1. To prevent mollusks and other sea things from sticking to submerged structures, like ships and docks, there are many kinds of coatings you can apply: one is a "peeling layers" coating, where you have polymers that are cross-linked via oxygen-metal ion bridges (Sn, Zn, Cu, etc-- Sn is banned in EU waters); these bonds hydrolyze relatively easily and when sea creatures go to attach, the polymer layers peel off. You can also teflon coat (or other super low surface tension substances, like certain silicon-based compounds) surfaces to prevent attachment; but these things depend on strong currents to sweep away animals. It works for shipping vessels, which are always on the go, but not for more stationary vessels (military). You can also create a dynamic/soft surface (like sea sponges don't get mollusk attachment) or certain patterned surfaces (like shark skin).
2. MRSA dosing of clinda: 40mg/kg.
3. Failure to thrive: first you fall off the growth curve for weight, then height, finally head circumference.
4. If someone presents with a neck mass + local lymphadenopathy: 
-Viral: (EBV, esp if they have strep throat since strep often happens in people with EBV), HIV (causes parotitis and generalized LAD), VZV, CMV, Adeno
-Fungal: histo, blasto, TB, atypical mycobacteria like MAI
-Parasitic: toxo
-Bacterial superinfection- staph, strep
-Rheum: sarcoid (parotid mass- can be sarcoid even if ACE is normal), kawasaki
-Superinfected congential lesion: brachial cleft cyst/cervical sinus, hypoglossal duct cyst or other thyroid anomaly
-Neoplastic: hodgkin's/non-hodgkin's.
-Abscess: retropharyngeal (look for pain on extension of neck, difficulty/painful swallowing, drooling), paratonsillar.
5. Elevated alk-phos in a pediatric population, think about where alk-phos comes from: 
-Liver: check LFTs, GGT, bili, to see if there's any sort of hepatic or biliary process. Check for clinical stigmata of cholecystitis or stones (murphy's sign, colicky URQ pain)
-Bone: check PTH, Ca (tchovek's sign), phosphate levels to look for primary bone dx; check renal function.
--Ask about pain, fully examine (press on) all bones to elicit point tenderness-- to r/o fracture or cancer (primary/met)
--Check vitamin D levels (check 25-OH vit D which is the storage form; 1,25 is active form with v short half life) for rickets. Clinical stigmata of rickets: genu varum, thickening of wrists (one of the first signs), cuffing/fraying of distal ends of long bones on xray esp radius/ulna, rachitic rosary; also ask the kid about his diet, is he eating enough ca/vit D, does he get enough sunlight, is he chubby and active or failure to thrive?
-Placenta: pregnancy test.
-Leukocytes: tumor lysis syndrome, chemo, mono.
-Gut- ask about GI sx (pancreatic CA, celiac can present like this)
6. Isolated ulnar fractures are rare, unless the pt raises his arm to block a hit (i.e. from a blunt object). If you see an ulnar fracture, check for radial head dislocation -- "monteggia fracture"
7. Salter-Harris fractures: 
diaphysis -> metaphysis -> physis -> epiphysis. Physis is another term for epiphyseal/growth plate.
I: Straight through the physis
II: Above the physis (diaphysis) + physis
III: Lower than the physis (epiphysis) + physis
IV: Through all 3: metaphysis/physis/diaphysis
V: Ram- compression fracture of physis.
It can be hard to tell the difference between S-H 1 and 5, but the outcomes are different. 3,4, and 5 are worse.
8. To fix nursemaid's elbow: flex the affected arm 90 degrees, grasp radial head in one hand, and either hyperpronate or flex/supinate simultaneously; some people think the former is less painful. Do it fast, because it hurts and you want the pain to be as quickly over as possible. The kid should be no longer in pain and able to use the arm again in a few minutes. Counsel parents on not letting the injury recur (i.e don't swing your kid around by the arms, etc)
9. If someone is in the ICU and needs inotropes and sedatives, you should put them in different lines. If you only have one line, put the sedative in front of the inotropes. If the sedatives are behind, when you bolus them (i.e. for acute pain control for an exam or quick procedure), you will push everything in front of the sedatives on the line into the patient, i.e. bolusing the inotropes too, and that's dangerous. You can't just temporarily stop whatever is in front of the sedatives-- if they're sick enough to need inotropes, even a few seconds off of the IV drip will lead to hemodynamic instability.
10. TPN causes cholestasis and subsequent liver damage. The pathogenesis is incompletely understood, but here are some theories:
-Loss of enteral intake: reduced release of GI hormones/growth factors that are normally released by peristalsis/food in gut that maintain overall GI health, no CCK -> bile stasis in GB, bacterial overgrowth due to stasis/less developed GI immuno (also worsens cholestasis by deconjugating bile acids), bacteria also stimulate inflammation.
-TPN components may be toxic, too high, or too low: i.e. lipids may lead to hepatic steatosis and cholestasis (lipids >1g/kg/day corr with inc hepatic dmg), certain amino acids are not metabolised well by preemies and must be dropped (methionine) or are missing and need to be replaced (taurine), less vitamin antioxidants, certain minerals/metals may be toxic.
Finally, whatever underlying dx that necessitated TPN, such as short gut, will contribute to the poor outcomes. (clin liv disease)