HY lecture notes:
Normal pressure hydrocephalus (NPH) = wet, wacky, wobbly – urinary incontinence, CNS dysfunction, gait instability
NPH also often has Parkinsonism. This is really HY on 2CK.
So NPH = wet, wacky, wobbly +Parkinsonism
Mechanism for incontinence = “failure to inhibit the voiding reflex” or “impingement on corona radiata.”
Mid-shaft fracture of humerus fracture = radial nerve –> wrist drop in a pronated arm; also Saturday night palsy (e.g., with crutches or falling asleep on a chair.).
Supracondylar fracture of humerus injury = median nerve; lateral hand/forearm function
Surgical neck of humerus = axillary nerve = flattened deltoid or loss of sensation over deltoid
Medial epicondylar = ulnar nerve = medial hand/forearm
Musculocutaneous nerve palsy = loss of sensation lateral forearm; decreased biceps function
Erb-Duchenne = upper brachial plexus injury = C5/6 dysfunction = “Waiter tip” positioning
Klumpke palsy = lowre brachial plexus injury = C8/T1 = claw hand
Ulnar nerve entrapment syndromes on the USMLE are super HY and under-emphasized in resources.
Cubital tunnel syndrome = ulnar nerve entrapment at the elbow; paresthesias of medial forearm and hand; do splint as treatment; always start with conservative Tx on the USMLE for these MSK presentations.
Guyon canal syndrome = ulnar nerve entrapment at the wrist –> hook of hamate fracture, or ongoing compression due to handle bars (i.e., in avid cyclists).
Polycythemia vera is a primary bone marrow overproduction problem due to JAK2 mutation. Causes high Hb, splenomegaly. Basophils are often elevated, causing pruritis after showers. Can get flushing and signs of hyperviscosity syndrome –> pain in fingertips / Raynauds, blurry vision, headache. EPO is down because it’s suppressed.
In contrast, EPO is elevated in in secondary polycythemia due to low oxygen tension, e.g., COPD, cystic fibrosis. In this case, only RBCs would be elevated, and you’d expect O2 saturation certainly under 90%. These patients would presumably be chronic CO2 retainers as well, with elevated bicarb to reflect chronic respiratory acidosis. Can also be seen in obesity hyperventilation syndrome.
Interstitial nephropathy is the renal answer when pt takes beta-lactam or cephalosporin and gets a rash + eosinophils in the urine. Rash need not be present all of the time, but makes the Q super easy.
NSAIDs can also cause interstitial nephropathy, but eosinophils won’t be seen in urine.
Acute tubular necrosis causes classically muddy brown granular casts, but “granular casts” as a general term can also be seen in other things, e.g., pyelonephritis.
For example, 82 yr old granny with costovertebral angle tenderness, fever, and “granular casts” (not muddy brown) on lab report. ATN and pyelo are both answers. Answer = pyelo, not ATN.
ATN also is due to ischemia, e.g., from blood loss during surgery. Super HY. PCT has high concentration of ATPase pumps that require a lot of O2, so ischemia causes sloughing of PCT.
ATN also due to myoglobinuria (nephrotoxic) secondary to rhabdomyolysis, e.g., from electrical burns, alcoholism, McAardle syndrome, drugs like fibrates+statin combo
Gentamicin (aminoglycoside) is highest yield cause of ATN on the USMLE probably. Don’t confuse this with NSAIDs/cephalosporins, which, as we said, cause interstitial nephropathy (aka interstitial nephritis; tubulointerstitial nephritis) instead. Drugs like gold salts or sulfa drugs can cause regular membranous glomerulonephritis.
Low blood flow to kidney can cause ATN (intra-renal failure) or pre-renal azotemia. So you need to look at BUN/Cr ratio. If >20 –> pre-renal; if <20, intra-renal (ATN).
If they just tell you episode of low BP during surgery and blood was given, and they give you no other information whatsoever, choose ATN over hypovolemia as the cause of renal failure.
Pre-renal is usually due to congestive heart failure or chronic NSAIDs. BUN/Cr >20; FeNa <1%; high urine osmolality. This is because the PCT is trying to absorb more water to compensate for what is perceived as low blood volume. In order to reabsorb water, cations are reabsorbed, namely Na, and then water follow sodium. So there’s lower sodium in the urine in prerenal –> indicates PCT is trying to retain water.
One can even go on to say that this causes low Na flow distally at the macula densa (DCT), which is a trigger for renin release from JGC. That is, if the macula densa senses low sodium, it means the PCT is trying to reabsorb it, so our volume must be low (or the kidney just isn’t getting blood flow, e.g., renal artery stenosis or fibromuscular dysplasia), so RAAS is upregulated.
In intra-renal, BUN/Cr is <20. FA for Step 1 had said <15 for intra-renal, 15-20 for post-renal, and >20 for pre-renal, but I can tell you that there are various questions on 2CK NBMEs where you’ll get ratios of, e.g., 17, where the answer is ATN, clearly intra-renal.
So I just go with >20 = pre-renal; <20 = not pre-renal.
Post-renal could be due to BPH or urethral stricture, etc. Hydronephrosis can occur. USMLE likes “increased Bowman capsule hydrostatic pressure” as an answer in post-renal failure. Iow, since the latter is increased, there’s decreased ability to filter through the glomerulus. Renal failure by definition is decreased GFR. So that’s the mechanism.
Answer for BPH and urinary retention / post-renal insufficiency always = insert a catheter as the next best step, even if he’s got a fever of 100F and 1+ bacteria in the urine. Insert the catheter before giving Abx.
