IM Pulmonary Quiz PDF
Document Details
Uploaded by ResoluteCactus9736
Spelman College
Tags
Summary
This document provides information on pulmonary terminology, obstructive and restrictive lung diseases, and concepts like shunt and dead space. It explains concepts in detail and includes key points for USMLE preparation.
Full Transcript
MEHLMANMEDICAL.COM IM Pulmonary Annoying lung volume terminology - Forced Expiratory Volume in 1 second. FEV1 - The amount of air one can forcefully exhale in one second following a maximal inspiration. - Forced Vital Capac...
MEHLMANMEDICAL.COM IM Pulmonary Annoying lung volume terminology - Forced Expiratory Volume in 1 second. FEV1 - The amount of air one can forcefully exhale in one second following a maximal inspiration. - Forced Vital Capacity. FVC (VC) - The total volume of air one can maximally exhale following a maximal inspiration. FEV1/FVC - Ratio used to differentiate between obstructive and restrictive lung disease. - Total Lung Capacity. TLC - The total amount of air in the lungs following maximal inspiration. - Tidal Volume. TV - The amount of air inhaled + exhaled during normal/casual breathing. - Inspiratory Capacity. IC - The maximum amount of air that can be inhaled after a normal/casual exhalation. - Inspiratory Reserve Volume: Additional amount of air that can be inhaled after a normal IRV inhalation. - Expiratory Reserve Volume. ERV - Additional amount of air that can be exhaled after a normal exhalation. - Functional Residual Capacity. FRC - Volume of air remaining in the lungs after a normal exhalation. RV - Residual Volume. Volume of air remaining in the lungs after a maximal exhalation. - Not a lung volume term. But you’ll handle it. - Diffusion capacity of the lungs for carbon monoxide. Reflects extent to which gas exchange is occurring across the pulmonary capillaries. - For USMLE purposes, it is decreased in every pathologic lung condition, but increased in DLCO asthma. This is thought to be due to a combination of transient in blood flow through the pulmonary capillaries + additional hyperinflation during acute episodes. - In other words, if you get a big paragraph Q where you’re not sure what’s going on, but they say DLCO is reduced, you can say, “Cool, not asthma.” Or if they say DLCO is high, you can just select asthma without even reading the question basically. MEHLMANMEDICAL.COM 40 MEHLMANMEDICAL.COM Obstructive vs restrictive lung disease Obstructive Restrictive - Asthma. - Pulmonary fibrosis due to any cause - COPD (chronic bronchitis + emphysema). (i.e., idiopathic; radiation; drugs; auto HY conditions - Old age (i.e., healthy person age 70 vs 20). immune disease). - Pneumoconioses. FEV1 ¯ ¯/« FVC ¯ ¯ FEV1/FVC ¯ (70-80%) TLC ¯ FVC (VC) «/¯ ¯ TV « «/¯ IC «/¯ ¯ IRV «/¯ ¯ ERV ¯ ¯ FRC (due to air trapping) ¯ (due to ¯ lung compliance) RV (due to air trapping) ¯ (due to ¯ lung compliance) DLCO ¯ (but in asthma on USMLE) ¯ (« if neuromuscular) - The reason FEV1/FVC is /« in restrictive, as compared to ¯ in obstructive, is because of radial traction, which is a “stickiness” on the outside of the airways (such as from fibrosis) that prevents them from closing as rapidly as in obstructive. - If you feel iffy on lung volumes, a general point to remember is that they’re basically all decreased in restrictive due to ¯ compliance, but various ones are in obstructive because air can’t get out. - Lifetime inhalation of particulates (i.e., non-smoker simply living in a city) causes an accreted effect on the lungs akin to very slow-onset COPD. So if the USMLE asks for lung volumes in a healthy 70-year-old versus a 20-year-old, select arrows for the former consistent with obstructive lung disease. MEHLMANMEDICAL.COM 41 MEHLMANMEDICAL.COM Flow-volume loop garbage - Don’t freak out about the above flow-loops. For USMLE, I’d say the most important point is that you know the expiratory component of the obstructive curve (purple) has a scooped-out/concave shape. This is because obstruction causes the flow rate to be significantly reduced throughout the expiration. - What USMLE will do is give you a real bootleg Windows 95-type spirometry curve as per above in a 34- year-old + no family Hx + 5-year smoking Hx. You look at curve and say, “No idea what I’m looking at, but top of curve is scooped-out/concave, and I know that means obstructive. So if I’m guessing between COPD or asthma here, which are both obstructive, I’ll choose asthma as more likely over COPD in young patient.” Obstructive Restrictive Shape - Scooped-out/concave appearance. - Smaller and more symmetric. - Airway obstruction causes big reduction - Peak expiratory flow rate relatively preserved, Expiratory in flow rate, which is why it drops but overall size of the loop is reduced due to less flow rate precipitously and results in scooped curve. volume in the lungs on maximum inspiration. Inspiratory - Less affected compared to expiratory - Significantly reduced due to diminished flow rate curve. Can be normal or reduced. pulmonary compliance. - Wider curve, due to increased TLC from - Narrower curve, due to diminished TLC from Volume air trapping. reduced compliance. MEHLMANMEDICAL.COM 42 MEHLMANMEDICAL.COM Shunt versus dead space - When we discuss V/Q mismatch, V = ventilation; Q = perfusion. - ¯ V/Q (ventilation/perfusion) = reduced ventilation relative to perfusion. - V/Q = reduced perfusion relative to ventilation. - Shunt = ¯ V/Q à refers to almost all lung conditions on USMLE. - Dead space = V/Q à refers to just pulmonary emboli on USMLE. - If you hear the term “shunt” used in isolation, this refers interchangeably to “pathologic shunt,” where ¯ V/Q occurs to the point that the patient’s arterial oxygen becomes decompensated. In other words, the reason why a patient has ¯ O2 sats is because there’s some sort of lung problem where aeration of the alveoli is ¯. But there’s nothing wrong with perfusion (i.e., blood flow isn’t cut off to the lungs). - ¯ V/Q can also refer to the physiologic (i.e., normal) shunt we see at the lung bases, where V/Q is 0.6. This is because despite both ventilation and perfusion apex à base, gravity pulls blood down more greatly than air, so perfusion toward the bases, whereas ventilation only . So V/Q is ¯ at the bases (shunt). - Areas of lung with ¯ V/Q attempt to compensate via hypoxic vasoconstriction, where blood vessels constrict in order to redirect (i.e., shunt) blood to better-ventilated areas. In other words, if an area has low ventilation, constriction of blood vessels in that area lowers Q in order to increase the V/Q ratio and prevent wasting of blood flow. - If you hear the term “dead space” used in isolation, this refers interchangeably to “pathologic dead space,” where V/Q occurs to the point that the patient’s arterial oxygen becomes decompensated. In other words, the reason why a patient has ¯ O2 sats is because blood flow is cut off to the lungs. This will be PE (and air, fat, amniotic fluid emboli) on USMLE because the clot that embolizes to the pulmonary arteries compromises blood flow to the pulmonary tissue. - V/Q can also refer to dead space processes that are non-pathologic: - Alveolar dead space = natural, physiologic V/Q within the alveoli, where some areas of lung receive more ventilation than perfusion – i.e., the apices (V/Q of ~3.0) compared to the bases (~0.6). This is because gravity pulls blood down more than air, so at the apices of the lungs, there’s relatively less blood flow in comparison to how much those areas are ventilated. - Anatomic dead space refers to parts of the respiratory tree that are naturally ventilated but do not partake in gas exchange, such as the trachea, bronchi, and terminal bronchioles. These areas do not receive perfusion where gas exchange occurs for respiratory purposes, despite being ventilated by air moving in and out. - Physiologic dead space is the sum of anatomic and alveolar dead space. - To understand shunt vs dead space better, both involve a right-to-left mixing of deoxygenated blood (right) with oxygenated blood (left). Shunt is a R-to-L mixing where “R” is created by areas of alveoli not receiving enough oxygen; dead space is a R-to-L mixing where “R” is due to ¯ perfusion to areas of lung. - An area of lung under-ventilated or -perfused could be said to represent a “zero” in terms of the oxygenation it contributes to the blood. That zero is mixed in with all of the other areas of normal lung. This means the average of all areas of lung cannot achieve normal oxygenation because that zero is mixed in. This is why arterial O2 will be decreased when we have pathologic shunt or dead space. - In both pathologic shunts (e.g., COPD, pneumonia, asthma) and dead space (PE), there are still areas of lung that have normal V/Q. Administering oxygen to these patients will have differing effect, where shunt is less effectively remedied often due to the extent of hypoxic vasoconstriction, which causes a high fraction of blood to bypass normal V/Q areas altogether, even though a small fraction is diverted appropriately to them. The net result is oxygen administration still fails to increase PaO2 in shunt. In dead space, where hypoxic vasoconstriction doesn’t occur because ventilation is normal, administered oxygen to normal V/Q areas helps because it comes into contact with more blood overall. - This can essentially be simplified as: dead space by definition is a primary ¯ in perfusion; shunt causes a secondary ¯ in perfusion. But we don’t call the secondary ¯ in perfusion “dead space.” Hypoxic vasoconstriction due to shunt is a mere compensatory response to ¯ ventilation, but it happens to be the case that the blood that is shunted away from the lungs can be greater in volume than the primary ¯ in perfusion in the setting of a pathologic dead space. MEHLMANMEDICAL.COM 43 MEHLMANMEDICAL.COM Alveolar-arterial (A-a) gradient stuff - A is alveolar oxygen; a is arterial oxygen. - In settings where the patient’s arterial oxygen is low, the A-a gradient (normally 5-10 mmHg) tells us whether there’s an actual lung pathology or if the patient is merely hypoventilating. In other words, - A-a gradient = the lungs are fucked up = the patient is breathing normally but there is a problem such as impediment of gas exchange, poor lung compliance, or pathologic shunt or dead space. The patient has low arterial oxygen despite sufficient respirations, where alveolar pO2 is normal in unaffected areas of lung. The normal “A” in unaffected areas of lung minus the low “a” in the blood makes A-a high. - Normal A-a gradient = the lungs are normal = patient is just not breathing enough – i.e., quality and/or quantity of respirations is insufficient. This refers to opioids, heroin, benzos, and barbiturates because these agents cause respiratory depression. Normal A-a gradient is also sometimes seen in patients on ventilators. The patient has low arterial oxygen merely because of insufficient respirations, where alveolar oxygen is low throughout the lungs. The low “A” throughout the lungs is due to poor respirations, minus the low “a” in the blood, making A-a not elevated. - The NBME doesn’t expect you to know the exact numbers for A-a gradients. The Q might give you answer choices where A-a gradient is either 40 or 10, where you have to say, “Well clearly the answers with 40 are high and the ones with 10 are normal.” So if the Q is a patient who has opioid toxicity with low O2 sats, you’d select the answer choice with 10 for A-a rather than 40. Not dramatic. - USMLE also wants you to know that the mechanism for a patient’s hypoxemia in pulmonary edema is “high A-a gradient”; this makes sense, as the transudate in the alveolar spaces impedes gas exchange, but the patient’s respirations are otherwise fine. - Old age in healthy persons causes: A-a gradient, ¯ arterial pO2, TLC. This combo is answer on NBME – i.e., even if people are non-smokers, as we live out life inhaling particulates from car exhaust, etc., the lungs experience obstructive changes with age (essentially “very slow COPD”). - Choose normal A-a gradient in patients on ventilators who have pCO2. The latter tells us the arterial pO2 is low because of insufficient respirations. - My biggest advice is to not automatically assume “high A-a gradient” for every scenario of low O2 sats. The mistake I see students make is they just think “any issue causing low O2 sats = A-a gradient must be high.” HY pulmonary / respiratory tract cancers for IM - Small basophilic (purple) cells. NBME can describe these cancer cells as “twice the size of lymphocytes.” Small cell bronchogenic carcinoma - Occurs centrally in the lung (i.e., hilar / medially). Smoking biggest risk factor. - Paraneoplastic syndromes exceedingly HY: 1) SIADH (ADH secretion); 2) Cushing syndrome due to ACTH secretion; 3) Lambert-Eaton syndrome (production of antibodies against presynaptic voltage-gated calcium channels); 4) Cerebellar dysfunction / ataxia (anti-Hu/-Yo antibodies). - Treatment on 2CK is “chemotherapy.” Do not do surgery. I believe this is the only time I’ve seen straight-up “chemotherapy” as correct answer on NBME. MEHLMANMEDICAL.COM 44 MEHLMANMEDICAL.COM - Stains positive for keratin; may have keratin pearls on histo (pink circles). - Similar to small cell, occurs centrally in the lung (i.e., hilar / medially). Smoking biggest risk factor. In other words, the two cancers that start with an “ssss” sound for “central” (i.e., Small cell and Squamous cell) are Central. - Can cavitate à if USMLE gives you lung cancer with a cavitation (i.e., cavity/hole), Squamous cell the answer is squamous cell. carcinoma - Highest yield point is that it secretes PTHrp (parathyroid hormone-related peptide). This acts like PTH and increases calcium / decreases phosphate, but this is not the same as PTH. Endogenous PTH is suppressed due to negative feedback from high calcium. In other words, choose a down arrow for PTH in squamous cell carcinoma of the lung. - Adenocarcinoma means cancer of glands. If the Q says something about biopsy showing glandular morphology, you know they’re talking about adenocarcinoma. - The answer on USMLE for lung cancer in a non-smoker; classically “female non- smokers,” but I’ve seen NBME Qs with this in men. - Normal ground/Earth radiation due to radon is accepted cause of lung cancer in non-smokers. There is NBME Q where they mention non-smoker living in a Adenocarcinoma basement and develops lung cancer. The correlation is probably nonsense in real of the lung life, but it’s in an NBME question somewhere. - Does not occur centrally on NBME exam, unlike small cell and squamous, and hence will be described as apical or peripheral lung lesion in non-smokers. - Apical tumors can are known as Pancoast tumors and cause Horner syndrome (miosis, ptosis, anhidrosis) due to impingement on C8 superior cervical ganglia (sympathetic nerves). They can also cause SVC syndrome (flushing of the face + congestion of neck veins) or brachiocephalic syndrome (only right side of MEHLMANMEDICAL.COM 45 MEHLMANMEDICAL.COM face/neck) due to impingement on venous return. (+) Pemberton sign is worsening of flushing + neck vein congestion when raising the arms above the head. - Can be associated with migratory thrombophlebitis (Trousseau sign of malignancy). The latter is not limited to head of pancreas cancer. Adenocarcinomas in general are known to be associated with hypercoagulable state due to malignancy. USMLE won’t ask specific mechanism, but liberation of tissue factor (factor III) by these cancers is a proposed etiology. - Associated with hypertrophic osteoarthropathy (clubbing + hand pain due to lung cancer); mechanism is fibrovascular proliferation. Literature says adenocarcinoma of lung is most common cause, although the association isn’t 100% specific. - Nonexistent lung cancer on USMLE. Bogus/garbage diagnosis. I don’t think I’ve Large cell carcinoma ever seen this assessed. - Pulmonary nodule that secretes serotonin or serotonin-like derivatives, resulting in carcinoid syndrome (i.e., tachycardia, flushing, diarrhea). Bronchogenic - A type of neuroendocrine tumor. carcinoid tumor - Carcinoid tumors are classically appendiceal and of the small bowel, but you should be aware that bronchogenic carcinoids exist. - USMLE wants urinary 5-hydroxy indole acetic acid (5-HIAA) for initial step in Dx. - Cancer of “mesothelial cells” (answer on NBME) seen in patients with prior occupational exposure to asbestos. - Asbestosis occurs first, which then gives rise to mesothelioma years later. - Shipyard and construction workers are buzzy for prior occupational exposure. - Asbestosis will be described as pleural or supradiaphragmatic plaques (“soft tissue plaques seen on CXR”). Pulmonary biopsy shows ferruginous bodies. - Calretinin (+); a protein that is highly indicative of mesothelioma on staining. - Mesothelioma appears as a whiteish cancer and is described as an “encasing rind of pleural-based tumor” (i.e., circumferentially surrounds/wraps around the lungs). Mesothelioma Nasopharyngeal - Can be caused by EBV. carcinoma - A type of squamous cell carcinoma of the airway. - Squamous cell carcinoma of vocal cords. Laryngeal cancer - Smoking is major risk factor. - New NBME Q wants you to know this spreads to cervical lymph nodes. - Pediatric condition characterized by warts of the vocal cords. Laryngeal - Lesions will have papillary structures on biopsy. papillomatosis - Due to HPV 6/11 exposure from maternal vaginal canal. MEHLMANMEDICAL.COM 46 MEHLMANMEDICAL.COM Pneumoconioses for IM - As already mentioned above in the mesothelioma section, this is associated with shipyard workers, construction workers, and electricians. It can give rise to mesothelioma later in life. Asbestosis - The above ferruginous body is dumbbell-shape. Choose macrophage as the answer on USMLE for the cell that initiates pulmonary fibrosis (in response to asbestos and in general). - Causes restrictive lung pattern. - Occupational exposure to beryllium in the aerospace / aeronautical industry. Berylliosis - Causes restrictive lung pattern. - Can cause granulomas. - Occupational exposure to silicon (sand) in foundry or stone quarry workers. - Can cause egg-shelf calcifications in upper lobes. Silicosis - Increases risk of tuberculosis infections. - Avoid anti-TNF-a agents (i.e., infliximab, adalimumab, etanercept) in these patients due to increased TB risk (TNF-a needed to suppress/fight TB). - Aka “coal miner’s lung.” Anthracosis - Black discoloration of the lung. - Can be either obstructive or restrictive. - Rheumatoid arthritis + any pneumonociosis, presenting as pulmonary nodules. Caplan syndrome - Clinical relevance is that patients with RA are at increased risk for developing pneumoconioses if they have a workplace exposure. MEHLMANMEDICAL.COM 47 MEHLMANMEDICAL.COM HY General lung conditions for IM - The answer on USMLE for a patient over the age of 50 who has 6-12+ months of unexplained dry cough. This is how it shows up 4/5 times. - Textbook restrictive lung disease, with « or FEV1/FVC. The reason for the FEV1/FVC being greater than in obstructive lung disease is radial traction, as mentioned earlier. - CXR and CT scan show “reticular” or “reticulonodular” pattern. These descriptors are exceedingly HY on USMLE, where students will overlook them in the vignette, but they are hugely buzzy for restrictive lung disease. They are colloquially known as “honeycombing,” but I have not seen the USMLE give a fuck about the latter colloquialism. They frequently just say “reticular” and “reticulonodular,” and then you know right away, “Boom. Restrictive lung disease,” i.e., fibrosis, etc. Tangentially, it’s to my observation that NBME will say “reticulogranular” frequently for NRDS, but the two vignettes are clearly disparate anyway. - After the CXR and spirometry are performed, 2CK wants “high- Idiopathic pulmonary fibrosis resolution CT of chest” as answer for next best step. (Usual interstitial pneumonitis) “Honeycombing” = reticular / reticulonodular pattern. - New 2CK NBME wants “lung biopsy” as answer to confirm diagnosis of interstitial lung disease (i.e., idiopathic pulmonary fibrosis) after imaging. - Vignette can also mention loud P2 (means pulmonary hypertension) with “dry inspiratory crackles heard bilaterally.” - 1/10 times, the Q will be patient over 50 with increasing fatigue and shortness of breath over 6-12 months, with only 1 month of cough, where it initially sounds like heart failure, and they’ll say CXR shows “interstitial markings” instead of reticular/reticulonodular patterning. MEHLMANMEDICAL.COM 48 MEHLMANMEDICAL.COM However, they say patient has “ FEV1/FVC showing restrictive pattern” in the stem, which gives it away. - You need to know that “usual interstitial pneumonitis” (UIP) is another name for idiopathic pulmonary fibrosis. Yes, the name is weird, but it’s not my opinion and it’s asked twice on the NBMEs, where instead of writing “idiopathic pulmonary fibrosis” as the answer, they write “usual interstitial pneumonitis.” UIP is technically a broad term that can refer to many restrictive lung conditions, but as I said, on NBME they use this synonymously with idiopathic pulmonary fibrosis. - Tx on 2CK = pirfenidone à anti-fibrotic agent that inhibits TGF-b- mediated synthesis of collagen. - COPD = chronic bronchitis + emphysema. - Smokers will have combination of the two. When we say a smoker has COPD, we are saying he/she has chronic bronchitis + emphysema at the same time. - The term COPD can in theory apply to any obstructive disease of the lung that is chronic (e.g., asthma, Kartagener, etc.) but when the term is used without any specific condition attached, it refers to the combo of chronic bronchitis and emphysema. Chronic obstructive pulmonary disease (COPD) - Hyperinflated lungs in COPD (due to air trapping) can push the heart to the midline. NBME will say there’s a “long, narrow cardiac silhouette,” or a “point of maximal impulse palpated in the sub-xiphoid space.” In left ventricular hypertrophy, in contrast, there will be a lateralized apex beat, or a point of maximal impulse in the anterior axillary line. - Home oxygen is indicated on 2CK if O2 sats are: - 0.6. - Pleural fluid LDH >2/3 upper limit of normal of serum LDH. - In other words, transudate contains less protein and LDH as the two main distinctions. - Transudates contain fewer WBCs than exudates, but I routinely see 500 WBCs/µL in transudate Q on NBME. - Highest yield cause of transudate on USMLE is left heart failure, as discussed in the Cardio PDF. - ARDS, pulmonary emboli, and infections can cause exudative pleural effusions (due to inflammation). - Progression to empyema HY (see below). - Two ways empyema presents on NBME: - 4 out of 5 questions, it will present as a sequence of pneumonia à parapneumonic effusions (i.e., exudative pleural effusions that occur due to pneumonia) à empyema. In other words, if a patient has a pneumonia that then leads to an exudative pleural effusion, we simply call that a parapneumonic effusion. This effusion can become progressively worse and purulent, to the point that the pH of the pleural fluid falls below ~7.1ish. We now call it empyema, Empyema which is frank pus in the pleural space. Low pH of the pleural fluid to < ~7.1 is very HY on 2CK forms. I’ve seen Qs where they say 7.12, 7.11, and 6.99, and they want empyema. - 1 out of 5 Qs will not mention anything about Hx of pneumonia. They will give patient who has persistent fever + recurrent pleural effusions in someone who has cirrhosis (i.e., ¯ oncotic pressure à transudative pleural effusions). Then the answer is just empyema. - NBME wants tube thoracostomy to drain the purulence. - Chyle (lymph fluid) in the pleural space. - The answer when they tell you a patient has milky or white-cloudy fluid in the pleural space where the pH is significantly above 7.1. - For instance, they might give you 15-line paragraph where they say milky fluid + Chylothorax tons of lab values, but you notice the pH of the pleural fluid is 7.40. This means it’s chylothorax and empyema is wrong. - Can be caused iatrogenically by insertion of central line via the left internal jugular vein, or by cancers, e.g., lymphoma. - Blood in the pleural space. - Apart from massive trauma, the way this shows up on USMLE is as malignant pleural effusion. - They’ll give you massive paragraph with tons of info + tell you patient has Hemothorax history of breast or lung cancer + has dullness to percussion à answer = malignant pleural effusion. - Patient can have hypotension and muffled heart sounds, similar to cardiac tamponade, but rather than JVD (to complete Beck triad), can have flattened neck veins (due to loss blood from the circulation). MEHLMANMEDICAL.COM 61 MEHLMANMEDICAL.COM HY Alveolar fluid conditions - Due to left heart failure on USMLE. - There is such thing as “non-cardiac pulmonary edema” (i.e., ARDS, TRALI [discussed below in this table]), but for USMLE purposes, if you see “pulmonary edema” as an isolated phrase, it refers to transudation of fluid into the alveolar spaces due to pulmonary capillary hydrostatic pressure from left heart pathology. - PCWP and LAP are both elevated. Pulmonary edema - USMLE can give you vignette of, e.g., MI with dyspnea, and they ask for the mechanism of the dyspnea in the patient à answer = “increased alveolar- arteriolar oxygen gradient” – i.e., the patient can breathe just fine so alveolar O2 is normal, but fluid impairs the gas exchange, so we have low arterial/arteriolar oxygen. - “Cephalization of pulmonary vessels” is buzzy and synonymous with pulmonary edema on USMLE. Shows up in some NBME vignettes. - The answer on USMLE for bilateral exudative chest infiltrates and ¯ O2 sats in patient following: pancreatitis; aspiration of vomitus; near-drowning episodes (aspiration of fresh/sea water); improper insertion of NG tube into the lungs with feeding initiated; toxic shock syndrome; or general trauma / sepsis. - 2CK NBME Q gives vignette of toxic shock syndrome and then asks most likely cause of death in this patient à answer = ARDS. - Pulmonary decompensation associated with pancreatitis is very buzzy. - Another 2CK Q gives patient who is brought to hospital following near- drowning episode + they ask what the patient needs to be monitored for à Acute respiratory distress answer = ARDS. syndrome (ARDS) - ARDS is technically defined as a PaO2/FiO2 10mm (+): Health care worker or prisoner/prison worker; immigrant from endemic area; TB laboratory personnel, children 15mm (+): everyone else. - If a PPD test is (+), never repeat it. If it is negative, it must be repeated in 1-2 weeks (i.e., sometimes false-negatives). - Answer on a 2CK form for a guy who moves into a new apartment building Hot tub lung with a hot tub and gets bilateral chest infection à inhalation of fumes with Mycobacterium avium complex (MAC). MEHLMANMEDICAL.COM 66 MEHLMANMEDICAL.COM - Exceedingly HY on USMLE. - USMLE wants “aspiration of oropharyngeal normal flora,” or “aspiration of oropharyngeal anaerobes” as the cause. - Q will give aspiration risk factor, such as alcoholism, dementia (can cause loss of gag reflex), Hx of stroke (leading to dysphagia), or epilepsy. - Q can also mention broken or missing teeth (hypodontia) as risk factor. - Often described on NBME as pulmonary lesion with an air-fluid level. This is buzzy, but not a mandatory descriptor. This refers to the top half of the circle being air, and the bottom being pus, the latter settling due to gravity. Pulmonary abscess - The stem can say the patient has “foul-smelling sputum.” This descriptor is exceedingly HY and is synonymous with anaerobes on USMLE. - Oropharyngeal normal flora = Bacteroides (strictly anaerobic gram-negative rods); as well as Peptostreptococcus and Mobiluncus. The latter two are not HY, but Bacteroides is. I mention all three, however, because the Q can say sputum sample shows “gram-negative rods, gram-positive cocci, and gram- positive rods,” which refers to all three. But the bigger picture concept is, this = mixed normal flora. - Tx = clindamycin. USMLE loves this. - If Q tells you patient was treated for pulmonary abscess + a year later there’s still a lesion seen on CXR à answer = “failure of maintenance of basement membranes.” Acute bronchopulmonary - Presents as asthma-like presentation in patient with sensitivity to aspergillosis (ABPA) aspergillus skin antigen. - Answer on USMLE for bilateral lung condition + fever in farmer who has exposure to hay (on new NBME). Hypersensitivity - They will tell you the fever self-resolves after 2 days and he now is afebrile. pneumonitis - Byssinosis (pneumoconiosis from hemp) is wrong answer, since this won’t present with fever + classically presents in textile workers. - Idiopathic restrictive lung disease where patient has pneumonia-like presentation that fails to improve with antibiotics. Not actual pneumonia. Cryptogenic organizing - Formerly known as bronchiolitis obliterans organizing pneumonia (BOOP). pneumonia (COP) - Nonexistent yieldness on USMLE, but I mention it because you will sometimes see this as a wrong answer choice, particularly on hard 2CK Qs, and I’ve seen enough students erroneously pick it. - Infection of portion of ear just deep to tympanic membrane. Otitis media (OM) - Most commonly Strep pnuemo. MEHLMANMEDICAL.COM 67 MEHLMANMEDICAL.COM - Will present as red, immobile tympanic membrane. Immobility of the tympanic membrane is highly sensitive for OM, meaning that if the Q says mobility is normal, we can rule out. - “Ear tugging” can be a sign in children of either otitis media or externa. - Tx is amoxicillin or penicillin. - Augmentin (amoxicillin/clavulanate) is classically given for recurrent OM. So if you are forced to choose between amoxicillin/penicillin alone or Augmentin, go with the former. - For 2CK Peds, a tympanostomy tube (aka grommet) is used if the kid has >3 OM occurrences in 6 months, or >4 in a year. - Aka otitis media with effusion. - Presents as fluid behind the tympanic membrane in a kid weeks after Serous otitis media resolution of 1 or 2 otitis media infections. - Almost always benign and self-resolves in 4-8 weeks. Answer is observation. - “Tympanic membrane perforation” is the answer on new 2CK NBME for 2- year-old who had 3-day Hx of viral infection followed by awakening with severe ear pain + has dried blood on ear lobe and pillow + otoscopy cannot Tympanic membrane visualize tympanic membrane because of seropurulent fluid draining from the perforation ear canal. - Can occur due to otitis media, although vignette on NBME doesn’t sound like classic OM and is as described above. - Inflammation of mastoid bone caused by untreated otitis media. - The mastoid process is the posterior part of the temporal bone that is felt just behind the ear. - Can present as a painful ear pinna that is displaced (e.g., upward and Mastoiditis outward). - Diagnosis is made by CT or MRI. X-ray is wrong answer. - 2CK IM Q gives a 2-year-old with mastoiditis where the answer is “CT of the temporal bone.” Sounds wrong, since this is radiation for a kid, but it’s what they want. - Isolated inflammation of the tympanic membrane. Myringitis - Can be bullous (i.e., bullous myringitis). - Caused by Strep pneumo or Mycoplasma. - Infection of ear superficial to tympanic membrane. - Classically caused by Pseudomonas. - Increased risk in swimmers and diabetics. - An NBME form has “necrotizing otitis externa” as answer for black skin Otitis externa (OE) within the ear canal in a patient. This is aka “malignant otitis externa.” - USMLE wants “acetic acid-alcohol drops” as prophylaxis in college student who does crew + continues to have water exposure. - Tx (not prophylaxis) = “topical ciprofloxacin-hydrocortisone” drops. - The answer if they tell you a school-age kid has a lingering fever after an upper respiratory tract infection (URTI) for 10-14+ days. - Whenever a URTI lingers for more than ~10ish days, you want to think about sinusitis as a differential. - A 2CK vignette gives nocturnal cough (reflects aspiration; in this case, from the sinuses) and grey membranes in the oropharynx. - The grey oropharyngeal membranes detail sounds weird, since that is Sinusitis normally buzzy for Diphtheria, but it shows up on an NBME Q where the answer is sinusitis and Diphtheria isn’t listed. - IgA deficiency Qs, which presents as recurrent sinopulmonary infections, can say patient has Hx of pneumonias + presents today with sore left cheek à reflects sinusitis. - For 2CK, CT scan is done if chronic sinusitis >12 weeks. After CT is performed for chronic sinusitis, nasal endoscopy can be performed. MEHLMANMEDICAL.COM 68 MEHLMANMEDICAL.COM - Tx is amoxicillin/clavulanate (Augmentin). This is in contrast to OM and Strep pharyngitis, which are treated with just amoxicillin or penicillin alone, without the clavulanate (unless recurrent). - Causes respiratory distress, fever, and myalgias (muscle pain). For USMLE purposes, the myalgias are exceedingly HY as a vignette finding that usually suggests the flu over other diagnoses. - Has 8 segments, two of which are hemagglutinin and neuraminidase. - Hemagglutinin mediates viral attachment to the cell by enabling its binding at sialic acid receptors. - If a question asks about the molecule most flu vaccines are targeted against, the answer is hemagglutinin. - Neuraminidase allows for newly synthesized viral particles to leave the host cell. This enzyme cleaves sialic acid residues, which normally bind the new viral particles within the cell. Once these residues are cleaved, the viral particles can leave the cell. - Drugs such as oseltamivir and zanamivir are sialic acid analogues that function as neuraminidase competitive inhibitors. In other words, they prevent the virus from leaving the cell. If the USMLE asks which drug prevents viral spread within a community, or they tell you a drug is given and now host cells are "packed with virions" (because they can't leave the cell), the answer Influenza is one of the -mivirs. - Antigenic drift is point mutations in hemagglutinin and/or neuraminidase, where the virus has changed slightly. It leads to seasonal epidemics. Antigenic shift is due to two influenza viruses entering a cell, one of human origin, the other of animal origin (such as bird or swine), where they engage in reassortment of viral segments, leading to a completely novel influenza virus. It leads to generational pandemics. - If a patient gets a bacterial lobar pneumonia following recent convalescence from influenza infection, USMLE likes S. aureus as a HY cause. The USMLE will not play trivia where they list S. aureus alongside S. pneumo and you're forced to choose. What they'll do is say something about how a guy recently recovered from a viral illness in which he had high fever and myalgias, and now he has a pneumonia caused by a gram-positive coccus in clusters --> answer = S. aureus. In contrast, S. pneumo is gram-positive diplococci. - IM killed vaccine: start age 6 months, then give yearly in the fall or winter throughout life; safe to give during pregnancy. - Intranasal live-attenuated vaccine: ages 2-45; immunocompetent, non- pregnant persons only. - The virus specifically known as SARS-CoV-2, or COVID-19, caused the 2019 global pandemic. - SARS stands for Severe Acute Respiratory Syndrome. - The pandemic is believed to have started following a laboratory leak in Wuhan, China, although this has been a source of political debate, where initial explanations asserted that there was a natural, zoonotic origin for the virus (i.e., originating from animals, e.g., bats). - Has characteristic spike proteins that create a crown-like appearance on electron microscopy. Coronavirus - The spike proteins bind to ACE2 receptor, allowing for viral fusion with host respiratory epithelium. - Presentation can range from mild respiratory symptoms similar to the common cold (rhinovirus) all the way to severe respiratory disease with multi- organ failure. - Many different vaccine types exist - i.e., mRNA (Moderna; delivers mRNA coding for the spike protein), viral vector (AstraZeneca; delivers mRNA in a harmless viral capsid), and killed (Sinovac; delivers inactivated, killed virus). - Both live viral infection as well as vaccination are known to cause rare adverse effects, such as Bell's palsy and myocarditis, although these effects MEHLMANMEDICAL.COM 69 MEHLMANMEDICAL.COM are not unique to coronavirus and can rarely happen with many viral infections and vaccines. - Vaccination mandates and their political implications were (and still are) a source of contentious debate. - Prior to the 2019 pandemic, coronavirus was known to cause SARS in China in 2002 and Middle Eastern Respiratory Syndrome (MERS) in Saudi Arabia in 2012. - Vaccination schedule for children now recommends IM vaccine starting at 6 months; 2-3-doses. Vaccine stuff - PCV15 at 2, 4, 6 months, then again 12-15 months. - Age ³65: PCV20 once; OR, PCV15 then PPSV23 a year later. S. pneumo - For asplenia/surgical splenectomy, sickle cell, cochlear implant, CSF leak, chronic renal failure/nephrotic syndrome, HIV, and immunosuppressed patients: extra dose of PCV15, followed by PPSV23 8+ weeks later. - IM killed vaccine: start age 6 months, then give yearly through life; safe to give during pregnancy. Influenza - Intranasal live-attenuated: ages 2-45; immunocompetent, non-pregnant persons. Coronavirus - IM vaccine starting at 6 months; 2-3-doses. HY Pediatric-related respiratory stuff - HY pediatric condition in which the proximal esophagus ends in a blind pouch + the distal esophagus connects to the trachea. Tracheoesophageal fistula (TEF) - Will present as a neonate who coughs up milk with initial feeding. - Highest yield point about TEF is that diagnosis is made via insertion of nasogastric tube (which cannot be inserted fully because it hits the blind pouch of the esophagus). - An NBME Q wants “endoderm” as the abnormal embryology for TEF (makes sense, since esophagus is epithelial lining of the gut à endoderm). - Weird condition in which the nasal passages don’t develop patency, so Choanal atresia the neonate is an obligate mouth-breather. MEHLMANMEDICAL.COM 70 MEHLMANMEDICAL.COM - Will present as a child who becomes blue/hypoxic while breast feeding (because he can’t breathe through the nose), then cries/becomes pink once detaching from the breast. - Similar to TEF, diagnosis is made via insertion of nasogastric tube. - Part of CHARGE syndrome à Coloboma of the eye (hole in the eye), Heart defects, Atresia of the choanae, Renal defects, Genitourinary anomalies, Ear anomalies. - One of the highest yield Peds conditions on USMLE. - Caused by failure of formation of pleuroperitoneal membranes. - Always occurs on the left, where bowel from the abdomen can herniate up into the left-chest. - Can present as ¯ bowel sounds in the abdomen + bowel sounds in the left hemithorax. Congenital diaphragmatic hernia - Vignette might say there are cystic-appearing areas in the left hemithorax seen on CXR (loops of bowel). MEHLMANMEDICAL.COM 71 MEHLMANMEDICAL.COM - Aka hyaline membrane disease. - The answer on USMLE for respiratory distress in kid who is born 38 C. - 3) Tonsillar exudates. - 4) Lymphadenopathy (cervical, submandibular, etc.). - There is a version of the criteria that includes age, but on the USMLE it can cause you to get questions wrong. So just use the simplified above four points. - If 0-1 point, answer = “supportive care”; or “no treatment necessary”; or “warm saline gargle” (same as supportive care); or “acetaminophen.” Latter is answer for 3M with viral URTI + fever on NBME form. - If 2-4 points, next best step = “rapid Strep test.” If rapid Strep test is negative, answer = throat culture, NOT sputum culture. - While waiting on the throat culture results, we send the patient home with amoxicillin or penicillin for presumptive Strep pharyngitis. - If child is, e.g., 12 years old, and develops a rash with the beta-lactam, answer = beta-lactam allergy. - If the vignette is of a 16-17 year-old who has been going on dates recently (there will be no confusion; the USMLE will make it clear) + gets a rash with the beta-lactam, the answer = EBV mononucleosis; therefore do a heterophile antibody test (Monospot test). - EBV is the odd virus out that usually presents with all four (+) CENTOR criteria and presents like a bacterial infection. - This is why it’s frequently misdiagnosed as Strep pharyngitis. It is HY to know that beta-lactams given to patients with EBV may cause rash via a hypersensitivity response to the Abx in the setting of antibody production to the virus. EBV, in a patient who does not receive Abx, can cause a mild maculopapular rash. But the rash with beta-lactam + EBV causes a more intense pruritic response generally 7-10 days following Abx administration on the extensor surfaces + pressure points. Ventilator settings nonsense - Students will sometimes nag about pedantic ventilator settings info. The vast majority of it is garbage for USMLE. What I can basically say is that increasing PEEP (positive-end expiratory pressure) is probably the answer 4 out of 5 times for any ventilator settings-type of question. The Q might give you a big 15-line rambling paragraph where you’re not sure what’s going on, and then the answer is just “increase PEEP.” - PEEP keeps the alveoli open longer, thereby facilitating gas exchange. - When the patient is on a ventilator, the general aims are: - Keep FiO2 as low / as close to room air as possible (i.e., high O2 can cause free radical damage); - Keep tidal volume as low/normal as possible (i.e., 400-500-ish mL); high tidal volumes can cause ventilator-associated barotrauma. - Increase PEEP if it means lower FiO2 and tidal volumes can be achieved. - But the above needs to be taken with a caveat. For example, the Q might say the patient is on a ventilator and has arterial pO2 of 40 mm Hg (normal is 80-100) + FiO2 is 100% + tidal volume is 1000 mL, and the answer will be “increase PEEP.” The student says, “Wait but I thought you said we want to reduce FiO2 and tidal volume.” à Sure, but we can’t do that here because pO2 is super-low, so that would only exacerbate it further. - As I talked about for ARDS earlier, you could be aware the triad of 1) prone positioning, 2) low-tidal volume mechanical ventilation, and 3) permissive hypercapnia can be implemented. - A very HY point is that ¯ CO2 causes ¯ cerebral perfusion (this is why patients faint in panic attacks, which is asked on NBME). The first step in managing intracranial pressure is “intubation + hyperventilation.” MEHLMANMEDICAL.COM 74 MEHLMANMEDICAL.COM - They also ask the inverse of this on NBME – i.e., they say an anesthesiologist wants to a patient’s cerebral perfusion, and the answer is “decrease respiratory rate” à causes CO2 à cerebral perfusion. - Ventilator-acquired pneumonia (VAP) should be treated with vancomycin PLUS either ceftazidime or cefepime. Vancomycin not only covers MRSA but also is effective against some high-resistance S. pneumo strains. Ceftazidime (3rd generation ceph) and cefepime (4th gen ceph) are very effective against Pseudomonas, which is a HY nosocomial organism for VAP. - Patients should ideally be weaned from ventilators as quickly as possible. USMLE also likes patients who are sick on ventilators as sometimes having euthyroid sick syndrome – i.e., they will say patient cannot be weaned from ventilator + has ¯ T3 and normal TSH à answer = euthyroid sick syndrome. The full array of arrows are: ¯ T3, rT3, « T4, « TSH. If you have no idea what I’m talking about, then I recommend going through my HY Arrows PDF. - If a patient ever has a high CO2 (NR 33-44 mmHg) à answer can = “ventilatory insufficiency.” This applies to both patients on and off ventilators. Don’t be confused if they give you respiratory rate. New NBME form gives RR of 40 with CO2 as an example. Sometimes patients have shallow breathing despite RR. HY Pulmonary drug points - Endothelin-1 receptor antagonist used for pulmonary hypertension. - Endothelin is a vasoconstrictor in pulmonary hypertension. - There is an NBME Q where guy is shaving + cuts himself + they ask what will be Bosentan seen at site of injury à answer = endothelin. So be aware that even though 14/15 times this relates to pulmonary vascular constriction, it is technically a vasoconstrictive mediator not isolated to the lungs. - Dihydrofolate reductase inhibitor. - 1st-line DMARD for RA + 1st-line oral agent for psoriasis that fails topicals. Methotrexate - Causes pulmonary fibrosis (and hepatotoxicity and neutropenia). - Toxicity can be mitigated with “leucovorin rescue,” aka folinic acid (not folic acid). - Short-acting b2-agonist used for asthma. Albuterol - Can cause tremor (asked on NBME). - Inhaled corticosteroids (ICS) used for asthma and COPD. Fluticasone, - Used for prevention / to decrease recurrence of episodes. They have no role in Beclomethasone acute exacerbations. For the latter, IV methylprednisolone is used. - Most effective at ¯ recurrent asthma attacks, but used last resort because oral Prednisone steroids can cause Cushing syndrome and growth stunting. - Leukotriene receptor antagonists (LTC, D, and E4). - Leukotrienes normally cause bronchoconstriction. So these agents ¯ airway constriction. Montelukast, - LTB4 is special and is a neutrophilic chemotactic molecule. For immuno, you can Zafirlukast memorize that LTB4, IL-8, and C5a are HY neutrophilic chemotactic molecules. - Can be used for asthma in patients with aspirin-induced asthma (blockage of COX shunts arachidonic acid down the lipoxygenase pathway toward leukotrienes), or for asthma in general in between a LABA and prednisone. - Lipoxygenase inhibitor. Blocks synthesis of leukotrienes. Zileuton - Use-case same as the -lukasts. Nedocromil, - Mast cell stabilizers used for asthma. Prevent release of histamine. Cromolyn sodium Tiotropium - Long-acting muscarinic receptor antagonist (LAMA) used first-line for COPD. - Long-acting b2-agonist (LABA) used first-line for COPD. Olodaterol - As discussed earlier, either a LAMA or LABA can be used first-line for COPD. - Short-acting muscarinic receptor antagonist (SAMA) used for COPD. Ipratropium - Not first-line anymore, but still shows up on 2CK material as an agent that’s used. Some old-school practitioners still use it, so don’t disregard it. Epoprostenol - PGI2 prostacyclin that can be used for pulmonary hypertension. Sildenafil - Viagra; PDE-5 inhibitor that can also be used for pulmonary hypertension. MEHLMANMEDICAL.COM 75 MEHLMANMEDICAL.COM - Dihydropyridine calcium channel blocker that can be used for pulmonary HTN. Nifedipine - As discussed in the Cardio PDF, can cause peripheral edema/fluid retention. - Monoclonal antibody against IgE. Omalizumab - Can be used in theory in severe asthmatics who have high IgE levels. Dornase alfa - Nucleotidase used to break down airway mucous in cystic fibrosis patients. Guaifenesin - Mucolytic agent that softens mucous in cystic fibrosis. Ivacaftor - Helps localize CFTR channel to membrane and correct its folding (in CF clearly). - Used for idiopathic pulmonary fibrosis. Pirfenidone - Anti-fibrotic agent that inhibits TGF-b-mediated collagen synthesis. MEHLMANMEDICAL.COM 76