to snoo-finity ... and beyond!
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Fibrates inhibit VLDL secretion (by inhibiting 7-a Hydroxylase) and they increase HDL. However, this patient has chronic pancreatitis, which decreases enzymes that allow for fat absorption. Because a large portion of HDL is synthesized in enterocytes from newly absorbed fat, HDL content is unlikely to increase in patients with chronic pancreatitis from any of the lipid-lowering agents. Hope this helps!
fibrates cause decreased VLDL as well as niacin. They increase the activity of LpL by activating PPARa causing increase catabolism of VLDL and chylomicrons. since VLDL are rich in triglycerides, this is how they decrease triglycerides.
but fibrates also decrease bile acid production by inhibiting 7alpha hydroxylase, which is how they cause increased cholesterol gallstones.
Increased blood HCO3 could have easily been interpreted as increased blood pH aswell. FOllowing your explanation, since the pt had acidosis, the increased HCO3 will just make it a normal pH.
Another way to think of the question is: if there is decreased exhalation due to COPD --> increased CO2 --> increased CO2 transported in blood by entering the RBC's with Carbonic Anhydrase and HCO3 is released into blood stream. So increased CO2 -> increased HCO3 seeing as this type of CO2 transport is 70% of total CO2 content in blood.
I thought you could never fully compensate, so your pH will never normalize.
Primary problem = respiratory acidosis → pH low. Compensatory metabolic alkalosis will increase blood HCO3-, but not enough to normalize pH, it will just be 'less' low, but still an acidosis.
Thats myosatellite cells. Satellite cells are also glial cells that form around damaged nerve cells and lie close to neuron bodies in the CNS
Myosatellite cells are also called satellite cells so it is not clear which definition they were using.
That makes that glucose needs to be given with sodium. But, what about bicarb? Isn't the patient losing lots of bicarb from diarrhea?
Had the same debate. I knew glucose/sodium was the textbook answer for rehydration but also was wondering if we just ignore the bicarb loss in diarrhea...?
@pg32 - Sure, they are losing bicarb in the diarrhea, and yes this can effect pH, but it doesn't matter that much. You're not going to replace the bicarb for simple diarrhea in a stable, but hydrated previously healthy 12 year old. You're gonna give him some oral rehydration with a glucose/sodium-containing beverage. Don't overthink the question :)
it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ?
according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf)
Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb?
How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis??
normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis
"Down Syndrome has high HI (hCg and inhibin)"
the relationship between the words down/high really stuck for me
An easy way to remember the other aneuploides is that the "lower" ones (e.g. lower than 21 = 13,18) have "lower" values (e.g. LOW hCg and LOW inhibin)
How is Tuberous Sclerosis the most likely given that it is an AD disorder and there is no family history of "seizure disorder or major medical illnesses"?
@fcambridge variable expressivity of TSC allows for many different phenotypes.
Ilioingual covers part of the medial thigh, base of penis and anterior scrotum
Posterior scrotal nerves are a branch of pudendal and cover said area
Doral nerves cover the dorsum of the penis which are also from the pudendal
I thought it was the Genitofemoral nerve because the genital branch supplies the cremaster and scrotal skin, but I looked it up and: The genital branch passes through the *deep inguinal ring* and enters the inguinal canal; also, Ilioinguinal wraps around the spermatic cord just like the question stem says.
"The structures which pass through the canals differ between males and females:
in males: the spermatic cord and its coverings + the ilioinguinal nerve." from wiki "Inguinal canal", which means the ilioinguinal nerve lies on the external surface of spermatic cord. https://en.wikipedia.org/wiki/Inguinal_canal
The contents of spermatic cord includes, "nerve to cremaster (genital branch of the genitofemoral nerve) and testicular nerves (sympathetic nerves). It is worth noting that the ilio-inguinal nerve is not actually located inside the spermatic cord, but runs along the outside of it, in the inguinal canal." from wiki spermatic cord.
dysphagia from hit of nucleus ambiguus (CN IX/X/XI)
Sensation changes due to hit of lateral spinothalamic tract and spinal trigeminal
Check out rule of 4s if you haven't already
Yup, lateral meduallary syndrome or Wallenburg Syndrome. Whatever you want to call it. The hemifacial analgesia is from damage to the spinal trigeminal nucleus/tract, and you get the hoarseness from damage to the vagus and the body loss is from the spinal thalamic tract. You can also get Horner’s syndrome with this.
Lateral medullary syndrome = Wallenberg's syndrome