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158 Cards in this Set

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What is the mechanism of extrinsic asthma?
inhaled antigens cross-link IgE on mast cells on mucosal surfaces --> release histamine/preformed mediators --> bronchoconstriciton, mucus production, leukocyte involvment. Late phase: eosinohils --> major basic protein --> epithelial damage & airway constriction

Other: leukotriene C4, D4, E4 --> prolonged bronchoconstriction; acetylchline --> airway smooth ,muscle contraction
What are the histopathologic changes in asthma?
basement membrane thickening
hypertrophy of submucosal glands, goblet cell metaplasia/hyperplasia, mucus plugs
hypertrophy/hyperplasia of smooth muscle cells
edema, mixed inflammatory infiltrate
Curschmann spirals: shed epithelial cells
charcot-Leyden crystals- precipitated crystalline granules form eosinophils
What are cause of intrinsic asthma?
respiratory infections (viral)
stress
EXERCISE
COLD AIR
Medications (ASA or NSAIDs)
What are the signs/Sx of asthma?
SOB, wheezing, chest tightness, cough (worse at night)

Attacks: tachypnea, diaphoresis, wheezing, use of accessory muscles
Paradoxical movement of abdomen and diaphragm
Pulsus Paradoxus: decrease of bp w/ inspiration (also w/ tamponade, pericarditis, croup, COPD)
How do you dx asthma?
PFTS (decreased FEV1, FVC, FEV1/FVC. increased RV, FRC, TLC)

Bronchodilator (increase in FEV1 or FVC)

Peak flow- mild persistent >300, moderate 100-300, sever <100.

Bronchoprovocation test (methacholine challenge)- lower PD50.

ABG- hypocarbia, hypoxemia, fatigue --> normal paCO2 --> intubation indication
What are the treatments for asthma?
SABA, LABA, ICS, B2 nonselective, leukotriene antagonists, mast cell stabilizers, systemic cortico steroids
What is the treatment of acute sever asthma exacerbation?
inhaled B2, systemic corticosteroids, 3rd line, supplemental oxygen, antibiotics
What are complications of asthma?
status asthmaticus, Acute respiratory failure, pneumothorax, atelectasis, pneumomediastinum
What is the mechanism of interstitial fibrosis?
injury --> alveolitis -->

loss of type I pneumoytes --> proliferating type II (loss of surfactant) -->

thrombosis and
thrombolysis changes endolthelium

recruitment of neutrophils and lymphocytes

cytokines --> fibroblasts proliferation --> tissue remodeling and increased tissue matrix deposition --> scarring --> alveolar destruction

non-homogenous (patchy) diffuse parenchymal lung scarring

increasing tissue leukocytosis (T cells and mast cells)

cuboidal epithelium lines airspaces --> honeycombing

fibrosis --> decreased lung compliance and increased eleasticity

poor gas exhanged and pulmonary vascular abnormalities
What are the sx and signs of interstital fibrosis?
nonproductive cough, exertional dyspnea, fatigue (diffusion defect and V/Q mismatching), tachypnea (from hypoxemia)

crackles (due to fibrosis and loss of surfactant), clubbing, cardiac abnormalities (prominent P2, right hear toverload, elevated JVD, tricuspid regurg murmur, right sided S3, cyanosis)
How do you diagnose interstital fibrosis?
CXR: bilateral reticulonodular infiltrates (patchy), ground glass opacities, honeycombing

PFTs: all lung volume decreased. Normal to increased FEV1/FVC
Reduced diffusing capacity (edema/ BM thickening)

ABG: respiratory alkalosis (hyperventilation secondary to hypoxia and fibrosis)
hypoexemia (dead space)
oxygen desaturation during exercise(cardiac output reduces transit time for blood through alveolar capillary bead)
hypercapnia (poor ventilation or excess breathing work)

bronchoalveolar lavade

tissue biopsy

urinanalysis (glomerular injury- Goodpasture's syndrome, Weener's gramulomatosis)
What is honeycomb lung?
scarred and shrunken lung iwth dilated airspaces and fibrous interstitial scars, signifying poor prognosis
What is complicated CWP?
may have necrotic centers, massive progressive fibrosis, may have cor pulmonale
What is the is the class CXR of silcosis?
egg-shell calcifications(dystrophic calcifications in hilar nodes)
What are the increased risk of silicosis? What are the sx?
TB and lung cancer
exertional dyspnea, productive cough
What are the CXR finding of asbestosis?
pleural plaques, hazy infiltrates w/ bilateral linear opacities.
What 2 cancers does asbestosis predispose you to?
bronchogenic carcinoma, malignant mesothelioma
Why is berylliosis similar to sarcoidosis? What is the diagnostic test? What is the tx? What are the risks?
both have diffuse interstital fibrosis w/ non-caseating granulomas
beryllium lymphocyte proliferation test
Cor pulmonale and primary lung cancer
What is the pathophysiology of sarcoidosis?
CD4 TH response to unknown antigen --> noncaseating granulomas.
Schaumann bodies (laminated calcificaiton)/ asteroid bodies (stellate inclusion)
What are the clinical features of sarcoidosis?
malaise, fever, anorexia, weight loss.
Pulmonary: dry cough, dyspnea
dermatologiuc (erythema nodosum), plaques, maculopapular eruptions
opthalmic: anterior uveitis, posterior uveitis, conjunctivitis, glaucoma, corneal opacities
musculoskeletal: arthralgias/arthritis, bone lesions
cardiac: arrythmias, heart blocks, sudden death
Neurologic: Bell's Palsy, optic nerve dysfunction, papilledema, peripheral neuropathy
Endocrine/immune: enlarged salivary/lacrimal glands, diabetes insipidus, hypercalccemia
How you dx sarcoidosis?
CXR: bilateral hilar adenopathy, skin anergy, incrased ACE, hypercalcemia, PFTs
What is the tx of sarcoidosis?
systemic corticosteroids (methotrexate)
What is histiocystosis X? What are variants of the disease? What are the clinical s and signs?
chronic interstial pneumonia cause by histiocyte proliferation
eosiniophilic granuloma, Letterer-Siwe disease, Hand-Schuller-Christian syndrome

dyspnea, nonproductive cough, spontaneous penumothorax, lytic bone lesions, diabetes insipidus

CXR: honeycomb, Ct: cystic lesion
Corticosteroids or lung transplant
What is Wegener's gramulomatosis? What areas does it effects? What is the marker?
Necrotizing granulomatous vasculitits
Lungs, kidneys, UR

LRI/URI, glomerulonephritis, pulomnary nodules

C-ANCA
What is Churg-Strauss Syndrome? What areas does it effects? What is the marker?
Granulomatous vasculitis in pts w/ asthma
skin, muscles nerves
pulmonary infilitrates, rash, eosinophili
pANCA
What is Goodpasture's Syndrome
IgG against BM --> hemorrhagic neumonitis and glomerulonephritis (hemotypsis and dyspnea)
Dx: biopsy, anti-GBM antibodies
tx: plasmaperesis, cyclophosphamide, corticosteroids
What is pulmonary alveolar proteinosis?
surfactant-like protein accumulation in alveoli
Clinical manifestations:- dry cough, dyspnea, hypoxia, rales
CXR: bat-shaped ground-glass appearance w/ bilateral alveolar infiltrates
BIOPSY
Tx: lung lavage, do notgive steroids( infections)
What is miscellaneous interstitial lung disease?
repeared cycles of alveolitis by unknown agent causes progress interstital fibrosis and proximal dilation of small airways
Diagnosis: CXR- ground glass or honeycomb appearance
What is hypersensitivity pneumonitis?
allergic alveolities by known inhaled agent --> type III hypersensitivity

farmer's lung
What is pneumoconiosus with rheumatoid lung nodules?
Caplan syndrome
What are the signs of SLE in young women?
pleuritis, unexplained pleural effusion, serositis
What is the treatment for COP?
steroids, unresponsive to antibiotics
What is readiation penumonitis?
interstial pulmonary inflammation after radiation
What medications are associated with ILD?
amiodarone, bleomycin, busulfan, cyclophosphamide, metotrexate, methysergide, nitrosurea, nitrofurantoin
What is the air inspired and expired during normal breathing?
tidal volume
What is the volume inspired with maximal respiratory effort beyond tidal volume?
inspiratory reserve volume
What is the volume expelled with maximal respiratory effort beyond passive exhalation?
expiratory reserve volume
What is the volume at end of maximal forced expiration?
reserve volume
What is the volume at the end of quiet, passive expiration?
functional residual capacity
What is FRC the sum of?
RV + ERV
What is the volume inspired w/ maximal inspiratory effort after passive expiration? What is the formula?
Inspiratory capacity
IC = TV + IRV
What is the volume expired from maximal inspiration to maximal expiration? What is the formula?
Vital capacity
VC= IRV + VT + ERV?
What is TLC?
TV + IRV + ERV + RV
When is maximal mid-inspiratory flow rate achieved?
50% of vital capacity MIF50%
When does maximal air flow occur in expiration? Why?
Early, incrased airway resistance limits expiratory low
What occurs to the airway in COPD because of destruction of elastic tissue?
increased resistance and increased lug compliance created an equal pressure point and dynamic compression (collapse)
What is bronchodilator test for asthma?
Increase of FEV1 by 12% = reversible = asthma
What is the methacoline challenge?
Doe to reduce FEV1 by 20% < 8mg/mL
What 2 lung volume increase in COPD much more than the others?
RV and FRC
How doe diagnose restrictive lung disease by FEV1 and FVC?
FEV1/FVC = increased or normal

FEV1 & FVC = decreased
What is body plethymography?
measuring lung volumes and FRC. FRC cannot be measured by spirometry.
What are the major sites of airway resistance?
medium siozed bronchi
How do you measure airway resistance?
pneumotachograph
What happens to inspiration/expiration during fixed, variable extrathoracic and variable intrathoracic upper airway obstruction?
fixed: inspiration and expiration rates decrease

variable extrathoracic: inspiration decrease, expiration normal

variable intrathoracic: inspiration normal, expiration decreased
How is diffusion inhibited in fibrosis and emphysema? What gas is used to measure pulmonary diffusion capacity?
fibrosis- thickened barrier
emphysema- decreased surface area
CO
What cause increased and normal extrapulmonary A-a gradient?
pulmonary and extrapulmonary hypoxemia
What is the alveolar gas equation?
PAO2 = PIO2 - (PCO2/R)
What is chylothorax and psuedochylothorax?
lymphatic fluid and cholesteral in the pleural space
What are causes of pleural effusions?
increased hydrostatic pressure (CHF), decreased oncotic pressue )nephrotic, cirrhosis, hypoalbuminemia)
obstruction of lymphatic drainage from visceral pleura (lung tumor)
increased vessel permeability (infarction, ARDS)
metastasis to pleura (breast cancer)
What forms from alteration of Starling's law?
transudate
What are light's cirteria for exudative?
pleural fluid protein > 0.5
pleural LDH > 0.6
Pleural LDH > 2/3 upper limit normal serum
What are the sx and signs of pleural effusion?
pleuritic pain, dyspnea, peripheral edema, orthopnea, PND

Signs- dullness to percussion, decreased breath sounds, bronchial breathing over compressed area, egophony, decreased tactile fremitus, pleuritic friction rub
What the dx signs on CXR?
meniscus sign, blunting of costophrenic angle
What are the positions in order of increasing sensitivity for CXR diagnosis of pleural effusion?
supine, P/A, lateral, lateral decubitus (lie of the bad lung side)
Besides CXR, what are the other imaging techniques used for pleural effusion?
ultrasound and CT
What do you look for in thoracentesis in pleural effusion?
CBC (neutrophils- acute, lymphocyte-TB or cancer)
gram stain/smear/Cx
glucose: low in RA
LDH: inflammation
cytology: cancer
TB markers: IFN-g, PCR
pH- (urinothorax has low pH, low pH in inflammatory conditions, parapneumonic effusion or malignancy has poor prognosis)
What is the complication of thoracenteses?
pneumothorax
What are the treatments for pleural transudates, exudates, and parapneumonic effusion?
transudates- diuretic, Na restriction, thoracentesis for palliative relief
exudative- underlying cause
parapneumonic- antibiotics or empyemia: drainage, injection of thrombolytic agents, and surgical lysis of adhesions
What are causes of primary/ secondary spontaneous pneumothorax? Pathophys?
idiopathic, paraseptal emphysema, Marfan

rupture of subpleural/intrapleural bleb --> escape of air into pleural space

secondary: underlying lung disease (COPD, asthma, ILD, CD, TB, and malignancy)
What are the signs and sx of spontaneous pneumothorax?
sudden dyspnea w/ pleuritic chest pain.
decreased or absent breath sound, hyperresonance, mediastinal shift and tracheal deviation toward pneumothorax. DxL displaced visceeral pleural line

Tx: primary- observation or small chest tube/oxygen.
secondary- chest tube drainiage due to poor pulmonary reserve.
What are the causes of tension pneumothorax?
penetrating trauma, rupture of tension pneumatocysts, mechanical ventilation, CPR
What is the pathphys of tension pneumothorax?
flap-like pleural teat allows atmospheric air to enter but not escape (one-way) --> compression atelectasis
What are the sx and signs of tension pneumothorax? tx?
sudden onset severe dyspnea

absentbreath sounds, hyperresonance, hypotension, JVD, mediastinal shift away from affected side

chest decompression (need in 2nd or 3rd intercostal space)
What is a strider and what are the types and what are they caused by?
abnormal high-pitched sound produced by turbulwent airflow through partially obstructed airway at larynx or trachea

inspiratory- laryngeal obstruction
expiratory-tracheobronchial obstruction
biphasic- subglottic or glottic
What is stertor?
harsh discontinuous crackling sounds heard over the larynx or trachea
What are the causes of tracheal stenosis?
extrinsic: masses, vascular anaomalies, lymphadenopathy
intrinsic: intubation, autoimmune, amyloidosis, foreign bodies infection/TB, masses, trauma
What is the treatment of tracheal stenosis?
dilation with rigid bronchoscope, laser surgery, resection and reconstruction
What are causes of laryngeal carcinoma?
smoking, alcohol, HPV, GERD, Toxic, race, poor nutrition, weak immune
What are sx of laryngeal cancer?
persistent cough, sore throat. Breathing difficulties, globus sensation, lump or mass, ear pain, hemoptusis, voice changes
How do you diagnose and tx laryngeal cancer?
history and physical, direct visualisation, CT w/ contrast, MRI and PET-CT, chemo vs surgery
What 2 bacteria normally cause epiglottitis?
h. flu type B and strep pneumoniae
What are the sx of epiglottitis?
triad: drooling, leaning forawrd, dysphagia, toxic appearance, anxious, and tripod position

odynophagia and dysphagia most common in post-vaccine era
What is the dx and tx of epiglottitis?
dx: thumb sign on XR, secure airway --> blood Cx and sputum culture, fiberoptic laryngoscopy, percutaneous transtracheal ventilation

secure airway and ventilate, 3rd gen cephalosporin to cover most organisms
What does aspiration pneumonitis represent?
chemical damage
What is caused by chronic, unwitnessed, inhalation of small oropharyngeal contents that leads to infectious process?
aspiration pneumonia
What are chronically impaired airway defense mechanisms that cause aspiration pneumonia?
impaired gag reflex, cough reflex, ciliary action, immune mechanisms
What is the tx for aspiration pneumonia?
stabilize airway, oropharyngeal/trracheal suctioning, antibiotics, surgical airway deviation
What are risk factors for DVT?
age >60, lupus, malignancy, hx, immobilization, CHF, obesity, major surgery, trauma, pregnancy, estrogen, nephroticc, hypercoaguable states

virchow's triad
What are the clinical features of DVT?
LE edema and pain, Homan's sign, palpable cord, erythema, fever
How do diagnose DVT?
Doppler/Duplex ultrasound, venography (accurate but invasive_, impedance plethysmography (not specific), D-dimer (not specific)
What are the complications of DVT?
DVT, postthrombotic syndrome (chronic venous insufficiency), phelgmasia cerulea dolens,
What is the tx of PVT?
Anticoagulant: heparin or LMWH
Thrombolytic: streptokinase urokinase, or tPA
IVC filter
How do you prevent DVT?
compression, ambulation, heparin or LMWH
Besides DVT, what are the causes of PE?
fat, amniotic fluid, air, oil, and septic
What is the pathology of PE?
venous thrombi are firable masses of fibrinous exudate that can produce red-blue, raised, wedge shaped areas of obstruction extending to pleural surface.
What is the difference between patients w/ and w/o pre-existing cardiopulmonary disease?
pre-existing disease causes pressure to increase out of proportion and they can't compensate
What happens to V/Q ratio, dead space, ventilation, and surfactant in PE?
high, high, hyper, low --> atelectasis
What is the effect of PE on the heart and what are the signs?
acute right ventricular strain, chest pain, tachycardia, S4 heart sound, prominent P2
How do you diagnose Pe?
ABG- low PCO2 (hyperventilation), low PaO2 (hypoxemia)
CXR: r/o other stuff, Westermark's sign and Hampton's hump
V/Q: preferred when pregnant to spiral CT
Spiral CT: best test, but may miss small sub segmental defects in periphery, CI in unstable or RF pts
Pulmonary Angiography: gold, but invasive
EKG: sinus tachycardia, S1Q3T3
D-dimer- not specific
What is the prognosis of PE?
resolution with lytics or recurrent/chronic PE and pulmonary HTN
What is the Tx of PE?
supplemental oxygen, anticoagulant: heparin or LMWH (aPTT), warfarin (PT/INR), lutics, IVC filter.
What is HIT? What is the pathophys?
platelet destruction or consumptive coagulation after heparin administration w/ resultant thrombocytopenia. Association w/ thrombosis.

Heparin bind to platelet factor 4 --> IgG production --> heparin-PF4-IgG complex

Type I (aggregation and consumption) < 48hrs
Type II splenic platelet destruction (Type II hypersens) 5-14 days
What are the clinical features of HIT? Tx?
cutaneous bleeding, mucosal bleeding, post-op bleeding

Type I- nothing
II- discontinue (protamine sulfate reversal), direct thrombin hinhibtors (lepirudin, argatroban) or factor Xa inhibitors (fondaparinux)
What is the process of Type I hypersensitivity?
sensitization: antigen --> APc --> Th2 --> b cell maturation/switching --> IgE production

re-exposure: allergen crosslink w/ IgE on mast cells
early: histamine and other preformed --> bronchoconstriction and edema
late: mast cells PRODUCE prostaglandins and leukotrienes --. prolong acute inflammation
What are the tests to evaluate type I hypersensitivity?
scratch test (wheal and flare reaction) and radioimmunosorbent test
What is the treatment for type I hypersensitivity?
Desensitization therapy: IgG antibodies that attach to allergens to prevent IgE cross-linking
What is the process of type II hypersensitivity?
Lysis: IgG or IgM antibodiese against on cell membrane activates COMPLEMENT MEDIATED MEMBRANE ATTACK COMPLEX AND SUBSEQUENT LYSIS
Phagocytosis: macrophages phagocytose RBCs coated by IgG and/or complement C3b
Complement-Independent reactions: leukocytes (NK or eosinophils) w/ IgG or IgE receptors lyse but do not phagocytose antibody coated cells
IgG autoantibodies directed against cell surface receptors
What are diagnostic tests to evaluate type II hypersensitivity?
Coombs (direct and indirect)
What are the stages of type III hypersensitivity? What is the reaction associated with type III?
First exposure: antibody synthesis
Second exposure: deposition of antigen-antibody --> complement activation --> C5a attracts neutrophils --> inflammatory damage

Arthus reaction: localized immunocomplex reaction
What is the diagnostic test to evaluate type II hypersensitivity?
immunofluorescent staining of tissue
What are the 2 subtypes of type IV hypersensitivity?
delayed reaction hypersensitivity: CD4 helpter T cells interact w/ APCs --> cytokine mediated tissue injury
Cell mediate hypersensitivity: CD8 cytotoxic T cells neoplastic, virus-infected, or donor graft cells
What are the diagnostic tests for type IV hypersensitivity?
Pach test and skin reaction to candida
A newborn has meconium ileus and nasal polyps at birth. The doctor runs a PCR and detects a mutation: deltaF508 detected. What other technique could he have used to diagnose both the mutation or the suspected condition? What will he show in early childhood? What is the prognosis?
Allele specific nucleotide or Sweat chloride test/ pilocarpine iontophoresis
steatorrhea, fat soluble vitamin deficiency (ADEK)

Live to 30s
What is the NaCl content on skin and in secretions?
high, low
Where are the regions with dehydration in CF?
bronchioles, pancreatic ducts, bile ducts, intestines, and seminal fluid
A patient has thick mucus secretions and nasal polyps. The are coughing, wheezing, have clubbed fingers, general malaise, decreased appetitie, and fever. What bacteria would you expect to find in their sputum? What disease would you expect secondary to these infections?
P. aeruginosa, S. aureus, B. cepacia
chronic sinopulmonary and bronchiectasis/ endobronchial disease
A patient comes in with coughing, wheezing, have clubbed fingers, general malaise, decreased appetitie, and fever. They are thin, have steatorrhea, and are sterile. What do you expect on CXR and spirometry?
CXR: central bronchiectasis, bronchial wall thickening, mucus plugging

spirometry: obstructive lung disease, FVC downward trend
A patient shows the following results:
CXR: central bronchiectasis, bronchial wall thickening, mucus plugging
spirometry: obstructive lung disease, FVC downward trend

How would you tx the patient?
annual CXR, sputum (2x), spirometry
physiotherapy, N-acetylcysteine, recombinant human DNAse, bronchodilators, antibiotics
A sterile patient with salty sweat and central bronchiectasis on CXR will die of what? If they live long enough, what is a complication?
respiratory infection around 30
cor pulmonale
A patient with dry pancreatic secretions will have steatorrhea, but rarely type I diabetes because __________. What is a consequence of their dry secretions?
exocrine function is compromised, but endocrine remains

--> atrophy and damage to pancreas
deficiency of ADEK, malabsorption of fat (steatorrhea) and protein --> failure to thrive
loss of HCO3- and H2O to assist in absorption
A pt presents with asymptomatically high LFTs and difficulty conceiving. What yearly tests/ daily maintenance should you run on him?
LFT, stool quality/frequency, weight gain and growth, vit deficiencies
A sweaty baby has failure to thrive with steatorrhea. What could help correct this problem?
Pancreatic enzyme replacement therapy and H2 blockers
What are causes to bronchiectasis?
cystic fibrosis (MC), TB, infection, bronchogenic tumor (obstruction), Kartagener's, aspergillosis
A SMOKER comes in with productive cough over 3 months over the last 2 years. What condition is he immediately diagnosed with? What do you expect in his histologically bronchi? Bronchioles?
chronic bronchitis

mucus gland hypersecretion/hypertrophy (Reid index), loss of ciliated epitelium (squamous metaplasia)

mucus plugging --> CO2 retention --> respiratory acidosis
goblet cell metaplasia, mucus gland hypertrophy
chronic inflammation and fibrosis of terminal bronchioles with luminal narrowing
A patient has a productive cough for 3 months per year for over 2 years. When do you expect hypoxemia and dyspnea to occur? What do you expect to see clinically?
early (cyanosis- blue bloaters) COR PULMONALE
late (they don't try)

stocky, prolonged expiratory phase, wheezing, decreased breath sounds, crackles, tachypnea, tachycardia
You have a patient with a constant chronic productive cough and thin, rosy cheeked patient who is constantly hyperventilating. Who will develop cor pulmonale first?
the first (chronic bronchitis --> hypoxemia --> vasoconstriction --> pulm HTN --> RVH --> RHF)
A patient with a constant chronic productive cough with cyanosis will have what findings on CXR?
hyperinflated lungs, depressed diaphragms, cardiomegaly (hypoxemia --> pulm HTN), thickened bronchial wall markings "tram track lines"
A pt with hyperinflated lungs and cardiomegaly on CXR with prolonged expiratory will have what ABG/blood pH and why?
chronic respiratory acidosis
PaCO2 > 45
HCO3-> 30 (compensatory metabolic alkalosis)
A patient shows emphysema with elastic tissue destruction in distal terminal bronchioles and respiratory bronchioles. Why do they show large lungs? Where are lesions primarily?
air trapping due to loss of normal radial traction and airway collapse
apical segments of upper lobes (air)
A patient shows emphysema with elastic tissue destruction in distal terminal bronchioles and the entire respiratory bronchioles? Where do you tend to see the lesions? What is the condition called? What causes it?
lower lobes (more neutrophils)
panacinar emphysema
alpha1 antitrypsin deficiency (abnormal piZZ versus normal piMM)
A smoker with a piZZ mutation and no crackles displays dyspenea and hypoxemia when?
early, late
A patient has hyperinflated lungs, flatened diaphragms, prolonged expiratory phase, no cor pulmonale, deminished peripheral vascular markings, what do you expect in ABGs?
high V/Q, normal to decreased PaCO2 (hyperventilation), late hypoxemia
What are the non-pharmalogical tx of COPD?
stop smoking, oxygen therapy, vaccines
A pt is in the hospital with a COPD flare-up. What do you suspect? Wht non-pharmalogical tx do you give?
infection, noncompliance, and cardiac disease
BIPAP or CPAP, intubation
After a pt develops hypoxemia in COPD, what do you start testing them for?
elevated hematocrit, pulmonary HTN, cor pulmonale
What characterizes each stage of sleep/waking?
awake- beta waves
awake- relaxed, eyes closed- alpha waves
stage 1: theta
2: K complexes, sleep spindles
3: delta waves
4: delta waves
When does REM occur?
every 90-100 minutes, lasting 10-30 minutes
What controls respiration during sleep? What does it receive information from (3)?
central respiratory pattern generator in medulla
higher cortical centers
mechanical receptors in chest wall and lung
central and peripheral chemoreceptors
What happens to alveolar ventilation, PaCO2, PaO2, Vt, Resistance, Oxygen consumption, and ventilatory response? Which of these decreases less in REM?
all of them decrease except resistance. oxygen consumption
Duriong night, a person with COPD/CF/IPF displays respiratory acidosis. During the day, he's normal. Why?
blunted response to hypoxia and hypercapnia
What occurs hemodynamically during sleep?
pulm artery p increases
SVR decreases
HR/CO decrease
How do you expect a pt with asthma to worsen at night?
nocturnal bronchoconstriction
How do you expect a patient w/ COPD to worsen at night?
hypercapnia, hypoxemia, oxy sat falls
What are indications for non-invasive positive pressure ventilation support in COPD?
severe COPD and persistent Sx despite medical therapy
severe daytime CO2 retention or hospitalization for recurrent hypercapnic respiratory insufficiency
nocturnal oxygen desaturation > 5 min while receiving oxygen therapy
motivated pateint
What are indications for non-invasive positive pressure ventilation support in restrictive and neuromuscular disease?
worsening of dyspnea or orthopnea, Vt<50%, morning HA, maximal inspiratory force <60 cmH2O, daytime hypersomnolence
Define the following terms:
apnea, hypopnea, respiratory effort related arousal, apnea-hypopnea index, respiratory disturbance index
apnea: cessation or near >10 sec
hypopnea >30% reduction of airflow >10 sec w >4% desaturation
RERA- breathing wakes you up shown by progressively negative esophagel pressure or flattening of nasal pressure waveform >10 sec
AHI- total number of apnea & hypopnea / hr
RDI- average apnea + hypopnea + RERAs/hour
Define normal, mild, moderate, and severe sleep apnea?
AHI<5
5<AHI<15
15<AHI<30
>30
What are the 2 sleepiness scales?
Stanford and Epworth
What is measured during polysomnography?
EEG: sleep stage scoring
EOG: REM determination
chin EMG: REM determination
anterior tibilias EMG: detect periodic limb movement (PMLS)
respiratory monitors
video monitors
A pt presents with intermittent obstruction of airflow which produces apnea. They snore excessively and have daytime sleeping (hypersomnolence).l They show respiratory effort, but an occlusion prevents airflow. What are possible causes?
obstructive sleep apnea
obesity collapses pharyngeal muscles
Structural abnormalities: enlarged tonsils, uvula, or soft palate, nasal obstruction (polyps, turbinates, deviated septum), hypertrophy of pharyngeal muscles, enlarged tongue base, retrognathia, micrognathia
An obese pt comes in with hypersomnolence, excessive snoring, morning HA, decreased intellectual function and libido, and respiratory acidosis. What do you expect to find with their heart in several years? Blood?
pulmonary HTN, cor pulmonale, systemic HTN, cardiac arrhythmias
secondary polycythemia (chronci hypoxemia)
A pt comes in w/ obstructive sleep apnea. Besides sleep hygiene and positioning, what is the most effective non-invasive or medical tx?
WEIGHT LOSS, you fat fuck
What is the preferred noninvasive therapy for obstructive sleep apnea?
nasal continuous positive airway pressure
What are drastic surgical therapies used after CPAP in obstructive sleep apnea?
uvulopalatopharyngoplasty
septoplast, turbinoplast
tongue base radiofrequency ablation
genioglossus advancement
hyoid suspension
A morbidly obese pt comes in hypersomnolence, dyspnea. His tests show hypoxemia, cyanosis, polycythemia, cor pulmonale, and peripheral edema. He shows hypoventilation during wakefulness. What 2 concurrent syndromes does he likely have? What are the 2 possible treatments?
obesity-hypoventilation syndrome (Pickwickian syndrome) and obstructive sleep apnea

weightloss and phelbotomy
A pt has episodes sleep apnea w/ frequent arousal from sleep, difficulty maintaining sleep, and hypersomnolence. You bring the patient in for a polysomnography and they don't appear to have respiratory muscle effort. What are possible causes?
Central sleep apnea

idiopathic
CHF or CVA --> Cheyne-Stokes
acromegaly, hypothyroidism, renal failure
high altitidue
drugs
CNS disorders (autonomic dysfunction, neuromuscular disease, poliomyelitis, myasthenia gravis, encephalitis, brain stem infarction
What are Cheyne Stoke respirations and what causes it? What kind of apnea is it seen in?
crescendo-decrescendo hypernea alternating with apnea/hypopnea
longer in pts w/ CHF
central
What apnea is CPAP or oxygen not useful in?
Central