would anyone be able to clarify what the others would be? A) Allergen mediated vasoconstriction, leading to ischemic tissue injury: Type I B) Binding of antigen to IgE on the surface of mast cells leading to mast cell degranulation: Type I C) deposition of antigen-antibody complexes within postcapillary venules, leading to activation of complement: Not sure D) Phagocytosis of antigen by neutrophils, leading to oxidant mediated tissue damage: Type III?
Somehow I was able to convince myself that increased testosterone --> decreased estrogen --> decreased negative feedback on LH/FSH secretion --> increased FSH. Does anyone care to explain why this logic is wrong? Thanks :)
So alpha was the answer so my fatigued mind put "A"...well done. You're going to be a doctor. lol
Almost got tricked by this one because osteosarcoma also causes osteoblastic lesion. Osteosarcoma most commonly metastasizes to lungs though.
You have to think about this using the concept of CONDITIONAL PROBABILITY. Another way to ask this type of question is like this: “I show you a patient with spontaneous pneumothorax. Which other thing is most likely to be true about that person?” Or you can phrase it these ways:
spontaneous pneumo), what other finding is most likely to be the case? In other words, of all people who end up with spontaneous pneumo, the most common other thing about them is that they are MALE & THIN.
If I gave you a bucket of spontaneous pneumo patients -- and you reached your hand in there and pulled one out -- what scenario would be more common: In your hand you have a smoker or in your hand you have a thin male? It’s the latter.
The answer is due to an exception outlined here where niacin is used in pts w/o diabetes who have refractory hypertriglyceridemia at high risk or has a hx of pancreatitis.
I agree that fibrates are first line (and so does that article) but NBME was honing in on a specific exception that niacin can also be used since VLDL and TGs are high in hypertriglyceridemia.
The "clue" they had was "recurrent pancreatitis" which is supposedly a lead towards niacin.
I also put increase HDL....
Goljan stresses the Boards giving the leukemia questions away based on the age given in the question stems.
ALL = 0-14
AML = 15-39; 40-59
CLL = 60+
CML = 40-59
https://forums.studentdoctor.net/threads/goljan-on-leukemias.303605/
Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.
Hyperventilation decrease PaCO2. Central chemoreceptors respond to low PaCO2 by vasoconstricting cerebral blood vessels.
A) Arterial Blood Oxygen Concentration: Blood Oxygen Concentration is directly related to Hb concentration and saturation (SaO2) FA2019, p. 653. Via the Bohr Effect, decreased PaCO2 will increase SaO2, thus increasing blood oxygen concentration.
B) Arterial Blood PO2: PaO2 changes in response to decreased PAO2, PIO2, or diffusion. There would be no change in PaO2 during hyperventilation (theoretically).
C) Aterial Pressure: Decreased PaCO2 is associated with vasoconstriction, which would increase blood pressure.
E) Cerebral Tissue pH would increase due to respiratory alkalosis.
I've never been good at converting units :( lol so had to ask my brother. He told me that distance x distance = distance^2 = area, and distance x distance x distance = distance^2 x distance = distance^3 = volume. Gotta love public school for never been taught that... geesh (obviously I've done the equations and stuff, just never been told it that way/that simple before). Knowing that makes figuring out the equation much easier.
Flow rate = velocity x CSA = 20 cm/sec * 2cm^2 = 40cm^3/sec. To convert to L/min, just multiply: 40cm^3/sec X 60 sec/min X 1L/100cm^3 = 240 L/100 min = 2.4 L/min
Hope this helped!
is this question asking what we physically pass through or by?
is this question asking what we physically pass through or by?
Per First Aid 2018 (pg 421) & Merck Manual
a) CML is not the answer because in CML you have HIGH WBCs & Platelets. In the stem there is only high platelets. b) Is the answer because in Essential Thrombocythemia we have normal WBCs and RBCs, just high platelets. c) Myeloid metaplasia refers to well a metaplasia in myeloid cells which are basophils, eosinophils, etc. d) In Polycythemia Vera we have HIGH RBCs, WBCs, and Platelets. e) Reactive thrombocytosis- is a elevated platelet count that occurs secondary to another disorder like:
-Chronic inflammatory disorders (eg, rheumatoid arthritis, inflammatory bowel disease, tuberculosis, sarcoidosis, granulomatosis with polyangiitis) -Acute infection
-Hemorrhage
-Iron deficiency
-Hemolysis
-Cancer
-Splenectomy or hyposplenism
Beta-2 receptors are coupled to Gs proteins, which activate adenylyl cyclase and increase cAMP. Cyclic AMP then increases activity of protein kinase A, which phosphorylates myosin light chain kinase, ultimately resulting in smooth muscle relaxation. Albuterol, a B2 agonist, is therefore useful in treating bronchospasm.
Can someone explain properly how we know that this trait follows Mendelian genetics and is autosomal recessive and furthermore how the parents were heterozygous?
I guessed a lot on this question and got lucky :(
Process of elimination on this one.
out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)
My poverty education didn't ingrain this in me.
So...case-control studies compare a group of people with the disease and a group of people without the disease. I'm not sure I understand why you can call people randomly and call that a control group. What if among those called randomly, some of them have also had hemorrhagic strokes?
so its reassurance bc some boys can have mild breast development at 13? I've never heard or seen this before can someone please clarify. Basically reassuring that this is (relatively) normal?