Pulmonary 3

Question 1

What is hypersensitivity pneumonitis?

Answer 1

“extrinsic allergic alveolitis”
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

Question 2

What are some clues that strongly suggest a dx of hypersensitivity pneumonitis?

Answer 2

recurrent pneumonia, particularly with regularity or a pattern
respiratory symptoms after move to a new place
contact with birds - “bird fancier’s lung”
water damage home or school facility (mold)
use of a hot tub, sauna, or swimming pool
exposure to other people with similar symptoms
improvement of symptoms when the pt is away extended period, eg vacation

Question 3

What is the etiology of hypersensitivity pneumonitis?

Answer 3

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 4

What are the SSxs of hypersensitivity pneumonitis?

Answer 4

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

Question 5

What are the 3 types of hypersensitivity pneumonitis?

Answer 5

i. Acute hypersensitivity pneumonitis: acute onset, usually within 4-6 hrs after exposure.
fever, chills, dry cough, chest tightness, malaise, headache, ill appearance, tachypnea, crackles (often heard at the lung base), dyspnea, 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)
cough (which may be productive), dyspnea, fatigue, anorexia, weight loss, ill appearance, tachypnea, crackles
iii Chronic hypersensitivity pneumonitis: insidious onset
cough, progressive dyspnea, fatigue, weight loss, and exercise intolerance; crackles, possible digital clubbing, and an inspiratory squawk in some patients

Question 6

What are lab/imaging results associated with hypersensitivity pneumonitis?

Answer 6

CBC, allergy testing, PFT (restrictive changes), BAL (shows lymphocytosis)
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
Lung biopsy

Question 7

What are complications of hypersensitivity pneumonitis?

Answer 7

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 8

What is acute eosiniphilic pneumonia and the SSxs involved?

Answer 8

unknown etiology, does not recur
rapid eosinophilic infiltration of lung interstitium
SSxs: < 7days of fever, dry cough, dyspnea, malaise, myalgia, night sweats, pleuritic chest pain. Tachypnea, crackles,. Possible pleural effusion. May progress to respiratory failure.

Question 9

What are labs/imaging results associated with acute eosinophilic pneumonia?

Answer 9

CT, CBC (eos), pleural fluid analysis (eos, high pH), CXR (opacities, Kerley-B lines), Bronchoscopy (eos seen)

Question 10

What SSxs are associated with chronic eosinophilic pneumonia?

Answer 10

fever, weight loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort
NOTE: Clinical picture may lead to misdiagnosis of community acquired pneumonia

Question 11

What drugs are associated with ILD?

Answer 11

over 150 drugs or categories have toxic pulmonary effects leading to respiratory symptoms, CXR changes, decreased respiratory function, histological changes
Drugs involved: Antibiotics, chemotherapy, anti-arrythmics, statins, illicit drugs (cocaine, heroin, methadone), anticoagulants
Diagnosis based on response to withdrawl of the suspected drug

Question 12

Asbestosis - SSxs/PE?

Answer 12

inhalation of asbestos fibers. Source: mining, milling, manufacture
leads to pulmonary fibrosis - dose dependent, pleural thickening
Also can lead to bronchogenic carcinoma (10x > risk in non-smokers; 60-90x in smokers) or malignant pleural mesothelioma (seen on CXR and staged with chest CT)
SSxs: 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

Question 13

Silicosis - SSxs/PE?

Answer 13

inhalation of very fine silica particles– Source: mining, pottery, sand-blasting, brick-making, foundries (cast metals), glassmakers etc.
occurs 5-20 yr. after 1st exposure, ≥1 cm nodules in upper lobes seen on CXR, eggshell calcification of hilar nodes
smoking or mycobacterium infection increase effect
SSxs: insidious onset of dyspnea, exercise limitation, dry cough (unless 2° infection)
later weight loss, hemoptysis
PE: mid to late inspiratory crackles, tachypnea
late findings: cyanosis, pulmonary hypertension leading to cor pulmonale

Question 14

Anthracosis - SSxs/PE?

Answer 14

“black lung” >15 yr. exposure, worse in smokers
SSxs: may be no respiratory symptoms or 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

Question 15

Berylliosis - SSxs/PE?

Answer 15

mineral beryllium dust from older fluorescent light bulbs, ceramics, chemical plants, electronics, aerospace industry
SSxs: insidious onset of dyspnea, exercise limitation, dry cough (unless 2° infection), weight loss
PE: mid to late inspiratory crackles, tachypnea
late findings: cyanosis, pulmonary hypertension leading to cor pulmonale

Question 16

What are other environmental causes of pneumoconiosis/ILD?

Answer 16

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

Question 17

What is occupational asthma? SSxs?

Answer 17

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

Question 18

What is irritant gas inhalation injury? Some gases involved?

Answer 18

Inhaled gases dissolve in respiratory tract fluids, release acidic or alkaline radicals which cause inflammation in trachea, bronchi, bronchioles, alveoli (into interstitium)
May be from industrial accidents, mixing household ammonia with bleach (chloramine)
Directly toxic agents: cyanide, carbon monoxide
Displace O2 leading to asphyxia: methane, carbon dioxide
Others: chlorine, sulfur dioxide, hydrogen sulfide, nitrogen dioxide, ammonia

Question 19

What are SSxs and potential complications of irritant gas inhalation?

Answer 19

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 20

What are characteristics of air pollution related illness?

Answer 20

Airway hypersensitivity to Agents: oxides of nitrogen and sulfur, ozone (irritant and oxidant), carbon monoxide, lead, volatile organic compounds (eg methane), chlorofluoro carbons, 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 21

What are the 2 pulmonary vasculitides disorders?

Answer 21

Wegener’s granulomatosis
autoimmune condition that affects lung, nose, kidneys
Pulmonary infiltrates, rhinosinusitis, alveolar hemorrhage, glomerulonephritis
SSxs: Cough, dyspnea, hemoptysis, pleuritic pain, hematuria, proteinuria

Churg-Strauss syndrome
“Allergic granulomatosis and angiitis”
allergic rhinitis, asthma, alveolar hemorrhage
Also can affect GI, liver, and heart

Question 22

What connective tissue disorders are associated with pulmonary manifestations?

Answer 22

Goodpasture’s syndrome
RA - Rheumatoid Lung disease
Lupus (SLE)

Question 23

What are the characteristics of goodpasture’s syndrome?

Answer 23

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

Question 24

What are the characteristics of rheumatoid lung disease?

Answer 24

Autoimmune disease of joints (pain, stiffness, deformity), skin (nodules), lungs, kidney
usually in a pt. with sero-positive rheumatoid factor
Pulmonary SSxs: pleuritic chest pain, pleural effusion
CXR shows nodules in lungs, interstitial fibrosis, vasculitis

Question 25

What are the characteristics and pulmonary findings of lupus?

Answer 25

Autoimmune disease of blood, heart, joints, skin, lungs, liver, kidneys Pulmonary SSX: pleuritic chest pain, cough, dyspnea, URIs, dec lung volume, hemoptysis

Question 26

What are the characteristics and pulmonary findings of amyloidosis?

Answer 26

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

Question 27

What is sarcoidosis? Incidence and etiology?

Answer 27

Chronic disease of unknown cause that affects multiple systems, characterized by non-caseating granulomas, (nodules filled with macrophages) leading to inflammation of the involved tissues - lungs are usually first affected, maybe leading to pulmonary fibrosis Incidence: found worldwide, in all races and both sexes. F>M, 20-40 yrs most common African descent (10-20:1 over Caucasian)Scandinavian, Northern European, Puerto Rican ethnicities most susceptible Etiology: inflammatory response (T lymphocytes, macrophages, cytokines) to environmental exposure (viral, bact. infection, organic or inorganic agent) in a genetically susceptible person leads to the development of non-caseating granulomas

Question 28

What are the SSxs of sarcoidosis?

Answer 28

vary depending on the area involved, and may be mild, moderate, severe First sx are often vague: fever, weight loss, or joint pain, SOB, persistent cough Other symptoms include: Skin: erythema nodosum on the legs Eyes, conjunctivitis, tearing (rarely cataracts, glaucoma, and blindness) Also affects the brain, nerves, heart, liver, and endocrine system

Question 29

What systems are involved/what are the PE findings associated with sarcoidosis?

Answer 29

- Skin erythema nodosum (most common) Plaques, subcutaneous nodules Granuloma formation in old scar or tattoo - Neuro Cranial nerve VII involvement (unilaterally or bilaterally) Bell’s palsy, basal granulomatous meningitis (ie, aseptic meningitis), or peripheral neuropathies - Ocular Uveitis: blurry vision, tearing, and photophobia. Conjunctival infiltration: appearance of a yellowish nodule - Musculoskeletal Myositis, polyarthritis, spondyloarthropathy - HEENT dry cough, crackles tonsillitis, parotitis, or epiglottitis --hoarseness, stridor, or cough nasal involvement (may present as damage to septum and turbinates) Nontender lymphadenopathy - Cardiac cor pulmonale (most common cardiac complication) complete heart block, ventricular tachycardia (most common arrhythmia), bundle branch block (BBB), ventricular aneurysm, myocarditis, pericarditis, and congestive heart failure (CHF) - Abdominal Splenomegaly, hepatomegaly, nephrolithiasis (hypercalcemia and hypercalciuria secondary to increase in 1,25-dihydroxyvitamin D)

Question 30

What is labs/imaging should be ordered for sarcoidosis dx?

Answer 30

PFT - restriction/obstruction CBC - anemia, eos, leukopenia CMP (check serum calcium levels*) LFTs CXR - non-caseating granuloma, hilar adenopathy CT Bronchoscopy (granulomas may occasionally make excess vitamin D leading to elevated calcium levels in serum and urine - precipitating kidney stones) biopsy of granuloma during bronchoscopy

Question 31

What is the course of sarcoidosis?

Answer 31

60-70% - the disease appears briefly and disappears 20-30% - permanent lung damage (fibrosis) 10-15% - chronic disease 5% - death (serious damage to a vital organ)

Question 32

What are the different types of lung tumors and the prevalence/distribution of each?

Answer 32

Small Cell Carcinoma - (15%) arise in large airways Adenocarcinoma - (40+%) arise from glandular tissue in periphery Bronchoalveolar carcinoma (subtype of adenocarcinoma) - solitary peripheral nodule, multifocal disease, or rapidly progressing form Squamous cell carcinoma - (30%) arise on large airways Large cell carcinoma - (9%) large peripheral

Question 33

What are risk factors associated with lung tumors?

Answer 33

- Smoking - Smoker’s risk 13.3 times greater than non-smoker (varies with the # of cigarettes smoked - 10x risk with ≤20/d; 20x risk with >20/d) - Second-hand smoke – 15% of lung cancers - Asbestos exposure - strongly associated with the lung cancer, malignant pleural mesothelioma, and pulmonary fibrosis (80-90x risk with smoking AND asbestos exposure) - Radon exposure – (2-3% of lung cancers) well-established risk factor for lung cancer in uranium miners - Other environmental agents - polycyclic aromatic hydrocarbons , beryllium, nickel, copper, chromium, cadmium, diesel exhaust - Genetics?

Question 34

What are SSxs of central tumors/tumors in airway?

Answer 34

(Small cell carcinoma/SCC) | cough, dyspnea, atelectasis, wheezing, hemoptysis

Question 35

What are SSxs of peripheral tumors?

Answer 35

(adenocarcinomas or large cell carcinomas) cough, dyspnea, and symptoms due to pleural effusion and severe pain as a result of infiltration of parietal pleura and the chest wall

Question 36

What are other potential SSxs/complications associated with lung tumors?

Answer 36

superior vena cava obstruction paralysis of the recurrent laryngeal nerve, and phrenic nerve palsy, causing hoarseness and paralysis of the diaphragm pressure on the sympathetic plexus (Horner’s syndrome - ptosis, miosis, anhidrosis) dysphagia resulting from esophageal compression pericardial effusion (ie, Pancoast tumor). Superior sulcus tumors can cause compression of the brachial plexus (TOS) Squamous cell carcinomas - associated with hypercalcemia from to PTH-like hormone) Adenocarcinomas - clubbing and Trousseau syndrome (hypercoagulability/venous thrombosis)

Question 37

What cancers lead to lung mets (secondary tumor)?

Answer 37

breast, stomach, pancreas, colon, thyroid, prostate, kidney, cervix, rectum, testis, bone

Question 38

Where does lung cancer (primary tumor) like to spread in the body?

Answer 38

Liver, Brain, Bone

Question 39

What are some potential PE findings associated with lung cancer?

Answer 39

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

Question 40

How is lung cancer Dx made?

Answer 40

CXR, PET, or CT shows mass Cytology of sputum or pleural fluid Chem panel: high serum calcium (esp. if metastasis) Bronchoscopy-guided biopsy for intralumenal cancer (SCC)

Question 41

What is a DDX for lung cancer (other solid lesions on CXR)?

Answer 41

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

Question 42

What is lung cancer prognosis? 5 yr survival?

Answer 42

Overall prognosis is poor. less 10% 5 yr. survival, if untreated survive 9 months

Question 43

What is ARDS?

Answer 43

Adult Respiratory Distress Syndrome Sudden, life-threatening respiratory failure from inflamed alveoli, causing them to fill with fluid and collapse, gas exchange ceases, and the body hypoxic. Duration and intensity of the condition varies considerably

Question 44

What are some potential causes of ARDS?

Answer 44

``` serious infection in blood or other tissues (sepsis; > 30% of cases) primary bacterial, viral, or aspiration pneumonia inhalant injuries (smoke, chemicals) shock drug overdose burns acute hemorrhagic pancreatitis multi-transfusions ABO trauma to chest/lung uremia head injury emboli of fat, air, amniotic fluid cardiopulmonary bypass surgery near-drowning ```

Question 45

What are SSxs/PE findings associated with ARDS?

Answer 45

``` SSxs: 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 lethargy followed by obtundation ```

Question 46

What labs/imaging findings are associated with ARDS dx?

Answer 46

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

Question 47

What is the prognosis of ARDS? What are some complications?

Answer 47

Prognosis - Mortality rate from ARDS ranges from 35–50%. In most cases, death results from underlying disease, sepsis or multiple organ failure In patients who survive, normal lung function usually resumes within 6 to 12 months. multi-organ failure (or multiple organ dysfunction syndrome) Complications - The same inflammatory processes injure liver, kidney, brain, blood, and immune system Shock

Question 48

What is atelectasis? Who is at risk?

Answer 48

Collapse or closure 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, asthma, CF May be acute (sudden onset of airless lung area) or chronic (infection, bronchiectasis, scarring)

Question 49

What are the different types of atelectasis?

Answer 49

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

Question 50

What are SSxs/PE findings associated with atelectasis? What does imaging show?

Answer 50

SSxs variable with cause, may come on rapidly or gradually Cough, chest pain, dyspnea, cyanosis, tachycardia Rapid onset - pain on affected side, sudden onset of dyspnea & cyanosis, shock Slowly developing - maybe asymptomatic at first 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 dull or flat percussion note over involved area decreased or absent breath sounds chest excursion decreased or absent if large area trachea and heart deviated to affected side if large area rib spaces narrowed, diaphragm elevated Low O2 on pulseox/ABGs Imaging: CXR shows airless lung, CT and bronchoscopy (visualize, remove foreign body)

Question 51

What is a pulmonary embolism? Acute vs chronic?

Answer 51

obstruction of pulmonary artery or branch by material originating from other part of body (eg thrombus, tumor, air or fat); 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)

Question 52

What risk factors are associated with PEs?

Answer 52

post surgery, trauma to lower extremity, prolonged immobilization, cast on leg, malignancy, CHF, abnormal clotting, obesity, birth control pills (estrogen increases clotting)

Question 53

What are SSxs and PE findings associated with pulmonary embolism?

Answer 53

SSxs: (need > 50% of pulmonary vascular bed occluded to produce sx) Sudden onset SOB, dyspnea with or without exertion Pleuritic pain Cough Hemoptysis anxiety and restlessness may be present PE: (normal chest exam is possible) Tachypnea, tachycardia Hypotension Low fever crackles, decreased breath sounds Maybe abnormal splitting of S2 or S4 gallop JVD seen on right side of neck If DVT is cause: edema, erythema, tenderness, palpable cord in calf or thigh < 10% develop infarction, start to have signs of consolidation: cough, hemoptysis, pleuric chest pain, fever

Question 54

What labs/imaging findings are associated with pulmonary emboli?

Answer 54

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

Question 55

How are pulmonary emboli diagnosed?

Answer 55

Gold standard for dx is pulmonary angiography ``` Along with modified Well's criteria (likely with >4): Clinical symptoms of DVT (3 pts) Other Dx less likely than PE (3 pts) Heart rate >100 bpm (1.5 pts) Immobilization > 3 days or surgery in previous 4 weeks (1.5 pts) Previous DVT or PE (1.5 pts) Hemoptysis (1 pt) Malignancy (1 pt) ```

Question 56

What is the prognosis associated with pulmonary emboli?

Answer 56

> 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

Question 57

What are some important DDXs for pulmonary emboli?

Answer 57

acute MI, tension pneumothorax, pericardial tamponade, pleurisy, bacterial pneumonia

Question 58

What are the characteristics of pulmonary hypertension?

Answer 58

Elevated pulmonary arterial pressure and secondary right ventricular overload and failure (cor pulmonale). Pulmonary vessels constrict, hypertrophy, and become fibrotic. Usually from increased pulmonary vascular resistance and/or increased pulmonary venous pressure Etiology: Idiopathic, familial, L heart failure, parenchymal lung disease, Sleep apnea, connective tissue disorders, pulmonary embolism, HIV infection, thyroid disorders SSxs: fatigue, DOE, chest discomfort, syncope, hemoptysis, hoarseness, possible concomitant Raynaud’s syndrome PE: Wide split S2, S3, tricuspid murmur, JVD, 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, survival rate of 2.5 yrs. Good response to Ca channel blocker therapy.

Question 59

What is the difference between central and peripheral cyanosis?

Answer 59

- Central: (more serious) due to hypoxemia caused by acute or chronic cardio/ pulm dz., COPD, 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 (atherosclerosis) Arterial O2 is normal in blood (unless cardio-pulm dz. also present) but not getting to the tissue Seen in diabetics, intermittent claudication, Raynaud’s syndrom PE: pallor and cyanosis of hands, ears, nose, cheeks, feet Decreased peripheral pulses, pain, ulcers can develop, cold to touch

Question 60

What are risk factors for sleep apnea?

Answer 60

Obesity increased neck circumference (overweight) alcohol/sedatives sleeping on back and using one or more pillows smoking endocrine disorders (hypothyroidism and acromegaly) Family history deformities (scoliosis, Marfan's syndrome, Down syndrome) Menopause

Question 61

What are SSxs associated with sleep apnea?

Answer 61

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 problems with memory and concentration irritability, fatigue personality changes morning headaches hypertension GERD symptoms low libido