respiratory pt 3

Question 1

INTERSTITIAL LUNG DISEASES (ILD)

Answer 1

General clinical features of ILD:
• Insidious/Progressive dyspnea, which leads to limited physical activity
• Persistent non-productive cough, may be hemoptysis
• May be extrapulmonary sx: musculoskeletal pain, weakness, fatigue, fever, photosens
• History of occupational exposure?

Physical exam:
• crackles are common
• heart exam in advanced cases may reveal signs of pulmonary hypertension
• general: clubbing can be present, check skin for rashes, joints for nodules
• PFT show restrictive ventilatory pattern (reduced TLC and FVC)

Question 2

HYPERSENSITIVITY PNEUMONITIS: “extrinsic allergic alveolitis”

Answer 2

• allergic response after inhalation of organic dusts, or simple chemicals in sensitized patient, leading to granulomatous inflammation of the alveolar epithelium
• Delayed reaction 4-6 hrs after exposure

Clues that strongly suggest the diagnosis
• history of recurrent pneumonia, particularly with regularity or a pattern
• respiratory symptoms after move to a new home or new school
• history of contact with birds “bird fancier’s lung”
• water damage to the patient’s home or school facility
• use of a hot tub, sauna, or swimming pool
• mprovement of symptoms when the pt is away extended period, eg vacation

Etiology: inhaled organic particulates—fibers (cotton, flax) bagasse (sugar cane), hemp, coffee, animal dander, mold, hay, maple bark, saw dust, flour, brewer’s yeast, mites, compost, detergent, paints/resins

Sxs: often nonspecific – chronic cough and SOB or a history of recurrent episodes/exacerbations of acute respiratory symptoms without definite infectious triggers.

Work-up:
• CBC, allergy testing, PFT (restrictive changes)
• BAL (broncho-alveolar lavage) shows lymphocytosis
• Lung biopsy

Imaging studies
• Radiographic studies may show irreversible pulmonary fibrosis.
• Acute: diffuse interstitial micronodular “ground-glass” opacities
• Subacute: micronodular or reticular opacities
• Chronic: loss of lung volume, alveolar destruction (“honeycombing”)
• High resolution CT scan—ground-glass opacities

Complications:
• permanent lung damage with pulmonary fibrosis
• subpleural blebs may rupture, leading to spontaneous pneumothorax
• chronic respiratory insufficiency can lead to cor pulmonale and premature death

Question 3

Three varieties of hypersensitivity pneumonitis:

Answer 3

i. Acute hypersensitivity pneumonitis: acute onset, usually within 4-6 hrs after exposure.
• Sx: fever, chills, dry cough, dyspnea, chest tightness, malaise, headache
• PE: ill appearance,tachypnea, crackles (at lung base), often NO wheezing
• resolves within 12 hrs to days after the antigenic exposure is eliminated

ii. Subacute hypersensitivity pneumonitis: gradual onset (less severe, lasts longer)
• Sx: cough (which may be productive), dyspnea, fatigue, anorexia, weight loss
• PE: ill appearance, tachypnea, crackles

iii Chronic hypersensitivity pneumonitis: insidious onset
• Sx: cough, progressive dyspnea, fatigue, weight loss, and exercise intolerance
• PE: crackles, possible digital clubbing, and an inspiratory squawk in some patients

Question 4

EOSINOPHILIC PULMONARY DISORDERS

Answer 4

accumulation of eosinophils in lung interstitium (aveoli possibly) (considered allergic response to parasite, drug (antibiotics, phenytoin, L-tryptophan), inhaled toxins?)

Disorders:
i) Acute Eosinophilic Pneumonia—does not recur
• rapid eosinophilic infiltration of lung interstitium
• SSX: less than 7days of fever [mild], dry cough, dyspnea, malaise, myalgia, night sweats, pleuritic chest pain.
• PE: Tachypnea, crackles. Possible pleural effusion. May progress to respiratory failure.
• Work-up: CT, CBC (eos), pleural fluid analysis (eos, high pH), CXR (opacities, Kerley-B lines), Bronchoscopy (eos seen)

ii) Chronic Eosinophilic Pneumonia—may be recurrent
• abnormal chronic accumulation of eosinophils in lung interstitium
• SSX: fever, weight loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort
• NOTE: Clinical picture may lead to misdiagnosis of community-acquired pneumonia
• Work-up: CBC (eos), inc ESR, CXR shows characteristic opacities in mid/upper lobes

Question 5

IDIOPATHIC INTERSTITIAL PNEUMONIAS

Answer 5

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

Question 6

DRUG-INDUCED ILD

Answer 6

• many drugs/drug categories have direct toxic pulmonary effects (unknown mechanism leading to:
o respiratory symptoms
o CXR changes
o decreased respiratory function
• Examples: Antibiotics, chemotherapy, anti-arrythmics, statins, illicit drugs (cocaine, heroin, methadone), anticoagulants
• Dx based on response to withdrawal of the suspected drug

Question 7

ENVIRONMENTAL CAUSES of ILD

Answer 7

group of diseases (various inhalants) causing replacement of normal lung tissue by abnormal tissue. Restrictive pulmonary changes. Get clear and complete occupational/exposure history!

General:
• SX: insidious onset of dyspnea, exercise limitation, dry cough (unless 2° infection)
• PE: mid to late inspiratory crackles, tachypnea. late findings: cyanosis, pulmonary hypertension leading to cor pulmonale
• Work-up: CXR shows patchy, subpleural, bibasilar interstitial infiltrates, cystic radiolucencies, “honeycombing” – indicates chronic fibrosis

Question 8

TYPES OF PNEUMOCONIOSIS

Answer 8

i) Asbestosis:
• inhalation of asbestos fibers. Source: mining, milling, manufacture (insulation)
• leads to pulmonary fibrosis - dose dependent, pleural thickening
• Also can lead to: bronchogenic carcinoma (10x > risk in non-smokers; 60-90x in smokers); malignant pleural mesothelioma (seen on CXR and staged with chest CT)
• Sx: insidious onset of dyspnea; may also have coughing and wheezing

ii) Silicosis:
• inhalation of silica particles. Source: mining, pottery, sand-blasting, brick-making, foundries (cast metals), glassmakers etc.
• occurs 5-20 yr. after 1st exposure [long time before presentation], worse in smokers
• SSx: dry cough, dyspnea, tachypnea, later weight loss, hemoptysis
• Imaging: CXR shows ≥1 cm nodules in upper lobes; eggshell calcification of hilar nodes
• DDx: COPD, lung cancer (hemoptysis and weight loss)

iii) Anthracosis
• (anthracite=coal) “black lung” >15 yr. exposure, worse in smokers
• SSx: may be no resp. symptoms, productive cough possible
• More severe state leads to progressive massive fibrosis

iv) Berylliosis:
• (mineral beryllium dust)
• Source: older fluorescent light bulbs, ceramics, electronics, aerospace industry
• SSx: dyspnea, cough, wt. loss

v) Miscellaneous sources: talc, Fe oxides, tin oxide, titanium, Cd, aluminum, iron, cotton

Question 9

Irritant Gas Inhalation Injury

Answer 9

• Inhaled gases dissolve in respiratory tract fluids, release acidic or alkaline radicals which cause inflammation in trachea, bronchi, bronchioles, alveoli (and into interstitium)
• May be from industrial accidents, mixing household ammonia with bleach (chloramine)
• Directly toxic agents: cyanide, carbon monoxide
• Others: chlorine, sulfur dioxide, hydrogen sulfide, nitrogen dioxide, ammonia
• Displace O2 leading to asphyxia: methane, carbon dioxide
• SSX depends on extent and duration of exposure: severe burning of eyes, nose, trachea, bronchi with cough, hemoptysis, wheezing, retching, dyspnea
• May leads to ARDS or Bronchiolitis obliterans (granulation tissue accumulates in bronchioles and alveolar ducts)

Question 10

Air Pollution-Related Illness

Answer 10

• Airway hypersensitivity to pollutants: oxides of nitrogen and sulfur, ozone (irritant and oxidant), carbon monoxide, lead, volatile organic compounds (eg methane), chlorofluorocarbons, particulates
• Triggers exacerbations in asthmatics, COPD
• Most vulnerable: elderly, kids, those with underlying lung disease
• Airway inflammation, bronchoconstriction, may be permanent decrease in lung function

Question 11

PULMONARY VASCULITIDES (vasculitis)

Answer 11

Inflammatory leukocytes in pulmonary (and other) blood vessel walls with reactive damage to mural structures, leading to bleeding (hemoptysis), ischemia and necrosis

Conditions:
i. Wegener’s granulomatosis
• autoimmune condition that affects lung, nose, kidneys
• Pulmonary infiltrates (seen on CXR), rhinosinusitis, alveolar hemorrhage (dyspnea hemoptysis), glomerulonephritis
• SSX: Cough, dyspnea, hemoptysis, pleuritic pain
• Lab: hematuria, proteinuria

ii. Churg-Strauss syndrome
“Allergic granulomatosis and angiitis”: allergic rhinitis, asthma, alveolar hemorrhage (impacting microvasculature of the lungs – hemoptysis). Alternating periods of asx.

Question 12

CONNECTIVE TISSUE DISORDERS with pulmonary manifestations

Answer 12

i) Goodpasture’s syndrome
• pulmonary hemorrhage with severe and progressive glomerulonephritis (often in young men)
• present with severe hemoptysis with secondary Fe deficiency, dyspnea and rapidly progressive renal failure

ii) Rheumatoid Lung disease
• associated with Rheumatoid Arthritis (RA) – Autoimmune disease of joints (pain, stiffness, deformity), skin (nodules), lungs, kidneys
• usually in a pt. with sero-positive rheumatoid factor
• Pulmonary SSX: pleuritic chest pain
• CXR shows pleural effusion, nodules in lungs, interstitial fibrosis, vasculitis

iii) Lupus (SLE)
• Autoimmune disease of blood, heart, joints, skin, lungs, liver, kidneys
• Pulmonary SSX: pleuritic chest pain, cough, dyspnea, recurrent URI, hemoptysis
• CXR: dec lung volume

Question 13

PULMONARY AMYLOIDOSIS (relatively rare)

Answer 13

• Amyloid protein deposition in lung (also commonly in heart, spleen, intestine, kidney)
• Unknown cause
• 3 main pulmonary types: tracheobronchial, nodular pulmonary, alveolar septal
• Pulmonary SSX: (chronic and mild) fever, dyspnea, cough, hemoptysis
• CXR shows multiple pulmonary nodular opacities, low density, irregular contours (Biopsy will confirm)

Question 14

SARCOIDOSIS

Answer 14

• Chronic, idiopathic dz that affects multiple systems, characterized by non-caseating granulomas, (nodules filled with macrophages) leading to inflammation of the involved tissues (in genetically susceptible persons)
• lungs are usually the first area to be affected, may lead to pulmonary fibrosis

Incidence: found 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
Age: most common 20- 40yo
Sex: F>M

S/Sx:
• vary depending on the area involved, and may be mild, moderate, severe
• First sx are often vague: fever, weight loss (unintended), or joint pain, SOB, persistent cough
• Other symptoms include:
o Skin: erythema nodosum on the legs
o Eyes, conjunctivitis, tearing. blurry vision, and photophobia. Rarely, blindness.
o Also affects the brain, nerves, heart, liver, and endocrine system

Laboratory: PFT, CBC, CMP (check serum calcium levels – granulomas may occasionally make excess vitamin D leading to elevated calcium levels in serum and urine [precipitating kidney stones]), LFTs

Imaging: CXR, CT, Bronchoscopy

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

Course: varies. majority of cases (2/3), the disease appears briefly and disappears. 20% to 30% have some permanent lung damage (fibrosis). although not common, death from sarcoidosis can occur if the disease causes serious damage to a vital organ.

DDX: TB, Aspergillosis, Histoplasmosis, Rheumatoid arthritis, lymphomas, Wegener’s granulomatosis, hypersensitivity pneumonitis

Question 15

SARCOIDOSIS - other findings

Answer 15

• Skin: (involvement common in blacks), erythema nodosum (most common), Plaques, subcutaneous nodules
• Neuro: Cranial nerve VII involvement (unilaterally or bilaterally), Bell’s palsy, basal granulomatous meningitis, peripheral neuropathy
• Ocular: Uveitis, glaucoma
• Musculoskeletal: myositis, polyarthritis: spondyloarthropathy - assoc.with positive HLA-B27 – back or SI pain
• Head, neck, and upper respiratory tract: Crackles on lung auscultation, tonsillitis, parotitis, or epiglottitis –hoarseness, stridor, or cough. Nontender LAD.
• Cardiac: cor pulmonale (most common cardiac complication), complete heart block, arrhythmias, bundle branch block (BBB), myocarditis, pericarditis, congestive heart failure (CHF)
• Abdominal: Splenomegaly, hepatomegaly (elevation in LFTs), nephrolithiasis–caused by hypercalcemia and hypercalciuria secondary to increase in 1,25-dihydroxyvitamin D

Question 16

TUMORS OF THE LUNG

Answer 16

Incidence:
2nd most common cancer in men and women
Most common 50-60 yr., rarely seen before age 35

DDX of Solid lesion seen on CXR: 15-50% CA (esp. if pt > 50 yr), benign tumor, granuloma (TB), histoplasmosis, coccidiomycosis,

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

Etiology
• Smoking - Smoker’s risk 13.3 times greater than non-smoker
• Second-hand smoke (~15% of lung cancers)
• Asbestos exposure (malignant pleural mesothelioma, and pulmonary fibrosis)
• Tobacco smoke + asbestos exposure– risk 80-90 times
• Radon exposure—uranium miners
• Other environmental agents: Polycyclic aromatic hydrocarbons PAHs, beryllium, nickel, copper, chromium, cadmium, diesel exhaust; Genetics? Polymorphisms or shared exposures?

~7-10% are asymptomatic; advanced dz — unintended wt loss, respiratory distress

SX Vary by type and location/source of tumor:
Primary tumor:
• Central tumors are usually squamous cell carcinoma (in airways) SX: cough, dyspnea, atelectasis, wheezing, hemoptysis.
• Peripheral tumors are usu adenocarcinomas or large cell carcinomas. SX cough, dyspnea, and symptoms of pleural effusion (pleuritic chest pain)

From loco-regional spread and tumor growth could lead to:
• superior vena cava obstruction (growth in apices) – peripheral edema, central cyanosis
• paralysis of the recurrent laryngeal nerve or phrenic nerve, causing hoarseness and paralysis of the diaphragm
• pressure on the sympathetic plexus, causing Horner’s syndrome (ptosis, miosis, ipsilateral dec in face sweating)
• dysphagia resulting from esophageal compression
• pericardial effusion (ie, Pancoast tumor)

Superior sulcus tumors can cause compression of the brachial plexus roots as they exit the neural foramina, resulting in severe, radiating neuropathic pain in the ipsilateral upper extremity.

Squamous cell carcinomas - associated with hypercalcemia from to parathyroid-like hormone production

Adenocarcinomas - clubbing and Trousseau syndrome (hypercoagulability and venous thrombosis)

Metastasis from: breast, stomach, pancreas, colon, thyroid, prostate, kidney, cervix, rectum, testis, bone.
SSX from primary CA organ
Lab: high serum calcium

Metastasis to:
Liver: RUQ pain, GI symptoms
To Brain: behavioral changes, confusion, aphasia, seizures, paresis, (coma)
To Bone: bone pain, pathological fractures

PE:
• may find local wheezing over tumor
• decreased breath sounds (distal to tumor)
• dullness to percussion with large tumor
• enlargement of axillary and supraclavicular nodes
• hepatomegaly

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

Prognosis: Based on type, staging and grading. Overall prognosis is poor, often b/c of advanced stage at dx

Question 17

ARDS- ADULT RESPIRATORY DISTRESS SYNDROME

Answer 17

Sudden, life-threatening respiratory failure from inflamed alveoli, causing them to fill with fluid and collapse, gas exchange ceases, and the body becomes hypoxic.

Etiology: 
variety of acute processes that directly or indirectly injure the lung
Conditions that predispose: 
•	Sepsis  (> 30% of cases)
•	primary bacterial or viral pneumonia	aspiration pneumonia
•	inhalant injuries- smoke, chemicals	
•	shock
•	drug overdose	
•	burns
•	acute hemorrhagic pancreatitis
•	head injury
•	trauma to chest/lung	
•	uremia
•	emboli	
•	cardiopulmonary bypass surgery	

S/Sx: usu. develop within 72hrs of initial injury/illness, then acute onset of urgent distress: dyspnea, tachypnea, pulmonary hypertension

PE: 
•	labored breathing and tachypnea (almost universally present)
•	cyanosis and moist skin
•	tachycardia			
•	scattered crackles
•	agitation, then lethargy/ obtundation

Laboratory: arterial blood gases
Imaging: CXR shows abnormal bilateral diffuse infiltrates

Dx:
• presence of fluid in the alveolar spaces of both lungs
• changes on x-ray may lag several hours behind functional changes seen on ABGs
• abnormal arterial blood gas analysis: severe hypoxemia (CO2 may be normal or low)
• respiratory acidosis

Tx: ARDS requires treatment with mechanical ventilation

Complications: multi-organ failure: same inflammatory processes injure liver, kidney, brain, blood, and immune system; Shock.

Prognosis: Mortality rate from ARDS ranges from 35–50%. (from underlying disease, sepsis or multiple organ failure). In patients who survive, normal lung function usually resumes within 6 to 12 months

Question 18

ATELECTASIS

Answer 18

Collapse of alveoli leading to diminished lung volume (airless areas) affecting all or part of a lung. Result is reduced or absent gas exchange in that area
Higher risk: smokers, post-surgical, elderly, pulmonary embolism, asthmatics, CF
May be acute (sudden onset) or chronic (infection, bronchiectasis, scarring)

Types:
• Obstructive atelectasis—airway blockage. Air trapped distal to the blockage is resorbed, and the region becomes completely airless, then collapses. Eg. mucus plugs, foreign body, airway mass, aneurysm, kinking of bronchial tree, CF, bronchospasm and/or airway inflammation in asthmatics
• Non—obstructive atelectasis:
o Relaxation atelectasis: loss of contact between parietal and visceral pleura (eg. pleural effusion or pneumothorax)
o Compression atelectasis: space occupying lesion presses on lung
o Adhesive atelectasis: surfactant dysfunction (eg Preemies, ARDS, radiation)
o Cicatriceal atelectasis: lung parenchymal scarring leads to dec lung volumes (eg. sarcoidosis, radiation)
o Replacement atelectasis: alveoli of entire lobe filled with tumor
o Rounded atelectasis: distinct finding of pleural damage from asbestos exposure

S/Sx:
variable with cause, may come on rapidly or gradually
• Acute: Cough, chest pain, dyspnea
• Chronic form: middle lobe syndrome—asymptomatic at first, then severe, nonproductive cough from bronchial compression by surrounding lymph nodes or tumor. The RML may then develop pneumonia that does not fully resolve.

PE:
• Low BP
• high temp
• tachycardia
• Cyanosis
• signs of shock
• dull or flat percussion note over involved area
• decreased or absent breath sounds
• trachea and heart deviated to affected side if large area
• rib spaces narrowed, diaphragm elevated
• Low 02 on pulse ox

Labs: ABGs

Imaging: CXR: airless lung, CT and bronchoscopy (used to see & remove foreign body)

Question 19

PULMONARY EMBOLISM

Answer 19

obstruction of pulmonary artery or branch by material originating from other part of body causing obstruction of blood supply to lung parenchyma. Pulmonary infarction and necrosis may follow.
Acute PE: SSX develop immediately
Chronic PE: progressive dyspnea—may be over years

Etiology:
• most common: embolized thrombus (blood clot) from leg or pelvic vein (DVT)
• septic material from septicemia, tumors, parasites
• sickle cell, polycythemia vera,
• fat emboli from fractured long bone
• amniotic fluid emboli (pregnancy)
• air emboli very common in hospital pt., post- abd surgery, surgery lower extremities, trauma to lower extremity, hip fracture, prolonged immobilization, cast on leg
• malignancy
• abnormal clotting
• birth control pills- estrogen increases clotting, thrombophlebitis (esp smokers)

Sxs: (need > 50% of pulmonary vascular bed occluded to produce sx)
• Sudden onset SOB
• dyspnea with or without exertion
• pleuritic pain
• Cough (pink, frothy sputum)
• hemoptysis
• anxiety and restlessness may be present

PE: (normal chest exam is possible)
• Tachypnea, tachycardia
• Hypotension: systolic BP 40mmHg drop from baseline
• may have low fever
• crackles, decreased breath sounds
• may have abnormal splitting of S2 (accentuated pulmonic component)
• S4 gallop may be present (due to acute RV strain)
• may cause ventricular heave (R ventricle)
• jugular venous distention (JVD)
• If DVT is cause: calf edema, erythema, tenderness, palpable cord

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

Procedures: ECG may show right ventricular strain, RBBB, atrial arrhythmia; Pulmonary Angiography “gold standard”

Imaging: CXR may be non specific, may see infiltrates, pleural effusion, atelectasis, elevation of diaphragm

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

Prog: > 25% fatal in a compromised pt.; without tx, 30% mortality rate. 50% recurrence rate. if pt has no previous heart/lung problems, developed from surgery, death is rare. prophylaxis is important- to prevent after surgery use elastic stockings to prevent venous stasis, active leg exercises, early ambulation

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

Question 20

PULMONARY HYPERTENSION

Answer 20

Elevated pulmonary arterial pressure and secondary right ventricular overload and failure (cor pulmonale). Pulmonary vessels constrict, hypertrophy, and become fibrotic.

Etiology: 
•	Idiopathic
•	Familial
•	L heart failure
•	parenchymal lung disease
•	Sleep apnea
•	connective tissue disorders
•	pulmonary embolism
•	HIV infection

SSX: 
•	Fatigue
•	dyspnea on extertion
•	chest discomfort
•	syncope (insufficient cardiac output)
•	Other possible concomitants: Raynaud’s syndrome, hemoptysis, hoarseness

PE: 
•	Wide split S2, S3, tricuspid murmur
•	jugular venous distention
•	hepatomegaly
•	peripheral edema

Work-up: CXR (enlarged hilar vessels), ECG, echocardiography, spirometry (restrictive), CBC, Pulmonary artery catheterization (measures arterial pressures)

Prognosis: if untreated, leads to right ventricular failure. Good response to Ca channel blocker therapy.

Question 21

CYANOSIS (CENTRAL and PERIPHERAL)

Answer 21

Blue discoloration of skin and mucus membranes, usu due to at least 5 g of reduced Hb in arterial blood.

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

Peripheral: due to stagnant circulation through peripheral vasc. bed due to exposure to cold, emotional tension, decreased cardiac output, peripheral artery disease (arteriosclerosis). Arterial O2 is normal in blood (unless cardio-pulm dz. also present). Seen in: diabetics, intermittent claudication, Raynaud’s syndrome
PE: pallor and cyanosis of hands, ears, nose, cheeks, feet. Decreased peripheral pulses, pain, ulcers can develop, cold to touch

Question 22

SLEEP APNEA

Answer 22

periodic cessation of breathing during sleep for 10 seconds or more, sometimes more than 300x/night (5 - 50 x an hour)

M:F 3:1, most common 30+ yr
Ethnicity – greater risk in African Americans, Hispanics, Pacific Islanders

Etiology:
blockage (obstruction) in the nose, mouth, or throat from: altered bone structure of the face, eg birth defect or injury affecting the head and face swollen nasal, oral or throat tissues

  contributing factors include: •	Obesity •	increased neck circumference (overweight may have extra tissue around neck)  •	alcohol or other sedatives  •	sleeping on back and using one or more pillows  •	smoking •	endocrine disorders - hypothyroidism and acromegaly •	deformities of the spine such as scoliosis, may interfere with breathing  •	conditions that may cause head and face (craniofacial) abnormalities such as Marfan's syndrome and Down syndrome  

S/Sx:
• most common symptoms –loud snoring and excessive daytime somnolence (often sleeping partner will report nighttime signs)
• restless tossing and turning during sleep
• nighttime choking spells, sweating, and chest pain
• waking unrefreshed after sleep, morning headaches
• problems with memory and concentration, irritability, personality changes
• hypertension
• GERD symptoms
• low libido

Work-up: polysomnography: measures several diff. factors while sleeping: arterial O2, rib motion, ocular motion (REM), EEG

Often treated with C-PAP machine (continuous positive airway pressure)