Respiratory Exam 2 Flashcards

Question

acute effects high altitude

Answer 1

hypoxia causes deterioration of nervous system - sleepiness, laziness, impaired judgement, loss of consciousness, or even death moderate - acute mountain sickness (headache, dizziness, breathless, weak) bc hypoxemia/hypocapnia/cerebral edema/alkalosis increased rate and depth of breathing increase work of breathing, greater transpulmonary pressures needed, may have active expiration

Answer 2

renal compensation for respiratory alkalosis within a day erythropoiesis within 3-5 days to increase hematocrit and oxygen carrying capacity increased 2,3 BPG to help release oxygen at tissues

Answer 3

few hours up to 2 days acute cerebral edema bc hypoxia causes vasodilation acute pulmonary edema bc hypoxia causes pulmonary arterioles to constrict

Answer 4

stay at high altitude too long red cell mass and hematocrit increase which increases blood viscosity high pulmonary artery pressure enlarged right side of heart peripheral arterial pressure falls congestive heart failure death occurs unless person removed to lower altitude

Answer 5

increased ambient pressure, gecreased effects of gravity, altered respiration, sensory impairment, hypothermia volume of gas in lungs inversely proportional to depth as gasses compressed partial pressures of gas increase so amount of gas dissolved in tissues increases pressure on chest decreases elastic recoil and decreases FRC by 50% at expense of ERV intrapleural pressure less negative at FRC bc decreased outwar elastic recoil greatly increase work to bring air into lungs

Answer 6

bradycardia (often arrhythmias and increased systemic vascular resistance) decrease workload of heart and limit perfusion to all vascular beds except heart and brain spleen contracts releasing erythrocytes as they descent PCO2 increases pushing CO2 from alveoli into blood during ascent pressure falls so CO2 flows from blood into alveoli and rapid decrease in arterial PO2

Answer 7

ambient pressure increases or decreases but pressure in closed unventilated area cannot equilibriate "the squeeze" middle ear, sinuses, lungs must exhale as ascending or things will rupture

Answer 8

gas bubbles form in blood and body tissues as pressure decreases arterial gas embolism - bubbles in arteries can cause embolism obstructing airway and can travel to cerebral vessels decompression sickness - bubbles in tissues, affects venous blood or joints nitrogen narcosis - high pressures of nitrogen affect CNS oxygen toxicity - CNS, visual system, alveolar damage bc superoxide anions or other free radicals high pressure nervous system - caused by helium replacing nitrogen causing tremors, decreased mental ability, nausea, vomiting, dizziness, decreased dexterity

Answer 9

autosomal recessive variable presentation mutation in cystic fibrosis transmembrane regulator protein (CFTR)

Answer 10

transmembrane, form channel for Cl nucleotide binding domains bind ATP for transport function regulating domain has phosphorylation site for cAMP regulated by protein kinase A

Answer 11

many different, most common delta F 508 (deletion of phenylalanine)

Answer 12

1 - no protein 2 - protein not folded or processed properly in ER or golgi 3 - no ATP binding and hydrolysis, no transport 4 - low conductance (mild) 5 - less protein (promoter, splicing defects, mild) 6 - increased rate of turnover at cell surface class 1-3 have <10% residual activity and severe manifestations class 4-6 have <20% residual activity and milder manifestations

Answer 13

sweat glands - no CFTR to bring Cl into cells, ENaC stops bringing Na into cells, sweat has high Na and is Cl (salty) airway/gut epithelium - no CFTR to push Cl out of cell into airway, ENaC still brings sodium into cells, water follows sodium and dehydrates mucus

Answer 14

CFTR interacts with many proteins to regulate their function beta adrenergic receptor, SLC26A, ENaC

Answer 15

electrolyte and water transport disturbed airway secretions thick and difficult to clear mucus accumulates chronic infections (staph aureus and pseudomonas) bronchiectasis recurrent nasal polyps, chronic sinusitis, pulmonary HTN, chronic hypoxia, terminal respiratory insufficiency mucus plugging and dilation of tracheobronchial tre lung parynchema green w pseudomas

Answer 16

severe persistent cough with expectoration of foul smelling blood dyspnea and orthopnea massive hemoptysis can be triggered by new infection paroxysmal couh cyanosis improvement with antibiotic and PT therapy

Answer 17

pancreatic ducts get blocked leading to trapped pancreatic enzymes, digestion of pancrease, cystic and fibrotic changes liver - plugging of bile canaliculi by mucus can cause hepatic steatosis and cirrhosis can have azoospermia and infertility

Answer 18

clinical symptoms in at least 1 organ system, positive newborn screen, or sibling with CF AND evidence of CFTR dysfunction

Answer 19

potentiators - keep gate open, help class 3,4,5 correctors - assist in proper folding, help class 2 amplifiers - increase amount, help class 5

Answer 20

panacinar emphysema inheritance codominant (M normal, S moderately low levels, Z very little) missense mutation: glutamate (acidic) to lysine (basic) prolonged hyperbilirubinemia and elevated transaminases liver disease COPD bc chronic breakdown of alveolar septa dramatically exacerbated by smoking autophagic response, mitochondrial dysfunction, activation of NF-kB path PAS positive/acidophilic globular inclusions near portal tracts

Answer 21

volume of air moved into and out of lungs per unit time tidal volume x breaths/min

Answer 22

volume of air entering and leaving alveoli per minute gas exchange between alveoli and external environment V in V/Q (tidal volume - dead space) x breaths/min

Answer 23

volume of gas that enters unperfused alveoli per breath alveoli ventilated but not perfused no gas exchange dead space = tidal volume x (PaCO2-PeCO2)/PaCO2 approximately persons weight

Answer 24

increase total and alveolar ventilation dead space constant

Answer 25

increase total ventilation more than alveolar ventilation increased dead space

Answer 26

PAO2 = 104 mm Hg PACO2 = 40 mm Hg

Answer 27

alveolar ventilation pulmonary capillary diffusion oxygen consumption carbon dioxide production

Answer 28

hypothermia decreases PACO2 and considered hyperventilating ventilation increases CO2 decreases ventilation decreases CO2 increases

Answer 29

PO2 decreases, alveolar ventilation decreases

Answer 30

PAO2 = (FiO2 x (Patm - PH2O)) - (PaCO2/RespQ) FiO2 = fraction inspired O2 (0.21) Patm = atmospheric pressure (760) PH2) = H2O vapor pressure (47) PaCO2 = CO2 from ABG RespQ = respiratory quotient (0.8) since FiO2 x (Patm-PH2) = PIO2 PAO2 = PIO2 - (PACO2/RespQ)

Answer 31

PO2 increases, alveolar ventilation increases

Answer 32

alveoli in lower regions receive more ventilation than uper regions (intrapleural pressure less negative in lower regions so transpulmonary pressure less negative in lower regions) alveoli in upper regions have larger volume so most alveolar air in uper regions at FRC and ERV most IRV and IC in lower regions

Answer 33

loss of alveolar elastic recoil increased elastic recoil of chest wall decreased respiratory muscle strength loss of alveolar surace area increased FRC increased RV decreased FEF 25-75%

Answer 34

capillaries and vessels surround alveoli increase lung volumes increases resistance

Answer 35

does not surround alveoli increase lung volumes decreases resistance

Answer 36

alveoli expand vessels between alveoli elongate and decrease diameter pulmonary vascular resistance through alveolar vessels increases

Answer 37

intrapleural pressure becomes more negative vessels increase radius and distend decrease pulmonary vascular resistance of extra alveolar vessles

Answer 38

alveoli decrease in size alveolar vessels no longer elongated and return to normal position pulmonary vascular resistance decreases in alveolar vessels

Answer 39

intrapleural pressure becomes more positive extra alveolar vessels compressed pulmonary vascular resistance increases in extra alveolar vessels

Answer 40

decreases pulmonary vascular resistance recruitment of unperfused pulmonary capillaries distention increases radii as perfusion increases

Answer 41

Pa>PA>PV dead space

Answer 42

hypoxia high PCO2 low pH

Answer 43

alveoli perfused but not ventilated ET tube

Answer 44

alveoli perfused and ventilated

Answer 45

deadspace ventilation alveoli ventilated but not perfused cardiac arrest

Answer 46

abnormal from the start pulmonary AVM - abnormal connections/shunts between arteries and veins can be associated with hereditary hemrrhagic telangiectasia bc mutations in TGF beta signaling path can see vascular malformation elsewhere in GI, urinary, or skin can cause dyspnea, fatigue, cyanosis, pulmonary hemorrhages, paradoxical embolization risk

Answer 47

blood clots travel into pulmonary circulation virchows triad increases risk embolism respiratory compromise - not perfused but ventilated causing hypoxemia hemodynamic compromise - major block, sudden increase in pulmonary artery pressure, diminished cardiac output, right sided heart failure, ischemia of lung parynchema lines of zahn

Answer 48

fat embolism - long bone fracture air embolization - iatrogenic procedure, diving issues, trauma amniotic fluid embolism - maternal labor

Answer 49

significant pulmonary embolism tend to be in lower lobes and often multiple significant cardiopulmonary compromise wedged shaped occluded vessel, hemorrhagic, necrosis, infeected emboli lead to septic infarcts

Answer 50

increased pulmonary vascular blood flow, pulmonary vascular resistance, or left sided heart resistance to blood flow lesions similar to atherosclerosis, arterioles with medial hypertrophy and intimal fibrosis, arterioles affected by capillary proliferation in lumen of arterioles tx - treat underlying condition, vasodilators, lung transplant

Answer 51

gene encoding BMPR2 dysfunction and proliferation of endothelial cells and vascular smooth muscle cells

Answer 52

bleeding into alveolar spaces from pulmonary microvasculature originates in pulmonary interstitium idiopathic or secondary to disease cause hemoptysis, decreased hematocrit, diffuse pulmonary infiltrates, hypoxemic respiratory failure

Answer 53

autoimmune, predisposition with HLA DRB 1501 and 1502 antibodies against basement membrane of renal glomeruli and pulmonary alveoli causing glomerulonephritis and necrotizing hemorrhagic interstitial pneumonitis death often by uremia hemoptysis and progressive renal failure tx - plasmaphoresis, immunosuppressive therapy

Answer 54

insidious onset of productive cough, hemoptysis, anemia diffuse alveolar hemorrhage mainly young children

Answer 55

autoimmune, t cell mediated with granulomas, PANCA necrotizing granulomas of upper respiratory tract, necrotizing granulomatous vasculitis, hemorrhages tx - immunosuppression

Answer 56

leakage of excessive interstitial fluid which accumulates in alveolar spaces hemodynamic (starling forces) - increased hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction microvascular injury - damage to alveolar endothelium or epithelial cell with secondary microvascular damage (direct or indirect injury) can be of undetermined origin

Answer 57

major systemic insult, develops over short period, hypoxemic respiratory failure, diffuse respiratory infiltrates stages: exudative (leakage of fluid and necrotic cells from hyaline membrane), proliferative (type II pneumocytes undergo hyperplasia), fibrosis

Answer 58

ICS - formoterol SABA as alternate route SAMA can be used alone for rescue never use LABA alone

Answer 59

LABA for prophylaxis and maintenance exacerbations treated with antibiotics

Answer 60

preferred reliever - ICS formoterol (albuteral alternate) step 1 - as needed ICS formoterol (low dose ICS when SABA taken) step 2 - daily low dose ICS or as needed ICS formoterol (leukotriene receptor agonist or low dose ICS when SABA taken) step 3 - low dose ICS LABA (medium dose ICS or low does ICS LTRA) step 4 - medium dose ICS LABA (high dose ICS, add on tiotropium or LTRA) step 5 - high dose ICS LABA (phenotypic assessment for add on)

Answer 61

symptoms less than twice a month control = as needed ICS formoterol reliever = as needed low dose ICS formoterol ALTERNATE = control take ICS whenever SABA taken, rescue as needed SABA

Answer 62

symptoms less than 4-5 days a week control = as needed ICS formoterol reliever = as needed low dose ICS formoterol ALTERNATE = control low dose maintenance ICS, rescue as needed SABA

Answer 63

symptoms most days or waking with asthma once or more a week control = low dose maintenance ICS formoterol reliever = as needed low dose ICS formoterol ALTERNATE = control low dose ICS LABA, reliever as needed SABA

Answer 64

daily symptoms or waking with asthma once a week or more and low lung function control = medium dose ICS formoterol reliever = as needed low dose ICS formoterol ALTERNATE = maintenance high dose ICS LABA, reliever as needed SABA

Answer 65

uncontrolled after step 4 tx may need short dose OCS for severly uncontrolled asthma control = add on LAMA, consider high dose ICS formoterol reliever = as needed low dose ICS formoterol ALTERNATE = add on LAMA, reliever as needed SABA

Answer 66

albuterol (preferred in pregnancy) levalbuterol pirbuterol relax muscles in narrowed airways anxiety, tremors, tachycardia, hypokalemia, hyer/hypotension possible dont take with MAO inhibitors

Answer 67

salmeterol formoterol indacaterol vilanterol combo w ICS - should not use as monotherapy for asthma can cause cough

Answer 68

terbutaline - selective beta 2 agonist, reverse bronchospasm epinephrine - stimulate alpha 1&2, beta 1&2, increase HR & heart contractility, vasoconstrict many vascular beds, dilate skeletal muscle vessels, bronchodilation, anaphylaxis!!

Answer 69

ipratropium quaternary derivative of atropine dont use with MAO inhibitors

Answer 70

tiotropium aclinidinium umeclidinium

Answer 71

theophylline - inhibit adenosine receptors, high doses inhibit PDE 2 and PDE 4 stimulating bronchodilation aminophylline - prodrug of theophylline can cause vomiting, seizures, arrhythmias, death interact w erythromycin, cimetidine, fluoroquinolones

Answer 72

betamethasone budesonide fluticasone mometasone ciclesonide bind intracellular glucocorticoid receptor and modulate gene expression, inhibit inflammatory cells and release of inflammator mediators can cause thrush, hoarseness, throat irritation, URI

Answer 73

prednisone only in severe asthma cant use in fungal infections, if receiving prednisone for immunosuppression, live vaccines

Answer 74

cromolyn nedocromil prevent degranulation of pulmonary mast cells and decrease release of histamine, PAF, LTC4 for allergen induced asthma and exercise induced asthma can cause throat irritation/cough, bronchospasm, drowsiness

Answer 75

montelukast zafirlukast deukotrine D4 receptor antagonist

Answer 76

zileuton inhibit 5 lipoxygenase which decreases airway edema, constriction, inflammation

Answer 77

monoclonal antibody for IgE reduce eosinophilic bronchial inflammation

Answer 78

dual inhibitor of IL4 and IL13

Answer 79

all receive SABA can get short acting muscarinic agonis as alternative or in combo w SABA systemic glucocorticoids antibiotics if increased dyspnea, increased sputum volume, increased sputum purulence O2 with hypoxemia (target 88-92)

Answer 80

selective phosphodiesterase 4 inhibitor reduce risk of COPD exacerbation

Answer 81

HCO3/PaCO2 HCO3 on metabolic panel PaCO2 on ABG

Answer 82

decrease in HCO3

Answer 83

increase in HCO3

Answer 84

increase PCO2

Answer 85

decrease PCO2

Answer 86

6-12 hours for respiratory compensation 3-5 days for metabolic compensation

Answer 87

7.35 - 7.45

Answer 88

pH > 7.4 primary alkalosis pH < 7.4 primary acidosis

Answer 89

acidotic patient has metabolic acidosis if PCO2 < 35 acidotic patient has respiratory acidosis if PCO2 > 45 alkalotic patient has metabolic alkalosis if PCO2 > 45 alkalotic patient has respiratory alkalosis if PCO2 < 35 if PCO2 close to normal look at HCO3 the one consistent with pH and furthst from normal will account for primary disorder

Answer 90

predicted PCO2 = (1.5 x HCO3) + 8 +/- 2 chronic metabolic acidosis PCO2 = HCO3 + 15 actual PCO2>predicted PCO2 then additional respiratory acidosis actual PCO2 < actual PCO2 then additional respiratory alkalosis

Answer 91

Na - (HCO3 + Cl) normal is 12 or less over 12 means metabolic acidosis

Answer 92

corrected HCO3 = (anion gap - 12) + measured HCO3 corrected HCO3 > 26 then underlying metabolic alkalosis corrected HCO < 22 then underlying non AG metabolic acidosis

Answer 93

urine sodium + urine potassium - urine chloride normal is 30-50 positive indicates kidney origin negative indicates extrarenal origin

Answer 94

expected PCO2 = 0.7 [HCO3] + 20 +/- 5 actual PCO2 < expected PCO2 then additional respiratory alkalosis actual PCO2 > expected PCO2 then additional respiratoyr ecidosis

Answer 95

blood flow and ventilation increased dead space ventialtion/perfusion mismatch hypoxemia increased A-a gradient rspiratory alkalosis, hyperventilation

Answer 96

lung ischemia/infarction increased vascular resistance/RV afterload

Answer 97

dyspnea, chest pain, cough, hemoptysis, syncope, palpitaions, diaphoresis, leg pain and swelling tachycardia, tachypnea, hypoxemia, loud P2, fever, diaphoresis, JVD, cyanosis, hypotension elevated d-dime (>500) loss of vein compressibility on ultrasound ABG - hypoxemia, hypocapnia, respiratory alkalosis normal CXR ECG - tachycardia, RBBB, right axis deviation, S1-Q3-T3 CT w contrast gold standard

Answer 98

0-4 PE unlikely >4 PE likely signs DVT = 3 points alternative diagnosis less likely = 3 points tachycardia = 1.5 points immobilization or sx in 4 weeks = 1.5 points previous DVT/PE = 1.5 points hemoptysis = 1 point malignancy = 1 point

Answer 99

unlikely = d dimer likely = CT or leg ultrasound if no CT then if no DVT do VQ scan

Answer 100

systolic BP > 90 and no signs cardiac instability

Answer 101

systolic BP > 90 with right ventricular strain and possible troponin?BNP elevation

Answer 102

systolic BP < 90, extensive thrombosis affecting at least half of pulmonary vasculature, dyspnea/syncope/hypotension/cyanosis

Answer 103

IV heparin or SQ lovenox bridge with warfarin until INR 2-3 OR oral anticoagulation with factor Xa inhibitor continue for 3-6 mo for provoked indefinite for unprovoked indefinite LMWH or DOAC as monotherapy for cancer

Answer 104

cardiopulmonary stress test pulmonary = peak exercise increase in dead space or hypoxemia or develops bronchospasm cardiovascular = high HR, early anaerobic threshold, excessively high BP, O@ pulse falls, ischemic changes on ECG

Answer 105

increase in resistance to airflow decreased FEV1/FEV

Answer 106

reduced expansion of the lund parenchyma and decreased lung capacity decreased in TLC and FEV, normal FEV1/FEV

Answer 107

loss of pulmonary parenchema (alveolar septa and walls of airways) and dilation of terminal airways loss of elastic recoil, airway collapses when breathe out trapping air centrilobular/acinar = smoking (upper) panacinar = alpha 1 antitrypsin deficiency (lower) distal = fibrosis/atelectasis irregular = fibrosis dilated acini with floating sections decrease capillary alveolar bed inflammation blebs flattened diaphragm and extended hyperlucent lungs hyspnea, hypoxemia, hypercapnia, hyperventilation less V/Q mismatch can cause pulmonary HTN, cor pulmonale

Answer 108

secondary to noxious/irritating substances mucus hypersecretion inflammation infection CFTR dysfunction bronchi/bronchioles affected hyperemia, swellind, edema of mucous membranes with excessive secretions lumens filled w heavy casts chronic inflammation increased size/hyperplasia of mucous glands bronchioles w mucus plugging, inflammation, fibrosise

Answer 109

max thickness of bronchial mucous glands divided by bronchial wall thickness b to c/a to d

Answer 110

overinflation and atelectasis eosinophilic infiltrate occlusion of bronchi by mucus plugs sputum contains curshmann spirals and charcot leyden crystals airway remodeling

Answer 111

progressive disorder with patchy bilateral interstitial fibrosis trichome stain - blue = fibrosis fibrosis and honeycombing start as dyspnea on exertion, dry cough, and velcro like crackles on auscultation

Answer 112

inhaled coal dust lesions vary from arthracosis to coal macules/nodules to broad scars in lungs usually not mjor decline in lung function

Answer 113

slow gradual progression phagocytized silica activates macrophages and releases proinflammatory factors of fibrogenic mechanisms asbests bodies, fibrosis, pleural plaques, tumors can be exaggerated by smoking mesothelioma and pleural neoplasm

Answer 114

silica particles ingested by macrophages and activate inflammatory cells and release mediators acute resemble pulmonary alveolar proteinosis (lung lavage) chronic fibrosis with hard collagenous scars, uper lobes

Answer 115

granulomatous disease cell mediated immunity increased incidence with certain HLA genotypesr difuse interstitial fibrosis and pulmonary hypertension signs and symptoms of organ involvement hilar lymphadenopathy unpredictable course diagnosis of exclusion

Answer 116

starts with inhalation then affects alveoli pigeon breeders, bagassosis, heating/air conditioner, farmers noncaseating granulomas, interstitial pneumotitis, interstitial edema cough and crackles, symptoms worse after exposure

Answer 117

defects in GM CSF causing accumulation of surfactant in alveolar/bronchial spaces

Answer 118

cigarette use bc most people who vape have never smoked

Answer 119

strongly considered to possibly be associated with the pathogenesis of EVALI

Answer 120

higher rates of wheezing development of bronchiectasis greater prevalence and exacerbation of asthma changes in gene expression indicative of immunosuppression in bronchial biopsies susceptible to infections

Answer 121

inflammation and increase inflammatory cytokines lung and systemic damage stimulation of sympathetic nervous system DNA damage exacerbation of chronic disease decreased defense mechanism

Answer 122

empiric antibiotics supportive care NOT GLUCOCORTICOIDS

Answer 123

chronic bronchitis airway inflammation and remodeling immediate bronchodilator but poor control of asthma spontaneous pneumothorax and hypersensitivity pneumonitis lung cancer?

Answer 124

cardiomegaly, pulmonary venous hypertension and bilateral effusions continuum edema and interlobular septa

Answer 125

batwing appearance, enlarged heart stage 1 - redistribution of pulmonary vessels, cardiomegaly, broad vesicle pedicle stage 2 - kerley B lines, peribronchial cuffing, hazy contour of vessels, thickened interlobular fissure stage 3 - consolidation, air bronchogram, cotonwool appearance, pleural effusion

Answer 126

nonsocomial community acquired determined by etiology

Answer 127

atypical typical determined by presentation

Answer 128

interstitial determined by CXR

Answer 129

lobar bronchopneumonia determined by CXR usually bacterial febrile pattern not diagnostic of organism most common S. pneumoniae

Answer 130

fairly homogenous consolidation lobe/multiple lobes peripheral strep pneumoniae - most common community acquired klebsiella - voluminous exudate, bulging fissures legionella - smokers, elderly, immunosuppressed, contaminated water moraxella - elderly, COPD

Answer 131

bronchogenic spread patcy areas of consolidation several lobes areas of inflammation seperated by normal lung strep pneumoniae staph aureus - most connon after influenza haemophilus influenzae - elderly or COPD klebsiella moraxella - elderly and COPD

Answer 132

mild fever/dry cough may be confined or begin in pulmonary interstitium may progress to patchy or diffuse opacities mycoplasma - 20% community acquired (+ agglutinin) chlamydophila - 10% community acquired legionella - contaminated water, coccobacillary and grows in buffered cahrcoal yeast viruses PJP - immunocompromised

Answer 133

fungus nearly all infected in infancy methenamine silver stain

Answer 134

CT for underlying mass/complications

Answer 135

intermitent fever/productive cough/weigh loss/night sweats foul sputum hemoptysis anaerobes/gram negative bacilli/staphylococci

Answer 136

acid fast bacilli cough, hemoptysis, fever, night sweats consolidation, adenopathy, pleural effusion ghon focus nodular or patchy opacity post primary = upper lung zones due to reinfection

Answer 137

hyperinflated lungs, flat diaphragm, hyperlucent lung fields increased AP diameter panacinar in lower lobes bullae and blebs - cystic air containing spaces

Answer 138

usually normal xray abnormal will have hyperinflation, bronchial wall thickening, peribronchial cuffing, rarely pulmonary edema complications - pneumonia, pneumothorax, pneumomediastinum

Answer 139

dilated bronchi kartageners syndrome - autosomal recessive, ciliary dyskinesia and citus inversus, bronchiectasis/sinus disease/infertility

Answer 140

fibrosis/cysts bronchiectasis

Answer 141

bilateral hilar adenopathy and mediastinal adenopathy stage 1 - adenopathy stage 2 - adenopathy and opacities stage 3 - parenchymal densities

Answer 142

ferruginous bodies stain with prussian blue risk of bronchogenic carcinoma and mesothelioma calcified pleural plaques

Answer 143

nonspecific bilateral lung opacities

Answer 144

hyperresonance diminished breath sounds hyperlucent pleural space can have shift of mediastinum small/simple = at top tension - all over

Answer 145

most common lung cancer in non smokers

Answer 146

central, cavitation, calcium

Answer 147

central aggressice paraneoplastic syndrome (cushings) lamber eaton myasthenia neuroendocrine neoplasms

Answer 148

incomplete expansion volume loss of section of lung obstructive and compressive types

Answer 149

spirometry lung volumes diffusing capacities respiratory muscle strength testing FENO ABG exercise testing

Answer 150

air exhaled with forced expiration normal varies based on age, sex, size, race abnormal due to lung issues, pleural issues, chest wall issues, muscle issues

Answer 151

normal 75 to 85% FEV1 is low and ratio < 70 obstructive FEV1 is low and ratio > 75 restrictive ratio decreases with aging

Answer 152

FEF 25-75% - average flow rate over the middle 50% of FVC, effort dependent, always low with obstruction, low and FEV1 normal small airway disease PEF - effort dependent PFT, monitor asthma with portable device

Answer 153

fixed - inspiratory and expiratory flow curves flat variable intrathoracic - expiratory flow curve flat variable etrathoracic - inspiratory flow curve flat

Answer 154

static lung volumes measure RV most important measures are TLC and RV nitrogen washout, inert gas dilution, plethysmography, radiographic

Answer 155

must be low (<70%) to confirm restriction usually increased in COPD, can be increased or normal in asthma

Answer 156

obstructive - increased, determined by airway collapse and gas trapping restrictive - variable decreased or normal, determined by limit of chest wall compression

Answer 157

measured using CO increased DLCO - exercise, asthma, polycythemia, alveolar hemorrhage, CHF decreased DLCO - SA issues (emphysema, lung resection, decreased blood volume) and thickness issues (pulmonary fibrosis, CHF, sarcoidosis, interstitial lung disease, alveolar proteinosis)

Answer 158

volume of air measured after hard and fast breathing for 10-15 sec extrapolatd to 60 differentiate neuromuscular disease (if MVV < FEV1 x 40)

Answer 159

respiratory muscle strength low MEP - weak cough, skeletal muscle weakness low MIP - hypercapnia, diaphragm dysfunction

Answer 160

measure of allergic (eosinophilic) airway inflammation useful in asthma to determine response to steroids

Answer 161

reduced minute ventilation - reduced TV, increased PaCO2, reduced PaO2 reduced FRC, reduced PEFR increased supraglottic resistance altered set points for ventilatory response mechanical and chemical arousal thresholds

Answer 162

snoring - 20% all ages, 60% over 60 OSA prevalence - men 15-30%, women 10-15%, increase wtih age and BMI

Answer 163

cessation of airflow for 10 sec or more obstructive - continued respiratory effort central - lack of respiratory effort mixed - combo of both

Answer 164

abnormal respiratory event with 10 sec duration, 30% reduction in airflow or thoraces abdominal movement, 4% oxygen desaturation

Answer 165

people with UARS have RERA increase airway resistance leads to progressive respiratory effort and arousal no oxygen desaturation no reduced airflow esophageal monitoring

Answer 166

AI = apneas per hour

Answer 167

AHI = apneas + hypopneas per hour 5-15 mild 16-30 moderate >30 severe

Answer 168

RDI = apnea + hypopnea + RERA

Answer 169

unexplained dyspnea, fibromyalgia, nocturnal reflux, ADHD in children, motor vehicle collision, nocturia, impotency, unexplained weight gain

Answer 170

education sleep hygeine weight loss positional therapies avoid alcohol and sedating medications

Answer 171

first line treatment pneumatically stent upper airway increase end expiratory lung volume CPAP, APAP, BiPAP, adaptive sero ventilation

Answer 172

continuous positive airway pressure

Answer 173

auto adjusting positive airway pressure

Answer 174

bilevel positive airway pressure

Answer 175

oral appliance hypoglossal nerve stiulation

Answer 176

optimize CHF rx, oxygen, seroventilation, pharm (acetazolamide, theophylline, benzodiazapines, diaphragm pacing)

Respiratory Exam 2 Flashcards

(208 cards)