Core Flashcards
Rhabdomylysis electrolyte effects
lysis of cells leads to hyperkalemia –> can lead to peaked T waves; hyperphosphatemia which binds to calcium resulting in hypocalcemia
cerebral salt wasting vs SIADH
Syndrome of inappropriate antidiuretic hormone (SIADH): pass urine with concentrated sodium but increased plama volume
Cerebral salt wasting occurs after intracranial injury. pass lots of urine with sodium and end up volume depleted. It responds to fluid and sodium replacement. It differs from syndrome of inappropriate antidiuretic hormone (SIADH) where you pass urine with concentrated sodium therefore also results in hyponatremia but increased plasma volume:
Curreri formula
25kcal/kg/day + 40 kcal/%TBSA/day
should also get 1-2 gm/kg/day of protein
Aspirin (acetylsalic acid)
inhibits cyclooxygenase which forms arachidonic acid compounds including thromboxane and prostacyclin. Thromboxane is a platelet aggregator and vasoconstrictor. Prostacyclin is a platelet aggregator.
Dextran
polysaccharide decreases platelet aggregation by altering electric charge of platelets and decreases blood viscosity. Also volume expander. Can cause renal injury and pulmonary edema.
Heparin
glycosaminoglycan that binds to antithrombin III and enhances its ability to inactivate thrombin (which converts fibrinogen to fibrin), as well as clotting factors IX, X, XI, and XII. May also cause NO-mediated vasodilation.
Hirudin
derived from leech Hirudo medicinalis and directly inhibits thrombin.
Streptokinase (first generation) and tissue plasminogen activator (second generation)
converts plasminogen to plasmin which breaks down fibrin within a clot
Glycoprotein IIb/IIIa inhibitors
antiplatelet agent like aspirin
vonWillebrand disease
treat with desmopressin (DDAVP). Can measure levels of von Willebrand factor ristocetin cofactor and coagulation factor VIII. Note DDAVP is a derivative of ADH so restrict fluid to avoid hyponatremia and seizures.
Factor V Leiden
most prevalent hypercoagulation disorder. Activated protein C cleaves factor V in three sites; a mutation in the first site is known as factor V Leiden. Factor Va is inactivated 10 times slower than normal.
Protein C and S deficiencies
Activated protein C with cofactor protein S inhibits coagulation cascade by inactivating factor V and factor VIIIa. May be associated with warfarin-related skin necrosis and purpura fulminans in neonatal period.
Antiphospholipid syndrome
most common acquired coagulation disorder. Autoimmune disorder with antibiodies to phospholipids including anticardiolipin, lupus anticoagulant, anti-beta-2-glycoprotein I.
Tetracyclines
contraindicated children under 8, effect growing teeth and bones
Quinolones
contraindicated children under 18, effect cartilage and joints
Third generation cephalosporins
cefotaxime, cephtriaxone
Antibiotic prophylaxis for leeches
aeromonas hydrophila so prophylaxes with fluoroquinolone or in children Bactrim (or ceftriaxone)
Fungal infections
- Coccidiomycosis (Southwest US)
- Histoplasmosis (Ohio-Mississippi river valley)
- Blastomycosis (Ohio-Mississippi river valley)
- Mucormycosis (rhizopus species)
- Crytococcus
- Chromomycosis (tropics)
Statistical error
- Type I: false positive; reject the null hypothesis and falsely conclude there is a treatment effect (guard against with low significance/alpha level of <0.05)
- Type II: false negative; failing to reject a null hypothesis that should be rejected due to inadequate sample size/power
- Type III: correctly reject the null hypothesis for the wrong reason
- Type IV: incorrect interpretation of a correctly rejected hypothesis
Levels of evidence
- High quality, multicentered or single-centered, randomized controlled trial with adequate power
- Lesser-quality, randomized controlled trial; prospective cohort study
- Retrospective comparative study; case control study
- Case series
- Expert opinion; case report
Autonomic dysreflexia
Uncontrolled sympathetic response (headache, hypertension, bradycardia, flushing, blotching, sweating) to stimulus (bladder distention, rectal distention, fractures, heterotopic ossification, dislocations, infections, pregnancy, labor). Patients with paralysis above T6. Treatment to remove stimulus (foley catheter), nifedipine.
Malignant hyperthermia
caused by inhalational agents like isoflurane and depolarizing muscle relaxants like succinylcholine. Results in skeletal muscle rigidity, tachycardia, fever, cardiac arrhythmias, acidosis, hypotension, hyperthermia, increase in end-expired CO2 concentration. Treat with dantrolene.
Succinylcholine side effects
only depolarizing muscle relaxant
can trigger malignant hyperthermia
can result in hyperkalemia in paralytics, burns, crush, rhabdomylitis, lower motor neuron injury due to upregulation of nicotinic acetylcholine receptors in denervated or traumatized muscle. Treat with sodium bicarbonate, glucose with insulin, calcium.
FENa
FENa = ((UNa x PCr)/(PNa x UCr)) x 100% calculates percent of filtered sodium excreted
FENa below 1% prerenal where appropriate reabsorption due to decreased renal perfusion
FENa above 2% inappropriate salt wasting indicating ATN or if intrinsic damage so less sodium reabsorbed. In postrenal disease the FENa is high initially then as there is renal damage the value increases. Diuretics and chronic renal failure alter reliability
