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179 Cards in this Set
- Front
- Back
What are 5 causes of hypoxemia?
|
Shunt
V/Q mismatch Diffusion abnormality Alveolar hypoventilation Reduced FiO2 |
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What are 3 causes of hypercapnia?
|
Alveolar hypoventilation
Increased dead space ventilation Increased CO2 production in setting of fixed ventilation |
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Obstructive Disease Mnemonic
|
Foreign body
Asthma Chronic bronchitis + bronchiectasis Emphysema Small vessel disease |
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Restrictive Disease Mnemonic
|
Pleural
Alveolar filling Interstitial lung Neuromuscular Thoracic cage |
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What is the most common reason for hypoxemia in ILD?
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V/Q mismatch
|
|
Broad-based budding and multiple nuclei
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Blastomycosis
|
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Pleomorphic yeast with mucinous capsule
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Cryptococcus
|
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Necrotizing granulomas with small yeast on silver or PAS
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Histoplasmosis
|
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Spherules with endospores
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Coccidiomycosis
|
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How does inflation of the lung effect blood flow?
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Alveolar vessels are compressed as lung expands
Extraalveolar vessels are pulled open by the lung parenchyma |
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Transmural pressure of alveoli
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P_intravascular - P_alveolar
|
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Lung zones 1,2, and 3
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Zone 1: PA > Pa > Pv = DEAD SPACE
Zone 2: Pa > PA > Pv Zone 3: Pa > Pv > PA |
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Effect of high PACO2 and low pH on pulmonary vascular resistance
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Vasoconstriction but weaker than hypoxemia
|
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NO and Atrial natriueretic factor
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Relax pulmonary smooth muscle
|
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Prostaglandin I and platelet activating factor effect on pulm vascular tone
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Decrease
|
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Starling's law for pulmonary capillaries
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(P_cap - P_interstitial) - (Oncotic_cap - Oncotic_interstitial)
|
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Pulmonary arterial pressure equation
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Pa = PVR*CO + PCWP
|
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Causes of pulmonary hypertension (use equation) (3)
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Increased CO - left -> right shunts
Increased PVR - hypoxic vasoconstriction, tumor, inflammation Increased PCWP - left ventricular disease (mitral stenosis) |
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Fetal circulation shunts
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Ductus arteriosus - Pulmonary artery to aorta
Foramen ovale Hypoxic vasoconstriction in utero is released at birth allowing flow through lungs |
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Minute ventilation
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Respiratory rate X Tidal volume
Normal is 5-6 L/min |
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Physiologic dead space equation
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VD/VT = (PaCO2 - PeCO2)/PaCO2
Usually = .3 ((40-28)/40) |
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Pressure of oxygen starting from atm thru venous
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Atm - 160
Trachea - 150 Alveolus - 104 Arterial - 100 Venous - 40 |
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Factors regulating bronchial smooth muscle tone
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Parasympathetic - constriction
Sympathetic - dilation Inflammatory mediators (leukotrienes, prostaglandins), chemical irritants, immediate hypersensitivity response (histamine) -> constriction |
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Where is the majority of airway resistance?
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Large airways due to small total cross sectional area
|
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Collapsing tendency of lung is due to what 2 forces?
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Elastic recoil - 1/3
Surface tension - 2/3 |
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As radius decreased does surface tension get bigger or smaller?
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Bigger
P= 2T/r More pressure is required to keep it from collapsing Surface tension makes T vary with r so that P is constant and smaller alveoli dont collapse into larger |
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Function residual capacity
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Relaxation volume.
Tendency for lung to recoil inward and for chest wall to spring outward is balance Palv = Patm |
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Factors that increase airways resistance
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Smooth muscle hypertrophy/hyperplasia
Abnormal smooth muscle contraction Mucus gland/goblet cell hypertrophy Excess mucus Inflammatory cell infiltation Edema of airway wall |
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What causes hyperinflation?
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B/c of expiratory flow limitation, cannot expire all of air and is still expiring when have to take next breath. They increase lung volume so that the airways can stay open long enough to breathe
|
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Factors that decrease compliance (6)
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Fluid or air in pleural space
Thickening or fibrosis of pleural space Flooded alveoli Fibrotic interstitium Infiltration of interstitium Thoracic cage less mobile or more difficult to expand |
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How is most O2 and CO2 transported in blood?
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O2 on hemoglobin
CO2 as bicarbonate |
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Haldane effect
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Oxygenation of blood decreases the amount of CO2 bound to hemoglobin
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Causes of increased PaCO2 using the alveolar ventilation equation
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Decr minute ventilation (cant breathe due to muscle weakness or wont b/c of cns depression
Incr dead space Incr VCO2 alone does not incr PaCO2 in health, only w/ underlying disease due to inability to increase minute vent |
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Shunt vs dead space
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Shunt - perfusion w/o ventilation
Dead space - ventilation w/o pefusion |
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Pulsus paradoxus
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Abnormally large decrease in systolic pressure upon inspiration
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Around what PaO2 is hemoglobin saturated?
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60 mmHg
|
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4 causes of v/q mismatch
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COPD
Pulmonary embolism Pulmonary edema Pneumonia |
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Equation for carrying capacity of oxygen
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CaO2 = 1.34(Hgb)(SaO2) + .003(PO2)
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Equation for oxygen delivery
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DO2 = CaO2 X CO
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Classic sign for PAH
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Dyspnea on exertion
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Two explanations for reduced DLCO
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Membrane component - interstitial lung disease
Capillary component - pulmonary hypertension |
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What makes sputum green?
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Neutrophils
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What is the mechanism for hypoxemia in COPD?
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V/Q mismatch due to airway disease
|
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Key criteria for ARDS (4)
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Bilateral infiltrates
PaO2/FiO2 < 100-200 Decreased compliance No evidence of cardiogenic |
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Effects of hyperinflation on diaphragm
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Fibers shorten and decrease force ->
Inability to increase ab pressure, paradoxical inward movement of abs on inspiration |
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Consequences of respiratory muscle dysfunction (3)
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Hypoventilation
Aspiration (malfunction of upper airway muscles) Impaired cough |
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Dorsal respiratory group
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Inspiratory ramp signal cycling
|
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Ventral respiratory group (3)
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PreBotzinger complex - rhythm generator w/ pacemaker cells that excite DRG
Inspiratory neurons receive input from DRG Expiratory neurons output to expiratory muscles for exercise |
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Apneustic center
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Excitatory effect on VRG to prolong ramp action potentials
(triggered if a-pneu) |
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Pneomotaxic center
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Switch off inspiration
(triggered if pneumo) |
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Ventilatory response to hypercapnia
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Linear in the physiologic range of PaCO2
PO2 levels affect sensitivity of response of CO2 receptors so there is a stronger response to hypercapnia if hypoxemia is present |
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Ventilatory response to hypoxemia
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Aortic and carotid bodies sense PO2 drops < 60 mmHg
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Central chemoreceptors
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Increased CO2 ->
CO2 crosses BBB -> Elevated H+ detected in CSF |
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Hering-Breuer Reflex
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Slowly adapting pulmonary stretch mechanoreceptors in tracheobronchial tree
Fire when lung volume increases Sends signal via CN X to pneumotaxic center to terminate inspiration |
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Rapidly adapting stretch receptors
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In upper airways
Respond to tissue distension and irritation (cough) |
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J receptors
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In alveoli and small conducting airways
Respond to interstitial edema and engorgement of pulm caps -> closure of larynx and apnea and rapid shallow breathing |
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Apnea vs hypopnea and apnea-hypopnea index
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Apnea = complete lack of airflow for < 10 s
Hypopnea = airflow reduction of > 30% assoc w/ oxy desat of > 4% AHI = #apneas+hypopnease / total sleep time OSA = AHI >5 |
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Obstructive sleep apnea
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Central drive is working but upper airway collapse obstruct breathing during sleep
|
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Obesity-hyperventilation syndrome
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Progressive accumulation of CO2 over time and brainstem no longer response to hypercapnia
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OSA associated features (6)
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Depression
EDS GERD Impotence Anxiety Cognitive |
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OSA treatment (3)
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Avoid alcohol, depressants
Weight loss CPAP |
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OHS (3)
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BMI > 30
Daytime PaCO2 > 45 No other causes (mech = leptin resistance?) |
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OHS presentation
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Sleepiness
Morning headaches Mood Dyspnea |
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OHS treatment (2)
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Respiratory stim
Mechanical vent |
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Albuterol (SE?)
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Short acting B2 agonist ->
Incr cAMP -> Relaxes smooth muscle B1 side effects: tachycardia, HTN OSA: 10-20 min for 4-6 hr |
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Salmeterol
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Long acting B2 agonist
Slow onset Long duration |
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Ipratropium
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Short acting anticholinergic (blocks muscarinic action)
More effective in COPD than asthma since more enhanced parasymp tone in COPD |
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Tiotropium
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Long acting anticholinergic
Less affinity for M2 which is inhibitory for negative feedback so greater bronchodilatory effects |
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Theophylline
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Methylxanthine phosphodiesterase inhibitor ->
Incr cAMP Weak bronchodilators but might also be anti inflammatory, respiratory stimulant CYP450 metabolism so lots of drug interactions |
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Leukotriene antagonists
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Inhibiit 5-lipoxygenase or block LT receptors
Leukotrienes enhance inflammatory response and cause bronchoconstriction |
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Inhaled corticosteroids
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Principally anti inflammatory but have lots of systemic SE: cataracts, osteoporosis, oral thrush from deposition in mouth
|
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Cromolyn
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Blocks release of histamine and leukotrienes from mast cells
For exercise-induced asthma and pediatrics |
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Nedocromil
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Blocks release of mediators from eosinophils, macrophages, platelets, and mast cells
|
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Broncho vs lobar pneumonia
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Broncho is patchy distribution in terminal and resp bronchioloes
Lobar is diffuse uniform CONSOLIDATION of an entire lobe |
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Stages of lobar pneumonia
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Congestion - vasc dilation and fluid accumulation in alv
Red hepatization - consolidated and red w/ vascular congestion and intra alv exudate (protein, RBC, PMNs) Gray hepatization - firm lobe, bloodless septa and alv spaces filled w/ PMNs + fibrin Resolution - enzymatic digestion of exudate and restoration of normal lung |
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Gram positive diplococcus
Most common cause of CAP |
Strep pneumococcus
|
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Gram negative rod
Exacerbations of COPD |
H. influenzae
|
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Gram positive cocci
Infections in IVDA Abscesses |
Staph aureus
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Gram negative rod
Alcoholics or debilitated patients |
Klebsiella
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Gram negative rod
CF or nosocomial Invades blood vessels |
Pseudomonas pneumoniae
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Weakly gram negative rod
Lives in H2O reservoirs Causes severe disease |
Legionella
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Aerobic gram positive rod
Filamenous Acid fast red In immunocompromised |
Nocardia
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Anaerobic gram negative
Filamentous In normal hosts oral cavity Acid fast neg |
Actinomyces
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Lung abscesses (what do they contain and what causes them?)
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Localized area of necrosis containing neutrophils
Aspiration of infective material, post infectious, septic emboli, tumors |
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Mycobacterium avium intracellulare complex
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AIDS patients w/ CD4 < 60
Disseminated Acid fast bacilli in macrophages if AIDS - no granulomas if no AIDS - caseating granulomas |
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Emphysema (2)
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Abnormal permanent distal (to terminal non resp bronchiole) airspace enlargement
Destructive changes in alveolar wall w/o fibrosis Smoking -> neutrophils -> proteases or ROS |
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Centrilobular vs panlobular emphysema (common causes for each)
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Centri - respiratory bronchioloes only, upper lobes, most common in smokers
Pan - whole acinus, lower lobes, a1 anti trypsin |
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Chronic bronchitis clinical diagnosis
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Clinical diagnosis:
Excess mucous Cough most days for 3 mo for 2 years Not necessary to have airflow obstruction |
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3 mechanisms of COPD
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1. Chronic inflammation - neutrophil recruitment and CD8s
2. Proteinase/antiproteinase imbalance 3. Oxidative stress - free oxygen radicals |
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Pathophys of COPD dyspnea (3)
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Increased WOB
Decreased diaphragm function Hypoxemia - due to airway obstruction -> v/q mismatch |
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Why is there hypercapnia in COPD?
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Increased dead space
|
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COPD treatment (4)
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Smoking cessation improves survival and O2 therapy if hypoxemic
Short acting bronchodilators for dyspnea Long acting bronchodilators and ICS Pulmonary rehab |
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Bronchiectasis (definition and etiologies)
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Permanent abnormal dilatation and destruction of bronchial walls
Requires infectious insult plus impairment of drainage, airway obstruction, and/or defect in host defense |
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Pathogenesis of cystic fibrosis lung disease
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Defective CFTR does not put Cl- into lumen, Na goes into cell and water follows leaving dry mucus ->
Infection and inflammation |
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PFTs in CF and treatment
|
Mixed
Airway toilet via chest PT Antibiotics - inhaled tobimycin DNase B2 agonists NOT anticholinergics (Pseudomonas infections may be lethal) |
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Pathophys hallmarks of asthma (4)
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Airflow obstruction caused by bronchoconstriction
Airway edema AHR Airway remodeling |
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Clinical hallmarks of asthma (3)
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Intermittent cough
Dyspnea Wheezing |
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Asthma pathogenesis (5)
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APC in airway epithelium bind allergen via IgE -> activate (overexpressed Th2 cells -> IL secretion -> eosinophil recruitment and mast cell activation -> AIRWAY INFLAMMATION
|
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Asthma: early vs late bronchospasm
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Early - 30 minutes, activated macrophages, cells release inflammatory mediators -> bronchospasm, vasodilation, edema, mucus secretion
Late - 4-6 hr, recruit and activation of eosinophils -> lots of cytokines and mediators -> AIRWAY INFLAMMATION, mucus secretion, edema, bronchoconstriction |
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Asthma: causes of chest tightness and dyspnea
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Airflow obstruction (2/2 inflam, b/c, mucus, remodling) -> increased w.o.b, v/q mismatch, hyperinflation
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Asthma PFTs
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Obstructive but improve w/ BD
Normal DLCO Lung volumes can be increased |
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Asthma: 4 features of airway remodling
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Loss of ciliated epithelial cells and increase in mucus by goblets
Thickened BM Fibroblast activation w/ collagen Smooth muscle hyperresponsiveness and hypertrophy |
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Asthma differential
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Children - foreign body asp, CF
Adults - GERD, postnasal drip, bronchiectasis, sarcoid, copd . . . |
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Asthma treatment steps (5)
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SABA
ICS ICS + LABA ICS + LABA + LTM Anti IgE |
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Chronic bronchitis histology (4)
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Increased size and # of mucus glands
Increased Reid index Goblet cell hyperplasia Chronic inflammation |
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Bronchiectasis gross and histo
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Dilated bronchi and bronchioles
Ulceration Inflammation + fibrosis of bronchial wall Squamous metaplasia |
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ILD: Physiology (3 steps, O2 and CO2)
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Decreased compliance (due to fibrosis) ->
Increased w.o.b. -> Decreased PaO2 (w/ exercise) Hypercapnia as disease worsens b/c CO2 is more diffusible V/Q mismatch |
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What is major cause of hypoxemia in ILD
|
V/Q mismatch
|
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ILD Radiology (two key findings)
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Diffuse bilateral infiltrates
"Ground glass" -> inflammation Honeycomb -> fibrosis |
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Smoking related ILDs (3)
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DIP, RB-ILD, Langerhans cell histiocytosis
|
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Pulmonary fibrosis complications (5)
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Respiratory failure
PE Lung cancer Pneumothorax PH/cor pulmonale |
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Cryptogenic organizing pneumonia (presentation, etiology, Rx)
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Pres: cough, dyspnea, weight loss, flu
Can be secondary or idiopathic Rx: steroids |
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Sarcoidosis (3 findings)
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Findings: enlarged hilar lymph
Well-formed non caseating non necrotizing granulomas Eleveated ACE |
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Diffuse alveolar hemorrhage (2 examples)
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Goodpasture's - anti GBM
Wegener's - c-ANCA Both are systemic |
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IFN-gamma vs TGF-beta
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IFN - proinflammatory and antifibrotic
TGF - profibrotic and antiinflammatory |
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Hypersensitivity pneumonitis (granulomas?)
|
Type III and IV (granuloma formation
CD8 proliferation Chronic can progress to fibrosis |
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UIP vs COP
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UIP - diffuse (also AIP)
COP - patchy (also sarcoid) |
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Viral pneumonia histology
|
Chronic interstitial infiltrate: lymphocytes, plasma cells, macrophages
DAD - hyaline membranes |
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Fungal pneumonia infection histo
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Necrotizing granulomas w/ rim of histiocytes
Silver stains identify fungus |
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Miss. river and bat droppings
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Histoplasmosis
|
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Waterways, Central US
|
Blastomycosis
|
|
Southwest US, Mexico
|
Coccidiomycosis
|
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Cysts with black dot in center
Low CD4 count AIDS patients |
Pneumocystis jiroveci
|
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Aspergillosis (immunocompetent vs compromised)
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Competent - allergic bronchopulmonary aspergillosis (mucoid impaction of bronchi, eosinophils), fungus ball
Compromised - invasive |
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If necrotizing granuloma in fungal pneumonia . . .
|
Histoplasmosis
Coccidiomycosis Blastomycosis |
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Physiologic response to hypoxemic respiratory failure (type I)
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Increased catecholamines -> incr HR
Incr carotid body stim -> tachypnea -> incr vent |
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Physiologic response to hypercapnic respiratory failure (type II)
|
decr pH
incr ICP -> CO2 necrosis |
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Physiologic adaptation to chronic resp failure (2)
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Incr erythropoietin -> incr hgb
Incr bicarbonate so less severe acidosis |
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Causes of acute respiratory failure type I (6)
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anything that can cause shunt or v/q mismatch
ALI - ARDS Pneumonia Cardiogenic pulm edema PE Pneumothorax Severe acute ILD |
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Causes of acute resp failure type II (5)
|
Drugs
Spinal cord injury Acute neuromuscular disease (guillan barre, als) COPD exacerabation Status asthmaticus |
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O2 therapy for acute vs chronic hypoexmia
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Acute - high flow high FiO2
Chronic - low flow, lower FiO2 |
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O2 therapy complications (3)
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Resorption atelectasis
Hypercapnia in COPD (due to incr dead space, haldane effecte) ALI |
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Indications for mechanical ventilation (3)
|
Refractory hypoxemic respiratory failure: shunt, atelectasis
Ventilatory (hypercapnic) resp failure Inability to protect airways |
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NIV indications
|
COPD exacerbations and immunocompromised hosts
|
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What causes resorption atelectasis in O2 therapy
|
High concentration of O2 washes out NO which was helping to keep airways open
|
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3 things that cause hypercapnia in COPD when given O2 therapy
|
1. O2 releases hyopemic vasoconstriction
2. Haldane effect 3. Abnormal respiratory drive means COPDers cant correct minute ventilation when VCO2 goes up |
|
Causes of ARDS
|
Pulmonary - pneumonia, aspiration, inhalation, chest trauma
Extrapulmonary - sepsis, shock, trauma, transfusion |
|
ARDS pathophys (3 steps with 5 results)
|
Acute lung injury ->
Increased permeability -> Increased lung water in interstitium and alveoli -> Decr compliance, shunt, hypoxemia, incr PA pressure from vasoconstriction, injured type II cells differentiate to type I |
|
Barotrauma, volutrauma, atelectrauma
|
Barotrauma - air leaks into pleural space -> pneumothorax
Volutrauma - overdistension of alveoli -> release of mediators -> biotrauma Atelectrauma - shearing force from constant opening and closing |
|
Granulomatous vasculitis with palisading histiocytes
|
Wegener's granulomatosis
|
|
Eosinophils, Birbeck granules
|
Langerhans
|
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UIP path (3)
|
Cobblestone pleura
Young = fibroblastic foci w/ spindle cells, Old = collagen |
|
COP path
|
Collagen plugs of fibroplastic tissue elongated in bronchioles
|
|
Acute interstitial pneumonia path
|
DAD w/ hyaline membranes like ARDS
|
|
DIP path
|
(similar to RB-ILD)
Alveoli filled w/ pigmented macrophages Not much fibrosis |
|
Alveoli filled w/ pigmented macrophages
|
DIP
|
|
Hypersensitivity pneumonitis path
|
Lymphocytic infiltrates around bronchioles extending to alv septae
Poorly formed, non necrotizing granulomas |
|
Definition of pulmonary hypertension
|
mean PA > 25 w/ PCWP < 15
If PCWP > 15, pulmonary venous hypertension |
|
How does hypoxia cause pulmonary hypertension?
|
Vasoconstriction leading to remodeling of vessels and abnormal presence of smooth muscle (peripheralization)
|
|
WHO PH groups
|
I - idiopathic PAH and PAH in setting of conn tissue disease (scleroderma), HIV, cirrhosis, portal HTN . . .
2 - PVH from left heart disease 3 - From hypoxia (sleep apnea, OHS, high altitude) or parenchymal (COPD) 4- - Thromboembolic |
|
PH treatment (3)
|
By pathogenesis:
Vasodilators (Ca blockers, endothelin antag, NO, prostacyclins, PDE5 inhibitors) Oxygen Anticoagulants |
|
Pathophys of PH (5)
|
Endothelial injury ->
Increase in vasoconstrictors/decrease in vasodilators -> Vasoconstriction -> Remodeling w/ smooth muscle -> In situ thrombosis |
|
Pulmonary embolism risk factors
|
Virchow's triad:
Stasis Inflammation Hypercoagulability |
|
Pulmonary edema path
|
Congested alv cap
Pink precipitate in alveolar spaces Heart failure cells = macs w/ hemosiderin |
|
ARDS path: acute (5)
|
Exudative
Edema Hemorrhage Hyaline membranes |
|
ARDS path: subacute (when and 2 features)
|
7-10 days after injury
Type II replaced by type I Fibroblasts in interstitium and alv spaes |
|
ARDS path: chronic (when and 2 features)
|
2-3 wks
Fibrosis w/ architectural distortion Cyst formation |
|
PAH histo (4)
|
Medial hypertrophy
Intimal thickening Muscularization of arterioles Angiomatoid and plexiform lesions |
|
Pleura blood supply
|
Visceral - arterial from bronchial systemic and venous to pulmonary (low pressure)
Parietal - arterial and venous both systemic (high pressure) |
|
Pleura lymphatics
|
Visceral - not involved in clearage
Parietal - via stoma |
|
Pleura innervation
|
Visceral - no sensory nerve endings
Parietal - richly innervated w/ sensory: costal and peripheral diaphragmatic via intercostal and central by phrenic for referred pain |
|
Identifying Exudate
|
Pleural fluid protein/serum protein > .5
Pleural fluid LDH/serum LDH > .6 |
|
Principle causes of transudative effusion (4)
|
CHF -> RV failure/increased systemic - increased parietal, LV failure/increased venous - visceral pleura
Hepatic -> transdiaphragmatic flow Nephrotic -> hypoalbuminemia Atelectasis -> decreased pressure in pleural space |
|
Why is gas absorbed from pleural space?
|
Because the sum of pressures in the venous blood in lower than the sum of pressure in the pleural space
|
|
Principle causes of exudative effusion (4)
|
Malignancy - disruption of mesothelium and caps
Inflammation Chylothorax - lymphatic obstruction of parietal pleura somata PE |
|
Parapneumonic vs empyema
|
Parapneumonic - infection in adjacent lung -> pleural effusion
Empyema - infection in pleural space |
|
Pleural effusion treatment: trans vs exudate
|
Transudate - underlying cuase
Exudate - can drain |
|
Pneuthorax presentation
|
Acute onset of pleuritic chest pain and dyspnea
Tension --> CHEST TUBE ASAP if large tension |
|
Pneumothorax types (4) and etiologies
|
Primary - idiopathic, in tall thin young men secondary to subpleural blub
Secondary - w/ underlying lung disease: COPD, CF, astham . . .rupture of distended alveoli w/ leakage of air into interstitial then pleural space Traumatic - penetrating wounds Iatrogenic - visceral pleura punctured during invasive procedures |
|
Pneumothorax Rx
|
If small, nothing or O2 to displace N2 in cap blood and reduce pressure so air goes into blood
If large, chest tube drainge or catheter aspiration |
|
Squamous cell carcinoma path (4)
|
Central
Cavitate Hypercalcemia Keratin pearls |
|
Adenocarcinoma (3)
|
Most common
Peripheral (Broncheoalveolar adenocarc grows in septae and doesnt invade) |
|
Large cell lung cancer (2)
|
Poorly differentiated
Central or peripheral |
|
Carcinoid
|
Has neuroendocrine differentiation
Low grade malignancy Can look like SCLC but w/ much fewer cells |
|
TTF-1 and CEA
|
Adenocarcinoma
|
|
Calretinin-1
|
Mesothelioma
|
|
Nasopharyngeal carcinoma
|
Associated w/ EBV
Upper cervical lymphadenopathy |
|
Key radiographic features of malignancy (4)
|
Increased size - > 2.5 cm
Ragged/spiculated margins Double time is b/w 2wks and 200 days Absence of calcification |
|
Equations for metabolic acidosis and alkalosis
|
dPaCO2 = dHCO3 X 1.25 (acidosis)
dPaCO2 = dHCO3 X .6 (alkalosis) |