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)
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)
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)
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)
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
The posterior columns (Fasciculus cuneatus/Fasciculus gracilis) carry information to the brain regarding proprioception, vibration, discriminative touch and pressure. Physical exam findings suggest a lesion here (the spinothalamic tract carries pinprick/pain and temperature, and these were normal). Since the patient has abnormal findings in the lower extremities, and normal findings in the upper extremities, the answer is Fasciculus gracilis. This is because information from body areas below the level of T6 is carried by gracilis and information from body areas above the level of T6 is carried by cuneatus.
so I was stuck on this because his BUN /creatinine ratio led me to think he had an intrinsic renal dysfunction. And a PGI2 inhibition would lead to a pre-renal azotemia, where the BUN/ creatinine ratio would be more than 20. I know that NSAIDs inhibit PGIS. But how are you supposed to cross out induction of distal tubular acidosis?
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.
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
https://www.ncbi.nlm.nih.gov/pubmed/22417016
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
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)
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)
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 (https://neurology.testcatalog.org/show/ACRN)
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.
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.