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Comments ...

 +0  (nbme19#0)

An AP is generated once the summation of charge at the axon hillock reaches a threshold voltage. Once the threshold voltage is passed, an AP is generated. However, the peak amplitude of the AP above threshold can still vary depending on the number of Na channels that are simultaneously open while the AP is present.

Thus, after the AP threshold has been reached and the AP is generated, the peak voltage attained can be reduced in amplitude if the first Na channels that opened begin to close because of a short inactivation time.

 +1  (nbme19#41)

The thymic cortex is where positive selection of T cells takes place. Positive selection is a process that tests if T cells can bind to self-MHC well enough above a certain threshold to function properly. If the binding is too weak, the T cell undergoes apoptosis.

Bcl-2 is an anti-apoptosis gene. If cells that reach the thymic cortex have a constitutively active Bcl-2 gene, they would not undergo apoptosis despite weak self-MHC binding. Thus, you would have failure of positive selection and "decreased cell death in the thymic cortex" which was the correct answer.

Also, remember that after positive selection in the thymic cortex, the T cells go on to the thymic medulla for negative selection where the cells undergo apoptosis if they bind to self-MHC too strongly (ie risk for auto-immunity)

 +0  (nbme17#2)

The answer is factor VII because it has the shortest half-life of all the Vit K dependent coagulation factors. Warfarin inhibits epoxide reductase -> no more activated Vit K -> no more activation of coagulation factors 2,7,9,10,C,S -> factor VII degrades first =(FA 2018 p 402)

solidshake  Answered the wrong question here. My bad. +1

 +0  (nbme17#0)

If you need more convincing that this is an Epidural hematoma, note that the blood collection does not cross the suture lines. Compare against subdural hematoma which does cross the suture lines and can be seen creeping along the length of the inner surface of the skull. Pictures in First Aid show good examples. (FA 2018 pg 497)

 +0  (nbme17#0)

Also good to know that only Unfractionated Heparin has the ability to (1) bind to factor Xa and therefore potentiate Anti-coagulation and (2) bind to Anti-thrombin III and Thrombin thus bringing them together and therefore potentiate Anti-coagulation

Fractionated Heparin can only do (1)

Reasoning is due to the difference of size between the heparin molecules and what they can bind to

(see Uworld Qid# 2132)

 +2  (nbme18#22)

Acute stress disorder involves flashbacks of traumatic event, avoidance of triggers, depressed mood, and nightmares; lasts 3 days - 1 month; can evolve to PTSD if lasts >1 month

Panic Disorder is recurrent and happens unexpectedly without known triggers

Biploar and Histrionic easily ruled out

Alcohol Withdrawal is left as the right answer. Symptoms also match with time course. Delirium tremens 2-4 days after last drink

Subcomments ...

submitted by cbrodo(60),
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kai  kick Goals (gracilis) with your feet Cook and eat (cuneatus) with your hands +3  
temmy  i remember gracilis is for legs by saying i have graciously long legs and they are inside while arms can spread out to remember their orientation on the spinal cord +4  
jess123  I remember it as gracilis = grass so feet haha +4  
link981  Just to add found on page 492 on FA 2018. +  
charcot_bouchard  Hey Temmy, I can spread my legs too :) +  
maxillarythirdmolar  I can't feel GRACIE's ~fine touch~ as she ~vibrates~ my balls. +3  
cat5280  Could someone please explain why you were able to eliminate the spinocerebellar tracts? +1  
drzed  Lmao I remember gracilis because of the gracilis muscle in the legs! +3  
alexxxx30 spinocerebellar tract does 4 things to know 1. proprioception in the Romberg test 2. intention tremor if damaged 3. shin to knee test 4. dysdiadochokinesia (being able to rapidly pronate/supinate the upper extremity) yes the patient has proprioception issues, but the other symptom of vibration loss points us more to a fasciculus gracilis issue. If the patient had presented with proprioception and and intention tremor then we would think spinocerebellar +2  
alexxxx30  adding to my comment^ I would commit these 4 things to memory as I have gotten several questions concerning this topic (there were 2 questions on this exam where spinocerebellar tracts are involved). Memorize them and it might get you 1-2 extra points! +  
solidshake  Just to clarify a point, Spinocerebellar tracts are not tested by the Romberg Test. Romberg tests conscious proprioception that is done by the dorsal columns. Spinocerebellar tracts are used for Unconscious proprioception. Look up tabes dorsalis in First Aid. One of the positive indicators is a positive romberg test, which shows that the dorsal columns have been damaged thus affecting conscious proprioception and thus impaired balanced on standing with the eyes closed +  

submitted by brise(51),
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so I asw kcust on thsi aeubces shi UBN /ecteiainrn oirat edl em ot nktih eh dha na tcinrinis rlean iydocstfn.un nAd a 2IPG oiinibnthi uodlw lead to a el-parern miaozaet, ehewr het /BUN aircneniet aorti lduow eb mreo hnta .02 I wnko hatt ANDIsS iinhbit .SGIP utB who era yuo pdusepso to ssrco tou dinuiotcn of satidl ubrutla csisaid?o

purdude  You can cross out Distal RTA because the urine pH is 5. In Distal RTA, urine pH becomes greater than 5.5 because a-IC cells can't secrete H+ +1  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +1  
thotcandy  pH > 5.5 is only true for Type I RTA. Type 2 RTA is proximal so that wouldn't be considered anyways. Type 4, however, urine pH would be < 5.5 and can be caused by NSAIDs, so how do we eliminate that? +1  
underd0g  @thotcandy Distal RTA is another name for Type 1 RTA, so that is the type of RTA that they are specifically referring to in that answer choice. +1  
solidshake  ^agreed. Type 4 RTA is not an option as an answer. Type 4 is a result of low aldosterone or aldosterone resistance -> hyperkalemia -> impaired NH3 synthesis in the Proximal tubule -> impaired NH4 formation -> high tubule H+ -> tubular acidosis +  

submitted by brasel(13),

Overflow incontinence is present (bladder fills then leaks slightly), so either:

1.) something blocking outflow (e.g.; BPH)

2.) impaired contraction of bladder (e.g.; damaged nerves)

Only the pelvic nerve causes detrusor contraction, so it is the only possible answer. External sphincter, pudendal nerve, and skeletal muscle all does the same thing. Hypogastric nerve helps retain urine (relaxes detrusor) so it is clearly not damaged.

solidshake  I agree answer is the parasympathetic Pelvic Splanchnic nerve, but don't forget there are 2 mechanisms that are affected when it's damaged: 1. Impaired involuntary contraction of bladder and also 2. Impaired involuntary relaxation of the internal urethral sphincter. Pelvic Splanchnic nerve facilitates both of those + voluntary somatic relaxation of external urethral sphincter via pudendal nerve allows you to pee +  

submitted by cassdawg(1101),

Many opioids (like morphine) are potent histamine releasers, which can cause puritis and anaphylactoid reactions (such as seen in this patient with the facial flushing, drop in blood pressure and corresponding increase in heart rate). Puritis is actually a common side effect of morphine.

Source: First Aid and

solidshake  Opioids (morphine), radio contrasts, some antibiotics (vancomycin), and several other medications can trigger IgE independent mast cell degranulation. (Uworld Qid# 11852) +  

submitted by kevin(24),

Tubocurarine competitively antagonizes nAchR. Phrenic nerve was still functioning, so the problem was at the neuromuscular junction. Of the answer choices, the only pure NMJ blocker was this

solidshake  Just to show why the other answers are wrong: Lidocaine - Blocks Na channels, Morphine Sulfate - mu opioid receptor blocker, Pentobarbitol - increased duration of GABA-A channel thus increased Cl thus decreased nerve firing, Potassium Chloride - replenish K, Tetrodotoxin - Blocks Na channels. Question shows Phrenic nerve trying to make the diaphram move with Ach release but fails because Tubocurarine is a competitive antagonist of Ach at the NMJ. +5  

submitted by mannan(8),

Why would it not be answer C) Lutenizing hormone?

My thought process was this:

Leydig cells make testosterone (internal genitalia) that also gets converted to DHT (external genitalia)

Without the leydig cells working you don't have internal genitalia (patient in stem) and you dont have male external (patient in stem)

solidshake  Androgen insensitivity is the better answer because it is more specific for the findings given. A deficiency of LH secretion would point to a problem with Gonadotropic cells in the anterior pituitary which would present with problems with LH and FSH, but the sertoli cells are working here. If you say its because of LH insensitivity, i suppose this is plausible, but Androgen insensitivity is a well known condition that gives this presentation. +  

submitted by solidshake(10),

The answer is factor VII because it has the shortest half-life of all the Vit K dependent coagulation factors. Warfarin inhibits epoxide reductase -> no more activated Vit K -> no more activation of coagulation factors 2,7,9,10,C,S -> factor VII degrades first =(FA 2018 p 402)

solidshake  Answered the wrong question here. My bad. +1  

submitted by cassdawg(1101),

The two most common defects in fatty acid metabolism are systemic primary carnitine deficiency and medium-chain acyl-CoA dehydrogenase deficiency or MCAD [FA2020 p89]. Both can present with physically normally appearing babies as the primary issues occur later (MCAD between 3 and 24 months and some variations of carnitine deficiency don't present until adolescence). Often the main danger is "hidden" in neonates unless prolonged fasting occurs because the individuals will go into hypoketotic hypoglycemic and can die. Thus, they are put on the newborn screens along with other disorders of fatty acid metabolism.

Thus, this neonate would have likely normal appearing physical exam and general labs. The best test of the list would be to look at acylcarnitine concentrations, which can be used to detect many disorders of fatty acid metabolism and some organic acidemias (

Amino acids are not associated with fatty acid metabolism. ABG and electrolytes would likely be normal and would not be helpful in diagnosis. Lactic acid levels would be useful in neonates to give an idea of oxygen delivery to tissues, but is not useful here.

solidshake  Just adding to comment above In the setting of a suspected defect in fatty acid oxidation, test for carnitine to find the cause: If carnitine is low/absent -> primary carnitine deficiency If carnintine is present/normal -> MCAD (deficiency with acyl-coa-dehydrogenase) A big flag that you are in this scenario is an infant with Hypoketotic Hypoglycemia (characteristic of both diseases) +1  
sexymexican888  Just to add to this on how to differentiate MCAD from primary carnitine deficiency: (1) Primary carnitine deficiency: muscle weakness, cardiomyopathy, hypoketotic hypoglycemia, inc. muscle trygicerides. (2) MCAD: hypoketotic hypoglycemia +