NBME Answers : match95's page

Comments ...

+19 visit this page (nbme18#32)

get full access to all content ⋅ become a member

Transposition of the vanA gene from vancomycin-resistant Enterococcus is how it transfers resistance. They use transposons which are located on plasmids. If you have plasmid loss, you won't have transposons, and resistance will decrease.

get full access to all content ⋅ become a member

azibird Why can't this be a point mutation? +6

freenbme23 I don't think that this implies that it can't be point mutation, but rather plasmid loss is more likely. Also, the point mutation Would have to ultimately lead to the plasmid loss. +

thrawn FA says transposition is responsible for antibiotic resistance and plasmids are for transferring the genes of toxins (though UW says also antibiotic resistance). Make up your minds sheeple +2

mariame The most common Vancomicin resistant genes, vanA and vanB are found in a transposon. These have been transferred from Enterococcus to a multidrug resistance plasmid in Staph aureus. the super multidrug resistance plasmid now contains resistance genes against lactams, vancomycin, aminoglycosides, trimethoprim, and some desinfectants. +2

an1 @thrawn I recall that too, but I think it said transposition was antibiotic resistance and UW said transposons was for multi drug resistance +

uasid The plasmid is lost during bacteria replication – when DNA is being replicated, the plasmid is not always replicated and passed on to subsequent generations, especially if there are several generations of replication. +1

+4 visit this page (nbme18#37)

get full access to all content ⋅ become a member

Usually breaks down succinylcholine. Mutated pseudocholinesterase will not break down succinylcholine as well --> increased succinylcholine in your system --> longer to recover from the anesthetic.

get full access to all content ⋅ become a member

+17 visit this page (nbme18#32)

get full access to all content ⋅ become a member

This would just be the normal response of our kidneys to when we don't drink water enough (aka just normal).

Proximal tubule is isotonic because we are reabsorbing BOTH Na+ and H2O.

Macula densa is hypotonic because it is sensing the distal convoluted tubule -- the most DILUTE part of the nephron. Remember the countercurrent exchange system - thick ascending limb is losing NaCl (urine gets less concentrated as it ascends).

Medullary collecting duct is hypertonic because we are reabsorbing all the water making the urine more concentrated.

get full access to all content ⋅ become a member

baja_blast https://i.pinimg.com/474x/73/66/4f/73664f299be8964fb8f3e7e9d2fa1c93.jpg +1

epiglotitties The collecting ducts are the main site of urine concentration only when in the presence of ADH, right? Normally it wouldn't be hypertonic? +

fatboyslim @epiglotitties (great name btw) yes that is correct. UW# 1607 illustrates this nicely. In LOW ADH settings (i.e. not dehydrated), fluid in the collecting tubule has the LEAST osmolarity (i.e. dilute), and fluid between the descending and ascending loops of Henle has the HIGHEST osmolarity. +

+4 visit this page (nbme18#38)

get full access to all content ⋅ become a member

Question was tricky -- need to look ate FOLATE levels. Both B12 deficiency and folate deficiency will cause an increase in homocysteine. Only B12 deficiency will cause an increase in BOTH methylmalonic acid AND homocysteine.

get full access to all content ⋅ become a member

cheesetouch B12 deficiency 'BOTH be high' (and neuro sx) +

handsome WHAT IS THE significance of 14.6 difficulty score of this question? +1

drdoom What is the significance of 14 upvotes? It’s a relative scale. The higher the difficulty score, the greater the difficulty. +

+7 visit this page (nbme18#31)

get full access to all content ⋅ become a member

Inhaled anesthetics that have low blood:gas partition coefficient/blood solubility dissolve in blood more easily. Therefore, there is LESS gas needed to saturate blood -- aka faster saturation of blood. This leads to faster saturation of brain.

tldr; low solubility --> faster onset --> faster recovery

get full access to all content ⋅ become a member

pelparente great answer; just to add to it. Lipid solubility determines potency, not onset/offset (that is determined by blood solubility as stated above). The more lipid soluble the more potent the drug. The more lipid soluble the drug the higher the oil:gas partition (directly proportional to potency) and the lower the MAC (inversely proportional to potency). Source: Boards and Beyond General Anesthesia Neurology +6

cbreland I really went down a rabbit hole on this one... Convinced myself that it had something to do with mask v. IV anesthesia even though I haven't seen/heard that anywhere. Taking step in a week🙏🏼 +1

jer040512 I thought a low blood:gas partition coefficient meant that it has a low solubility and therefore DOESN'T dissolve in the blood that easily. +2

dhpainte22 Think onset/offset is about blood solubility and potency of drug higher with higher lipid solubility so low blood gas coefficient has faster onset and recovery. +

jurrutia Just to drill point home further: consider halothane, high lipid solubility (so high potency) and high blood solubility (slow onset). If you want fast onset, low solubility is the key. +2

+5 visit this page (nbme18#13)

get full access to all content ⋅ become a member

Immune thrombocytopenia (FA 2017, pg 405) - causes destruction of antibody-platelet complex by spleen leading to decrease in platelet QUANTITY and increased megakaryocytes on bone marrow biopsy.

get full access to all content ⋅ become a member

ellie0124 anti-GpIIb/IIIa antibodies +1

baja_blast FA 2019 p. 419 +

jurrutia May be secondary to viral illness... +