxin levels (relate to regulation of TH1 and TH2 response |
|
|
Term
| production if IgE in asthma may be associated with a certain class of? |
|
Definition
|
|
Term
| what is ADAM-33? what happens with polymorphisms of this gene? |
|
Definition
| metalloproteinase gene, expressed in lung fibroblasts and bronchial smooth muscle cells. polymorphisms in this gene accelerate smooth muscle cell proliferation and fibroblast proliferation. |
|
|
Term
| what is the significance of the beta-2 adrenergic gene? |
|
Definition
| different genotypes respond differently to asthma therapy |
|
|
Term
| what is the significance of the IL-4 gene? |
|
Definition
| certain polymorphisms are associated with asthma/allergies |
|
|
Term
| what is the significance of the mammalian chitiniase family of genes? |
|
Definition
| cleaves chitin found in the walls of fungi and parasites; acidic mammalian chitinase is upregulated in TH2 inflammation and YKL-40 levels correlate with the presence of asthma |
|
|
Term
| mucous plugs in asthmatic bronchioles contain? |
|
Definition
| curschman spirals (mucous and shed epithelium) and charcot-leyden crystals (derived from eosinophilic membrane protein) |
|
|
Term
| aspirin induced asthma is associated with a triad? |
|
Definition
| recurrent rhinitis, nasal polyps, urticaria |
|
|
Term
| which part of lung affected by bronchiectasis? |
|
Definition
| LOWER lobes (bilaterally) |
|
|
Term
| whats the clinical presentation of pertussis? |
|
Definition
| prodrome (1-2 weeks) resembling common cold. paroxysmal cough with vomiting/syncope/gagging |
|
|
Term
| death in pertussis is associated with what? |
|
Definition
|
|
Term
| what is the cardinal feature of pertussis in adults? |
|
Definition
|
|
Term
| what do we use to treat pertussis? |
|
Definition
| erythromycin (14d), use for prophylaxis for household and other contacts (azithromycin and clarithromycin alternatives) |
|
|
Term
| what are the common pathological agents causing sinusitis? |
|
Definition
| h. flu, strep pneumoniae, moraxella, viruses (s. aureus and s. pyogenes less common, more with trauma) |
|
|
Term
|
Definition
| antibiotics to pathologic agent (amox, cephalosporin) 14d |
|
|
Term
| what are the common and uncommon pathological agents responsible for tonsillopharyngitis? |
|
Definition
| GAS (most common); group b, c, g strep (uncommon), neisseria gonorrhea, neisseria meningitidis, s aureus, rhinovirus, coronavirus, adenovirus, parainfluenza virus, rsv |
|
|
Term
| what populations are most affected by sore throats? |
|
Definition
| school populations (children 6-12), military, closed communities (subject to reinfection by diff M types from people in close contact) |
|
|
Term
| what is responsible for the virulence of strep (in pharyngitis)? |
|
Definition
| M proteins (cell wall protein, more than 80 serotypes) |
|
|
Term
| what are 2 sx that are unlikely to be associated with pharyngitis? |
|
Definition
| rhinitis and sneezing (and usually not in children <3yo) |
|
|
Term
| what is a possible fatal complication of mono? |
|
Definition
| post-anginal sepsis (lemierres disease) involves bacterial superinfection from fusobacteria necrophorum, spreads along vascular planes |
|
|
Term
| what is the dx with someone who has sore throat and gray exudate that bleeds when removed? |
|
Definition
|
|
Term
| what sx characterize scarlet fever? |
|
Definition
| fever, sore throat, headache, "sandpaper" rash |
|
|
Term
| whats the only drug used against GAS pharyngitis to prevent rheumatic fever? |
|
Definition
|
|
Term
| what are our antibiotic choices for tx of GAS pharyngitis? |
|
Definition
| pcn, amox, cephalosporins, macrolids/clindamycin (10d tx) |
|
|
Term
| when are people with GAS pharyngitis considered noncontagious? |
|
Definition
|
|
Term
| is acute otitis media a primary disease/infection? |
|
Definition
| no, it's 94% of the time preceded by viral URI |
|
|
Term
| what are the pathological etiologies of acute otitis media? |
|
Definition
| s. pneumoniae (30%); h. flu (20%); moraxella (20%), group b strep (20% in neonates and young infants); viral (30%) - rhinovirus, rsv, adenovirus |
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Term
| what factors increase a childs risk for acute otitis media? |
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Definition
| passive smoke exposure, male gender, day care, anatomic, genetics (viral URI most common predisposing factor) |
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Term
| what are the complications of acute otitis media? |
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Definition
| hearing loss (with chronic otitis media with effusion), mastoiditis (6% of untx'd cases), brain abscesses (rare) |
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Term
| tx for acute otitis media? |
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Definition
| 70-90% resolve spontaneously. most cases just watch and give symptomatic tx (aspirin), only give antibiotics when child does not improve within 24-48 hrs (then give amox for 10d) |
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Term
| what can protect against acute otitis media (prevention)? |
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Definition
| breastfeeding!, vaccination (7-valent pneumococcal vaccine), avoid smoke exposure, avoid day care, use of antibiotic prophylaxis in SELECT cases |
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Term
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Definition
| aka laryngotracheobronchitis, VIRAL etiology, kids, subglottic mucosal swelling (does NOT interfere with swallowing), hoarse voice, barking cough, respiratory stress, stridor (important ddx to epiglottitis) |
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Term
| what is the tx for croup? |
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Definition
| humidified air, systemic steroids, rarely require intubation/tracheostomy |
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Term
| describe what epiglottitis is and waht causes it |
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Definition
| potentially lethal infection of epiglottis/supraglottic larynx usually caused by type b h flu. hib vaccine has almost eradicated this. also caused by nontypable h flu, s aureus, s pneumoniae |
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Term
| what are the clinical sx of epiglottitis? |
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Definition
| high fever, severe sore throat, inspiratory stridor, toxic appearance, airway obstruction --> acute resp failure, problem swallowing, muffled voice, drooling |
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Term
| describe the etiology of tracheitis |
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Definition
| it is a secondary bacterial infection of a primary viral infection that causes upper airway obstruction. viral causes = parainfluenza, influenza, enterovirus; secondary bacterial invaders = s. aureus, s. pyogenes, s. viridans, h flu, gram neg enteric bac, anaerobes |
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Term
| what is the pathophysiology of tracheitis? |
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Definition
| infection of the mucosa of the subglottic area and upper trachea. thick pseudomembranes develop, attached loosely, can be removed without bleeding, spontaneous detachment --> respiratory obstruction |
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Term
| what is the clinical presentation of tracheitis? dx? |
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Definition
| (children) croup, stridor, acute illness with severe resp distress, cough, high fever, toxic appearance after 1-5 day prodrome (URI sx); dx clinical confirmed by endoscopy |
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Term
| what is the quellung reaction? |
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Definition
| take organism, add antiserum --> if organism has capsule, the capsule will swell --> this identifies strep (this capsule makes strep resistant to phagocytosis) |
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Term
| why can't kids <2yo get the pneumococcal vaccine? what CAN they get? |
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Definition
| bc polysac-based vaccines are not immunogenic in kids <2yrs. these kids should get the HEPTAvalent conjugate vaccine beginning at 2 mos old. this conjugate vaccine reduces carriage of vaccine-type strains and indirectly results in reduction of invasive pneumococcal disease in elderly |
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Term
| what is the racial preference for strep pneumo pneumonia? |
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Definition
| alaskan, african american, native american |
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Term
| what is the antibiotic that strep pneumo is most resistant to and how does this happen? |
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Definition
| >40% of s. pneumonia are resistant to PCN (via mutations in pcn binding proteins). carriage of resistant strains is highly related to prior tx with beta-lactam antibiotics. resistance is limited to 5 capsular types, which are in the polysaccharide and conjugate vaccines |
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Term
| which 3 strains does the 13 valent vaccine (pneumococcal) protect us against that are dangerous? |
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Definition
| 19A in otitis media and invasive infections (many are multi-antibiotic-resistant); types I and 3, assoc with recent increase in complicated pneumococcal pneumonia (empyema, necrotizing pneumonia) |
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Term
| this organism causes a pneumonia that is not that common, but is very severe and life threatening. |
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Definition
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Term
| how does s. aureus evade host defenses? |
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Definition
| unique cell wall protein, protein A, antiphagocytic properties, high affinity for Fc portion of immunoglobulin subclasses. also, preceding viral respiratory infection may alter natural host defense and allow the development of staph pneumonia |
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Term
| 50% of community acquired staph pneumonia are of what type? |
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Definition
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Term
| what is panton-valentine leuocidin (PVL)? |
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Definition
| many CA-MRSA isolates are positive for this pore forming protein encoded by luk-F-Pv and luk-S-PV genes, linked to necrotizing pneumonia |
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Term
| what is the type of staph pneumonia that is fatal? |
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Definition
| necrotizing - either regular, or caused by CA-MRSA following influenza A |
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Term
| what do the radiographic findings of staph pneumonia look like? |
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Definition
| consolidation, pneumatoceles, empyema, abscesses |
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Term
| what 2 diseases do legionella species cause? |
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Definition
| legionnaires' disease and pontiac fever |
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Term
| who is at the highest risk for acquiring legionella pneumonia? |
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Definition
| people with defects in pulmonary defense mechanisms: secondary to general anesthesia, steroids, cig smoke, chronic lung disease |
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Term
| which organism is responsible for 70-90% of legionella disease? |
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Definition
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Term
| what is the most frequent "atypical" respiratory pathogen causing community acquired pneumonia? |
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Definition
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Term
| which populations of people are at risk for mycoplasma pneumoniae pneumonia? |
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Definition
| institutional settings: nursing homes, schools, military (frequent cause of outbreaks - tends to be endemic puncutated by epidemics at 4-7 year intervals) |
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Term
| what antibiotics do we use to treat mycoplasma pneumoniae? |
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Definition
| lack a cell wall --> not susceptible to pcn ,amox, cephalosporins. they are sensitive to antibioitcs that interfere with protein or dna synthesis (macrolides/erythromycin, tetracyclines, quinolones, but there's increasing macrolide resistance d/t mutations of rRNA gene) |
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Term
| how does mycoplasma pneumoniae attach to respiratory epithelial cells? |
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Definition
| slipping between cilia, attaching through 2 adhesion proteins (P1 evokes a homologous antibody response) --> cilio-stasis, cilio-lysis, exfoliation via H2O2, superoxide, and hydroxy radicals |
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Term
| how do we diagnose mycoplasma pneumoniae? |
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Definition
| cold agglutinins (although negative test does not r/o infection). serology for retrospect dx, takes 3-4 weeks. culture takes 10-14 days and is not widely available. |
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Term
| what characteristic feature would we see on a stain of chlamydial pneumonia? |
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Definition
| intracytoplasmic inclusions |
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Term
| why would a high dose of beta lactam drugs work against chlamydia (pneumonia) if chlamydia is gram neg? |
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Definition
| chlamydia is gram neg, lacks peptidoglycan, BUT encodes proteins forming a nearly complete peptidoglycan synthesis pathway, including penicillin binding proteins, so if we throw enough beta lactams at it, it might work |
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Term
| how do chlamydia spp get their energy? |
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Definition
| auxotrophic for 3/4 nucleoside triphosphates, BUT encode functional glucose-catabolizing enzymes which can be used for the generation of ATP |
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Term
| which drugs do we use to tx chlamydia? |
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Definition
| susceptible to antibiotics that affect protein or dna synthesis: macrolides, tetracyclines, quinolones |
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Term
| what is the one known serotype of chlamydia pneumoniae? |
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Definition
| TWAR (worldwide distribution), may be responsible for 5-20% of community acquired pneumonia in adults and children |
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Term
| which species frequently co-infects with m. pneumoniae and s. pneumoniae? |
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Definition
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Term
| how is chlamydia pneumoniae spread? |
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Definition
| respiratory droplets (outbreaks in military populations, nursing homes) |
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Term
| who is at risk for chlamydia trachomatis pneumonia and what are the sx? |
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Definition
| infants (through aspiration of infected birth canal): rales, hyperinflation, variable interstitial and alveolar infiltrates, eosinophilia |
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Term
| what are some examples of environmental chlamydia (chlamydia-like organisms)? |
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Definition
| parachlamydia acanthamoebae, neochlamydia hartmanellae, simkania negevensis, waddlia |
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Term
| how do people become infected with environmental chlamydia? |
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Definition
| through free living protozoa (endosymbionts). pneumonia associated with contaminated humidifiers ("hall's coccus""). free living amoeba colonize the nasal mucosa and these amoeba are colonized with chlamydia-like organisms. may be cause of ventilator-associated pneumonia |
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Term
| what is a probable natural reservoir for SARS? |
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Definition
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Term
| what is the important first line defense against viruses? (specifically SARS) |
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Definition
| mannose binding lectin (patients with SARS more likely to have low or deficient levels of MBL compared to controls) |
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Term
| describe the clinical manifestation of SARS |
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Definition
| biphasic illness with prodrome, fever, with/without rigots, malaise, headache, myalgias, diarrhea, mild resp sx; respiratory phase: 3-7d non productive cough, dyspnea with progression to resp failure, intubation, mechanical ventilation |
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Term
| what is the pathology of SARS |
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Definition
| diffuse alveolar damage with varying degrees of organization (early phase: hyaline membranes, interstitial and intraalveolar edema, vascular congestion. organizing phase: fibroblast proliferation in interstitium and alveolar spaces) |
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Term
| what is our protective immunity against RSV? |
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Definition
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Term
| what populations of people are at risk for RSV infection? |
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Definition
| infants <6mos (esp those born during first half of RSV season: oct-march), daycare, infants and kids with underlying heart or lung disease, infants born <35 weeks gestation, immunocompromised, significant asthma, elderly in nursing homes, elderly with chronic pulm disease |
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Term
| what are the clinical manifestations of RSV? |
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Definition
| infants/kids: bronchiolitis/pneumonia; older kids and adults: URI, tracheobronchitis; immunocompromised/elderly: pneumonia; recurrent wheezing, reactive airway disease |
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Term
| what are the subtypes of adenovirus that are associated with severe pneumonia? |
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Definition
| subgroup B, subtypes 3, 7, 21 |
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Term
| clinical manifestations of metapneumovirus? |
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Definition
| bronchiolitis, wheezing, pneumonia, exacerbations of asthma (severe infection in immunocompromised |
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