HY Internal Medicine Tester PDF

MEHLMANMEDICAL.COM IM Cardio Important basic heart failure points - Presents as pulmonary findings (i.e., dyspnea, orthopnea, paroxysmal nocturnal dyspnea). - This is because l...

MEHLMANMEDICAL.COM IM Cardio Important basic heart failure points - Presents as pulmonary findings (i.e., dyspnea, orthopnea, paroxysmal nocturnal dyspnea). - This is because left-heart problems cause a backup of pressure onto the pulmonary circulation, leading to increased pulmonary capillary hydrostatic pressure à transudation of fluid into the alveolar spaces (pulmonary edema). Sometimes this can also cause pleural effusion. - Left atrial pressure (LAP) = pulmonary capillary wedge pressure (PCWP). Left heart failure - Therefore, if there is left heart pathology, PCWP is high (exceedingly HY). - Conversely, if a Q gives you normal PCWP, you know there’s nothing wrong with the left heart. Qs will often give high PCWP and low BP, where you need to know immediately that means cardiogenic shock. - What USMLE will do is give you some sort of left-heart pathology + dyspnea, and then ask for the cause of the dyspnea à answer = “increased pulmonary capillary hydrostatic pressure.” Another answer in this case is “increased alveolar-arteriolar (A-a) oxygen gradient.” - Presents as systemic findings – i.e., jugular venous distension (JVD) and peripheral edema. - Since blood cannot enter the right heart as easily, it backs up to the neck veins (JVD) and venous circulation (increased hydrostatic pressure in veins à transudation of fluid into legs). The Q might mention that central venous Right heart failure pressure is high. - Hepatosplenomegaly can also be seen in RHF but is very rare on USMLE. - Normal jugular venous pressure (JVP) is 3cm above the sternal angle. JVD would be higher than this. Sometimes questions can write that jugular venous pulsations are seen 3cm above the sternal angle and the student erroneously thinks this means JVD, but this is not the case. - Congestive heart failure = left heart failure + right heart failure. - The most common cause of right heart failure is left heart failure. Simply adding the two together, we now call that congestive heart failure. Congestive heart failure - In congestive heart failure, we’ll see both left- and right-heart failure findings – i.e., patient will have dyspnea, JVD, and peripheral edema. - PCWP is elevated in these patients, since the left heart has pathology. - Cor pulmonale is defined as right-heart failure due to a pulmonary cause. In other words, the left heart is completely normal in cor pulmonale and PCWP is normal. - Cor pulmonale will be a patient who has JVD and peripheral edema in the setting of obvious and overt lung disease, such as 100-pack-year smoking history, cystic fibrosis, or pulmonary fibrosis. These can present with lung findings such as wheezes, where you as the student need to say, “It just doesn’t seem like they’re focusing on left-heart failure as the cause of the right-heart failure here. It seems the 100-pack-year smoking Hx causing COPD is why the Cor pulmonale right heart is failing.” - The patient can have a “boot-shaped” heart colloquially, which refers to right ventricular hypertrophy without left ventricular hypertrophy. - If the patient has COPD, the massively hyperinflated lungs will push the heart to the midline, causing a long, narrow cardiac silhouette, with a point of maximal impulse in the sub-xiphoid space. - You must know that pulmonary hypertension is the reason the right heart decompensates. In both cor pulmonale and congestive heart failure, the right heart experiences increased afterload because of pulmonary hypertension. MEHLMANMEDICAL.COM 4  MEHLMANMEDICAL.COM - Endothelin 1 is vasoconstrictor and key mediator in pulmonary hypertension. USMLE wants you to know this is increased in both cor pulmonale and left heart failure. Bosentin is an endothelin 1 receptor antagonist. - Nitric oxide synthase, in contrast, USMLE wants you to know is decreased in pulmonary hypertension (makes sense, since NO dilates). - A loud P2 and tricuspid regurgitation are HY findings in cor pulmonale. I discuss these in more detail in the tables below. Hyper-quick causes of bilateral pitting peripheral edema - Right heart failure (either due to cor pulmonale or congestive) à ¯ ability to fill right heart à ­ central venous pressure à ­ systemic venous hydrostatic pressure à transudation of fluid from systemic veins/venules into interstitium of legs. - Answer on NBME for why HTN doesn’t automatically cause peripheral edema à Cardiac answer = “increased pre-capillary resistance.” In other words, arterioles are responsible for the majority of peripheral resistance; in the setting of high BP, the reason capillary hydrostatic pressure isn’t automatically high enough where the transudation threshold is reached is because arterioles constrict, thereby ­­ resistance and reducing excessive blood flow through the capillaries. - Cirrhosis à ¯ hepatic production of albumin à ¯ intravascular oncotic pressure à Hepatic transudation of fluid from systemic veins/venules into interstitium of legs. - Proteinuria à hypoalbuminemia à ¯ intravascular oncotic pressure à transudation Nephrogenic of fluid from systemic veins/venules into interstitium of legs. - Dihydropyridine calcium channel blockers (i.e., amlodipine, nifedipine). Drugs - Imatinib (targets BCR/ABL tyrosine kinase in CML). - Miscellaneous mechanisms not important for USMLE. Just know above drugs do it. - Strict vegetarianism or veganism à ¯ dietary protein consumption à ¯ intravascular Dietary oncotic pressure à transudation of fluid from systemic veins/venules into interstitium of legs. Pregnancy - A little bit of peripheral edema is normal in pregnancy due to compression of IVC. Hyper-quick causes of unilateral non-pitting edema - Malignancy (e.g., peau d’orange of breast), Hx of surgery (e.g., mastectomy), Lymphatic insufficiency Wuchereria bancrofti (elephantiasis). - Pretibial myxedema (Graves) à mucopolysaccharide deposition in skin + surrounding edema. - Myxedma (severe hypothyroidism) à despite the name, it refers to general “severe hypothyroidism,” not just skin changes; can cause carpal tunnel Thyroid syndrome. - “Pretibial myxedema” is only seen in Graves. Paradoxical hyperthyroidism seen in Hashimoto causing pretibial myxedema is astronomically rare and will get you questions wrong on USMLE. HY Valvular / flow abnormalities on USMLE - Fixed splitting of S2. - Can sometimes be associated with a systolic flow murmur, since more blood L à R from the LA à RA means more blood flow across the Atrial septal defect pulmonic valve. So Q might say “fixed splitting of S2 and a systolic murmur.” - Sometimes can be seen in Qs as “wide, fixed splitting.” I only mention this because some students get pedantic / ask about this. “Wide splitting” MEHLMANMEDICAL.COM 5  MEHLMANMEDICAL.COM just means right ventricular hypertrophy. So if the Q says “wide, fixed splitting,” they’re saying the patient has RVH due to an ASD. - Patent foramen ovale = ASD on USMLE. Don’t confuse with patent ductus arteriosus (discussed below). - USMLE loves asking questions (on 2CK, yes) showing you change in oxygen in the chambers of the heart and making you choose ASD, VSD, etc. - For example, you can see above that somehow O2 increases from the SVC to the RA, which is ordinarily impossible. The only way this could occur is if an ASD is present, where oxygenated blood moved from LA à RA. - ASDs can sometimes be responsible for “paradoxical emboli,” where a DVT leads to stroke. This is ordinarily impossible, since a clot embolizing to the lungs via the venous circulation has no way of reaching the arterial circulation. But if an ASD is present, the clot can go RA à LA à LV à up to the brain, causing stroke. - ASDs do not need to be repaired unless patient has evidence of pulmonary hypertension, RVH, arrhythmia (usually AF), or paradoxical embolus. - Holosystolic (aka pan-systolic) murmur at lower left sternal border. - Can be associated with a diastolic rumble or enlarged left atrium (if more blood going L à R across VSD, then more blood is returning to the LA from the lungs à LA dilatation). - Seen as part of tetralogy of Fallot (VSD, RVH, overriding aorta, pulmonic stenosis). - If a VSD is repaired, USMLE wants ­ LV pressure, ¯ RV pressure, and ¯ LA pressure as the changes now seen in the heart. - VSD does not cause cyanosis at birth. Only years later after the higher blood flow to the lungs results in pulmonary hypertension, followed by right ventricular hypertrophy and reversal R à L (Eisenmenger) does the patient become cyanotic. Ventricular septal defect - Murmur can be silent or soft at birth, followed by loud at 7 days of life. The USMLE will ask why the murmur is louder now à answer = decreased pulmonary vascular resistance – i.e., the lungs open up during the first week of life, resulting in decreased RV pressure and an increase in the L à R pressure gradient (louder murmur). - Conversely, if they ask why the murmur was softer at birth compared to now, the answer is “increased pulmonary vascular resistance,” where the lungs were still closed at the time, so there was a lesser gradient L à R (softer murmur). - Similar to ASD Qs, USMLE loves giving you diagrams with changes in O2 between the chambers and then making you infer we have a VSD. Yes, this stuff is asked on 2CK. MEHLMANMEDICAL.COM 6  MEHLMANMEDICAL.COM - NBME loves this style of Q. You can see O2 somehow increased from RA to RV. The only way this is possible is if we have a VSD where oxygenated blood moves from LV à RV. - This one might initially appear a little more difficult. This is Eisenmenger syndrome, where we have a reversal of flow from RV à LV across the VSD. The NBME is known to show this diagram as well. - If you’re wondering why oxygen % goes from 99 to 96 from the pulmonary circulation to the LA, this is because of thebesian veins draining the myocardium itself, which open into the different heart chambers, including the LA. If you think that’s weird, take it up with NBME, not me, since they have the 99 to 96 drop-down on their diagrams. - VSDs are repaired if patient develops pulmonary hypertension, RVH, arrhythmia, Eisenmenger syndrome, recurrent endocarditis (turbulence of blood due to VSD can ­ risk of valve infections), or aortic regurgitation (if VSD located near the aortic valve). - Seen in Down syndrome. Atrioventricular septal defect - Between the atrium and ventricle, aka “endocardial cushion defect,” although this latter term can also apply to ASD and VSD in Downs. - Holosystolic (pan-systolic) or just regular “systolic,” 29 times out of 30. - Most USMLE questions will not mention it radiating to the axilla. - Highest yield cause of MR on USMLE is post-MI papillary muscle rupture. Mitral regurgitation USMLE is obsessed with this. They’ll say hours to days after an MI, patient has new-onset systolic murmur à answer = MR. - Seen acutely in rheumatic heart disease (valve scars over years later and becomes mitral stenosis). MEHLMANMEDICAL.COM 7  MEHLMANMEDICAL.COM - Can be caused by general ischemia / dilated cardiomyopathy. - Can cause JVD (i.e., back up all the way to the right heart); this is asked multiple times on the new NBMEs. - You do not do preoperative stress tests to determine perioperative MI risk if the patient has mere mitral regurg without other risk factors. For example, one of the 2CK forms gives a Q where smoker with MR has no shortness of breath or chest pain with exertion, and the answer is “no further management indicated,” where exercise stress test is wrong. - If the patient has Sx of heart failure or ischemia, then we do pre-op stress test to determine MI risk. I discuss stress tests later in this chapter. - The mitral valve is replaced if the patient develops severe pulmonary symptoms (i.e., shortness of breath / reduced exercise tolerance), reduced ejection fraction, arrhythmia, or endocarditis if valve function is destroyed. - Described as “rumbling diastolic murmur with an opening snap”; can also be described as “decrescendo mid-late diastolic murmur” (i.e., following the opening snap). - Can cause a right-sided S4 if the pressure backs up all the way to the right heart (seen on NBMEs sometimes; this confuses students because they think S4 must be LV, but it’s not the case). An S4 is a diastolic sound heard in either the LV or RV when there is diastolic stiffening due to high afterload. - 99% of mitral stenoses are due to Hx of rheumatic heart disease (i.e., the patient had rheumatic fever as a child, where at the time it was mitral regurg, but years later it has now become mitral stenosis). - One 2CK NBME Q mentions patient with history of rheumatic heart disease who, years later, now has 4/6 rumbling diastolic murmur without an opening snap; this is still mitral stenosis. Although opening snap is buzzy for MS, just be aware it’s not mandatory and that this Q exists on NBME. - Other HY presentation on USMLE is pregnant women with new-onset Mitral stenosis dyspnea in 2nd trimester and a diastolic murmur. This is because 50% increase in plasma volume by 2nd trimester causes the underlying subclinical MS to become symptomatic. Don’t confuse this with severe dyspnea and peripheral edema in late third-trimester, which is instead peripartum cardiomyopathy (antibody-mediated). - The 1% of MS that’s not due to Hx of RF can be marantic (non-bacterial thrombotic endocarditis; NBTE) à endocarditis seen due to hypercoagulable state in the setting of malignancy, where the vegetations are small and verrucous, on both sides of the valve. This is in contrast to bacterial endocarditis, which causes large, floppy vegetations that lead to MR, not MS. - Libman-Sacks endocarditis seen in SLE is due to antiphospholipid antibodies and is a type of NBTE. - Balloon valvuloplasty is the 1st-line Tx for mitral stenosis. This is done if patient has minimal calcification of the valve + has pulmonary HTN. - Mitral valve replacement is done if balloon valvuloplasty fails, if patient has severe MS with dyspnea, arrhythmia, or calcification of the valve. - Most common murmur. - Described as mid-systolic click. - “Myxomatous degeneration” is buzzy term that refers to connective tissue degeneration causing MVP in Marfan and Ehlers-Danlos. Mitral valve prolapse - Almost always asymptomatic. On 2CK forms, they want you to know about “mitral valve prolapse syndrome,” which is symptomatic MVP that presents as repeated episodes of “fleeting chest pain” on the left side in an otherwise healthy patient 20s-30s. They might say there is Hx of MI in the family, but this is MVPS, not MI. Answer on NBME is “no Tx necessary." MEHLMANMEDICAL.COM 8  MEHLMANMEDICAL.COM - USMLE loves using MVP as a distractor in panic disorder questions. They will give long paragraph about panic attack/disorder + also mention there’s a mid-systolic click; they’ll ask for cause of patient’s presentation à answer = panic disorder, not MVP à student is confused because they say mid-systolic click, but the MVP isn’t the cause of the patient’s presentation; the panic disorder is; MVP’s are usually incidental, benign, and asymptomatic. - MVP does not progress to mitral regurg almost always. So don’t think that MVP and MR are the same. - Decrescendo holo-diastolic (pan-diastolic) murmur; can also be described as “early diastolic murmur,” or “diastolic murmur loudest after S2.” - Causes wide pulse pressure (i.e., big difference between systolic and diastolic pressures, e.g., 160/50, or 120/40) à results in head-bobbing and bounding pulses (don’t confuse with slow-rising pulses of aortic stenosis). - The bounding pulses can be described on NBME as “brisk upstroke with precipitous downstroke.” In turn, they can just simply say, “the pulses are brisk,” meaning the systolic component is strong. - I would say 4/5 times bounding pulses means AR. The other 1/5 will be PDA and AV fistulae (discussed below). Bounding pulses occur when blood Aortic regurgitation quickly leaves the arterial circulation. In AR, the blood quickly collapses out of the aorta back into the LV. In PDA, it leaves the aorta and enters the ductus arteriosus; in AV fistulae, it leaves for a vein. - Highest yield cause on USMLE is aortic dissection à can retrograde propagate toward the aortic root causing aortic root dilatation and AR. - Even though MVP is most common in Marfan and Ehlers-Danlos, AR is second most common in these patients, since if they get aortic dissection, this can lead to AR. - Can lead to volume overload on the LV and eccentric hypertrophy. - Valve is replaced if patient has EF