HY lecture notes:
Contact dermatitis –> type IV hypersensitivity –> linear vesicles / streak for poison ivy/sumac –> T cell-mediated
Cor pulmonale = right heart failure secondary to a lung pathology; PCWP must be normal to establish that the left heart is not the cause of the pulmonary hypertension (I talk more about PCWP in the Cardiology #3 lecture).
USMLE wants you to know straight up that cor pulmonale is caused by pulmonary hypertension. If you have any lung disease with chronic hypoxemia (e.g., COPD, CF, obesity hypoventilation syndrome) –> hypoxic vasoconstriction –> pulmonary hypertension –> RVH –> right heart failure secondary to a lung cause.
So in cor pulmonale, you’ll get a patient with, e.g., 80-pack-year smoking Hx who has a loud S2 + JVD + peripheral edema +/- hepatomegaly –> this says right heart failure secondary to COPD.
The loud S2 (P2 component) means the pulmonic valve is slamming shut because the pressure distal to it (in the pulmonary arteries) is high. The pulmonic valve will close when pressure in the RV falls below pressure in the pulmonary artery at the end of systole. In the case of pulmonary hypertension, this will be easier to achieve since the pulmonary artery pressure is greater.
After the RV hypertrophies, this process will begin to reverse as 1) the gradient becomes less pronounced, and 2) it actually takes longer for the pulmonic valve to shut because RV pressure increases –> wide splitting of S2 (P2 occurs much later than A2, rather than slightly after).
Bottom line is, if you see loud P2 in a question, just think that there’s definitely pulmonary hypertension in the setting of a right ventricle that hasn’t compensated sufficiently (right heart failure), regardless as to its absolute degree of hypertrophy.
The JVD + peripheral edema = right heart failure (right heart can’t handle the preload of the venous return).
I say +/- hepatomegaly because that’s a late finding for right heart failure (nutmeg liver). And by all means there can be splenomegaly too.
In prerenal failure –> BUN/Cr is >20, FeNa is <1%, urine osmolality is high –> some causes are heart failure (decreased perfusion to kidney), dehydration, and renal artery stenosis / fibromuscular dysplasia –> kidney increases PCT reabsorption of water to compensate for perceived (or real) low volume status –> it accomplishes this by reabsorbing Na in the PCT –> water follows sodium –> FeNa under 1% + high urinary osmolality (concentrated urine).
Intrarenal failure –> acute tubular necrosis is most common cause –> BUN/Cr is <20, FeNa >1%, urinary osmolality is low –> if you get a question where they say acute blood loss (e.g., in patient who needed resuscitation + packed RBCs) or acute ischemia (e.g., in episode of VF where the patient required defibrillation), and the patient goes on to get oliguria –> answer = acute tubular necrosis.
Postrenal failure –> BPH classically –> USMLE likes “increased Bowman capsule hydrostatic pressure” as the answer in an old man who has high BUN and Cr –> the BUN/Cr is <20, FeNa >1%, urinary osmolality low, same as intrarenal.
First Aid for Step 1 had made a distinction between intra- and postrenal as far as intrarenal being BUN/Cr <15, and postrenal 15-20, but I’ve seen several questions on 2CK-level NBMEs where these ranges were violated, most notably for ATN presenting with sometimes 16 or 17. So I always just teach the ranges as: prerenal >20, and the others <20.
Allergic bronchopulmonary Asperillosis (ABPA) –> asthma + eosinophilia –> hypersensitivity to Aspergillus antigen. Tx = combination of corticosteroid + fluconazole. The CXR for this lecture is ABPA.
