week 8- resp 3

Question 1

What is involved in Diffuse Parenchymal Lung dz?

Answer 1

o alveolar epithelium, pulm capillary epithelium, basement membrane, perivascular and perilymphatic tissues, surrounding tissue

Question 2

• what are the General clinical features of ILD?

Answer 2

o Insidious/Progressive dyspnea -> limited physical activity
o Persistent non-productive cough
o Mb hemoptysis
o Hx of occupational exposure?
o Mb extrapulm sx: MS pain, weakness, fatigue, fever, photosens

Question 3

• What is found on PE for ILD?

Answer 3

o crackles
o heart exam in advanced cases: pulm HTN
o general: clubbing, skin rashes, joint nodules
o PFT: restrictive ventilatory pattern (reduced TLC and FVC)

Question 4

• What is hypersensitivity pneumonitis?

Answer 4

o “extrinsic allergic alveolitis”
o Inhale organic dusts/chemicals in sensitized patient -> granulomatous inflammation of alveolar epithelium
o Delayed reaction 4-6 hrs after exposure

Question 5

• What are clues that strongly suggest dx of hyper. Pneum?

Answer 5

o hx of recurrent pneumonia (esp regular/pattern)
o resp sxs after move to a new home/school/etc
o water damage to the patient’s home/school/etc
o hx w/ birds: “bird fancier’s lung”
o hot tub, sauna, swimming pool
o exposure to others at home/school w/ similar sxs
o improved sxs on vacation

Question 6

• what is etiology of hyper. Pneum?

Answer 6

o inhaled organic dusts—fibers (cotton, flax) bagasse (sugar cane), hemp, coffee, bean dust, animal dander, mold, cheese, hay, maple bark, cedar oil, birds, moldy saw dust, wheat flour, brewer’s yeast, mites, compost, detergent, paints/resins

Question 7

• what are ssx of hyper. Pneum?

Answer 7

o often non-specific
o chronic or recurrent cough and SOB or hx of recurrent episodes/exacerbations of acute resp sxs w/o definite infectious triggers.

Question 8

• What are the 3 types of hypersensitivity pneumonitis?

Answer 8

o Acute: acute onset, usually w/i 4-6 hrs after exposure; fever, chills, dry cough, chest tightness, malaise, headache, ill appearance; tachypnea, crackles (often at lung base), dyspnea, often NO wheezing; resolves w/i 12 hrs to days after the antigenic exposure is eliminated
o Subacute: gradual onset (less severe, lasts longer); cough (mb productive), dyspnea, fatigue, anorexia, weight loss, ill appearance, tachypnea, crackles
o Chronic: insidious onset; cough, progressive dyspnea, fatigue, weight loss, and exercise intolerance; crackles, possible digital clubbing, and an inspiratory squawk in some patients

Question 9

• What is the work-up for hyper. Pneum?

Answer 9

o	CBC, allergy testing, PFT (restrictive changes)
o	BAL (broncho-alveolar lavage) shows lymphocytosis

Question 10

• What imaging is done/found for hyper pneum?

Answer 10

o may show irreversible pulm fibrosis.
o Acute: diffuse interstitial micronodular “ground-glass” opacities
o Subacute: micronodular or reticular opacities
o Chronic: loss of lung volume, alveolar destruction (“honeycombing”)
o HRCT: ground-glass opacities
o Lung biopsy

Question 11

• What are complications of hyper pneum?

Answer 11

o permanent lung damage with pulm fibrosis
o subpleural blebs may rupture -> spontaneous pneumothorax
o chronic resp insufficiency can lead to cor pulmonale and premature death

Question 12

• what are eosinophilic pulm d/os? Risk?

Answer 12

o allergic response with accumulation of eosinophils in lung interstitium (alveoli possibly)
o obtain a careful travel hx to assess the risk of fungal or parasitic infx. Areas endemic for parasites (e.g., Asia, Africa, Latin America, South America, SE US)

Question 13

• what is etiology of eos pulm d/os?

Answer 13

o Allergic reaction to filaria, drug rx (abx, phenytoin, L-tryptophan), intestinal parasites (ascaris lumbricoides roundworm) Candida albicans, Aspergillus fumigata (allergic bronchopulm aspergillosis) inhaled toxins (eg cocaine)

Question 14

• What are the eosinophilic pulm d/os?

Answer 14

o Acute or chronic eosinophilic pneumonia

Question 15

• What is acute eos pneumonia? Ssx? Work-up?

Answer 15

o unknown etiology, does not recur
o rapid eosinophilic infiltration of lung interstitium
o Ssx: < 7days of fever, dry cough, dyspnea, malaise, myalgia, night sweats, pleuritic chest pain. Tachypnea, crackles,. Possible pleural effusion. May progress to resp failure.
o Work-up: CT, CBC (eos), pleural fluid analysis (eos, high pH), CXR (opacities, Kerley-B lines), Bronchoscopy (eos seen)

Question 16

• What is chronic eos pneumonia? Ssx? Work-up? Ddx/mis-dx?

Answer 16

o unknown etiology, mb recurrent
o abn chronic accumulation of eosinophils in lung interstitium
o ssx: fever, weight loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort
o Work-up: CBC (eos), inc ESR, CXR shows characteristic opacities in mid/upper lobes
o NOTE: Clinical picture may lead to misdiagnosis of community acquired pneumonia

Question 17

• What are the idiopathic interstitial pneumonias? Ssx? Hx? Dx?

Answer 17

o Interstitial lung dzs with unknown etiologies, (but very common in smokers!) present similarly, suspect on history, lead to restrictive lung changes, seen on CXR
o 6 histological subtypes
o Common SSX: cough, dyspnea, tachypnea, reduced chest expansion, bibasilar crackles
o Hx: family hx, tobacco use, drug use, home and work environments
o DX: CXR or CT, PFTs (restrictive, though may be obstructive as well), Lung biopsy show specific histological patterns

Question 18

• What are the 6 histological subtypes of idiopathic interstitial pneumonias?

Answer 18

• -Idiopathic pulm fibrosis: most common, M smokers, gradual onset, poor px
• -non-specific interstitial pneumonia: 30 yo smokers; pigmented M0s in distal airways
• -acute interstitial pneumonia: healthy M & F >40; abrupt fever, cough, dyspnea. Poss resp failure

Question 19

• What is drug-induced ILD?

Answer 19

o over 150 drugs or categories have toxic pulm effects leading to: resp sxs, CXR changes, dec resp fxn, histological changes
o Mechanism not known: Abx, chemo, anti-arrythmics, statins, illicit drugs (cocaine, heroin, methadone), anticoagulants
o Dx based on response to w/d of suspected drug

Question 20

• What are the ILDs due to environmental causes?

Answer 20

o group of dzs from various inhalants, causing replacement of normal lung tissue by abn tissue. Restrictive pulm changes.
o Get clear and complete occupational/exposure hx!
o Pneumoconiosis; occupational asthma; irritant gas inhalation injury; air pollution-related illness

Question 21

• What is ssx, PE, work-up for environmental caused ILDs?

Answer 21

o SSX: insidious onset of dyspnea, exercise limitation, dry cough (unless 2° infx)
o PE: mid to late inspiratory crackles, tachypnea; late findings: cyanosis, pulm HTN leading to cor pulmonale
o Work-up: CXR shows patchy, subpleural, bibasilar interstitial infiltrates, cystic radiolucencies, “honeycombing”

Question 22

• What is pneumoconiosis? Types?

Answer 22

o Caused by the inhalation of inorganic “mineral” dusts

o Asbestosis; silicosis; anthracosis; berylliosis; miscellaneous sources

Question 23

• What is asbestosis? Consequences? Ssx?

Answer 23

o Inhale asbestos fibers: mining, milling, manufacture (insulation)
o -> pulm fibrosis - dose dependent, pleural thickening
o May -> bronchogenic carcinoma (10x > risk in non-smokers; 60-90x in smokers); malignant pleural mesothelioma (seen on CXR and staged with chest CT)
o Ssx: insidious onset of dyspnea; may also have coughing and wheezing

Question 24

• What is silicosis? Ssx? Ddx?

Answer 24

o Inhale very fine silica particles: mining, pottery, sand-blasting, brick-making, foundries (cast metals), glassmakers etc.
o occurs 5-20 yr. after 1st exposure, ≥1 cm nodules in upper lobes seen on CXR, eggshell calcification of hilar nodes
o smoking or mycobacterium infx increase effect
o SSx: dry cough, dyspnea, tachypnea, later weight loss, hemoptysis
o DDx: COPD

Question 25

• What is anthracosis?

Answer 25

o (anthracite=coal) "black lung" >15 yr. exposure, worse in smokers o SSx: may be no resp. sxs, productive cough possible o More severe state -> progressive massive fibrosis

Question 26

• What is berylliosis? Ssx?

Answer 26

o (mineral beryllium dust) o Source: older fluorescent light bulbs, ceramics, chemical plants, electronics, aerospace industry o SSx: dyspnea, cough, wt. loss

Question 27

• What are miscellaneous sources of pneumoconiosis?

Answer 27

o talc, Fe oxides, tin oxide, titanium, Cd, aluminum, iron, cotton

Question 28

• what is occupational asthma? Ssx? Detection?

Answer 28

o Reversible airway obstruction caused by workplace materials: castor bean, grain, detergent, red cedar wood, formaldehyde, antibiotics, epoxy resin etc. o Type 1 hypersensitivity affecting the bronchi o SSX: SOB, chest tightness, wheezing, cough and perhaps sneezing, rhinorrhea, tearing—which may not occur until several hours after exposure Temporal association with work o Can be detected by using Peak Flow Meter at work

Question 29

• What is irritant gas inhalation injury? Causes? Ssx? Consequences?

Answer 29

o gases dissolve in resp tract fluids, release acidic/alkaline radicals which cause inflammation in trachea, bronchi, bronchioles, alveoli (into interstitium) o Mb from industrial accidents, mixing household ammonia with bleach (chloramine) o Directly toxic agents: CN, CO o Displace O2 leading to asphyxia: methane, CO2 o Others: chlorine, SO2, HS, NO2, NH3 o Ssx: depends on extent and duration of exposure; severe burning of eyes, nose, trachea, bronchi with cough, hemoptysis, wheezing, retching, dyspnea o May leads to ARDS or Bronchiolitis obliterans (granulation tissue accumulates in bronchioles and alveolar ducts)

Question 30

• What is air pollution-related illness?

Answer 30

o Airway hypersensitivity to Agents: N and S oxides, O3 (irritant and oxidant), CO, Pb, volatile organic compounds (eg methane), chlorofluoro carbons, particulates o Triggers exacerbations in asthmatics, COPD o Most vulnerable: elderly, kids, underlying lung dz o Airway inflammation, bronchoconstriction, may be permanent decrease in lung fxn

Question 31

• What are pulm vasculitides? 2 Types?

Answer 31

o Inflammatory leukocytes in pulm (and other) blood vessel walls with reactive damage to mural structures, leading to bleeding (hemoptysis), ischemia and necrosis o Wegener’s granulomatosis: AI; affects lung, nose, kidneys; Pulm infiltrates, rhinosinusitis, alveolar hemorrhage, glomerulonephritis; Cough, dyspnea, hemoptysis, pleuritic pain, hematuria, proteinuria o Churg-Strauss syndrome: “Allergic granulomatosis and angiitis”: allergic rhinitis, asthma, alveolar hemorrhage

Question 32

• What are the 3 connective tissue d/os with pulm manifestations?

Answer 32

``` o Goodpasture’s syndrome: pulm hemorrhage with severe and progressive glomerulonephritis; M Fe deficiency, dyspnea and rapidly progressive renal failure o Rheumatoid Lung dz: assoc w/ RA; AI dz of joints (pain, stiffness, deformity), skin (nodules), lungs, kidney; usu in pt w/ sero-positive rheumatoid factor; Pulm Ssx: pleuritic chest pain, pleural effusion; CXR shows nodules in lungs, interstitial fibrosis, vasculitis o Lupus (SLE): AI dz of blood, heart, joints, skin, lungs, liver, kidneys; Pulm Ssx: pleuritic chest pain, cough, dyspnea, URIs, dec lung volume, hemoptysis ```

Question 33

• What is pulm amyloidosis? Ssx?

Answer 33

o relatively rare; unknown cause o Amyloid protein deposition in lung (also commonly in heart, spleen, intestine, kidney) o 3 main pulm types: tracheobronchial, nodular pulm, alveolar septal o Pulm ssx: (chronic and mild) fever, dyspnea, cough, hemoptysis o CXR shows multiple pulm nodular opacities, low density, irregular contours; Biopsy will confirm

Question 34

• What is sarcoidosis?

Answer 34

o chronic dz of unknown cause; affects multiple systems; non-caseating granulomas, (nodules filled with macrophages) leading to inflammation of the involved tissues o lungs are usually the first area to be affected, may lead to pulm fibrosis

Question 35

• what is incidence, age, sex of sarcoidosis?

Answer 35

o Incidence: worldwide, in all races and both sexes; young women of African descent (10-20:1 over Caucasian); also prone--Scandinavian, Northern European or Puerto Rican ethnicities o Age: most common 20- 40yo o Sex: F>M

Question 36

• What is etiology of sarcoidosis?

Answer 36

o inflammatory response (T lymphocytes, macrophages, cytokines) to environmental exposure (viral, bact. infx, organic or inorganic agent) in a genetically susceptible person leads to the development of non-caseating granulomas

Question 37

• what are ssx of sarcoidosis?

Answer 37

o vary depending on the area involved; mb mild, moderate, severe o First sx are often vague: fever, weight loss, or joint pain, SOB, persistent cough o Skin: erythema nodosum on legs o Eyes: conjunctivitis, tearing o Rare severe complications: cataracts, glaucoma, blindness o Also affects brain, nerves, heart, liver, endocrine system

Question 38

• What Skin PE is found for sarcoidosis? Neuro?

Answer 38

o Skin: (involvement common in blacks); erythema nodosum (most common); Plaques, subcutaneous nodules; Granuloma formation in old scar or tattoo o Neuro: CN VII involvement (unilaterally or bilaterally); Bell’s palsy, basal granulomatous meningitis (ie, aseptic meningitis), or peripheral neuropathies

Question 39

• What MS PE is found for sarcoidosis? Eye?

Answer 39

o MS: Myositis; polyarthritis: spondyloarthropathy - assoc w/ positive HLA-B27 – back or SI pain; bony lesions o Eye: Uveitis: blurry vision, tearing, photophobia; Conjunctival infiltration: yellowish nodule

Question 40

• What is found on PE for sarcoidosis for Head, neck, and upper respiratory tract?

Answer 40

o tonsillitis, parotitis, epiglottitis: hoarseness, stridor, cough o nasal involvement (may present as damage to septum and turbinates) o Non-tender LA o dry cough, crackles

Question 41

• What is cardiac PE for sarcoidosis? Abdominal?

Answer 41

o cor pulmonale (most common cardiac complication) o complete heart block, ventricular tachycardia (most common arrhythmia), bundle branch block (BBB), ventricular aneurysm, myocarditis, pericarditis, CHF o SM: hematological and general complications (e.g., rupture) o HP (in 25% of cases w/ hi LFTs (ALP, AST, ALT=liver fxn tests) o Nephrolithiasis: dt hypercalcemia and hypercalciuria 2nd to increase in active vit D

Question 42

• what labs are done for sarcoidosis? Imaging?

Answer 42

o PFT, CBC, CMP (check serum calcium levels*), LFTs o *granulomas may occasionally make excess vit D leading to hi serum and urine Ca (precipitating kidney stones) o CXR, CT, Bronchoscopy

Question 43

• How is sarcoidosis diagnosed?

Answer 43

o biopsy of granuloma during bronchoscopy o 90% of cases, CXR show characteristic non-caseating granuloma, hilar LA o CBC: anemia, eosinophilia or leukopenia o PFTs in advanced dz, possibly both restriction and obstruction

Question 44

• What is the course of sarcoidosis?

Answer 44

o varies o majority of cases (2/3), dz appears briefly and disappears o 20% to 30% have some permanent lung damage (fibrosis) o 10% to 15% have chronic dz o not common: death can occur if dz causes serious damage to a vital organ. (5%)

Question 45

• what is ddx of sarcoidosis?

Answer 45

o TB, Aspergillosis, Histoplasmosis, RA, lymphomas, Wegener’s granulomatosis, hypersensitivity pneumonitis

Question 46

• What is the incidence of lung tumors?

Answer 46

o 2nd most common cancer in men and women (1st are prostate 33%, breast 32%] o Mortality rates: ~30% of cancer deaths in men, ~25% in women o Most common 50-60 yr., rarely seen before age 35

Question 47

• What is ddx of solid lesion seen on CXR?

Answer 47

``` o 15-50% CA esp. if pt > 50 yr. o 10% benign tumor o 10% granuloma-TB o 10% histoplasmosis o 5 % coccidioidomycosis o 5% cysts or other changes ```

Question 48

• What are the types of lung cancer?

Answer 48

o Small Cell: ~15% of all lung cancers (arise in large airways) o Non-Small Cell: o Adenocarcinoma 40+% of all lung cancers (arise from glandular tissue in periphery) o Bronchoalveolar carcinoma is a distinct subtype of adenocarcinoma: manifests as a solitary peripheral nodule, multifocal dz, or rapidly progressing form. o SCC~ 30% (arise in large airways) o Large cell carcinoma ~9% - a large peripheral mass on a CXR.

Question 49

• What is etiology of lung cancer?

Answer 49

o Smoker’s risk 13.3 times greater than non-smoker; Risk varies with the # of cigarettes smoked - 10x risk with ≤20/d; 20x risk with >20/d Once a person quits smoking, the risk of lung cancer decreases gradually, but it never returns to the same level as that of a person who has never smoked. o Second-hand smoke: ~15% of LCA o Asbestos exposure: strong assoc w/ LCA, malignant pleural mesothelioma, pulm fibrosis. o Tobacco smoke + asbestos exposure; currently risk is 80-90x o Radon exposure: ~2-3% of LCA; well-established risk factor for LCA in uranium miners; (household exposure to radon has not been clearly linked to LCA) o Other environmental agents: Polycyclic aromatic hydrocarbons PAHs, beryllium, nickel, copper, chromium, cadmium, diesel exhaust o Genetics? Polymorphisms or shared exposures?

Question 50

• What are ssx of LCA?

Answer 50

o ~7-10% asx. Vary by type and location/source of tumor: o Primary tumor: central or peripheral o Central tumors usu SCC (in airways); cough, dyspnea, atelectasis, wheezing, hemoptysis. o Peripheral tumors usu adeno or LCC; cough, dyspnea, and sxs dt pleural effusion and severe pain as a result of infiltration of parietal pleura and chest wall.

Question 51

• What other problems can lung tumors cause, due to spread and growth?

Answer 51

o SVC obstruction o paralysis of recurrent laryngeal n, and phrenic n palsy, causing hoarseness and paralysis of diaphragm o pressure on sympathetic plexus, causing Horner’s syndrome (ptosis, miosis, ipsilateral anhidrosis, conjunctivitis); o dysphagia dt esophageal compression; o pericardial effusion (ie, Pancoast tumor).

Question 52

• What can superior sulcus tumors cause?

Answer 52

o compression of brachial plexus roots as they exit the neural foramina, resulting in severe, radiating neuropathic pain in ipsilateral upper extremity.

Question 53

• What are ssx of SCC? Adeno?

Answer 53

o SCC: assoc w/ hypercalcemia dt hi parathyroid-like hormone production o Adeno: clubbing and Trousseau syndrome (hypercoagulability and venous thrombosis)

Question 54

• Where does LCA metastasize from? Ssx? Advanced?

Answer 54

o breast, stomach, pancreas, colon, thyroid, prostate, kidney, cervix, rectum, testis, bone (pretty much anywhere) o Ssx from primary CA organ, high serum calcium o Advanced stage sxs (60-75% LCA cases)– unintentional wt loss, obvious resp distress.

Question 55

• Where does LCA metastasize to? Ssx?

Answer 55

o Liver: RUQ pain, GI sxs o Brain: behavioral changes, confusion, aphasia, seizures, paresis, (coma) o Bone: bone pain, pathological fractures

Question 56

• What is found on PE for LCA?

Answer 56

o may find local wheezing over tumor o decreased breath sounds o dullness to percussion with large tumor o enlargement of axillary and supraclavicular nodes o hepatomegaly

Question 57

• how is LCA diagnosed?

Answer 57

o CXR shows opaque mass o PET scan +IV imaging agent (F-18 fluorodeoxyglucose (FDG tracer)) o CT lungs, st w/ transthoracic needle aspiration biopsy (TNAB) o Cytology of sputum or pleural fluid o Chem panel: high serum calcium (esp. if metastasis) o Bronchoscopy-guided biopsy for intralumenal cancer (SCC)

Question 58

• What is Px for LCA?

Answer 58

o Based on type, staging and grading | o Overall, poor. less than 10% 5 yr. survival, if untreated survive 9 months.

Question 59

• What is ARDS?

Answer 59

o Adult resp distress syndrome o Sudden, life-threatening resp failure from inflamed alveoli, causing them to fill with fluid and collapse, gas exchange ceases, and body is hypoxic. o Duration and intensity of the condition varies considerably

Question 60

• What is etio of ARDS?

Answer 60

o variety of acute processes that in/directly injure lung. Usu ppl don’t develop ARDS. not clear why some people are at a higher risk o Conditions that predispose: o serious infx in blood or other tissues (sepsis; > 30% of cases) o primary bacterial or viral, aspiration pneumonia o inhalant injuries- smoke, chemicals o shock; drug overdose; burns o acute hemorrhagic pancreatitis; multi-transfusions ABO; trauma to chest/lung o uremia; head injury o emboli of fat, air, amniotic fluid o cardiopulm bypass surgery; near-drowning

Question 61

• what are ssx of ARDS?

Answer 61

o usu develop w/i 72hrs of initial injury/illness, then acute onset of urgent distress: o dyspnea; tachypnea; pulm HTN

Question 62

• what is found on PE for ARDS?

Answer 62

o labored breathing and tachypnea (almost universally present) o cyanosis and moist skin; tachycardia; scattered crackles o agitation; lethargy followed by obtundation (not fully aware)

Question 63

• what labs done for ARDS? Imaging?

Answer 63

o ABGs | o CXR: abnormal bilateral diffuse infiltrates

Question 64

• How is ARDS diagnosed?

Answer 64

o presence of fluid in alveolar spaces of both lungs o changes on x-ray may lag several hours behind functional changes seen on ABGs o abn ABG: severe hypoxemia (CO2 mb normal or low) o resp acidosis

Question 65

• what is tx for ARDS? Complications?

Answer 65

o requires tx with mechanical ventilation or some other form of assisted breathing. o Comp: multi-organ failure (or multiple organ dysfunction syndrome): The same inflammatory processes injure liver, kidney, brain, blood, and immune system o Shock

Question 66

• What is Px of ARDS?

Answer 66

o Mortality: 35–50%. o In most cases, death dt underlying dz, sepsis or multiple organ failure o In patients who survive, normal lung function usually resumes in 6-12 mos

Question 67

• What is resp failure? Causes? Tx?

Answer 67

o (inadequate gas exchange, low O2, high CO2) can result from other conditions, severe exacerbations, etc: o Asthma, COPD, pneumonia, pneumothorax, hemothorax, CF, pulm edema, cerebrovascular accident, cardiac arrythmia, CHF, drug intoxication (eg opioids, benzos, alcohol) o Tx will require immediate intervention: CPR, intubation/ventilation, resp stimulants

Question 68

• What is atelectasis? Risk?

Answer 68

o Collapse or closure of alveoli -> diminished lung volume (airless areas) affecting all/part of lung -> reduced/absent gas exchange in that area o Higher risk: smokers, post-surgical, elderly, pulm embolism, asthma, CF o May be acute (sudden onset of airless lung area) or chronic (infx, bronchiectasis, scarring)

Question 69

• What are the types of atelectasis?

Answer 69

o Obstructive and non-obstructive

Question 70

• What is obstructive atelectasis?

Answer 70

o airway blockage. Air trapped distal to blockage is resorbed, region becomes completely airless, then collapses. o Eg. mucus plugs, foreign body, airway mass, aneurysm, kinking of bronchial tree, CF, bronchospasm/airway inflammation in asthmatics

Question 71

• What are the types/causes of non-obstructive atelectasis?

Answer 71

o Relaxation: loss of contact between parietal and visceral pleura; eg. pleural effusion or pneumothorax o Compression: SOL presses on lung o Adhesive: surfactant dysfunction (eg preemies, ARDS, radiation) o Cicatricea: lung parenchymal scarring leads to dec lung volumes; eg. sarcoidosis, necrotizing pneumonia, radiation o Replacement: alveoli of entire lobe filled with tumor o Rounded: distinct finding of pleural damage from asbestos exposure

Question 72

• What are ssx of atelectasis?

Answer 72

o variable with cause, may come on rapidly or gradually o Cough, chest pain, dyspnea, cyanosis, tachycardia o Rapid onset- pain on affected side, sudden onset of dyspnea & cyanosis, shock o Slowly developing: mb asx at first o Chronic form: middle lobe syndrome—asx at first, then severe, nonproductive cough from bronchial compression by surrounding lymph nodes or tumor o RML may then develop pneumonia that does not fully resolve.

Question 73

• What is found on PE for atelectasis? Imaging?

Answer 73

o Low BP, high temp, tachycardia o Dull/flat percussion note over involved area o dec/absent breath sounds o if large area: chest excursion dec/absent; trachea and heart deviated to affected side o rib spaces narrowed, diaphragm elevated o Low O2 on pulse ox and ABGs o CXR: airless lung, CT and bronchoscopy (visualize, remove foreign body)

Question 74

• What is pulmonary embolism? Acute and chronic types?

Answer 74

o obstruction of pulm artery or branch by material originating from other part of body (eg thrombus, tumor, air or fat); -> obstruction of blood supply to lung parenchyma. Pulm infarction and necrosis may follow. o Acute PE: SSX develop immediately o Chronic PE: progressive dyspnea—may be over years

Question 75

• What is etio of PE?

Answer 75

o most common: embolized thrombus (blood clot) from leg or pelvic vein (DVT) o septic material from septicemia, tumors, parasites, sickle cell, PCV, fat emboli from fractured long bone, amniotic fluid emboli (pregnancy), air emboli o very common in hospital pt., post- abd surgery, surgery/trauma lower extremities, hip fracture, prolonged immobilization, cast on leg o malignancy; CHF; abnormal clotting; obesity predisposes o BCPs: estrogen increases clotting, thrombophlebitis (esp smokers) o Recent cases of previously healthy young adults (Michael Johns, Kelsey Stoneton)

Question 76

• What are ssx of PE?

Answer 76

o (need > 50% of pulm vascular bed occluded to produce sx) o Sudden onset SOB, dyspnea w/ or w/o exertion o Pleuritic pain; Cough ; hemoptysis; anxiety and restlessness may be present

Question 77

• What is found on PE for pulm embolism?

Answer 77

o (normal chest exam is possible); Tachypnea, tachycardia o Hypotension: systolic BP < 90mmHg or >40mmHg drop from baseline o Mb low fever; crackles, dec breath sounds o mb abnormal splitting of S2 (accentuated pulmonic component) o S4 gallop mb present (dt acute RV strain) o may cause ventricular heave as RV works hard to push blood into lungs o jugular venous distention (JVD) seen on right side of neck o If DVT is cause: edema, erythema, tenderness, palpable cord in calf or thigh o < 10% develop infarction, start to have signs of consolidation: cough, hemoptysis, pleuritic chest pain, fever

Question 78

• What labs are done for PE? Findings?

Answer 78

o d-Dimer assay: hi (degradation product of fibrin) o CBC: mild leukocytosis possible o ABG: hypoxemia, hypocapnea, respiratory alkalosis o CMP: hyponatremia o Brain Natriuretic Peptide BNP (hi) o Serum troponin (hi in 50%) o Cardiac enzymes high LDH in 85% of cases (also high with MI, not in 1st 12 hrs), o CPK normal & increased LDH, = pulm problems if w/i 24 hrs (CPK elevated 1st in MI )

Question 79

• What procedures are done for PE? Imaging?

Answer 79

o ECG may show RV strain, RBBB (bundle branch block), atrial arrhythmia o Pulm Angiography “gold standard” o CXR mb non-specific, may see infiltrates, pleural effusion, atelectasis, elevation of diaphragm

Question 80

• How is PE diagnosed?

Answer 80

``` o modified Well’s criteria: pulmonary embolism unlikely with 4: o Clinical sxs of DVT (3 pts) o Other Dx less likely than PE (3 pts) o Heart rate >100 bpm (1.5 pts) o Immobilization > 3 days or surgery in previous 4 weeks (1.5 pts) o Previous DVT or PE (1.5 pts) o Hemoptysis (1 pt) o Malignancy (1 pt) ```

Question 81

• What is px of PE?

Answer 81

o > 25% fatal in compromised pt. o w/o tx, 30% mortality rate. 50% recurrence rate o if pt has no previous heart/lung problems, developed from surgery, death is rare o prophylaxis is important- to prevent after surgery use elastic stockings to prevent venous stasis, active leg exercises, early ambulation

Question 82

• what is ddx of PE?

Answer 82

o acute MI, tension pneumothorax, pericardial tamponade, pleurisy, bacterial pneumonia (high fever, marked leukocytosis + other chest ssx)

Question 83

• what is Pulmonary hyptertension?

Answer 83

o Elevated pulm arterial pressure and 2nd RV overload and failure (cor pulmonale). Pulm vessels constrict, hypertrophy, and become fibrotic. o Usu from increased pulm vascular resistance or pulm venous pressure

Question 84

• What is etio of PH? Ssx?

Answer 84

o Idiopathic, familial, L heart failure, parenchymal lung dz, Sleep apnea, connective tissue d/os, pulm embolism, HIV inx, thyroid d/os o fatigue, DOE, chest discomfort, syncope (insufficient CO) o Other possible concomitants: Raynaud’s, hemoptysis, hoarseness

Question 85

• What is found on PE for PH? Work-up? Px?

Answer 85

o Wide split S2, S3, tricuspid murmur, JVD, HM, peripheral edema o CXR (enlarged hilar vessels), ECG, echocardiography, spirometry (restrictive), CBC o Pulm artery catheterization (measures arterial pressures) o Px: if untreated, leads to RV failure, survival rate of 2.5 yrs. Good response to Ca channel blocker therapy.

Question 86

• What is cyanosis? 2 types?

Answer 86

o Central and peripheral o Blu-ish discoloration of skin and mucus membranes, usu dt at least 5 g of reduced Hb in arterial blood. Mb also dt abn Hb: met-Hb (Fe3+,ferric) or sulf-Hb (HS binds to Fe3+) (Both usu drug- induced)

Question 87

• What is central cyanosis?

Answer 87

o dt hypoxemia caused by acute/chronic cardio/pulm dz., COPD (most common), cardiac- right to left cardiac shunt, pulm AV fistula o PE: skin and mucus membranes blue (lips, mouth); chronic- may see clubbing of finger tips/nails

Question 88

• What is peripheral cyanosis?

Answer 88

o dt stagnant circulation through peripheral vasc. bed dt exposure to cold, emotional tension, dec CO, peripheral artery dz (atherosclerosis) o Arterial O2 is normal (unless cardio-pulm dz. also present) but not getting to the tissue o Seen in: DM, intermittent claudication, Raynaud’s o PE: pallor and cyanosis of hands, ears, nose, cheeks, feet o Dec peripheral pulses, pain, ulcers can develop, cold to touch

Question 89

• What is sleep apnea? Epidem?

Answer 89

o periodic cessation of breathing during sleep for 10+ seconds, st >300x/night (5-50x/hr) o M:F 3:1, most common >30 yr o greater risk in African Americans, Hispanics, Pacific Islanders

Question 90

• What is etio of sleep apnea?

Answer 90

o blockage (obstruction) in the nose, mouth, or throat from: altered bone structure of the face, eg birth defect/injury affecting head/face; swollen nasal, oral, throat tissues o factors: Obesity/increased neck circumference; alcohol/sedatives; smoking; family hx; menopause o sleeping on back and using 1+ pillows o endocrine d/os – hypothyroidism, acromegaly o deformities of the spine such as scoliosis, may interfere with breathing o conditions that may cause head/face (craniofacial) abnormalities such as Marfan's and Down syndromes

Question 91

• what are ssx of sleep apnea

Answer 91

o most common: loud snoring and excessive daytime somnolence (often sleeping partner will report nighttime signs) o restless tossing and turning during sleep; waking unrefreshed after sleep o nighttime choking spells, sweating, chest pain o problems with memory and concentration o irritability, fatigue; personality changes; morning HAs; HTN; GERD sxs; low libido

Question 92

• what is work-up for sleep apnea? Tx?

Answer 92

o polysomnography: measures several diff. factors while sleeping: arterial O2, rib motion, ocular motion (REM), EEG o Often treated with C-PAP machine (continuous positive airway pressure)