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Pulm sb

clinical medicine

asthma chronic inflammatory disorder of the airways
atopy complex interaction between multiple genes and environmental factors, leading to IgE mediated response to allergens
asthma clinical findings cough, sob, wheezing, tachypnea, use of accessory muscles, wheezing, prolonged expiratory phase, agitation, cyanosis
differential of cough and wheezing in children CRADLE (cystic fibrosis, respiratory TI, aspiration, dyskinetic cilia, lung and airwary malformation, edema chf)
asthma evolution plasma cells in lung overreact and tell mast cells about it, in chronic esosinophils degranulate causing airway damage and eventually remodeling-fibrinoblasts lay down collagen
inhaled corticosteroid benefits sx diminish and improve gradually, decreases use of rescues, lung function improves, occurrence of exacerbations reduce
COPD many diseases characterized by chronic airflow obstruction
less than 0.7 post BD- fev1/fvc of_______ confirms COPD
Suspect COPD in patients over 40 with Dyspnea, chronic cough, chronic sputum production, exposure history, family history of COPD
Obstruction (PFT) FEV1 is reduced out of proportion to total volume of forced exhalation (FVC) Ratio of FVV1:FVC is reduced 70%
GOLD staging Gold 1- mild FEV1 >80% Gold 2- mod 50%<FEV1<80% Gold 3- Severe 30%<FEV1<50% Gold 4- very severe FEV1<30%
COPD risk factors Smoking, exposure to products of combustion, occupational dusts/fumes/vapors, airway hyper reactivity, genetics
COPD airflow obstruction Largely determined by resistance in small airways (airway remodeling, loss of elastic recoil, lumenal obstruction with mucous, bronchiolar lumenal narrowing
COPD hyperinflation Obstruction increases end expiratory volume (Increases elastic recoil, increases expiratory flow, mechanical disadvantage, positive alveolar pressure must be overcome to breath)
COPD V/Q mismatch variable from one pt to another, loss of hypoxic vasoconstriction, major determinant of decreases pao2
COPD decreased diffusing capacity loss of alveolar capillary bed, extent proportional to severity of emphysema
COPD alveolar hypoventilation Adaptive response to increase WOB, increase paco2 decrease pao2
Pink Puffer emphysema predominates, less alveolar surface are for gas exchange, hyperventilate to compensate, ABG normal
Blue Bloater Chronic bronchitis, alveolar space intact but airways obstructed, decrease ventilation, V/Q mismatch, air trapping, hypercanpia (CO increase)
COPD exacerbations amplification of baseline airway inflammation, precipitated by infections environmental pollutants smoking, major determinant of outcomes in pts
COPD tx, FEV1 >60% and no sx no pharm or a saba
COPD tx, FEV1 <60% saba, laba, ics, pulm rehab, oxygen, azithromycin
COPD exacerbation causes infections (most common), environmental pollution, unknown
Pulmonary Hypertension pathology small pulmonary arteries, vasoconstriction vascular remodeling
Pulmonary Hypertension diagnosis right heart cath, mean pulmonary artery pressure of greater than 25mmHg or mean pulmonary capillary wedge pressure of less than 15mmHg
Pulmonary Hypertension symptoms dizziness +/- syncope SOB chest pain ascities edema fatigue
mTB bacteria aerobic, nonmotile, bacillus with waxy lipid-rich outer wall (acid fast staining)
mTB pathogenesis TB hits alveoli, macrophages engulf, transport to hilar lymphnodes, CD4 Tcells try to kill create caseous granulomas
Primary TB refers to 1st exposure to inhaled infectious particles followed by flu-like illness, spread controlled sub pleural granulomas form, remain stable and no further spreading
Latent TB Infection mTB survive for decades in walled off lesions, not infectious, risk of reactivation
Reactivated TB causes Immune deficiency, AIDs, Immune modulated agents (occurs in 10-15% of pts half within 2 yrs of primary disease)
Reactivated TB symptoms worsen over months, cough with sputum, low grade fever, weight loss, fatigue, hemoptosis and pleuritic pain (severe disease)
Miliary TB initial exposure to mTB fails to incude cell-mediated immunity
Miliary TB physical exam chronically ill-appearing, LAD choroid TB in eyes (dx with transbronchial biopsy)
Screening for TB PPD (purified protein derivative) or interferon gamma release assay (IGRA)
Treating TB RIPE (rifampin, isoniazid, pyrazinamide, ethambutol) and vit b6
Fungal Pneumonia at risk populations neutropenics, lupus/RA, organ transplant recipients
Histoplasmosis transmitted by airborne spores inhaled from contaminated soil, primarily lungs and lymph chains (bat guano and chicken droppings)
Histobelt southern Ohio, Missouri, Tennessee, Arkansas, Kentucky, Illinois
Histo symptoms fever, fatigue, weight loss, hepatosplenomegaly, cough and dyspnea for greater than one month recurrent pneumonia
Histo dx testing urine histo ag or blood/BM cx
Histo, coccidiodomycosis, and blasto treatment liposomal amphotericin and itraconazole
Coccidiodomycosis geographic american southwest, mexico
Coccidiodomycosis transmitting by inhaling c immitis or c posadasil, 1-4 weeks of mild flu like illness, pleuritic chest pain resolves in a few weeks
Coccidiodomycosis DX IgM/IgG serologies, fungal comp fix panel, tissue biopsy
Blastomycosis geographic along mississippi, north, Canadian border
Blastomycosis least common, can infect lungs skin and bone
Ubiquitous fungi cryptococcus neoformans, aspergillosis
Cryptococcus neoformans more commonly meningitis, yeast, mostly infect immunocompromised
cryptococcus neoformans sx fever, weight loss, malaise, pleuritic pain, cough, wheeze, hemoptysis
Cryptococcus neoformans dx test serum cryptococcal
Crytococcus neoformans tx liposomal amphotercin, fluconazole
Aspergillosis mostly infects immunocompromised (leading cause of death in acute leukemia, bone marrow transplant)
Aspergillosis dx culture, serum galactomannan level, X-ray (solitary/multiple nodules, cavitary lesions) CT (halo sign, crescent sign)
Aspergillosis treatment empiric, surgical excision, once diagnosis is established variconazole and caspofungin
Normal pulmonary defense mucociliary clearance, cough and gag reflex, innate flora of oropharynx
Pneumonia pathophysiology inhalation of pathogen, macrophages overwhelmed, inflammatory mediators
Phases of pneumonia edema, red hepatization, gray hepatization, resolution
CAP pathogen strep pneumo (most common) H flu, M cat, M pneumo, RSV
MRSA risk factors (pneumonia) recent illness, flu, esrd, pleural effusion, multifocal infiltration, recent antibiotics, IVDA
Pneumonia typical acute, thick brown yellow sputum, productive cough, high fever shaking chills, consolidation on cxr
Pneumonia atypical gradual, clear sputum, low grade fever, no infiltrates
Pneumonia physical exam inspiration crackles, bronchial breath sounds, dull to percussion, e to a changes
CURB 65 confusion, uremia, rr (>30), bp (<90/<60), 65yo
Acute bronchitis inflammation of tracheobronchial tree, cough 1-3 weeks duration, usually viral
DVT thrombus usually found in the lower extremities, pelvic veins, and upper extremities
PE obstruction of the pulmonary artery or its branches by material (fat, air, tumor, or thrombus)
Virchows triad (DVT) venous stasis, venous injury, hyper-coagulability
Cause of death for PE r ventricle after load increases, rv dilates, rv dysfunction, rv ischemia, rv failure
PE "the great masquerader" non-specific symptoms, tachy, elevated neck veins, loud p2, pleural rub, humans sign (swollen, warm, erythematous)
PE EKG sinus tach, RBBB, right axis deviation, P wave pulmonale, new a fib, rt ventricle strain
Wells criteria clinical prediction model for PE
Gold standard for PE diagnosis pulmonary angiogram
Massive PE PE with systolic BP less than 90mmHg
Submassive PE PE with RHF with normal BP
Small Cell carcinoma extremely rapid growth, central location, almost always smokers, crush artifact
Non-small cell carcinoma squamous cell carcinoma, adenocarcinoma, large cell
Squamous cell carcinoma most common with hemoptysis, central location, exfoliates, aggressive
Adenocarcinoma Most common lung cancer, slow growing, peripheral location, "scar" tumor, more common in non smokers
Large cell carcinoma Poorly differentiated, peripheral, rapid growth
Cancer clinical presentation constitutional symptoms most common, other symptoms related to local tumor growth, local spread, metastasis
Pancoast tumor superior sulcus tumor, compresses brachial and cervical nerve roots, manifests as horners syndrome, anhydrosis, or arm pain
Paraneoplastic syndrome endocrine hormone secretion, clubbing, anorexia, weigh loss/ cachexia, fever
Gold standard for cancer diagnosis Surgical lung biopsy
TNM system Tumor size and invasion, lymph Nodes, Metastasis
Stage 1 no lymph nose involvement, surgical removal
Stage 2 and 3 lymph nodes involved, larger tumor, multiple lung tumors, surgery radiation and chemo
Small cell carcinoma staging limited or extensive both bad
Visceral pleura adheres to lung, covers each lobe, gets blood from the brachial artery, limited lymphatic drainage, no innervation
Parietal pleura adheres to chest wall, blood from systemic capillary, lymphatic drainage, innervated
Pleural effusion cause excess production of fluid, decreased drainage
Pleural effusion classification transudative, exudative
Transudative pleural effusion disorder of hydrostatic or oncontic or hydrostatic forces, fluid seeps from vessels
Exudative pleural effusion Disorder of inflammation, fluid exudes through wide gaps between cells, rich in cells and protein
Lights criteria protein/serum protein ratio >0.5 LDH/serum LDH ratio >0.6 LDH> 2/3 the upper limit of normal serum
Treatment of exudative pleural effusion bacterial infections (empyema) and malignancy need chest tube, chronic can lead to fibrosis, the rest of pts you drain or do surgically debride
Treatment of transudative pleural effusion no chest tube needed, treat underlying cause, can do a thoracentesis to help with dyspnea
Pneumothorax physical exam chest pain, dyspnea, hyperresonant, diminished tactile fremitis, decreased breath sounds
Pneumothorax Xray peripheral absence of lung markings and the presence of a pleural stripe
Pneumothorax classifications spontaneous, traumatic, tension
Primary Spontaneous no underlying lung disease, peak incidence in the 3rd decade of life
Blebs physical stress can cause small patches of irregular architecture which can rupture spontaneously
Secondary spontaneous pneumothorax in a lung with underlying disease
Traumatic pneumothorax penetrating chest injury, blunt chest injury, iatrogenic (healthcare on purpose or an oops)
Tension pneumothorax Rapid accumulation of air in the pleural space, rise in pleural pressure, pressure can reduce blood flow, decrease CO, shock and death
Tension pneumothorax exam low bp, absent/decreased breath sounds, hyperresonant, tracheal deviation
Tension pneumothorax treatment needle decompression, chest tube
Pleuritis pleural inflammation
Restriction causes P (pleural) A (alveolar) I (interstitial) N (Neuromuscular) T(thoracic cage abnormalities)
Interstitial lung disease diseases of the alveoli and interstitum
Usual Interstitial Pneumonia most common idiopathic interstitial pneumonia, worst prognosis, does not respond to anti-inflammatory tx
Idiopathic Granulomatous Sarcoidosis, second most common ILD, frequently a multi system disease
Sarcoidosis diagnosis and treatment transbronchial biopsy to find granulomas, treat with corticosteroids
ILD Granulomatous Chronic beryllium disease, hypersensitivity pneumonitis
ILD non-granulomatous autoimmune disease, occupational exposure, drugs, radiation
Created by: duanea00