Asthma Medical Overview PDF

MEHLMANMEDICAL.COM - The USMLE Q can absolutely say the patient is a smoker or drinks alcohol. For instance, they might say the patient is 34 and has been smoking for 5 years and has bullous changes on CXR, or that the father died from alcoholic cirrhosis, and th...

MEHLMANMEDICAL.COM - The USMLE Q can absolutely say the patient is a smoker or drinks alcohol. For instance, they might say the patient is 34 and has been smoking for 5 years and has bullous changes on CXR, or that the father died from alcoholic cirrhosis, and the student thinks, “Oh that can’t be a1-antitrypsin deficiency though because they said smoking/alcohol.” But the key point is that this condition increases the risk for early-onset emphysema and cirrhosis. Normally, COPD should take 20+ years of smoking to develop, not 5. - Bronchospasm that occurs either idiopathically/hereditarily, or in response to certain allergens or cold air. - One-third of patients with asthma only present with a dry cough and no problems breathing. This is called cough-variant asthma. It will often present as a patient with a dry cough that’s worse in the winter. - Can also present as part of atopy constellation – i.e., dry cough in winter, seasonal allergies / rhinoconjunctivitis / urticaria in spring, and eczema in summer. - Aspirin-induced asthma mechanism HY for USMLE à inhibition of COX by aspirin à shunting of arachidonic acid down lipoxygenase pathway à increased leukotrienes à increased bronchoconstriction. - Samter triad = aspirin allergy, asthma (due to aspirin), nasal polyps. - “Increased expiratory phase” is a buzzy phrase that will be thrown into quite a few asthma vignettes. It is not specific for asthma and can refer to any obstructive pathology, but I just make note of it here because you’ll see it quite a bit for asthma and say, “What’s that mean?” à in obstructive conditions, it takes us a lot longer to exhale (FEV1 is ¯¯). - Acutely, asthma causes ¯ CO2, ­ pH, « bicarb. This is an acute respiratory alkalosis. Even though the patient is having difficulty breathing, CO2 diffuses quickly, whereas O2 diffuses slowly, so insofar as the patient’s respiratory rate is ­, CO2 will be ¯. Bicarb is unchanged because it takes the kidney about a day to alter excretion. In contrast, CO2 is ­ in COPD because there is large amounts of hypoxic vasoconstriction due to excessive mucous (chronic bronchitis) or ¯ Asthma alveolar surface area, so CO2 can’t get out, even with faster breathing. In asthma, alveolar surface area is intact, and the degree of mucous production and hypoxic vasoconstriction is not nearly as bad as chronic bronchitis. - The combination of ¯ CO2 and ¯ O2 in acute asthma attack is known as type I respiratory failure. Eventually, the patient will begin to fatigue and breathing rate will slow. This will be observed as CO2 and pH rebounding to normal levels despite O2 remaining low. This means the patient is in transition to a type II respiratory failure (i.e., hypoventilation), where we have ­ CO2 and ¯ O2. USMLE wants intubation as the intervention. - 2CK Q gives vignette of asthma and then asks for best initial step in diagnosis à answer = “spirometry.” The expiratory component of the curve, as discussed earlier, will appear concave. - Should be aware methacholine challenge can also be done to diagnose. This is a muscarinic agonist that bronchoconstricts and can induce symptoms. Never give during acute episode. This can be tried between episodes. But if you’re forced to choose diagnostic modality, go with simple spirometry. - USMLE cares about both outpatient management of asthma as well as acute attacks. - For outpatient management: 1) First-line Tx is b2-agonist (albuterol) for acute attacks. 2) If the Q says the patient has weekly episodes, or they ask for what could decrease risk of future episodes if patient is already MEHLMANMEDICAL.COM 51  MEHLMANMEDICAL.COM on albuterol, the answer is inhaled corticosteroid (ICS; i.e., fluticasone). 3) If the combo of albuterol + ICS is insufficient, the next step is increasing the dose of the ICS. 4) If that doesn’t work, adding a LABA (i.e., salmeterol) is the next step. 5) If insufficient, agents such as mast cell stabilizers, leukotriene blockers, etc., can be tried. If patient has Hx of aspirin allergy, the latter in particular can be effective. 6) Last resort for outpatient asthma is oral prednisone. It is most effective at decreasing recurrence of episodes, but we want to avoid it if at all possible because of the risk of Cushing syndrome and ¯ linear bone growth in Peds. - Acute management of severe asthma attack (i.e., not outpatient) is nebulized albuterol, oxygen, and IV methylprednisolone. Inhaled corticosteroids have no role in acute asthma management. - NBME for 2CK wants you to know that any asthma patient who requires hospital management for an acute episode must automatically be given ICS (i.e., fluticasone) on discharge. In other words, if patient isn’t currently on an ICS, it must be commenced at discharge. I’m explicit here because this particular NBME Q doesn’t mention albuterol anywhere in the stem, but inhaled fluticasone is the answer. - Another 2CK NBME Q gives a patient who is currently not receiving any asthma medications but who gets 2+ episodes weekly à answer = “inhaled fluticasone + albuterol.” Students think this is weird because they jump straight to dual management + are even audacious enough to put the ICS before albuterol in the wording of the answer, but it’s what they want. Any patient with 2+ episodes per week needs ICS in addition to the albuterol and can be commenced right away on dual therapy. - Dilation of the airways (ectasia means dilation) that occurs due to “loss of musculature of the airways.” - Transverse CT scan will show cystic dilation of the airways. Bronchiectasis - Most common cause worldwide is TB. Most common cause in western countries is CF. But on USMLE, it will usually be a smoker. Asthma does not cause bronchiectasis. - Presents almost always as “cups and cups of foul-smelling sputum.” - “Foul-smelling” means anaerobes, such as Bacteroides. - One question on 2CK form gives bronchiectasis as the answer in a child who has right middle lobe syndrome, where they say there is scant white sputum (not cups and cups) and a thin, linear opacity visualized in the right middle lobe. If you think it’s weird, complain to NBME not me. - Clubbing tends to be seen in these patients. It’s not mandatory, but it’s to my observation USMLE likes it for bronchiectasis. MEHLMANMEDICAL.COM 52  MEHLMANMEDICAL.COM - Confusing word that refers to “lung collapse,” or “collapse of alveoli.” - Highest yield point for USMLE is that it is the most common cause of fever within 24 hours of post-surgery. If this is the first time you’re reading this, that might sound weird, but this is pass-level and extremely important for 2CK. - There is one 2CK Q I’ve seen where they say a woman had a C-section two days ago and the answer was still atelectasis, so even though it’s most common 60 mEq/L). The sweat chloride test is more accurate for diagnosis than genotyping due to allelic heterogeneity of CFTR gene, where many different mutations cause the disease and can be difficult to detect with routine screening panels. - A transepithelial nasal voltage test can also be done, where there is ­ nasal potential difference. - Male patients can have congenital bilateral absence of vas deferens (CBAVD), leading to absent sperm in a sample. - Since this is an AR condition, there is a 2/3 chance a phenotypically normal sibling of a CF patient is a carrier. This applies to any AR disorder, but USMLE likes to use CF as the archetypal example. If this 2/3-point sounds confusing, I talk about this stuff in detail in my HY Genetics PDF. MEHLMANMEDICAL.COM 54  MEHLMANMEDICAL.COM - CF medications not HY for Step, but you could be aware that -caftor agents (e.g., ivacaftor, lumacaftor) facilitate with proper CFTR channel localization to the cell membrane + structural folding. - Dornase-alfa (correct, not alpha) is a nucleotidase that softens mucous. - Guaifenesin is also a mucous-softening agent. - Answer on USMLE for a question that sounds like CF but patient has situs inversus or dextrocardia – i.e., patient will have recurrent pneumonias and organs (or just heart) on opposite side of body. - Abnormality of cilia function due to defective dynein arm. This is a HY point, where sometimes the answer will just be “dynein.” - A cilium on cross-section has a 9x2 microtubule configuration. Dynein is a molecule that is necessary for cilia function. Primary ciliary dyskinesia (Kartagener syndrome) - Patient will sperm in sample, but motility will be decreased. This is in contrast to CF, where sperm are absent due to CBAVD. - Women can get ectopic pregnancy due to abnormal Fallopian tube cilia. - This diagnosis sounds straightforward enough, but I’ve seen plenty of students miss these questions. For the situs inversus, they will describe this as cardiac sounds loudest on the right, or there being a large mass palpable beneath the left costal margin (liver on the opposite side). - Answer on USMLE for a woman 20s-30s, non-smoker, who has increased pulmonary vascularity/markings and either a loud P2 or triscupid regurg (as I talked about in cardio section, these are HY findings for pulmonary hypertension). - “Primary” means the pulmonary hypertension inherently starts with the lungs and is not due to a secondary (i.e., external) cause such as smoking, CF, systemic sclerosis, etc. - Due to mutations in BMPR2 gene. - Do not confuse this with cor pulmonale. Recall that the latter is right heart Primary pulmonary failure findings or RV structural changes due to a pulmonary cause. If the hypertension (PPH) question gives evidence of RVH (i.e., RBBB, right-axis deviation on ECG, boot- shaped heart on CXR), or has overt right heart failure findings (i.e., JVD or peripheral edema), then we can say the patient now has cor pulmonale due to primary pulmonary hypertension. A loud P2 and tricuspid regurg, however, are HY findings for pulmonary hypertension that don’t necessarily mean cor pulmonale. - One of the highest yield points is that endothelin-1 is ­ in these patients. This is a vasoconstrictor that is ­ in pulmonary hypertension from any cause, but notably USMLE likes it for PPH. - Bosentan blocks endothelin-1 receptors and is HY Tx. MEHLMANMEDICAL.COM 55  MEHLMANMEDICAL.COM HY Autoimmune-related pulmonary conditions - Idiopathic autoimmune disease characterized by multi-organ system fibrosis and hardening of tissues (i.e., sclerosis). - Divided into limited and diffuse subtypes. - Limited scleroderma = CREST syndrome (Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasias). - USMLE can describe Raynaud as color change of the fingers with cold weather. They describe sclerodactyly as tightening of the skin of the fingers. Esophageal dysmotility presents as GERD. I haven’t seen NBMEs give a fuck about calcinosis, which is abnormal Ca2+ deposition in tissues. - Diffuse scleroderma = CREST syndrome + renal involvement (presenting as ultra-HY BP, e.g., 220/120, due to renal involvement causing a surge in RAAS. If patient doesn’t Systemic Sclerosis have high BP, it’s not diffuse type on USMLE. (aka scleroderma) - Apart from just being able to diagnose these conditions, the highest yield point on USMLE is that both types cause pulmonary fibrosis, leading to pulmonary hypertension. - Pericardial fibrosis can also occur. - An offline NBME wants ¯ LES sphincter tone and ¯ esophageal peristalsis as an answer. - USMLE wants “dress warmly in cold weather” as an answer for how to ¯ recurrence of Raynaud. Dihydropyridine CCBs can also be used (e.g., nifedipine), which ­ arteriolar + capillary diameter. - USMLE wants to know which drugs you avoid in patients with Raynaud à answer = a1 agonists (e.g., phenylephrine, oxymetazoline), since these constrict arterioles/capillaries. - Idiopathic autoimmune disorder that is one of the highest yield conditions on USMLE. You must know this condition extremely well. - Characterized by non-caseating granulomas within lung tissue. These consist of activated macrophages called epithelioid macrophages, aka histiocytes. - These histiocytes in the lung secrete 1a-hydroxylase (normally produced in the PCT of the kidney in response to PTH), which will convert inactive 25-OH-D3 into active 1,25- (OH)2-D3 (i.e., causing high vitamin D; aka hypervitaminosis D), which then goes to the small bowel and ­ absorption of calcium, causing hypercalcemia. - Even though 1,25-(OH)2-D3 also ­ small bowel absorption of phosphate along with calcium, it’s to my observation that phosphate can be normal in sarcoidosis NBME Qs, Sarcoidosis so do not be confused if you see phosphate in the normal range and only see hypercalcemia. - PTH is suppressed in sarcoidosis due to the high Ca2+ (exceedingly HY). - In other words, on USMLE you will select ­ 1,25-(OH)2-D3 and ¯ PTH. - Archetypal presentation is African-American woman 20s-30s with 6+ months of dry cough and red shins (erythema nodosum). Other findings like low-grade fever with flares can occasionally be seen. - Bihilar lymphadenopathy seen on CXR or CT. They can also describe this as CXR or CT “shows hilar nodularity.” MEHLMANMEDICAL.COM 56  MEHLMANMEDICAL.COM - There is a 2CK Q that gives early-30s African-American woman with dry cough + they say CXR shows no abnormalities à answer = “activation of mast cells” (i.e., asthma is the answer); wrong answer is “non-caseating granulomatous inflammation.” So your HY point here is: if the vignette sounds like it could be sarcoidosis but they say CXR is normal or shows “mild hyperinflation” (also buzzy for asthma), choose asthma over sarcoidosis. - A 2CK IM CMS form gives a sarcoidosis vignette where they mention bihilar lymphadenopathy on a CT scan + high hepatic AST + ALP + weight loss; they don’t mention hypercalcemia. Unusual combo of findings, but the answer is inferable based on the CT. - Lupus pernio is an enlarged nose due to sarcoidosis (not SLE, despite the name). - USMLE wants steroids (i.e., oral prednisone) as treatment. - Rheumatoid arthritis can cause a restrictive lung disease known as rheumatoid lung. Rheumatoid lung - In addition, methotrexate, the first-line DMARD for RA, can cause pulmonary fibrosis. So patients with advanced RA can have pulmonary fibrosis from a combo of the two. HY Pulmonary embolic conditions - DVT that has embolized up the venous circulation to the pulmonary arteries. - Presents as acute-onset shortness of breath and tachycardia in patient with one of the following risk factors: post-surgery (including C-section); sedentation, e.g., due to trauma such as hip injury; OCP use; and thrombotic disorders (i.e., FVL, prothrombin mutation, MTHFR). - S1Q3T3 is most specific finding on ECG for PE that is nonexistent on USMLE and will get you questions wrong. What you want to remember is: sinus tachycardia (i.e., normal ECG but HR is simply high) is the most common ECG finding for PE. - First step in management (2CK) is heparin. - After heparin, do a spiral CT of the chest to diagnose. Pulmonary embolism - If the patient is already on warfarin and gets a PE, the first answer they want is CT to diagnose, followed by IVC filter. Do not choose IVC filter prior to confirming the PE with a CT. - One 2CK NBME Q has tPA as the answer for PE in patient who has obstructive shock (i.e., low BP due to PE). - V/Q scan is done instead of CT first-line in pregnancy. - One 2CK Q gives V/Q that is performed and shows “multiple sub-segmental perfusion defects” à answer = recurrent pulmonary emboli. - Most common cause of death from PE is ventricular fibrillation à acute right heart strain from a saddle embolus precipitates the Vfib. MEHLMANMEDICAL.COM 57  MEHLMANMEDICAL.COM - The acid-base arrows USMLE wants for PE are: ¯ CO2, ­ pH, « bicarb. In other words, we have an acute respiratory alkalosis from high RR. Bicarb is unchanged because the kidney requires minimum 12 hours to accomplish this. These arrows are the same as acute asthma attack. - One 2CK Q gives lab values in PE of ¯ CO2 and ¯ pH. What this means is: patient has lactic acidosis (hence ¯ bicarb) due to ischemia from poor perfusion. It’s HY for USMLE that you know any cause of shock, whether that be septic, hypovolemic, cardiogenic (or even obstructive from PE), can cause lactic acidosis and low bicarb. Don’t be confused by this. - PE is textbook example of dead space (as discussed earlier). - The answer on USMLE if they say 30 seconds to 2 minutes after delivery of the placenta, the patient gets shortness of breath and tachycardia à sounds like PE, but answer is amniotic fluid embolism to the lungs. In contrast, if they say a woman Amniotic fluid had a C-section 2 days ago + now gets up in hospital to use bathroom + now has embolism acute-onset SoB and tachycardia à answer = PE, not amniotic fluid embolism. - Can cause disseminated intravascular coagulation (DIC). It’s one of the weird causes for USMLE. They can say the patient has bleeding from IV sites / catheter lines following delivery of the placenta. - The answer on USMLE if they say long-bone fracture (i.e., usually femur) in patient who now develops shortness of breath + petechiae on the shoulders/chest. - The patient will also have thrombocytopenia, but only about half of vignettes mention this. Fat embolism - The petechiae on the shoulders/chest are not due to the ¯ platelets, since conditions like ITP, for instance, don’t present with this finding. Literature suggests it might be related to microvascular plugging by fat in the dermis. - Question can mention pulmonary biopsy stained with Oil Red O or Sudan black (stains for fat). - The answer on USMLE if they say patient has sudden death following insertion of Air embolism a central venous line à air goes to the lungs + kills patient. - Will present as two ways on USMLE: 1) violaceous lesions on the feet in someone who just had a AAA repair à cholesterol plaque launches off to feet + they show you image like this one below: Cholesterol embolism The second way (2CK NBME 10) has cholesterol emboli Q where they don’t show an image but describe the violaceous foot lesions in someone with mere Hx of AAA (rather than undergoing repair). They say “Maltese crosses are seen.” Obscure, but apparently refers to birefringence of cholesterol esters that can be visualized under polarized light. MEHLMANMEDICAL.COM 58  MEHLMANMEDICAL.COM HY Trauma and pleural space conditions - Difficult diagnosis on 2CK forms. - Diagnosis of exclusion, meaning all of these 2CK Qs require eliminating the other answer choices to get there. - The Q will say patient was in an accident + now has some form of difficulty breathing and patchy infiltrates in one or more areas of lung. They may or may not mention rib fractures just above the areas of infiltrates. Sounds vague as I said, but that’s what USMLE will say. Pulmonary contusion - Textbook descriptors such as “white-out of the lung” are nonsense. I don’t think I’ve ever seen this on NBME material. - Contused (bruised) lung is known to be fluid-sensitive, where the Q can say patient was given IV saline and now has worsening of O2 sats. This is classic, but I’ve also seen this in myocardial contusion questions, making the Dx difficult as I said. But you’ll be able to eliminate myocardial contusion if they don’t mention severe bruising or pain over the sternum or post-MVA arrhythmia (e.g., premature atrial contractions). - The answer on 2CK forms if they say a patient has paradoxical breathing (i.e., Flail chest the chest wall moves outward with expiration and inward with inspiration). - The answer on 2CK forms if they say there’s a “persistent air leak despite Ruptured bronchus placement of a chest tube.” This will be in a trauma patient. - The answer on 2CK forms for an MVA followed by CXR showing “obscured left hemidiaphragm and the NG tube present in the lower left side of the chest.” Diaphragmatic rupture - Don’t confuse with ruptured bronchus above, or with esophageal rupture, which will tell you water-soluble contrast swallow is visualized in the mediastinum. - Air in the pleural space. The terms almost always refers to a “spontaneous pneumothorax,” which will be acute-onset sharp chest pain in a tall, lanky patient in teens or 20s due to “ruptured subapical bleb.” Pneumothorax - Pneumothorax + low BP = tension pneumothorax. - Mechanism for tension pneumothorax is compression of the vena cavas leading to ¯ venous return à can cause JVD. - Simple/spontaneous pneumothoraces cause ipsilateral tracheal shift. - Tension pneumothoraces cause contralateral tracheal shift. - Tension pneumothorax need not be due to overt trauma. It will literally just be pneumothorax + low BP 9/10 times on USMLE. I’ve seen only one Q on a 2CK MEHLMANMEDICAL.COM 59  MEHLMANMEDICAL.COM form where BP is lower end of normal, but the patient is tachy around 120 bpm (implying barely holding BP in normal range). - Patient will have hyper-resonance to percussion, ¯ breath sounds, and ¯ tactile fremitus. Breath sounds are ¯ because the air in the pleural space masks the sounds of underlying air flow in the alveoli. Tactile fremitus is ¯ because the vibration of air in the alveoli is masked by the overlying air. - Treatment for pneumothorax is “needle decompression followed by chest tube.” That phrase is HY. - One 2CK Q just has “tube thoracostomy” as the answer without needle decompression being listed. So if they don’t list the needle, don’t be confused, and just choose the chest tube. Thoracostomy means making a hole in the thorax. - Pleurodesis I’ve never seen as correct answer on NBME material but can be listed as distractor à means putting talc into pleural space to obliterate it in patients who have recurrent pneumothoraces. - Should be noted that very small pneumothoraces in stable patients with minimal symptoms can be observed. There is one Q on a 2CK NBME form where the answer is observe. But the vignette goes out of its way to emphasize how unremarkable the patient’s presentation is. - There is a 2CK Q where pneumothorax is caused by barotrauma from ascending too quickly from underwater. This is different from Caisson disease (“the bends”), where nitrogen bubbles form in the blood. Pulmonary barotrauma from quick ascent, resulting in pneumothorax, can occur if some of the alveoli expand too quickly. - Fluid in the pleural space; often refers to “hydrothorax,” which means transudate or exudate of plasma-like fluid. Pleural effusion - USMLE wants: dullness to percussion, ¯ breath sounds, and ¯ tactile fremitus. Similar to pneumothorax, the latter two are ¯ because the fluid in the overlying pleural space masks air movement in the alveoli. - Many causes of pleural effusion on USMLE. I’ve observed left heart failure as a notable cause (i.e., patient will have pulmonary edema +/- pleural effusion). NBME can also give you pleural effusion with pneumonias, tuberculosis, and aortic dissection. - Meigs syndrome = triad of ovarian fibroma, ascites, right-sided pleural effusion. MEHLMANMEDICAL.COM 60