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362 Cards in this Set

  • Front
  • Back
What causes of chronic cough predominate in the mornings?
Chronic bronchitis, bronchiectasis.
What causes of common cough predominate at night?
CHF, Asthma, GERD, ACE inhibitor use.
What are some causes of chronic shortness of breath?
Chronic heart dz, emphysema, chronic anemia.
If a patient's cough is relieved by diuretic use, what is the likely etiology?
Congestive heart failure producing pulmonary edema.
If a patient's cough is relieved by inhaler use, what is the etiology?
Asthma.
Bronchorrhea? Presentation?
Broncho Alveolar Carcinoma (or bronchiectasis). Voluminous production of thin secretions, pts complain of "drowning inside", tons of sputum produced.
What disease has "tenacious mucoid" sputum, highly proteinaceous?
Asthma.
What are some subacute causes of shortness of breath?
Anemia, left-sided heart failure (dyspnea), asthma, chronic bronchitis, tuberculosis.
What are some acute/sudden causes of shortness of breath?
Acute exacerbation of asthma, pneumonia, pulmonary embolism, pneumothorax, acute MI, pulmonary edema, Ludwig's angina (SOB, epiglottitis and edema in sublingual and other regions).
What are some causes of massive hemoptysis?
Systemic lupus erythematosus, Wegener's granulomatosis, cocaine use, Goodpasteur's syndrome, IPH (pulmonary renal syndrome).
Classic presentation: 45-yr old male presents with acute SOB, wheezing. He's a farmer.
Thermophilic actinomyces, "Farmer's Lung", inducing HSP.
Classic presentation: 60-yr old male presents with progressive increase in SOB over the past two months. He works in a ship yard.
Asbestos exposure
Bitter almond smell?
Potassium cyanide gas poisoning.
Foul smelling sputum?
Anaerobic infection (requires pt to have teeth!). Also poor dental hygiene or lung abscesses, necrotizing pneumonia.
Rotten apple smell?
Diabetic ketoacidosis.
A patient is breathing 15 minutes using his intercostal muscles, and then 15 minutes using his diaphragm. What is this called and what condition is he about to submit to?
Respiratory alternans indicative of impending respiratory failure.
What is indicated by a Pink Puffer?
Severe COPD with an emphysema focus.
What is indicated by a Blue Bloater?
COPD of the chronic bronchitis subtype. Pt is blue bc right-sided heart failure, edema of feet, cyanosis.
What is paradoxical respiration and what does it indicate?
Only one group of respiratory muscles (intercostal or diaphragm) contract while the other is passive. Indicates impending respiratory failure.
Superior Vena Cava Syndrome is due to obstruction of the SVC by what? What is the symptom? How can it be relieved?
A lung cancer mass impinging on the SVC causing upper extremity and facial engorgement (turning red), relieved by raising the right arm.
What kind of percussional sound will emphysema have?
Hyperresonance.
What kind of percussional sound will pleural effusion have? What tissue will also sound like this when percussed?
Flatness. Any soft tissue area like the thigh or arms.
What kind of percussional sound will lobar pneumonia have? What tissue will also sound like this?
Dullness like the liver.
What is the relative intensity, pitch, and duration of percussion of a normal lung?
Loud intensity, low pitch, long duration. (Resonance).
What disease process is indicated by tympany upon percussion of the lungs?
Large pneumothorax.
What sounds do you expect to hear normally over most of the lungs?
Vesicular sounds, longer inspiratory than expiratory, soft, and low pitched.
Where would you expect to hear breath sounds that are nearly equal between inspiration and expiration?
Over the first and second interspaces anteriorly and btw the scapulae (bronchovesicular sounds) as well as anteriorly over the trachea (tracheal sounds).
What's the difference btw hyperresonance and tympany?
Tympany has a much higher pitch, almost a musical timbre.
Where would you expect to hear longer expiratory breath sounds than inspiratory?
Over the manubrium (tracheobronchial sounds).
In a patient with lobar pneumonia, what kind of breath sounds would characterize the majority of those heard in the fields with pneumonia involvement?
Bronchial or bronchovesicular.
How are transmitted voice sounds altered in the case of pneumonia? Fremitus?
Spoken and whispered words are louder and clearer (bronchophony). Ee's are heard as Ay's (egophony). Tactile fremitus is increased.
What two films are usually gotten in the case of pulmonary conditions?
PA and lateral films. Decubitus and other positions later on if indicated.
What is the most important risk factor for lung cancer and COPD?
Smoking.
What does stridor indicate?
Upper airway obstruction.
What conditions would the absence of fremitus indicate?
Pleural effusion, pneumothorax, or fibrothorax.
What adventitious lung sounds are due to obstructions in the smallest airways? Bronchi and bronchioles? Largest?
Smallest - crackles
Bronchi and bronchioles - wheezes/ronchi
Trachea/mainstem bronchi - stridor
T/F: The lower vertebral bodies should be visible on a normal PA CXR.
False.
T/F: With phrenic paralysis the diaphragm sags down.
False, it relaxes upwards (it contracts down). Other causes of elevated diaphragms: pleural collapse, subpulmonic effusion, subphrenic abscess, herniation of liver.
Between water and lipid, which one has a higher density on CXR?
Water. (Remember oil rises above water in solution, and darkness is always furthest up.)
T/F: Lower vertebrae on a lateral film CXR are darker than upper vertebrae.
True. This is because of the presence of soft tissue superiorly.
What's a pseudotumor?
Fluid accumulating in the fissures of the lungs due to CHF, cannot actually be resected.
Which hilum is usually lower?
Right hilum, because the left pulmonary artery is usu higher than the right.
Which sided decubitus film would you take to facilitate visualization of a right pneumothorax? What about right pleural effusion?
Pneumothorax - opposite side (left).
Pleural effusion - same side (right).
What is the Sniff test used to detect?
One-sided diaphragmatic paralysis (upon inhalation the active side will go down, the paralyzed side will paradoxically go up).
Ask patient to inspire/expire when doing PA and lateral films? What distance away?
Standing up, inspire to full capacity, six feet away.
What is the gold standard for detecting pulmonary emboli? What is used usu instead?
Angiography, but rarely used these days. SPIRAL CT or CT with PE protocol is the main method today. V/Q also prev was the modality of choice.
What is the final stage of intrauterine lung development?
Saccular development from 29wks-birth (inc complexity of saccules) as well as alveolar development from 36wks onward.
What are the histologic differences between bronchi and bronchioles?
No submucosal glands, cartilage, or goblet cells in bronchioles. Simple ciliated columnar epithelium in bronchioles vs pseudostratified respiratory epithelium in bronchi. Clara cells in the bronchioles.
What are the histologic differences between membranous and respiratory bronchioles?
No smooth muscle cells in the respiratory. No alveolar ducts/alveoli lining the membranous. Columnar in membranous (0.5-1mm) vs. cuboidal in respiratory (0.15-0.2mm).
What are the functions of type II pneumocytes?
1. Secretion of surfactant, reabsorption of surfactant. 2. Alveolar repair during injury to type I pneumocytes.
A pulmonary acinus consists of:
A functional unit comprising all the downstream branches of a respiratory bronchiole (as it first branches off the membranous bronchiole) including attached alveolar ducts and alveoli (~15k/acinus).
When does the surfactant amt reach an adequate level in the fetus? When do the respiratory bronchioles form, signaling the earliest possible point for respiration?
At 38 weeks term (2 weeks before normal birth). 24 weeks but survival is extremely low at this point.
What embryonic tissue does the lung develop from?
Laryngotracheal bud/diverticulum off the primitive pharynx.
Which mainstem bronchus is longer? Narrower? More likely to be obstructed by aspirated objects?
Left. Left. Right.
What is a panlobular disease of the lung?
Disease that affects the periphery but spares the central area of the lung (closer to the hilum).
What's the difference btw Pores of Kohn and Lambert's canals?
Pores of Kohn - collaterals btw alveoli;
Lambert's canals - collaterals btw alveoli and bronchioles;
Bronchial arteries supply what?
Lung parenchyma ranging from trachea to walls of the smaller airways as far as respiratory bronchioles (no alveolar supply), as well as the visceral pleura.
What vascular system has a dual elastic lamina in the lungs?
Pulmonary arteries accompanying bronchi/bronchioles.
What is the typical obstructive sleep apnea patient?
Male, middle-aged to elderly, obese, hypertensive, with a history of snoring and daytime sleepiness. Popular occupations are truck and bus drivers.
What phase of non-REM sleep is the most prevalent?
Stage 2.
What differentiates REM and non-REM sleep physiologically?
Dysregulation in REM accompanied by autonomic instability (manifested by BP fluctuation), relative muscle flaccidity, irregular respirations and reduced tidal volumes due to diaphragmatic paralysis.
What phase of sleep is apnea most likely to occur in?
REM due to the decrease in FRC and tidal volume.
What is the formal definition of apnea? What is the pathologic Apnea Index?
A >10 second pause in respiration during sleep. Over ten apneas in an hour is pathologic, although under 5 is normal.
What is the definition of hypopnea?
Reduction of airflow (not complete occlusion) accompanied by O2 desaturation of 4% or more.
What are some acquired risk factors to predispose to sleep apnea?
Alcohol (blunts physiological resposnes), tobacco (narrows airways), medications, hypothyroidism (affects soft tissues and hypopharynx).
What is the gold standard for diagnosing OSA?
Polysomnography (PSG), looking at respiratory rate, oxygen desaturation, and responses in diaphragmatic (AB) and intercostal (RC) muscles.
What is the most objective and accurate measure to quantitate "tiredness" (hypersomnolence)?
Multiple Sleep Latency Test (MSLT).
What are the physiologic conditions predisposed to in the setting of chronic sleep apnea (in the elderly)?
Hypertension, heart attacks, strokes, cardiac arrhythmias, cerebrovascular accidents, all due to frequent desaturation, inc heart rates and BP from vasoconstriction during apneas.
What's the current standard of care for OSA? Past? Surgical? Lifestyle?
CPAP, tracheostomy, UPPP (uvulopalatopharyngoplasty), weight loss, alcohol cessation, sedative cessation, TCA cessation, sleep on side not back.
What's the pharmacologic treatment of pts with Period Limb Movement in Sleep (PLMS)?
Dopaminergic agents like carbidopa/levodopa. Treat them like Parkinson's pts.
What's the most common cause of central apnea?
Congestive heart failure.
Hypoxemia induces what change in the pulmonary vasculature?
Vasoconstriction.
How does nitrous oxide act on smooth muscle cells in the vasculature?
Relaxation by 1. inc cGMP leading to inc cAMP and inc MLCP(hosphatase) activity, and 2. opening Ca-dependent K-channels hyperpolarizing the cell. Remember V>A!
What are the determinants of pulmonary blood pressure?
1. Blood volume
2. Flow rate determined by CO, fluid viscosity, vessel size
3. Left atrial pressure
What are four broad ways pulmonary artery pressure can be increased?
1. Decreased cross-sectional area to flow across (thrombosis, PE, pneumonectomy);
2. Lumenal narrowing (arteritis, hypoxia vasoconstriction)
3. Inc viscocity (polycythemia, leukemia)
4. Left-sided CHF (inc LAP)
What's the most common cause of pulmonary hypertension?
COPD (secondary, primary less common).
What is the pathology of primary pulmonary hypertension?
Vascular bed hypertrophy and fibrosis, with in situ thrombosis.
What are the most distinctive symptoms of pulmonary hypertension?
SOB, cough, syncope (fainting), hypotension, palpitations, JVD.
What is the radiologic finding for women in their 30's-40's with primary pulmonary hypertension?
Enlarged pulmonary arteries. Clear lung fields.
What are the side effects of PDE5 inhibitors?
Headaches, flushing, hypotension (V>A), vision changes.
What is the general treatment regimen for pts with pulmonary hypertension where treatable etiologies (COPD, cardiac problems) have been ruled out?
All: anticoagulants, diuretics, O2;
Responders: CCB transient vasodilators
Non-responders: Prostacyclins, ET-antagonists, PDE5-I's, gaseous NO. Transplantation.
What is the most common chronic cause of cor pulmonale?
COPD.
What are symptoms and signs of cor pulmonale?
Hepatojugular reflux, lower extremity edema, pulsatile liver, tricuspid regurg, ascites.
What's Virchow's triad.
Endothelial injury, circulatory stasis, hypercoagulable states.
What is Homan's sign and what is it pathognomonic for?
Dorsiflexion of foot causing pain in the calf, present in some pts with lower extremity DVT.
What are classic signs and sx's of DVT?
Pain, tenderness, swelling, and Homan's sign unilaterally in the lower extremity. Peau d'orange denoting texture of the skin like an orange peel.
Low D-dimer levels are a great prognostic indicator for what?
Negative predictive value for thromboemboli, if it's low then you can exclude DVT's and PE's with reasonable confidence.
What is the preferred diagnostic choice for detecting DVT?
Compression ultrasound. Gold standard is contrast venography which is more appropriate for asx pts.
Heparin-induced thrombocytopenia is associated with what complication?
Clotting due to the prothrombotic (yet thrombocytopenic) state.
What are the symptoms of severe PE?
Dyspnea, palpitations, LoC, tachypnea, tachycardia, low grade fever, acute heart failure (split of S2, presence of S3+S4), cyanosis, hypertension.
What is a notable EKG finding of pts with acute PE?
RAD with S1Q3T3 sign in <20% of pts.
In a patient with PE what numbers on the pulmonary function test do you want to pay attention to? Ignore?
Ignore the oxygenation and CO2, they may be normal. The A-a difference is what you want to pay attention to.
In a patient that presents with reasons for suspicion of PE, what is a good method for determining their risk?
The Wells Diagnostic Scoring.
What are some drugs that antagonize warfarin? Augment it?
Antagonist: vit K, carbamazepine, barbiturates, phenytoin, rifampin.
Augment: Amiodarone, Plavix, ethanol, fluconazole, metronidazole, Prozac.
When do you want to treat PE pts with thrombolytic therapy?
When they will die otherwise, there is a 25% risk of signif bleeds assoc with it.
The normal pleural fluid has what pH?
Alkaline, pH >7.60.
What are types of causes of transudative and exudative pleural effusions?
Transudative: Increased fluid diffusion to the pleura due to inc hydrostatic pressure or decreased serum oncotic pressure, both systemic.
Exudative: 1. Dysfnx/inc permeability of pleural membrane, or 2. Decreased lymphatic drainage of pleura, both local.
What are physical signs of pleural effusions?
Dec breath sounds, flatness/dullness to percussion, dec tactile fremitus, dec chest wall excursion, tracheal shift with massive effusions.
Always pierce ___ the ribs.
Above. Just below are nerves and vessels.
What is Light's criteria used to determine, and what are the criteria?
Used to differentiate transudative from exudative effusions. Pleural to serum ratios of 1. Fluid/serum protein >0.5, 2. Fluid/serum LDH > 0.6, and 3. LDH >2/3 upper limit. Exudates will have at least one of these criteria positive.
What are some specific common causes of transudative pleural effusion?
CHF, cirrhosis, peritoneal dialysis, nephrotic syndrome, ascites.
What is characteristic of a tuberculous effusion?
Exudative, early has a inc positive culture incidence with PMN's, late 90% WBC's are lymphocytes.
Blood-tinged effusion fluid should immediately raise your suspicion for:
Malignant metastatic effusion.
What is the classical presentation of spontaneous (idiopathic primary) pneumothorax?
Male, 20-30yo, smoker, tall, thin.
What is the most common cause of secondary pneumothorax? How do you diagnose it?
COPD. Not easy to diagnose, sx same as all others in COPD, look for exacerbation of SOB with a positive CXR sign.
Which direction do the trachea and great vessels shift during a tension pneumothorax?
AWAY from the pneumothorax, due to an accumulation of excess positive pressure within the pleural cavity.
What are physical signs of a tension pneumothorax?
Loud tympany ipsi. Absent breath sounds ipsi. Hypotension and cyanosis, sudden vascular collapse.
What are methods to sample mediastinal lymph nodes?
TBNA- transbronchial needle aspiration. Suprasternal and anterior mediastinoscopy.
What is Hamman's sign and what does it denote?
Crackling/crunching upon auscultation of the heart in synchrony with systole, best heard in the left lateral decubitus position, denoting pneumomediastinum.
What are the possible types of anterior mediastinal masses? Epidemiologies?
Thymoma, substernal thyroid gland, teratoma, other tumors (like lymphoma). Benign thymomas most common, in pts 40-60yo. Malignant ones more common in children.
What is the most assoc syndrome with a "parathymic syndrome" stemming from a thymoma?
Myasthenia gravis, in 10-50% of these pts.
What is the most common posterior mediastinal mass? What else is important to rule out?
Neurogenic mass in children, such as neurofibromas, neurogangliomas, and pheochromocytomas (usu benign in adults, 50% malignant in kids). Esophageal lesions must be considered, like megaesophagus, diverticula, or cancer.
Nerve compressions due to masses in the mediastinum may lead to what symptoms?
1. Hoarseness due to injury to L. recurrent laryngeal; 2. Diaphragmatic paralysis due to phrenic involvement; 3. Horner's syndrome due to injury to stellate ganglion or sympa chain.
What is the most common cause of SVC syndrome?
Lung cancer.
An 8yo pt presents with weight loss, chest pain, and difficulty swallowing (dysphagia). What do you suspect?
Posterior mediastinal mass such as neurogenic tumor.
What is the most common clinical situation where tension pneumothoraces occur?
Pts on mechanical ventilation with constant positive pressure into their lungs, developing a leak.
Why do leukemias present with hypoxemia?
WBC's use up oxygen at such a high rate that hypoxemia is artifactual. Not an actual hypoxemia but just a laboratory reading of one.
Which two cases of hypoxemia present with a normal A-a gap?
Decreased PIO2 (low barometric pressure, low FiO2), or hypoventilation (increased PCO2).
High A-a gradient respiratory acidosis has what broad etiologies as causes?
1. V/Q mismatch
2. Shunt defect
3. Diffusion barrier defect as in interstitial lung dz.
What are some causes of non-AG metabolic acidosis?
Diarrhea, ureteral diversion, renal tubular acidosis, mineralocorticoid deficiency, carbonic anhydrase inhibitor ingestion. Anything to remove bicarb essentially.
What are the causes of anion-gap metabolic acidosis?
A- aspirin
M- methanol
U- uremia (renal failure)
D- DKA
P- paraldehyde
I- ischemia/infarct
L- lactic acidosis
E- ethanol, ethylene glycol
S- salicylates, sepsis, starvation
After checking on whether an acidosis is metabolic or respiratory, what are the next two steps?
Is it an anion-gap acidosis? Is it properly compensated (Winter's formula matching bicarb and CO2)?
On a PFT, what is the quickest way to distinguish between obstructive and restrictive dz?
The FEV1/FVC ratio - normal or elevated in restrictive, diminished in obstructive. Next look for prolonged expiration and scooping on the obstructive breathform or steepness on the restrictive breathform. To exclude combined disorders, look at the TLC (elevated should be obstructive alone).
On obstructive disorders, which PFT reading differentiates btw COPD and asthma?
DLCO - elevated in asthma, normal in chronic bronchitis, reduced in COPD (and restrictive dzes).
What artery do they stick to get a measurement of arterial blood gas?
Radial artery so long as it is not the main one btw it and the ulnar (it usu isn't).
Arterial blood gas and A-a gap are affected by aging how?
Declines by 0.43 per year, increases by a variable amount.
What is a normal RR?
14-20 beats, higher in children and higher in stress.
What's the PCO2 VCO2 relationship?
PCO2 = VCO2/VA * .863

VA = alveolar ventilation
What effect does increased dead space have upon PaCO2?
Increased PaCO2.
What effect would hyperthyroidism have upon blood gas levels?
It would lead to excess CO2 production from hypermetabolism and thus inc PaCO2.
What is arterial oxygen saturation (SaO2)? The arterial oxygen content (CaO2)?
The % of heme binding sites saturated with oxygen in the arteries. The CaO2 is the total amount of oxygen in the arteries, combining the SaO2 with the PaO2.
What is it called when V/Q = infinity? Zero?
Infinity - dead space, pulmonary embolism, ischemia;
Zero - shunt.
What happens to V/Q as you move further superior in the lung?
V/Q increases the higher the elevation of the lung. This has to do with blood perfusion more than oxygen concentration in the alveoli.
What is a condition of hypoxia without hypoxemia?
Cyanide poisoning. Oxygen is in the blood but it doesn't diffuse to the tissues.
What are the three broad causes of hypoxia?
1. Hypoxemia (incl anemia, CO poisoning, lung dz)
2. Reduced delivery to tissues (CHF, systemic shunts)
3. Reduced uptake of oxygen (mitochondrial poisoning, high affinity Hb).
T/F: With metabolic acidoses or alkaloses you can determine whether or not the disease is acute or chronic by looking at the pH change expected based on the serum bicarb.
False. This only holds for respiratory acidosis/alkalosis since the kidney takes time to compensate for the disorder of the resp system. When the renal system is at fault, however, the resp system compensation is immediate.
What are the important measurements spirometry yields us and what exactly do they refer to?
FEV1 - the amount of air expelled after 1 sec;
FVC - forced vital capacity, the maximum amount of expelled air over the total exhalation;
What is the usual FEV1/FVC ratio, and if this is low what does it mean?
70%, low = obstructive pulmonary dz, normal or high w/ both FEV1 and FVC low = restrictive pulmonary dz.
Between spirometry of inspiration and expiration, which curve is skewed and in which direction?
Expiration skewed, to the right (the peak moves left but technically the skew is right).
What is the best measure in spirometry of the severity of airflow obstruction?
FEV1.
In spirometry, what does the FEF(25-75) measurement tell you if it is low and patient is otherwise normal?
Indicates small airway disease.
In obstructive pulmonary dz patients, how does the FVC, FEV1, and ratio look on spirometry?
FEV1 low, FEV1/FVC low, FVC may be low OR normal. If FVC is low suspect combined dz.
What disease is a positive bronchodilator reversibility test with an increase in FEV1 and FVC >12% indicative of?
Asthma and rarely COPD.
In spirometry truncation of the expiratory and inspiratory flow loops is indicative of what? Inspiratory or expiratory only?
Both - Fixed upper airway obstruction such as tracheal stenosis. Inspiratory - extrathoracic (vocal cord paralysis. Expiratory - intrathoracic (tracheal tumor above carina).
What test is used to measure total lung capacity?
Body plethysmography or helium dilution.
What pulmonary disease demonstrates large lung volumes in the pulmonary function lab?
Emphysema.
Low lung volumes combined with normal DLCO indicates what types of diseases?
Chest wall excursion diseases (pleural fibrosis, myasthenia gravis, Guillain-Barre). Potentially asthma too depending on severity.
Bronchoprovocation tests are used to measure what, and what is the most common challenging chemical?
Methacholine, used to determine mild forms of asthma with airway hyperresponsiveness.
A completely normal spirometry with decreased DLCO is indicative of what?
Pulmonary vascular disease.
In cases of acidosis where the change in bicarb is much greater the anion gap, what is going on? Who is the real hero?
A mixed disorder is causing an additional non-AG acidosis to require compensation via the bicarb increase, on top of the original AG acidosis.
In cases of acidosis where the change in bicarb is much less than the anion gap, what is going on? Who is the real hero?
A mixed disorder is leading to insufficient compensation of bicarb for the AG acidosis. This would be an additional primary metabolic alkalosis (e.g. diarrhea).
For respiratory alkalosis in acute situations, how much does the pH change with a 10 change in PCO2? How much does the bicarb drop in acute renal compensation for this?
pH - 0.08 per 10 PCO2 decrease.
HCO3 - 2 decrease per 10 PCO2.
What are some causes of metabolic alkalosis?
Volume contraction - (vomiting, diuretics, edematous states);
Mineralocorticoid excess - high renin (renal artery stenosis, estrogen therapy), low renin (primary aldosteronism, Cushing's dz).
T/F: Oxygen administration is a good way to treat chronic hypoxemia and CO2 retention.
False! For V/Q dead space hyperperfusion reasons, saturating a pts' airways with oxygen actually further exacerbates their high PaCO2 and resp acidosis.
What is Winter's formula for calculating expected PCO2?
PCO2 = 1.5*HCO3 + 8 +/- 2 only applicable in cases of metabolic acidosis with resp compensation.
Decreased DLCO in an emphysema pt indicates what disease pathology?
Destruction of alveolar walls.
Where in the lung does TB preferentially infect in reactivation dz?
Upper lobes (apices) due to the higher oxygen tension there. Posterior segments also preferred.
What are the hematogenous seeding sites for primary TB?
Apex of the lung, kidney, growing ends of long bones.
What does a positive PPD mean?
Someone was infected with TB in the past, or injected with the BCG vaccine in another country at some point. It speaks nothing to the disease state.
What are some risk factors that warrant the 5mm designation for a positive PPD?
HIV infection, immunosuppressed pts, close contacts of TB pts, pts with CXR findings.
What are some risk factors that warrant the 10mm designation for a positive PPD?
Any health worker, recent immigrant from high prevalence country, prison/nursing home/shelter resident, any other comorbid dz state like post-gastrectomy, diabetes.
What is prophylaxis therapy for a PPD+ person?
Daily INH 300mg for 9mos (12 for HIV), rifampin 4-6mos for close contacts.
What are the important side effects of TB drugs?
INH, pyrazinamide - hepatitis
INH - peripheral neuropathy
Rifampin - GI upset, inhibition of birth control and methadone
Ethambutol - optic neuritis
What is the risk of an HIV pt of getting TB?
5-10% per year.
What is the risk of a pt with a positive PPD (not related to BCG) of contracting TB disease?
10% lifetime, 2-3% with prophylaxis.
Risk factors for developing community-acquired pneumonia include?
Old age >70, smoking, malignancy, diabetes, chronic renal dz, alcoholism, hx of pulmonary dz, lymphoproliferative dz, aspiration risk factors, dementia, immunosuppression, asplenia, CHF.
What is the hallmark of pneumonia diagnosis?
A positive chest x-ray. Auscultation should also yield egophony, percussion should yield dullness.
What is the leading cause of pneumonia in the HIV+ patient?
Strep pneumonia. In AIDS pts with low CD4 counts, it becomes PCP.
What differentiates the presentation of typical and atypical pneumonia?
Atypical pneumonia is more gradual in onset, the cough is dry, and the fever and dz progression should be milder. The CXR will look worse though.
What presentation would make you suspicious of legionella pneumonia and how would you diagnose it?
High fever, lobar infiltrate like strep pneumo, more extrapulmonary sx like GI nausea, CNS confusion, hyponatremia. Diagnose with culture, DFA, and RIA for urinary antigen.
What are the most common HA-pneumonias?
Staph aureus (MRSA), pseudomonas, then the other gram - rods.
AIDS patients with CD4 counts below 200 will be prophylaxed with what to prevent what?
Trimethoprim/sulfa (bactrim) to prophylax against PCP.
What is used to diagnosis pneumonia in patients that fail to produce patent sputum?
Bronchoscope with bronchoalveolar lavage.
What kind of CXR does pneumocystis pneumonia display and what is the treatment?
Bilateral alveolar infiltrates. Treat with sulfa drugs (bactrim), steroids in the condition of hypoxemia to cut down on the inflammatory response.
What is the only adult pneumonia indication in which steroids are indicated?
PCP pneumonia with hypoxemia.
Prophylax HIV patients with CD4's <50 with what to prevent mycobacterium avium complex?
Macrolides (MAC for MAC).
What form of atelectasis is irreversible?
Contraction atelectasis.
In what forms of atelectasis does the mediastinum deviate, and to which side does it go?
Resorption - towards
Compression - away
What etiologies can lead to mucous plug formation and subsequent resorptive atelectasis?
Bronchial asthma, chronic bronchitis, bronchiectasis, post-operative states.
What are "heart failure cells"?
Hemosidern-laden macrophages deposited in alveolar cavities in the setting of pulmonary edema.
What is the most common cause of pulmonary edema caused by microvascular injury?
Pneumonia infection.
Which phase of alveolitis/ARDS is associated with granulation tissue? Hyaline membranes in alveolar spaces? Which cells proliferate in the organizing phase?
1. Organizing
2. Exudative
3. Type II pneumocytes
What are the causes of ARDS?
1. Diffuse pulmonary infections; 2. DIC/sepsis; 3. Trauma (esp to head); 4. Aspiration; 5. Inhaled agents - smoke, oxygen toxicity, toxic gases; 6. Chemotherapy, drugs; 7. Radiation; 8. Pancreatitis
What is respiratory distress of the newborn due to?
A deficiency in pulmonary surfactant.
DAD with significant type II pneumocytic hyperplasia is characteristic of what cause?
Radiation injury.
What immune cell type plays an important part in the pathogenesis of ARDS?
Neutrophils.
What grade of acute cellular rejection of a lung transplant involves lymphocytic infiltration of the interstitium?
Moderate (A3).
Chronic lung transplant rejection (bronchiolitis obliterans) involves what pathologic process?
Fibrosis of the small airways.
What are the criteria to differentiate acute lung injury from ARDS?
Both have diffuse pulmonary edema, but where ALI requires <300mmHg PaO2/FIO2, ARDS is below 200.
What are the differences between the pathophys of pulmonary edema and ARDS?
Pulm edema involves increased hydrostatic pressure or dec oncotic forces, where ARDS involves capillary damage and inc permeability. Pulm edema -> transudate, ARDS -> exudate which clogs the lymphatic drainage.
With proliferation of type II pneumocytes in the exudative phase of ARDS/alveolitis, what is a marker of pulmonary fibrosis?
Type III procollagen peptide.
What are some PFT findings in the setting of interstitial lung disease (ILD)?
Restrictive patterns, dec FEV1 and FVC but not FEV1/FVC, TLC reduction determines severity of dz. DLCO reduced.
What are the best modalities for diagnosing ILD?
High resolution CT and lung biopsy via bronchoscopy.
What does IPF look like on a high-resolution CT?
Patchy, subpleural and septal fibrosis, "cobblestone" appearance of pleura, basilar changes.
What is the one ILD that tends to occur more often in men than women?
Pleuropulmonary involvement of rheumatoid arthritis presenting as pleural effusions or nodules (Caplan's dz).
What ILD's are on the differential for pleural effusions/pleuritis?
Vascular etiologies like rheumatoid arthritis. Then think about sarcoidosis, asbestosis, silicosis.
What is the typical epidemiology and presentation for sarcoidosis?
Female, black, <40yrs, asymptomatic with CXR findings for lymph node involvement (stage I).
Classic presentation: A stone-cutting/polishing, mining, foundry work, sandblasting occupation for over 5 years coming down with SOB and dry cough?
Silicosis.
Which ILD's can present with upper lobe fibrosis and hilar adenopathy? What are these pts at increased risk of being infected with? Which ILD's present in the lower airways?
Silicosis @apex. TB since it loves the upper airways. IPF and asbestosis present @base.
T/F: Mesothelioma is assoc with smoking.
False.
What term in the Starling equation for flow across a permeable barrier is impaired in the case of ARDS?
The reflection coefficient, a constant multiplied against the oncotic pressure gradient.
What is the triad of Fat Embolism Syndrome with ARDS?
Respiratory failure, neurologic impairment, petechial rash.
What is the risk of acquiring post-ARDS fibrosis?
23% of all those that survive the initial acute attack, 3% being severe impairment requiring oxygen and perhaps death.
What interstitial lung diseases present with granulomatous formation?
Known causes - hypersensitivity pneumonitis (Farmer's lung), silicosis; unknown causes - sarcoidosis (non-caseating), Wegener's granulomatosis, Churg-Strauss-angitis, Behcet's dz, Goodpasture's syndrome.
What is Hamman-Rich Syndrome?
Acute intersitial pneumonia, a disease presenting like ARDS/DAD (diffuse uniform fibrosis) but with a rapidly progressing course (to Honeycomb lung) and likely end in death @3-6mo.
What is the most common lung involvement for SLE and rheumatoid arthritis?
Pleural effusions for both, SLE's #2 is NSIP (non-specific interstitial pneumonia) w/ variable interstitial fibrosis. #3 = chronic pleuritis.
Classic presentation: A 55yo coal-mining smoker male with rheumatoid arthritis presents with SOB, dry cough, fatigue and weight loss. CXR shows nodules. Differential diagnosis shows?
Malignancy and Caplan's syndrome if it's his arthritis.
Which vasculitis characteristically infects lung tissue in necrotizing fashion? Which characteristically avoids the lungs as a means for differentiating it from a similar vasculitis?
Wegener's granulomatosis. Polyarteritis nodosa very rarely hits the lungs unlike microscopic polyangiitis.
Out of dyspnea, tachypnea, wheezing, crackles, and cyanosis, what physical sign differentiates obstructive from restrictive lung dz?
Wheezing. Not present in restrictive.
What are the acute and chronic forms of IPF?
Chronic - UIP (usual interstitial pneumonia)
Acute - AIP (acute " ")
T/F: UIP involves a diffuse, homogeneous interstitial fibrosis that develops over years.
False, UIP is multifocal with fibroblastic foci and hetergeneous distribution.
What does Honeycomb Lung refer to?
The common end-stage pathologic state of fibrotic interstitial lung dz where gross cystic spaces separated by fibrous septae form.
What is the difference btw AIP and UIP and NIP?
AIP - acute, diffuse, uniform fibrosis leading to death in 3-6mo.
UIP - chronic, heterogeneous fibrosis, better course than AIP.
NIP - chronic, diffuse or patchy fibrosis, responds to steroids, better course than UIP.
Which interstitial lung dz involves polypoid plugs of loose mesenchyme in the acini, with myxoid stroma and fibroblastic infiltration?
Cryptogenic Organizing Pneumonia (COP or BOOP). Remember NO organized interstitial fibrosis or honeycomb lung!
Lymphocytic interstitial pneumonia has what as its causative disease? What separates from other interstitial pneumonias?
Autoimmune or lymphoproliferative disorders, i.e. Sjogren's syndrome. More cellular interstitial infiltrates with bluish giant cells and non-necrotizing granulomas.
Non-caseating granulomas in the lung?
Sarcoidosis, mycobacterial and fungal dz, pneumoconiosis, syphilis, berylliosis. Also giant cell inclusions which also be seen in Sjogren's, berylliosis, and TB.
Asteroid body? Schaumann body?
Sarcoidosis. Sarcoidosis.
Which ILD presents with bronchiolitis and airway-centered granulomas?
Hypersensitivity pneumonitis (HSP). Remember RBILD is in smokers but has no granulomas.
What inflammatory infiltrates predominate in Desquamative Interstitial Pneumonia?
Macrophage.
Classic pres: 45-yr old miner presents with SOB. Biopsy shows brown dumbbells.
Asbestosis. "Asbestos bodies".
What ILD involves nodular fibrosis and pigmented macrophages distributed within the lymphangiitic network?
Silicosis.
What ILD's are assoc with smoking?
RBILD (bronchiolitis-assoc) and DIP (desquamative).
What is the risk of TB infection for an HIV+ person? Non-HIV person infected in the past two years?
5-10% per year. 2-5% in those two years, 10% lifetime.
What is the definition of a multi-drug resistant strain of TB? What factors are more likely to predispose to the formation of MDR-TB?
TB resistant to both INH and rifampin. HIV, non-compliance, and antibiotic exposure breed resistance.
TB transmission occurs via:
Small droplet inhalation, usu in crowded, small spaces with poor ventilation.
During primary TB, where are some popular sites for hematogenous seeding?
Apex of lung, kidney, growing ends of long bone.
Which site in the lung is preferentially affected in primary TB? Secondary TB?
Primary - lower lobes, hilar adenopathy, pleura;
Secondary - apical posterior segment of lobes;
What is a difference between the physical presentation of pulmonary TB and interstitial lung diseases?
Pulmonary TB cough is productive, restrictive lung dzes like UIP and asbestosis employ dry coughs.
T/F: If a TB regimen is not improving a pt's dz course, then consider adding another drug like streptomycin.
False. Never add a single drug to a failing regimen.
The major determinant of TB outcome is:
COMPLIANCE.
The standard regimen for treatment of active TB dz mandates treatment for a minimum of how long? Latent infection? HIV+ pts?
6 months - 4 drugs/2mo + 2 drugs/4mo.
Latent - 9mos INH.
Latent and HIV+ - 12 months INH.
T/F: All first-line TB drugs are bacteriocidal.
False. Ethambutol is bacteriostatic.
What primary complication should one be on the watch for in a pt taking 4 drugs for TB treatment?
Hepatitis onset due to INH and pyrizinamide therapy.
What do the Quantiferon or ELISPOT tests measure and what disease do they diagnose?
IFN-gamma production in response to stimulation with TB-specific antigens to screen for TB.
Stimulation of the vagus nerve induces release in bronchial smooth muscle cells of what neurotransmitter?
Acetylcholine to constrict the airway.
Which NANC neuropeptides induces constriction? Dilation?
Constriction - neurokinin A, cacitonin gene-related peptide, substance P, bradykinin, tachykinin;
Dilators - NO, VIP;
What are the pathophysiologic sources of airway obstruction in the setting of emphysematous COPD?
1. Loss of alveolar tethering to keep airways open; 2. Mucus hypersecretion; 3. Mucosal inflammation + fibrosis;
What inflammatory cell types are responsible for early and late phase asthma?
Early - mast cells;
Late - eosinophils and neutrophils;
What drugs activate smooth muscle cAMP in the lungs?
Bronchodilators inc cAMP, either by beta-2 agonists like albuterol or PDE-I's such as theophylline.
What are the long acting beta-2 agonists?
Salmeterol and Formoterol.
T/F: Long-acting beta-agonists are only indicated in the setting of pts who are already on moderate doses of corticosteroids.
True. LABA are never indicated as a sole therapy, and increasing doses of corticosteroids has been proven to be less effective than dual therapy.
What are the side effects of long-acting beta-2 agonists?
Muscle tremor, tachycardia and palpitation, hyperglycemia, hypokalemia, V/Q mismatch. Tachyphylaxis (resistance to drug).
What are toxicities assoc with methylxanthines (like theophylline)?
GI sx (irritation, burning, nausea), CNS stimulation, tachycardia, tons of drug interactions.
Oral corticosteroids in the treatment of asthma have what side effects?
Osteoporosis, glaucoma, diabetes, adrenal suppression, skin fragility.
What is cromolyn sodium (Nedocromil) and what patient population is it for?
A mast-cell stabilizer, used in asthmatic children.
What drugs were covered in this block concerning smoking cessation and how do they work?
Buproprion - NDRI, antidepressant, increases dopamine to suppress cravings.
Varenicline (Chantix)- partial agonist of nAchR.
What are Zileuton and Zafirlukast/Monteleukast? What conditions are these not useful for?
Zileuton - 5-LO inhibitor.
Zafirlukast/Monteleukast - LTD4 receptor antagonists, longer-acting. Good for exercise-induced asthma, nocturnal sx, but bad for allergic rxn asthma.
What are common causes of respiratory acidosis?
CNS depression, chest wall dysfnx, obstructive lung dz, hypercapneic resp failure.
What are common causes of respiratory alkalosis?
Anxiety, sepsis, liver failure, acute pulmonary insult (PE, asthma).
What are common causes of metabolic alkalosis?
Diuretics or corticosteroids use, hypovolemic states/hyperaldosteronism, vomiting/NG suctioning, severe hypokalemia.
What are the three main symptoms of asthma?
Cough, SOB, wheezing.
What three airway findings are hallmarks of asthma?
Airway inflammation, obstruction, hyperresponsiveness.
T/F: Asbestos exposure is a risk factor for lung cancer.
True, but only in synergy with smoking.
What is the most common type of lung cancer?
Non-small cell carcinoma (70%), adenocarcinoma subtype (45%). Prev squamous cell carcinoma.
Which lung cancer presents with excessive sputum production?
Broncho-alveolar cell carcinoma, a subtype of adenocarcinoma.
Which lung cancer is assoc with gynecomastia and galactorrhea?
Large cell carcinoma.
Which cancers present centrally or peripherally?
Central - small cell CA and squamous cell CA.
Peripheral - adenocarcinoma, large cell CA.
What are the most common presenting symptoms of lung cancer?
Cough, SOB, hemoptysis (rarely severe), wheezing or stridor if an airway tumor, post-obstructive pneumonia sx, ill-defined chest discomfort.
A lymphocyte-predominant pleural effusion occurs in what two etiologies?
Lung cancer and TB.
For what stage of lung cancer and beyond is surgery not an option?
Stage IIIB and higher. Any small cell lung cancer falls under this designation.
What cancers involve common metastases to the lung?
Breast, thyroid, GI tract, kidney, germ-cell cancers (prostate, ovary), melanoma.
Most benign lung masses are:
Hamartomas or bronchial adenomas.
"Popcorn calcification"?
Hamartoma.
What is the standard treatment for pts with small cell carcinoma?
Radiation and chemotherapy only. Surgery is not an option.
What lung cancer has the best prognosis?
Bronchioloalveolar carcinoma.
What lung cancer would you suspect in a pt with a biopsied mass showing intercellular bridges and dense pink eosinophilic cytoplasm with intracytoplasmic keratin and sometimes keratin pearls?
Squamous cell carcinoma.
Which lung cancer is defined by a "cribriform pattern" of glandular formation?
Adenocarcinoma.
In poorly differentiated adenocarcinoma, what indication would lead one histologically to determine that it was in fact adenocarcinoma?
Intracytoplasmic mucin using special stains.
Which lung cancer demonstrates a "lepidic" growth pattern along alveolar septa?
Bronchioloalveolar carcinoma.
What lung cancer type is most frequent in nonsmokers?
Bronchioloalveolar carcinoma.
By EM which lung cancer does a large cell carcinoma look like more than the other?
Adenocarcinoma more than squamous cell carcinomas.
What stain can be performed on biopsied lung masses to detect a neuroendocrine etiology?
CD56 immunohistochemcal stain.
What is the most important prognostic factor for COPD?
FEV1. Others: continued smoking, age, weight status.
What are the etiologies of pneumonia in COPD pts?
1. Strep pneumo, 2. H. influenzae (higher than normal), 3. Moraxella catarrhalis
What are the etiologies of influenza?
Influenza virus, strep pneumo, staph aureus.
What are the three primary determinants of risk on the PORT score?
1. Age
2. Co-morbid dzes
3. Significant abnls on vital signs
When does Legionella peak?
Late summer, early fall.
What is the cutoff time in hospitalization for the pneumonia to become hospital-acquired?
48hrs inpt.
What is the dz progression for HIV+ pts with PCP? CXR finding?
Insidious onset, gradually inc cough, dyspnea over weeks, CXR showing bilateral alveolar infiltrates.
What is the best prognostic marker from the PFT of the severity of a restrictive lung disease?
TLC.
What organ systems does sarcoidosis affect?
Lungs, CNS, bone, cardiac, endocrine, skin.
T/F: COPD involves impaired airflow which is not fully reversible unlike asthma.
True.
What two diseases is COPD a mixture of?
Chronic bronchitis and asthma.
What kind of emphysema does alpha-1 antitrypsin deficiency classically lead to? Where does it typically localize? What other illness is assoc with it?
Panacinar emphysema of the lower lobes, assoc with hepatic cirrhosis. Smoking->Centrilobular, normal emphysema, classically upper lobe predominant.
What are the criteria for diagnosis of chronic bronchitis?
Chronic cough on most days for at least 3mos/yr, for at least 2 straight years, w/o other obvious causes.
Emphysema by definition involves what airspaces?
Distal airspaces to terminal bronchioes->enlargement.
Alveolar walls->destruction.
What is the primary risk factor for COPD? What is the best way to quantitate this risk? Others?
SMOKING. Pack years. Air pollution, poor nutrition, hx resp infxns, preexisting hyperreactivity (like asthma), A1AD, occupational exposures.
What is the % of smokers >60 pack-years with impaired FEV1?
80-85%.
What is the normal fnx of alpha-1-anti-trypsin? What does deficiency predispose pts to?
Protease inhibitor that protects lung tissue from elastases and proteases that degrade the parenchyma during inflammation or toxin exposure (smoking). COPD w/o smoking.
In the pathogenesis of COPD, what kinds of immune cells are active infiltrates?
Neutrophils, macrophages, and CD8 T-cells. (Asthma is eosinophils and CD4's).
What three processes contribute to cough and mucus production in the large airways in the setting of COPD?
1. Squamous metaplasia leading to impaired mucociliary clearance;
2. Glandular enlargement
3. Large airways goblet cell hyperplasia.
What three processes contribute to small airway narrowing in the setting of COPD?
1. Smooth muscle hypertrophy
2. Replacement of Clara cells with goblet cells
3. Small airway goblet cell metaplasia
T/F: COPD involves equal obstruction during inspiration and exhalation.
False. Exhalation has worse obstruction due to airway collapse from loss of supporting elastic tissue. This is seen on the PFT.
What happens to the DLCO in COPD and why?
DLCO goes down due to loss of total alveolar surface area in contact with the pulmonary microvasculature.
At what age does lung tissue atrophy (and thus most PFT volumes) begin?
30yrs.
At what FEV1's below normal do PaO2 and PaCO2 abnormalities occur? Pulmonary hypertension?
PaO2 goes down @ less than 50% (hypoxemia).
PaCO2 <25% leading to destruction of vascular beds and pulm hypertension.
What scoring system grades the degree of airway obstruction in chronic bronchitis/COPD?
Reid index, fraction of space in the wall occupied by bronchial glands (>.55 is bronchitis).
T/F: Clubbing in a pt with COPD means they have had severe chronic COPD for a prolonged time.
False. Clubbing never occurs in pure COPD, its presence = additional diseases.
What is Hoover's sign?
Inward movement of the ribcage on inspiration, occurs in severe COPD.
What auscultatory findings are present in COPD?
Decreased breath sounds, prolonged expiration, wheezing.
Between COPD subtypes, which one has the worst dyspnea? Cough? Sputum? Opportunistic infections? Resp insufficiency? Earlier age of onset? Cyanosis? RHF? Dec compliance? Airway resistance? DLOC?
Dyspnea - emphysema
Cough - bronchitis
Sputum - bronchitis
Infxns - bronchitis
Insufficiency - emphysema (terminal)
Age - bronchitis 50+/emph 60+
Cyanosis - bronchitis
RHF - bronchitis
Dec compliance - emphysema
Resistance - bronchitis
DLOC - emphysema.
Which COPD subtype is associated with an enlarged heart?
Chronic bronchitis - large heart
Emphysema - small heart
Which respiratory disease is associated with the cytokines LTB4, IL8, TNF?
COPD. Asthma is IL4, IL5, IL13.
T/F: Pulmonary vascular markings are increased on CXR in emphysema.
False.
What happens to exhalation times in COPD?
Pts require more time for full expiration, but are unable to do so. Overall, exhalation times increase but remain inadequate.
T/F: Smoking cessation can restore some of the FEV1 in COPD pts.
False, but it will reduce the decline to a normal rate of decline.
What pharmacologic options are available for pts that want to stop smoking?
Antidepressants (buproprion), Chantix, nicotine replacement therapy, clonidine patch.
What is the only therapy for COPD shown to improve clinical outcomes? What about decrease mortality?
1. Smoking cessation.
2. Long term oxygen therapy.
What pharmacotherapies help relieve the symptoms of COPD?
Bronchodilators - Anticholinergics (atropine), beta-2 agonists (albuterol), and methylxanthines (theophylline).
What is the most common cause of COPD exacerbation?
Pneumonia, vaccinate them for influenza and strep pneumo!
Bronchiectasis is irreversible dilatation of what secondary to what causes?
The bronchi, secondary to inflammation caused by infxn (pneumonia, influenza, pertussis, TB), endobronchial tumors, foreign body aspiration, stenosis, CF, or toxic inhalation.
What are findings of bronchiectasis?
Cough with purulent sputum. Hemoptysis, recurrent infxns, dyspnea/wheezing due to obstruction, clubbing.
What is the mutation for cystic fibrosis, and what does the gene regulate?
CFTR gene on chr7, a transmembrane conductance regulator for chloride (defects prevent chloride from exiting the cell resulting in thick sputum).
Cystic fibrosis involves impairment of which organ systems?
Lungs (viscous sputum- frequent infxns, obstructive dz), intestines (obstruction), panceas (insufficiency), GU tract (infertility).
Pts with cystic fibrosis will have what finding in their sweat?
Inc Na and Cl bc they can't excrete it in mucous form.
How many years does it take for a smoker to quit smoking and reduce his risk for lung cancer to that of a non-smoker? What is the risk of an active smoker over non-smoker for lung cancer? Passive smoker?
20 years. 13x. 1.5x.
For occupational exposure-based lung cancers, what is the mean interval between exposure and cancer?
30-35 yrs. 25-45 yrs for asbestos-related mesothelioma.
T/F: Prev acquired lung dz like COPD or ILD increase the risk of developing lung cancer.
True.
What lung cancer may present with multiple pulmonary nodules that look like "unresolving pneumonia" on CXR and HX?
Bronchioloalveolar carcinoma.
Which lung cancer carries with it paraneoplastic syndromes?
Small cell lung cancer, some with squamous cell carcinoma.
What are popular sites of metastasis for small cell lung cancer?
Liver, adrenal glands, bones, brain.
Which lung cancer involves spiculated chromatin with little cytoplasm?
Small cell lung cancer.
A solitary pulmonary nodule displaying fat on CT is a:
Hamartoma. High potential for calcification also.
A solitary pulmonary nodule with a contrast enhancement >25HU is probably:
Malignant.
A solitary pulmonary nodule with a doubling time of 25 days is probably:
Benign (the cutoffs are below 30 and above 490 days).
What are the constitutional symptoms of lung cancer?
Weight loss, fatigue, anorexia, weakness.
Where is a Pancoast tumor and what are the assoc symptoms?
Lung cancer at the apex of the lung, inducing a constellation of sx incl Horner's due to involvement of the stellate ganglion, also shoulder pain radiating down the arm (ulnar distrbn) and atrophy of the arm muscles due to brachial plexus involvement, finally compression of vasculature there.
What mediastinal-located nerves can be affected by lung cancers?
L. recurrent laryngeal - hoarseness.
Phrenic - elevated hemidiaphragm and dyspnea.
Sympathetic chain/stellate ganglion - Horner's syndrome.
Pleural effusions displaying lymphocyte predominant cells indicate which etiologies?
Lung cancer and TB.
What are the most common endocrine paraneoplastic syndromes assoc with lung cancer?
Hypercalcemia (more in squamous cell), ectopic ACTH and SIADH and Cushing's syndrome (more in small cell), gynecomastia and galactorrhea (large cell).
What are the most common skeletal paraneoplastic syndromes assoc with lung cancer?
Pulmonary hypertrophic osteoarthropathy (HPO) and clubbing more often in women.
What are the most common neuromuscular paraneoplastic syndromes assoc with lung cancer?
Eaton Lambert Syndrome (small cell lung cancer).
What disease is Eaton Lambert Syndrome often mistaken for and how do you differentiate btw the two?
Myasthenia gravis (weakness, fatigue, and aching), with repetition strength will return unlike in MG.
Give an example of a dermatologic, vascuar, and hematologic paraneoplastic syndrome assoc with lung cancer.
Derm - acanthoses nigricans (axilla, neck hyperpigmentation)
Vascular - Trousseau's syndrome
Heme - anemia/leukemoid rxn
What defines extensive dz in lung cancer?
Dz spread beyond one hemithorax. 5-7wk survival prognosis vs 12wks for limited.
Cancer staging takes what three factors into account?
TNM - tumor size, nodal involvement, metastasis presence.
Stage 4 of lung cancer is reached whenever:
Metastasis occurs, regardless of the tumor type and the T and N score.
What are contraindications to surgery in a pt with non-small cell lung cancer?
Metastases, SVC syndrome, malignant pleural effusion, recent MI, major arrhythmias, poor FEV1.
The most important factor in prognosis for lung cancer is:
Staging. Second is cell type.
Which lung cancer is assoc with the best prognosis?
Bronchioloalveolar carcinoma.
What is the best way to biopsy an adenocarcinoma?
CT guided transthoracic needle biopsy (bc it tends to be on the periphery).
Which cancer displays excessive desmosomes? Desmoplasia?
Desmosomes - squamous cell carcinoma (prickle cells, intercytoplasmic bridges);
Desmoplasia (fibrosis) - adenocarcinoma;
Vesicular/open chromatin pattern with prominent nucleoli? Hyperchromatic nuclei?
1. Squamous cell carcinoma, adenocarcinoma; large cell neuroendocrine CA;
2. Small cell carcinoma;
Subpleural lung cancer with no invasion of the stroma?
Bronchioloalveolar carcinoma.
What is a carcinoid tumor of the lung derived from? What is the most common type of this tumor? What is the most malignant type of this tumor?
Neuroendocrine cells. Small cell carcinoma. Large cell neuroendocrine carcinoma.
Which lung cancer displays nests, ribbons, trabeculae and pseudo-rosettes?
Typical carcinoids.
What differentiates a typical from atypical carcinoid tumor?
Atypicals include pleomorphism, mitotic figures, and tumor necrosis.
Crush artifact in a lung cancer biopsy?
Small cell carcinoma.
Nuclear molding (where cells hug together) in a lung cancer biopsy?
Small cell carcinoma.
What are the most common cancers involving the pleura?
Metastases.
Which asbestos fiber is the worst for inc risk mesothelioma?
Crocidolite subtype of the amphibole type fibers.
Pleural cancer with no parenchymal involvement of the lung indicates what?
Malignant mesothelioma.
T/F: Asthma involves decreased vascularization of the bronchial wall.
False. Increased vascularization due to remodeling.
How does asthma achieve airway obstruction?
1. Bronchoconstriction (incl SMC hyperplasia)
2. Mucous plugs and edema
3. Inflammatory infiltration
What is the theorized mechanism behind exercise-induced asthma?
Hyperemia of airway leading to reflex bronchoconstriction (NOT hyperventilation).
What is the best PFT indicator of asthma? What is the best histologic indicator for asthma progression?
FEV1 like all obstructive dzes.
BM thickening
T/F: GERD is a prominent cause of asthma.
True.
What is a peak flow meter useful for in asthma?
Monitoring dz progression rather than diagnosis.
What is pseudoasthma? How do you detect for it? What is the treatment?
Vocal cord dysfxn leading to asthma-like sx. Suspect it if PFT is normal with severe asthma sx, check with laryngoscopy. Speech therapy.
What are the pharmacologic choices for long-term control of asthma?
Mild - Inhaled corticosteroids.
Alternative mild - cromolyn, leukotriene modifiers, methyl-xanthines.
Severe - long-acting beta-agonist.
What are the pharmacologic choices for control of acute asthmatic attacks?
Mild - short-acting inhaled beta-agonists (albuterol); anticholinergics;
Severe - systemic corticosteroids, Omalizumab (anti-IgE).
Foamy eosinophilic edema in the alveolar space?
PCP pneumonia.