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 +1  (nbme22#37)

Why would deposition of fibrinoid deposits (i.e. fibrinoid necrosis/malignant HTN) be wrong?

amorah  Kidney is smaller than normal, suggesting less blood flow to it. Won't see shrunken kidney in the case of HTN.

 +0  (nbme22#37)

wouldn’t chronic hypertension of the L-renal artery induce RAAS activation, and hence tubular hypertrophy with cortical atrophy?

fcambridge  I had a similar thought regarding mesangial hypercellularity. I missed a UW question on a similar topic. Unilateral renal artery stenosis results in hyperplasia of modified smooth muscle cells (JG cells) due to reduced RBF. The hyperplasia is intended to correct the supposed deficiency via increased production of renin.

 +5  (nbme24#10)

Image shows Crescent Sign, a common finding in Abdominal Aortic Aneurysms due to mural thrombus occlusion.

happysingh  crescent sign is a finding on radiographs that is associated with avascular necrosis, NOT aneurysms !!! what you're seeing is Calcification of wall of the aortic aneurysm

 +3  (nbme24#31)

Answered my own question. Increased stress from a STEMI will activate the sympathetic nervous system -- Pulmonary vasodilation.


 +0  (nbme24#31)

Can somebody who understand why PVR decreases with a Left-Sided infarct please enlighten me. I would also appreciate it if you could relate it to right sided heart failure too (i.e. how would it change).

sajaqua1  I believe that keycompany's answer comes the closest. In an MI, consider it as cardiogenic shock. The heart is a pump, and it is failing to move blood out of the heart and into vasculature. This is why PCWP increases. Because of insufficient output, the body has a sympathetic response. The catecholamines then cause vasoconstriction in peripheral vasculature to keep blood pressure up and continue flow, leading to increased SVR. Meanwhile, the sympathetic response causes vasodilation in the lungs; this would be an appropriate autoregulatory response, because the body is trying to keep up the flow of oxygen throughout the system. This decreases PVR. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5715548/ Is a pretty good article on this. Of course the binding of catetcholamines changes depending on saturation and the response is not perfectly understood.
usmleuser007  My understanding is that the pulmonary circulation changes very little in terms of an acute MI. It is b/c pulmonary circulation has a lot more room to fill with blood much like the spleen in terms of blood accumulation. With higher volume of blood in pulmonary circulation, more blood vessels are able to be recruited specially the apex. With more recruited blood vessels = reduced pressure d/t circulation in parallel.

 +5  (nbme24#16)

This patient has a pneumothorax. Hyperventillation is not enough to compensate for the overall decrease in lung surface area.

_yeetmasterflex  Could the pneumothorax also cause less ventilation due to decreased lung surface, retaining more CO2 causing respiratory acidosis? That's how I got to the answer at least.
duat98  I think pneumothorax would increase RR because you're probably hypoxic. Also I'm sure when you have a lung collapse on you you'd be scared and that would trigger your sympathetic so your RR will go up either way.
kateinwonderland  Arterial blood gas studies may show respiratory alkalosis caused by a decrease in CO2 as a result of tachypnea but later hypoxemia, hypercapnia, and acidosis. The patient's SaO2 levels may decrease at first, but typically return to normal within 24 hours. (https://journals.lww.com/nursing/Fulltext/2002/11000/Understanding_pneumothorax.52.aspx)
linwanrun1357  How about choice C, --ARDS?
bullshitusmle  there is no bilateral lung opacities as you would see in ARDS

 +3  (nbme23#19)

This question is disguised. What they are really asking is "what is the sole determinant of species survival"? The only answer is the ability to procreate. Because DNA Polymerase has proof-reading activity, progeny will be unaffected by RNA Polymerases lack of proof-reading activity.

ls3076  the phrasing of this explanation doesnt make sense to me.
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA?
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication!

 +4  (nbme23#18)

Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.


 +0  (nbme23#39)

Figure it out after reading a review. UVA/UVB under normal circumstances is considered nonionizing. However, the only difference between nonionizing and ionizing radiation is the strength of the radiation rays. Because radiation does not dissipate from the body, prolonged UVB exposure can cause radiation to build up in the skin and cause an ionization effect. This is the same reason that repetitive X-Rays and CT Scans can increase your risk for cancer, even years down the line.


 +1  (nbme23#39)

Can somebody please explain how nonionizing radiation has an ionizing effect.

uslme123  "technically non-ionizing, can produce photochemical reactions that are damaging to molecules by means other than simple heat. Since these reactions are often very similar to those caused by ionizing radiation, often the entire UV spectrum is considered to be equivalent to ionization radiation in its interaction with many systems (including biological systems)." -- https://en.wikipedia.org/wiki/Non-ionizing_radiation#Near_ultraviolet_radiation I'm guessing NBME reads wiki lmao?

 +15  (nbme22#5)

Nitrogen balance is a measurement of protein metabolism in the body. A negative nitrogen balance indicates muscle loss, as increased amounts of amino acids are being metabolized to produce energy. This increases the amount of nitrogen secreted from the body. Because the amount of nitrogen you are taking in is less than the amount of nitrogen you are secreting, you have a negative nitrogen balance.

This man is malnourished, edematous, cachetic, and has hypoalbuminemia. These clinical findings point to protein malnutrition (Kawashkior Disease), which causes edema due to decreased serum oncotic pressure. Low oncotic pressure in this case is due to protein loss, and hence a negative nitrogen balance.

drdoom  Nice!
dubywow  I knew your last sentence and suspected Kwashiorkor. It's just everything else I did not know. I have not heard or thought of muscle/protein changes in terms of "nitrogen balance" before... and that's why I got this wrong. Nice explanation!

 +2  (nbme22#28)

While this question stem is vague, the most likely diagnosis is Hereditary Hemochromatosis.


 +2  (nbme22#16)

O, Rh-negative blood is the universal donor for blood plasma.

keycompany  Edit:: Blood RBCs***

 +1  (nbme22#7)

Loading Dose is the only answer that is independent of drug clearance.

nwinkelmann  I totally get this and understand it... but at the same time, couldn't loading dose differ due to renal function if patient has nephrotic syndrome so had less plasma proteins, because it would change the Vd of the drug, right? Per wiki: Volume of distribution may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid and plasma protein binding). Conversely it may be decreased in dehydration.

 +2  (nbme22#34)

Mandelian Genetics:

Man has 2/3 chance of being a carrier. (He does not have the disease). Woman carrier risk must be calculated with p^2 + 2pq + q^2. q^2 = 1/40,000 q = 1/200, p is roughly = 1 2pq = 1/100 = Carrier frequency .

Risk of having a child thus equals 2/3 x 1/100 x 1/4 = 1/600 Because: 2/3 = Man Carrier risk 1/100 = Female Carrier Risk 1/4 = Chance they each pass on the recessive gene to their offspring.

hello  See my explanation if you need more words to explain this explanation

 +10  (nbme22#41)

Answer: Increased Central Blood Volume (CBV), Decreased ADH, Increased ANP.

The physiological response to hypothermia is vasoconstriction of peripheral vessels (i.e. the ones in your extremities) in an effort to keep your core body temperature normal, and thus your organs functioning properly. Peripheral Vasoconstriction will increase CBV. Increased CBV will cause an increase in preload, and thus cause an increase in ANP/BNP. ANP/BNP has inhibitory effects on the Renin-Angiotensin-Aldosterone System, resulting in decreased ADH.


 +3  (nbme22#35)

Urinary tract infections are the most common acquired cause of Vesicouteric Reflux (VR) in children. VR can lead to Reflux Nephropathy, which is characterized by chronic tubulointerstitial inflammation with fibrosis and scarring, leading to renal failure.

lancestephenson  Can someone please explain what's going on in this picture? This is the SAME PICTURE used in NBME 20 and 21 with one of them being a 66 y/o with urothelial cell carcinoma and the other being tubular atrophy. I just don't know anymore
spacepogie  I'd be happy to send them a gift card to purchase more stock images of kidneys for use in future exams...

 +5  (nbme22#35)

Alteration of the thermostatic set point is a hypothalamic process mediated by prostaglandins and is independent of the sympathetic nervous system.

B, C, D, and E all require sympathetic nerves to ellicit a response.


 +12  (nbme22#9)

Flow Rate = Velocity x Cross-Sectional Area

2 cm^2 x 20 cm/sec x 60 sec/min x 1 L/1,000 cm^3 = 2.4 L/min

1,000 cm^3 = 1 L

seagull  Well, I missed this one. I don't even feel bad.
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L
hello  @keycompany how did you edit your original comment to fix your typo?

 +6  (nbme22#33)

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.

keycompany  EDIT: Via the **Haldane Effect**, not the Bohr Effect.
impostersyndromel1000  excellent response

 +6  (nbme22#10)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse."




Subcomments ...

I think I found what the disease was, though I honestly have no idea why they would test this rather than XLA. There’s a condition called Transient Hypogammaglobulinemia of Infancy. It presents w/low immunoglobulin levels post 6 months and can present w/small lymph nodes and tonsils in infancy BUT w/o any other findings of primary immunodeficiency including decreased counts.

Here’s an article about it: https://primaryimmune.org/about-primary-immunodeficiencies/specific-disease-types/transient-hypogammaglobulinemia-of-infancy/

You definitely don’t need to know the disease to get the correct answer since the link of lack of immunoglobulins would clue you into the lack of germinal centers, but I think this is more likely than XLA since every source I read implies that B cell counts are near 0 in the classic presentation (unless I’m missing a reason why leukocyte count w/diff wouldn’t show a significant decrease in lymphocytes due to near-zero B cells). Just wanted to put this here in case other people later came wondering, though I may still be wrong.

keycompany  I think we are all overthinking this question (and it is remarkably simple). I don't think this question is testing us on any of the UFAP immunodeficiency syndromes, per say. What they are really asking is "what would also be absent if there are no immunoglobulins and everything else is normal"? The answer is absent germinal centers b/c that's where Ig is synthesized. I think they put all other aspects of the history in this stem just to help you rule out any of the other answers. +1  


Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +8  
seagull  CML has blasts too but they tend to favor mature forms. +3  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +2  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +6  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  


The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +4  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +3  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  


Our little friend has a Parvovirus infection, which infects erythroid precursors, causing interruption of erythrocyte production. This is the same way it causes hydrops fetalis in unborn babies and aplastic anemia in sickle cell, etc.

gainsgutsglory  I get Parvo has tropism for RBC precursors, but wouldn’t it take 120 days to manifest? +  
keycompany  RBCs don’t just spill out of the bone marrow every 4 months on the dot. Erythropoesis is a constant process. If you get a parvo virus on “Day 1” then the RBCs that were synthesized 120 days before “Day 1” will need to be replaced. They can’t be because of parvovirus. This leads to symptomatic anemia within 5 days because the RBCs that were synthesized 125-120 days before the infection are not being replaced. +2  
drdoom  @gainsgutsglory @keycompany It seems unlikely that “1 week” of illness can explain such a large drop in Hb. It seems more likely that parvo begins to destroy erythroid precursors LONG BEFORE it manifests clinically as “red cheeks, rash, fever,” etc. Might be overkill to do the math, but back-of-the-envelope: 7 days of 120 day lifespan -> represents ~6 percent of RBC mass. Seems unlikely that failure to replenish 6 percent of total RBC mass would result in the Hb drop observed. +  
yotsubato  He can drop from 11 to 10 hgb easily +1  
ls3076  Apologies if this is completely left-field, but I didn't think this was Parvovirus. Parvo would affect face. Notably, patient has fever and THEN rash, which is more indicative of Roseola. Thoughts?? +2  
hyperfukus  @is2076 check my comment to @hello I thought the same thing for a sec too :) +  
hyperfukus  also i think you guys are thinking of hb in adults in this q it says hb is 10g/dL(N=11-15) so it's not relatively insanely low +  
angelaq11  @Is3076 I completely agree with @hyperfukus and I think that thinking of Roseola isn't crazy, but remember that usually with Roseola you get from 3-5 days of high fever, THEN fever is completely gone accompanied by a rash. This question says that the patient has a history of 4 days of rash and 7 days of fever, but never mentioned that the fever subsided before the appearance of the rash. And Roseola is not supposed to present with anemia. +  


submitted by lilamk(5),

I am so confused! The only logic I could come up w is that NSAIDs decrease dilation of afferent arteriole so this more constricted arteriole is interpreted as decreased blood flow and Renin increases? My issue w this is that when I google it and search UW for this renin affect nothing comes up only article I could find actually contradicts it and says renin would DECREASE from NSAIDs leading to the hyperkalemia we sometimes see ...

Any thoughts would be helpful! Thanks geniuses.

generic_login  I used that reasoning to pick C, but in looking it up now it seems like you are right ... There appear to be a bunch of mistakes on this test, and it’s not giving me a lot of confidence for the real thing. +  
mee48  I think it is because NSAIDs inhibit the local prostaglandin (PGE2) in afferent arteriole —-> less AA dilation —-> stimulation renin release. I think my reasoning came from sketchy pharm nsaid video but I can’t 100% remember +  
keycompany  NSAIDs constrict the afferent arteriole. ​ A. GFR would decrease due to decreased renal blood flow. B. Renal Blood flow would decrease. C. Renin would increase due to renal hypoperfusion. D & E. PGE2 and TXA would decrease (by MOA of NSAIDs). +1  
fallot4logy  UW says that Nsaids is one o +  
fallot4logy  UW says that Nsaids is one of the 5 drug categories that is able to cause hyperkalemia.Specificly ,Nsaids lower PG andrenin secretion .PGE2 stimulates JG cells to secrete renin...(how can i delete my previous unfinished message,lol?) +  


submitted by colonelred_(45),

Normally the arachnoid villi drains the CSF from the subarachnoid space to the venous system; if this part becomes defective then you can imagine all that CSF now building up in the subarachnoid space.

keycompany  Also take into account this patient had surgery that requires penetration into the subarachnoid space (hence through the arachnoid mater). This can lead to scarring of the arachnoid granulations and subsequent communicating hydrocephalus. +5  


submitted by calcium196(7),

NBME 20 has a question with a guy taking over the counter cough medication and now he has constipation. Want to guess the answer? It was dextro! -> https://nbmeanswers.com/exam/nbme20/458

So I’m pretty sure the NBME 22 question is just straight up wrong.

rockediny  No, not so. Dextro *is* the correct answer here. From the choices given, dextro is the least likely to cause constipation since its main mechanism of action is NMDA antagonism w/ *some* opioid activity -- it can cause constipation but the other choices are MUCH MORE likely to. As for diphenhydramine = it is not appropriate for elderly patients and it isn’t an antitussive. +  
surely_not_a_robot_  Agreed with @rockediny. Dextro would be the best to prescribe because it has the least amount of constipation out of the drugs that you could prescribe + Anti-cholinergics in the elderly have much more morbidity and risk of mortality. +  
keycompany  The only way to wrap your head around this is to conclude that Dextro is the "least wrong". I thought a lot about this, and I can't think of any drugs that can suppress cough without also causing constipation, so it makes sense that Dextro is the answer because it is the "least likely" to cause significant constipation. This is probably just a clinical correlate that will be learned during rotations/years in practice. +  


submitted by armymed88(15),

Shouldn't the treatment for hyperTG be a fibrates? Which would indicate the answer to be increasing HDL (FA.2017 p306)

I see decreasing VLDL as a function of niacin, which serves to decrease hepatic VLDL..

keycompany  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! +2  
mr_haib  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. +  
lordxrequiem  but fibrates also decrease bile acid production by inhibiting 7alpha hydroxylase, which is how they cause increased cholesterol gallstones. +  


Question is asking about encapsulated organisms infecting CGD patients. E.coli is also encapsulated. Can anyone expand on this?

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo. +  
keycompany  Sorry english is clearly not my shit, but you get the point +  
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head. +5  
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori +3  


Question is asking about encapsulated organisms infecting CGD patients. E.coli is also encapsulated. Can anyone expand on this?

keycompany  Step pneumonia is the most common pathogenic organism in CGD, and the most common cause of pneumonia, otitis media, meningits, and sepsis. While CGD are at an increased risk of encapsulated E. coli infections, however, they are at MOST risk for S. pneumo. This is kind of just a memorization fact that you need to know about S. pneumo. +  
keycompany  Sorry english is clearly not my shit, but you get the point +  
biliarytree220  CGD is susceptible against catalase-positive organisms (FA 109), of which S. aureus is the one to look out for. It's not about encapsulated organisms, like I had it confused in my head. +5  
.ooo.   You are completely right about E.Coli being encapsulated and is also a CAT+ organism and patients with CGD would have an increased risk of infection for both S. Aureus and E. Coli. How you narrow down the two is the most common infections are S. Aureus and Aspergillus (FA 109 like mentioned above) and also using the pneumonic "Cats Need PLACESS to Belch their Hairballs" (FA 128) Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E.Coli, Staphylococci, Serratia, B cepacia, H pylori +3  


submitted by keycompany(115),

O, Rh-negative blood is the universal donor for blood plasma.

keycompany  Edit:: Blood RBCs*** +  


Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +8  
seagull  CML has blasts too but they tend to favor mature forms. +3  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +2  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +6  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  


submitted by keycompany(115),

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.

keycompany  EDIT: Via the **Haldane Effect**, not the Bohr Effect. +  
impostersyndromel1000  excellent response +